DR AZAM'S Notes in Anesthesiology CARDIOVASCULAR - SYSTEM PDF

2011
Dr Azam's Notes in Anesthesiology

– Second Edition
Cardiovascular System
Dr. Mohammed Azam Danish
Consultant Anesthesiologist & Critical Care Specialist
www.DrAzam.com
Dr Azam's Notes In Anesthesiology 2011
-Second Edition
Dr Azam’s Notes in Anesthesiology

2nd Edition
CARDIOVASCULAR SYSTEM
By
Dr. Azam
Consultant Anesthesiologist & Critical Care
www.DrAzam.com Cardiovascular System

-Second Edition
PREFACE
This book grew from notes first written in 2003 - 2004 for the students at the J J M
Medical College in Davangere.
There are many textbooks to choose from when preparing for the “Anesthesiology
examination”. The candidate suffers not from the lack of information but rather from
being inundated with it. The candidate then has the task of information sorting and data
compression to memorize and utilize all this information.
Graphic representation of data is an excellent form of data compression; figures or

drawings are frequently asked about at the viva examination, particularly since the
candidate’s understanding of a problem comes across most clearly when drawing a
figure or a using a picture. Figures are also a good way of approaching a topic.
I constructed parts of Dr Azam’s Notes in Anesthesiology for Postgraduate students

when preparing for the Anesthesiology examination and later when preparing for
tutorials.
Dr Azam’s Notes is aimed primarily at trainees in Anesthesia though more experienced

practitioners may find it useful as a refresher in recent concepts and advances
Dr Azam’s Notes is not a substitute for the major anesthesiology text books but
concentrates on principles of management of the most challenging anesthetic cases.
The format is designed to provide easy access to information presented in a concise

manner. I have tried to eliminate all superfluous material. Selected important or
controversial references are presented as well as suggestions for further reading. Some
relate more to basic principles, physiology, pharmacology, etc. – bookwork. Others are
more practical in nature, discussing the principles of anesthetic techniques for certain
high-risk situations.
Dr Azam’s Notes have been created keeping the Postgraduate needs while preparing
for the exams, and also help in his day to day practice. I am sure that Dr Azam’s Notes
will not only help him to secure highest marks but also help him to gain knowledge to
its full.

-Second Edition
A NOTE TO THE READER
Anesthesiology is an ever-changing field. Standard safety precautions must be followed,

but as new research and clinical experience broaden our knowledge, changes in
treatment and drug therapy may become necessary or appropriate. Readers are advised
to check the most current product information provided by the manufacturer of each
drug to be administered to verify the recommended dose, the method and duration of
administration, and contraindications.
However, in view of the possibility of human error or changes in medical sciences,

neither the author nor the publisher nor any other party who has been involved in the
preparation or publication of this work warrants that the information contained herein
is in every respect accurate or complete, and they disclaim all responsibility for any
errors or omissions or for the results obtained from use of the information contained in
this work. Readers are encouraged to confirm the information contained herein with
other sources. It is the responsibility of the licensed prescriber, relying on experience
and knowledge of the patient, to determine dosages and the best treatment for each
individual patient. Neither the publisher nor the editor assumes any liability for any injury
and/or damage to persons or property arising from this publication.

-Second Edition
DEDICATION
To Mohammed Shafiulla, my father, my oxygen,

companion, and best friend; for being my major pillar of
support and making this vision a reality. Thank you for your
continual sacrifices with boundless love and limitless
gratitude, for the sake of your children. I owe you a debt I can
never repay.
I also would like to thank my mom (Naaz Shafi), my wife

(Roohi Azam), my two lovely kids (Falaq Zohaa &
Mohammed Izaan), for their support, ideas, patience, and
encouragement during the many hours of writing this book.
I also thank my Colleagues Dr Rajshekar Reddy & Dr

Sachin for their support.
Finally, I would like to thank my teachers. The dream begins

with a teacher who believes in you, who tugs and pushes and
leads you to the next plateau, sometimes poking you with a
sharp stick called "truth."

-Second Edition
Contributions
01. Dr. Rajshekar Reddy – UAE

02. Dr. Surendra – UAE
03. Dr. Nagaraj Chandy – Hubli
04. Dr.Kusuma – Bangalore
05. Dr Sachin Doijode – London
06. Dr Chandrashekar – Bangalore
07. Dr Sidhu – Bangalore
08. Dr Ravindra B K – Bangalore
09. Dr Harshavardhan – Mangalore
10. Dr Anil Kumar – Tamil Nadu
11. Dr Mashooda – Kerla
12. Dr Anusuya – Bangalore
13. Dr Sudhir – Bangalore
14. Dr Uma – Davangere
15. Dr Rajeev – UAE
16. Dr Surendra – UAE
17. Dr Shivananda – Shimoga
18. Dr Soujanya – Bangalore
19. Dr Aslam Faris – Kerla
20. Dr Nandakumar – Tamil Nadu
21. Dr Anuradha – Bangalore
22. Dr Arun G Pai – Kerla
23. Dr Geetha – Bangalore

-Second Edition
Table of Contents
PREFACE .......................................................................................................................................................... 3
DEDICATION .................................................................................................................................................... 5
CHAPTER 1 CARDIOVASCULAR SYSTEM PHYSIOLOGY .................................................................................... 25
CELLULAR CARDIAC PHYSIOLOGY:............................................................................................................................. 25

The Excitation System: ................................................................................................................................ 25
Initiation and Conduction of the Cardiac Impulse ....................................................................................... 27
ANESTHETIC IMPLICATIONS ..................................................................................................................................... 28
Excitation Contraction Coupling (ECC): ....................................................................................................... 28
RELAXATION / DIASTOLE: ....................................................................................................................................... 29
ANESTHETIC IMPLICATIONS: .................................................................................................................................... 30
The Cardiac Cycle: ....................................................................................................................................... 30
Length of Systole and Diastole: ................................................................................................................... 33
Clinical Importance: .................................................................................................................................... 33
Duration of diastole is important, as it is during diastole that: .................................................................. 33
Determinants of Ventricular Systolic Function: ........................................................................................... 33
Factors determining cardiac output: ........................................................................................................... 34
Cellular Basis: .............................................................................................................................................. 35
Factors affecting ventricular preload: ......................................................................................................... 36
Measurement of Preload / LVEDV ............................................................................................................... 36
After load: ................................................................................................................................................... 36
Measurement of After load: ........................................................................................................................ 39
Myocardial Contractility (Inotropism) ......................................................................................................... 39
Factors affecting Contractility: .................................................................................................................... 40
Measurement of Intrinsic Contractile Activity: ............................................................................................ 40
Ejection Fraction (EF): ................................................................................................................................. 42
Wall Motion Abnormalities ......................................................................................................................... 42
Assessment:................................................................................................................................................. 42
Neural Regulation of Cardiac Function: ...................................................................................................... 43
Hormones affecting cardiac function .......................................................................................................... 43
Coronary Circulation.................................................................................................................................... 44
Venous Drainage ......................................................................................................................................... 45
CORONARY BLOOD FLOW DURING CARDIAC CYCLE ................................................................................... 46
Coronary Blood Flow (CBF) .......................................................................................................................... 46
Auto-Regulation of CBF ............................................................................................................................... 47
Factors affecting the CBF: ........................................................................................................................... 47
Effects of Anesthetic Agents:....................................................................................................................... 48
Baro-receptor Reflex (Carotid Sinus Reflex) ................................................................................................ 49
Bainbridge Reflex ........................................................................................................................................ 50

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Marey’s Law: ............................................................................................................................................... 50
Chemoreceptor Reflex: ................................................................................................................................ 50
Bezold Jarisch Reflex: .................................................................................................................................. 51
Valsalval Maneuver: .................................................................................................................................... 51
Cushing’s Reflex: ......................................................................................................................................... 51
Positive pressure ventilation ....................................................................................................................... 53
CHAPTER 2 ADULT, PEDIATRIC AND NEWBORN RESUSCITATION ................................................................... 55
OVERVIEWS CARDIOPULMONARY RESUSCITATION (CPR): ............................................................................................. 55

CARDIAC ARREST ................................................................................................................................................... 55
Etiologies: .................................................................................................................................................... 55
Pathophysiology .......................................................................................................................................... 56
ADULT RESUSCITATION ........................................................................................................................................... 56
Basic life support: ........................................................................................................................................ 56
Airway and breathing:................................................................................................................................. 56
Circulation: .................................................................................................................................................. 57
Defibrillation: .............................................................................................................................................. 57
Defibrillation VT and VF (see Fig. 37.1): ...................................................................................................... 64
Pacing:......................................................................................................................................................... 65
Intravenous access: ..................................................................................................................................... 65
Drugs. .......................................................................................................................................................... 65
-Adrenergic blocking drugs: ........................................................................................................................ 67
Open-chest direct cardiac compression: ..................................................................................................... 70
Termination of CPR: .................................................................................................................................... 70
PEDIATRIC RESUSCITATION ...................................................................................................................................... 71
Table 37.2 Adult and pediatric cardiopulmonary resuscitation .................................................................. 72
Pediatric advanced life support: .................................................................................................................. 72
Neonatal resuscitation: ............................................................................................................................... 73
Four phases of newborn resuscitation: ....................................................................................................... 81
CHAPTER 3 “ANESTHETIC MANAGEMENT OF HYPERTENSIVE PATIENTS” ....................................................... 87
HISTORY: ..................................................................................................................................................... 87
INTRODUCTION ................................................................................................................................................ 87
PREVALENCE................................................................................................................................................ 87
DEFINITION ...................................................................................................................................................... 87
WHITE COAT HYPERTENSION ...................................................................................................................... 87
REVERSE WHITE COAT HYPERTENSION ....................................................................................................... 87
LABILE HYPERTENSION ................................................................................................................................ 87
PSEUDO HYPERTENSION ............................................................................................................................. 88
HYPERTENSIVE EMERGENCY ....................................................................................................................... 88
HYPERTENSIVE URGERNCIES ....................................................................................................................... 88
HYPERTENSIVE CRISIS .................................................................................................................................. 88
Classification of blood pressure for adults > 18 years (JNC – Classification) ............................................... 88
CLASSIFICATION........................................................................................................................................... 88
ETIOLOGY OF HYPERTENSION .......................................................................................................................... 89
MECHANISM OF HYPERTENSION ..................................................................................................................... 90
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INTRA VASCULAR VOLUME ......................................................................................................................... 90
GENETIC CONSIDERATION ........................................................................................................................... 90
AUTONOMIC NERVOUS SYSTEM ................................................................................................................. 91
AUTONOMIC NERVOUS SYSTEM ................................................................................................................. 92
VASCULAR MECHANISM .................................................................................................................................. 95
PATHOLOGICAL CONSEQUENSE OF HYPERTENSION ........................................................................................ 95
ANTIHYPERTENSIVE DRUG ............................................................................................................................... 97
ANESTHETIC CONSIDERATION: ................................................................................................................................. 98
BETA BLOCKERS FOR HYPERTENSION............................................................................................................... 98
ANESTHETIC CONSIDERATIONS: ................................................................................................................................ 99
MECHANISM OF ACTION OF BETA BLOCKERS ................................................................................................ 100
RENIN – ANGIOTENSIN – ALDOSTERONE MECHANISM .................................................................................. 101
ANGIOTENSIN RECEPTOR ANTAGONIST .................................................................................................... 102
ALPHA ADRENERGIC BLOCKERS ..................................................................................................................... 102
DIRECT VASODILATORS ............................................................................................................................. 103
CENTRAL ADRENERGIC INHIBITORS .......................................................................................................... 103
Recent Advances: ...................................................................................................................................... 103
GUIDELINES FOR SELECTING INITIAL DRUG TREATMENT FOR HYPERTENSION ........................................ 105
MECHANISM OF ACTION OF CALCIUM CHANNEL BLOCKERS .................................................................... 106
RECOMMENDED COMBINATIONS IN VARIOUS EMERGENCIES ................................................................. 107
PRE-ANESTHETIC EVALUATION: ................................................................................................................ 107
PRE OPERATIVE MANAGEMENT................................................................................................................ 108
MONITORING ................................................................................................................................................. 110
PREMEDICATION ............................................................................................................................................ 110
INDUCTION OF ANESTHESIA .......................................................................................................................... 111
MEASURES TO BLUNT THIS RESPONSE INCLUDE ............................................................................................ 111
INDUCTION AGENT.................................................................................................................................... 111
MAINTENANCE .......................................................................................................................................... 112
MUSCLE RELAXANT ................................................................................................................................... 112
INTRA OPERATIVE MANAGEMENT ............................................................................................................ 112
INTRAOPERATIVE HYPERTENSION............................................................................................................. 112
POST OPERATIVE MANAGEMENT ............................................................................................................. 113
CONCLUSION.................................................................................................................................................. 114
CHAPTER 4 ANESTHESIA FOR PATIENT WITH MS AND MR ........................................................................... 117
INTRODUCTION .............................................................................................................................................. 117

MITRAL STENOSIS ............................................................................................................................................... 117
Anatomy .................................................................................................................................................... 117
ETIOLOGY AND PATHOLOGY: ................................................................................................................................. 118
Other causes.............................................................................................................................................. 118
Simulating Conditions ............................................................................................................................... 118
PATHOPHYSIOLOGY ............................................................................................................................................. 119
MITRAL VALVE STENOSIS: ..................................................................................................................................... 122
Pressure Gradient across stenotic Mitral valve: ........................................................................................ 122
Hemodynamic alterations in rest and exercise ......................................................................................... 122

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History ....................................................................................................................................................... 123
(DISEASE PROGRESSION) ........................................................................................................................... 123
CLINICAL ASSESSMENT: ........................................................................................................................................ 125
NEW YORK HEART ASSOCIATION .............................................................................................................. 126
Laboratory finding ..................................................................................................................................... 130
Atrial fibrillation ........................................................................................................................................ 130
Chest Cardiograph ..................................................................................................................................... 130
TREATMENT ....................................................................................................................................................... 131
Medical treatment .................................................................................................................................... 131
Guideline recommends lifelong prophylaxis. ............................................................................................ 131
Surgical Correction .................................................................................................................................... 131
MITRAL STENOSIS – HEMODYNAMIC GOALS: ............................................................................................................ 136
Pulmonary artery catheters ...................................................................................................................... 136
Atrial fibrillation ........................................................................................................................................ 139
Treatment ................................................................................................................................................. 142
MITRAL REGURGITATION ...................................................................................................................................... 149
Causes ....................................................................................................................................................... 149
PATHOPHYSIOLOGY ............................................................................................................................................. 150
Acute phase ............................................................................................................................................... 150
Chronic compensated phase ..................................................................................................................... 150
Chronic de-compensated phase ................................................................................................................ 151
Comparison of acute and chronic mitral regurgitation ............................................................................. 152
Procedures................................................................................................................................................. 154
Cardiac catheterization ............................................................................................................................. 154
Complications ............................................................................................................................................ 154
Indications for surgery for chronic mitral regurgitation............................................................................ 155
Quantification of mitral regurgitation ...................................................................................................... 155
Determination of the degree of mitral regurgitation ................................................................................ 156
Treatment ................................................................................................................................................. 156
Main anesthetic Goals: ............................................................................................................................. 156
Anesthetic management ........................................................................................................................... 157
Goals ......................................................................................................................................................... 157
CHAPTER 5 ANESTHESIA FOR PATIENTS WITH AS AND AR (NON CARDIAC SURGERIES) ............................... 159
AORTIC STENOSIS ........................................................................................................................................... 159

ANATOMY ................................................................................................................................................. 159
CLASSIFICATION......................................................................................................................................... 160
AETIOLOGY ..................................................................................................................................................... 160
CLINICAL FEATURES........................................................................................................................................ 160
PATHOPHYSIOLOGY................................................................................................................................... 161
PRESSURE VOLUME RELATIONSHIP .......................................................................................................... 164
Normal In Aortic Stenosis .............................................................................................................. 164
ANESTHETIC MANAGEMENT ..................................................................................................................... 165
Mod to severe AS ...................................................................................................................................... 170
Aortic Regurgitation .................................................................................................................................. 172
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Common Features ..................................................................................................................................... 172
Pathophysiology: ....................................................................................................................................... 173
Acute AR .................................................................................................................................................... 174
Acute AR: ................................................................................................................................................... 174
Post –Operative Management: ................................................................................................................. 177
SUMMARY AND CONCLUSION: ................................................................................................................. 178
CHAPTER 6 PROPHYLACTIC REGIMENTS FOR VARIOUS PROCEDURES. FOR DENTAL, CARDIAC, RESPIRATORY
TRACT, OR ESOPHAGEAL PROCEDURES........................................................................................................ 179
CHAPTER 7 MANAGEMENT OF PERIOPERATIVE ARRYTHMIAS ..................................................................... 182
MANAGEMENT OF PERIOPERATIVE ARRYTHMIAS ......................................................................................... 182

NORMAL CARDIAC ELECTROPHYSIOLOGY: ................................................................................................ 182
ANATOMY OF THE CONDUCTION SYSTEM: ............................................................................................... 182
PHYSIOLOGY OF CONDUCTION SYSTEM .................................................................................................... 183
The electrical events: ................................................................................................................................. 183
MECHANISM OF CARDIAC DYSRHYTHMIAS ................................................................................................... 184
Cardiac dysrrhythmias can be explained mainly on the basis of: .............................................................. 184
HAEMODYNAMIC EFFECTS OF DYSRHYTHMIIAS ............................................................................................ 186
Lead systems: ............................................................................................................................................ 186
Diagnosis and management of dysrrhythmias: ........................................................................................ 188
SINUS BRADYCARDIA: .......................................................................................................................................... 188
SINUS TACHYCARDIA. ........................................................................................................................................... 189
Causes: ...................................................................................................................................................... 189
Significance: .............................................................................................................................................. 189
Treatment: ................................................................................................................................................ 190
ATRIAL PREMATURE BEATS: .................................................................................................................................. 190
Significance: .............................................................................................................................................. 190
Treatment: ................................................................................................................................................ 190
PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA (PSVT) ........................................................................................... 190
CLASSIFICATION OF SVT: ...................................................................................................................................... 190
Significance: .............................................................................................................................................. 191
Management:............................................................................................................................................ 191
ATRIAL FLUTTER ............................................................................................................................................. 192
Significance: .............................................................................................................................................. 192
Treatment ;................................................................................................................................................ 192
Alternative drugs include; ......................................................................................................................... 192
Multifocal (Multiform) atrial tachycardia: ................................................................................................ 193
Treatment: ................................................................................................................................................ 193
Atrial fibrillation: ....................................................................................................................................... 193
The characteristics are as follows; ............................................................................................................ 193
Significance: .............................................................................................................................................. 193
Treatment; ................................................................................................................................................ 193
JUNCTION RHYTHM ............................................................................................................................................. 194
High nodal rhythm: ................................................................................................................................... 194
Significance: .............................................................................................................................................. 194
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Treatment ................................................................................................................................................. 194
VENTRICULAR PREMATURE BEATS (VPB) ....................................................................................................... 195
Significance: .............................................................................................................................................. 195
Treatment: ................................................................................................................................................ 195
Treatment for VT with pulse: .................................................................................................................... 195
Stable patient: ........................................................................................................................................... 195
Management of pulseless ventricular tachycardia or ventricular fibrillation ........................................... 196
TORSADES DE POINTS: (TWISTING OF THE POINTS) ....................................................................................... 197
VENTRICULAR FIBRILLATION .......................................................................................................................... 197
The characteristic are: ............................................................................................................................... 198
Significance: .............................................................................................................................................. 198
Treatment: ................................................................................................................................................ 198
VENTRICULAR ASYSTOLE: ............................................................................................................................... 198
Significance: .............................................................................................................................................. 198
Management:............................................................................................................................................ 198
DIAGNOSIS AND MANAGEMENT OF CONDUCTION DEFECTS: ....................................................................... 198
CONDUCTION DEFECTS: ................................................................................................................................. 199
SA NODE BLOCK: ................................................................................................................................................ 199
AV CONDUCTION BLOCK:...................................................................................................................................... 199
FIRST DEGREE AV BLOCK: ..................................................................................................................................... 200
SECOND DEGREE AV BLOCK: ................................................................................................................................. 200
INTRAVENTRICULAR CONDUCTION DEFECTS ................................................................................................. 201
RBBB............................................................................................................................................................... 201
Marriott’s criteria for Left anterior Hemiblock are: .................................................................................. 201
AVF ............................................................................................................................................................ 201
The criteria for a left posterior hemiblock are as follows: ......................................................................... 201
BIFASCICULAR BLOCK:.......................................................................................................................................... 201
Trifascicular block: .................................................................................................................................... 202
CHAPTER 8 - ANESTHESIA FOR PATIENTS WITH IHD (NON CARDIAC SURGERY) ........................................... 204
RISK FACTORS FOR DEVLEOPMENT OF IHD: ................................................................................................... 204

MYOCARDIAL STUNNING: ..................................................................................................................................... 204
CAUSES OF IHD: ................................................................................................................................................. 205
CLINICAL PRESENTATION OF IHD: .................................................................................................................. 205
SYMPTOMS, SIGNS, DIAGNOSIS, TREATMENT FOR SA, UA, NSTEMIS STEMI ................................................. 206
PREOPERATIVE CARDIAC RISK ASSESSMENT: ................................................................................................. 208
ASA status - 1963 revised .......................................................................................................................... 208
GOLDMAN'S CRI - 1977. ..................................................................................................................................... 209
Detsky’s Modified CRI - 1986..................................................................................................................... 209
Lee’s revised CRI- 1999. ............................................................................................................................. 210
Intermediate predictors ............................................................................................................................ 211
NYHA Classification of heart failure .......................................................................................................... 211
Specific activity scale of cardiac function .................................................................................................. 211
Surgery specific approach ......................................................................................................................... 212
Cardiac functional capacity ....................................................................................................................... 212
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Estimated energy requirements for various activities ............................................................................... 213
APPROACH TO PRE-OPERATIVE CARDIAC ASSESSMENT: .......................................................................... 214
Laboratory testing: .................................................................................................................................... 215
PREOPERATIVE TESTING FOR RISK ASSESSMENT: ..................................................................................... 215
Ambulatory ECG monitoring: .................................................................................................................... 216
ECHOCARDIOGRAPHY: .............................................................................................................................. 216
Exercise stress testing: .............................................................................................................................. 216
MYOCARDIAL:............................................................................................................................................ 219
Pre-operative therapy: Surgical /medical percutaneous coronary intervention (PCI) ............................... 219
Pre-operative CABG: .................................................................................................................................. 219
THERAPEUTIC INTERVENTIONS IN ACTUE INFARCTION: ........................................................................... 220
Peri-operative NTG therapy: ..................................................................................................................... 220
Comparative CV effects of the calcium channels blocking drugs: ............................................................. 224
Side effects of anti anginal drugs: ............................................................................................................. 225
ANESTHETIC MANAGEMENT ..................................................................................................................... 226
INTRAOPERATIVE MONITORING ............................................................................................................... 227
HAEMODYNAMIC GOALS DURING ANESTHESIA ARE: ............................................................................... 229
Choice of anesthesia: ................................................................................................................................ 229
Regional Anesthesia/ Local Anesthesia ..................................................................................................... 230
Pre-medication: ......................................................................................................................................... 231
CHAPTER 9 - ANESTHESIA FOR OPEN HEART SURGERY ................................................................................ 241
HISTORY..................................................................................................................................................... 241
INDICATION FOR OPEN HEART SURGERY ................................................................................................................... 241
Ischemic heart disease .............................................................................................................................. 242
Congenital heart disease ........................................................................................................................... 242
Emergency open heart surgery ................................................................................................................. 242
PREOPERATIVE EVALUATION ......................................................................................................................... 242
Clinical Assessment of Cardiac Disease ..................................................................................................... 242
Angina pectoris: ........................................................................................................................................ 242
Prior myocardial infarction ....................................................................................................................... 243
Congestive heart failure: ........................................................................................................................... 243
Cyanosis: ................................................................................................................................................... 243
Dysrrhythmias: .......................................................................................................................................... 243
Non-invasive cardiac diagnostics studies: ................................................................................................. 243
CHAPTER 10 ANESTHESIA PROTOCOL FOR ADULT CARDIAC SURGERY ........................................................ 251
DUTY OF ANESTHESIOLOGIST ................................................................................................................................. 251

The room and set up: ................................................................................................................................ 251
Anesthetic check list for cardiopulmonary bypass: Boyle's machine: ....................................................... 251
ANESTHESIA FOR OPEN HEART SURGERY .................................................................................................................. 253
CHAPTER 11 PROTOCOL FOR OFF-PUMP CABG ............................................................................................ 266
CHAPTER 12 - CARDIAC INTENSIVE CARE ..................................................................................................... 267
REGIONAL ANESTHESIA:........................................................................................................................................ 267
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INTRAPLEURAL ANALGESIA: ................................................................................................................................... 267
POST OP MONITORING: ........................................................................................................................................ 267
POST OPERATIVE MI:........................................................................................................................................... 268
ANTIANGINAL DRUGS:.......................................................................................................................................... 268
Anemia Hypothermia ................................................................................................................................ 268
FAST-TRACKING ......................................................................................................................................... 268
Conclusion: ................................................................................................................................................ 269
CHAPTER 13 - CLINICAL PRACTICE OF CARDIAC ANESTHESIA ....................................................................... 270
ACUTE TREATMENTS FOR SUSPECTED INTRAOPERATIVE MYOCARDIAL ISCHEMIA ............................................................... 271
CHAPTER 14 - PAEDIATRIC INTENSE CARE UNIT ........................................................................................... 273
PEDIATRIC ICU INFUSIONS ............................................................................................................................. 275
CHAPTER 15 - ANESTHESIA FOR PATIENTS WITH CONGENITAL HEART DISEASE ....................................... 277
COMMON CONGENITAL HEART DISEASES AND ANESTHETIC MANAGEMENT OF THESE PATIENTS COMING FOR NON CARDIAC
SURGERIES ......................................................................................................................................................... 277
FETAL AND PERINATAL CIRCULATION: ...................................................................................................................... 277
Fetal circulation:........................................................................................................................................ 277
CHANGES IN CIRCULATION AFTER BIRTH: .................................................................................................................. 278
NORMAL CARDIAC CATHETERIZATION FINDINGS IN A CHILD: ......................................................................................... 279
ETIOLOGY OF CHD: ............................................................................................................................................. 279
EXTRACARDIAC ANOMALIES ASSOCIATED WITH CARDIAC LESIONS: ................................................................................. 280
CLASSIFICATION OF CHD: ..................................................................................................................................... 280
ATRIAL SEPTAL DEFECT (ASD): .............................................................................................................................. 282
PATHOLOGY:...................................................................................................................................................... 282
PATHOPHYSIOLOGY AND HEMODYNAMICS OF ASD: ................................................................................................... 282
Clinical Picture: .......................................................................................................................................... 283
AUSCULTATION: ................................................................................................................................................. 283
Natural history prognosis and complications: ........................................................................................... 284
Diagnosis: .................................................................................................................................................. 284
TREATMENT:...................................................................................................................................................... 285
VENTRICULAR SEPTAL DEFECT (VSD): ..................................................................................................................... 286
PATHOLOGY: TYPES OF VSD: ................................................................................................................................ 286
PATHOPHYSIOLOGY AND HEMODYNAMICS ............................................................................................................... 287
CLINICAL MANIFESTATIONS: .......................................................................................................................... 289
NATURAL HISTORY, PROGNOSIS AND COMPLICATIONS OF VSD: .................................................................................... 289
DIAGNOSIS: ....................................................................................................................................................... 290
MANAGEMENT ................................................................................................................................................... 291
CHAPTER 16 - PATIENT DUCTUS ARTERIOSUS (PDA): ................................................................................... 292
PATHOLOGY....................................................................................................................................................... 292
PATHOPHYSIOLOGY AND HEMODYNAMICS: .............................................................................................................. 293
CLINICAL MANIFESTATIONS: .................................................................................................................................. 294
Diagnosis: .................................................................................................................................................. 295
MANAGEMENT ................................................................................................................................................... 295
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TETRALOGY OF FALLOT (TOF): .............................................................................................................................. 296
ANATOMICALLY TOF CONSISTS OF ......................................................................................................................... 296
PATHOPHYSIOLOGY AND HEMODYNAMICS: .............................................................................................................. 296
CLINICAL MANIFESTATIONS: .......................................................................................................................... 297
MECHANISM:..................................................................................................................................................... 298
Treatment of Hypercyanotic spells: ........................................................................................................... 298
DIAGNOSIS: .................................................................................................................................................... 299
MANAGEMENT:.................................................................................................................................................. 300
ANESTHETIC MANAGEMENT OF PATIENT WITH CHD COMING FOR NON CARDIC SURGERIES ...................... 302
Symptoms and signs of cardiac-failure in a neonate and infant: .............................................................. 303
Laboratory studies: ................................................................................................................................... 303
Oral Regimen for Dental, Oral, or Upper Respiratory Tract Procedures ................................................... 307
Monitoring: ............................................................................................................................................... 309
 Thermal stabilization ....................................................................................................................... 310
 Fluid management:.......................................................................................................................... 310
ANESTHETIC MANAGEMENT: ................................................................................................................................. 310
CHD AND PREGNANCY: .................................................................................................................................. 315
Anesthesia consideration: ......................................................................................................................... 315
Anesthesia consideration: ......................................................................................................................... 316
CONCLUSION: ............................................................................................................................................ 316
CHAPTER 17 - ANESTHESIA FOR VASCULAR SURGERY .................................................................................. 318
INTRODUCTION:.................................................................................................................................................. 318
ANEURYSMS ................................................................................................................................................... 318
HISTORY OF AORTIC ANEURYSMS .................................................................................................................. 318
CLASSIFICATION OF AORTIC ANEURYMS ........................................................................................................ 319
Shape......................................................................................................................................................... 319
Size ............................................................................................................................................................ 319
Structure .................................................................................................................................................... 319
Location:.................................................................................................................................................... 319
ETIOLOGY ....................................................................................................................................................... 320
Degenerative: ............................................................................................................................................ 320
Congenital ................................................................................................................................................. 320
Infectious ................................................................................................................................................... 320
Inflammatory ............................................................................................................................................ 320
Trauma ...................................................................................................................................................... 320
Iatrogenic .................................................................................................................................................. 320
Dissecting .................................................................................................................................................. 321
ABDOMINAL AORTIC ANEURYSMS (AAA) ....................................................................................................... 321
PREVALENCE:............................................................................................................................................. 321
ANATOMY ................................................................................................................................................. 321
Risk Factors: .............................................................................................................................................. 322
HISTOPATHOLOGY..................................................................................................................................... 322
COMMON PRESENTATIONS ...................................................................................................................... 322
DIAGNOSIS ................................................................................................................................................ 323
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MANAGEMENT .............................................................................................................................................. 323
PRE-OP PULMONARY EVALUATION .......................................................................................................... 326
PREOP RENAL EVALUATION ...................................................................................................................... 326
AORTIC CROSS-CLAMPING ............................................................................................................................. 328
HEMODYNAMIC CHANGES............................................................................................................................. 329
PERCENT CHANGE IN CV VARIABLES ON INITIATION OF AORTIC OCCLUSION .......................................... 329
THERAPEUTIC INTERVENTIONS ................................................................................................................. 329
CONTROLLED CROSS CLAMPING: ............................................................................................................................ 330
After load Reduction ................................................................................................................................. 330
Normalizing Preload .................................................................................................................................. 330
RENAL PATHOPHYSIOLOGY DURING CROSS-CLAMPING ........................................................................... 330
AOTRIC UNCLAMPING .................................................................................................................................... 332
In case of refractory hypotension after Unclamping: ................................................................................ 332
ANESTHETIC MANAGEMENT .......................................................................................................................... 332
MONITORING: ........................................................................................................................................... 333
INTRAOPERATIVE MANAGEMENT............................................................................................................. 333
COMPLIATIONS OF AAA REPAIR ..................................................................................................................... 334
Intraoperative: .......................................................................................................................................... 334
POSTOPERATIVE MANAGEMENT .............................................................................................................. 335
ENDOVASCULAR ANEURYSM REPAIR ............................................................................................................. 335
RUPUTURED AORTIC ANEURYSM ................................................................................................................... 336
CHAPTER 18 - DELIBERATE HYPOTENSION ................................................................................................... 338
SYNONYMS: ....................................................................................................................................................... 338

DEFINITION:....................................................................................................................................................... 338
INDICATIONS: ..................................................................................................................................................... 338
CONTRA INDICATIONS: ......................................................................................................................................... 338
Routine monitors: ...................................................................................................................................... 342
Complications: ........................................................................................................................................... 343
COMMONLY USED HYPOTENSIVE AGENTS .................................................................................................... 344
SODIUM NITROPRUSSIDE:.............................................................................................................................. 345
TREATMENT:...................................................................................................................................................... 346
CHAPTER 19 - SHOCK ................................................................................................................................... 349
DEFINITION:....................................................................................................................................................... 349
PHYSIOLOGY (OF TISSUE PERFUSION): ..................................................................................................................... 349
STAGES OF SHOCK: .............................................................................................................................................. 350
PATHOPHYSIOLOGY OF SHOCK: .............................................................................................................................. 351
MICROCIRCULATORY FACTORS: .............................................................................................................................. 352
MICROCIRCULATORY RESPONSE IN SHOCK:................................................................................................... 352
CLASSIFICATION OF SHOCK: ........................................................................................................................... 353
Hypovolemic shock: ................................................................................................................................... 353
Cardiogenic shock: .................................................................................................................................... 353
EXTRACARDIAC OBSTRUCTIVE SHOCK:...................................................................................................................... 354
DISTRIBUTIVE SHOCK: .......................................................................................................................................... 354
ENDOCRINE: ...................................................................................................................................................... 354
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ORGAN DYSFUNCTION IN SHOCK: ........................................................................................................................... 354
GENERAL MANAGEMENT OF SHOCK: ....................................................................................................................... 356
HYPOVOLEMIC SHOCK: ......................................................................................................................................... 358
Etiology: .................................................................................................................................................... 358
Hemorrhagic shock: .................................................................................................................................. 359
VICIOUS CYCLE IN HEMORRHAGIC SHOCK: ................................................................................................................ 359
PATHOGENESIS OF HEMORRHAGIC SHOCK: ............................................................................................................... 360
NON HEMORRHAGIC SHOCK PATHOGENESIS: ............................................................................................................ 361
MANAGEMENT OF HYPOVOLEMIC SHOCK: ................................................................................................................ 362
TYPES OF FLUID AVAILABLE:................................................................................................................................... 363
Colloids: ..................................................................................................................................................... 363
Types: ........................................................................................................................................................ 363
CARDIOGENIC SHOCK: .......................................................................................................................................... 364
ETIOLOGY: ......................................................................................................................................................... 365
Clinical features: ........................................................................................................................................ 365
Management of cardiogenic shock: .......................................................................................................... 366
OBSTRUCTIVE SHOCK: .......................................................................................................................................... 369
Etiology: .................................................................................................................................................... 369
Pathogenesis: ............................................................................................................................................ 370
Clinical features and treatment: ............................................................................................................... 370
DISTRIBUTIVE SHOCK: .......................................................................................................................................... 370
Etiology: .................................................................................................................................................... 370
SEPTIC SHOCK................................................................................................................................................. 370
PATHOGENESIS: .................................................................................................................................................. 372
Features of septic shock: ........................................................................................................................... 373
MANAGEMENT OF SEPTIC SHOCK: .......................................................................................................................... 373
CHAPTER 20 - CARDIOMYOPATHIES ............................................................................................................. 375
ETIOLOGY:-........................................................................................................................................................ 375
Idiopathic .................................................................................................................................................. 375
Ischemic..................................................................................................................................................... 375
Classification of cardiomyopathies on morphologic and hemodynamic basis .......................................... 376
IDIOPATHIC DILATED CARDIOMYOPATHY:-................................................................................................................ 376
Clinical presentation:- ............................................................................................................................... 377
MANAGEMENT OF ANESTHESIA: ............................................................................................................................ 377
RESTRICTIVE CARDIOMYOPATHY: ............................................................................................................................ 378
Clinical presentation:................................................................................................................................. 378
HYPERTROPHIC CARDIOMYOPATHY:- ...................................................................................................................... 379
Clinical features:- ...................................................................................................................................... 379
TREATMENT:- .................................................................................................................................................... 379
Management of anesthesia:- .................................................................................................................... 380
OBLITERATIVE CARDIOMYOPATHY:- ........................................................................................................................ 382
PERIPARTUM CARDIOMYOPATHY:- ......................................................................................................................... 382
CHAPTER 21 - CARDIO PULMONARY BY PASS (CPB) ..................................................................................... 385
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HISTORY: .......................................................................................................................................................... 385
GOALS OF CPB ................................................................................................................................................... 385
TYPES ............................................................................................................................................................... 385
TOTAL CPB: ...................................................................................................................................................... 385
ROLE OF ANESTHESIOLOGIST ......................................................................................................................... 386
BASIC CIRCUIT FOR CPB: ...................................................................................................................................... 386
The path of blood flow is as follows: ......................................................................................................... 387
ANESTHESIA FOR THE SURGERIES WHERE CPB IS USED............................................................................ 401
CHAPTER 22 - CARDIOVASCULAR MONITORING .......................................................................................... 423
NON-INVASIVE MONITORING: ....................................................................................................................... 423

INVASIVE MONITORING: ................................................................................................................................ 423
STETHOSCOPY: .......................................................................................................................................... 423
Pulse oximetry: .......................................................................................................................................... 424
PULSE RATE MONITORING: ....................................................................................................................... 424
ELECTROCARDIOGRAPHY (ECG): ............................................................................................................... 424
SEGMENTS:................................................................................................................................................ 428
Right axis deviation: .................................................................................................................................. 428
Left axis deviation: .................................................................................................................................... 428
Intermediate: ............................................................................................................................................ 428
DETERMINATION OF AXIS: ........................................................................................................................ 428
ECG MONITORING SYSTEM: ...................................................................................................................... 429
Modified three electrode system: ............................................................................................................. 430
Five electrode system: ............................................................................................................................... 431
Combination and sensitivity of detection of ischemia:.............................................................................. 431
INVASIVE METHODS: ................................................................................................................................. 432
FACTORS AFFECTING ECG (Artifacts): ....................................................................................................... 432
BLOOD PRESSURE MEASUREMENT  Non-invasive................................................................................. 433
INVASIVE MONITORING ................................................................................................................................. 434
COMPLICATIONS: ...................................................................................................................................... 437
Arterial pressure monitoring system has number of components: ........................................................... 437
ARTERIAL PRESSURE WAVE FORM: ........................................................................................................... 437
CENTRAL VENOUS PRESSURE ......................................................................................................................... 438
INDICATIONS FOR CVP MONITORING: ...................................................................................................... 438
Wave forms of CVP:................................................................................................................................... 440
DIAGNOSTIC IMPORTANCE OF CVP: ............................................................................................................... 441
PULMONARY ARTERY PRESSURE MONITORING............................................................................................. 442
TRANSOESOPHAGEAL ECHOCARDIOGRAPHY: ............................................................................................... 449
Physical principle: ...................................................................................................................................... 449
INDICATIONS/PRACTICE GUIDELINES: ....................................................................................................... 451
CHAPTER 23 - WAVES IN ECG ....................................................................................................................... 455
P-WAVES: ......................................................................................................................................................... 455

PATHOLOGICAL Q WAVE  .................................................................................................................................. 455
Q – WAVE + ST SEGMENT ELEVATION  ................................................................................................................ 455
Q WAVE WITHOUT ST SEGMENT (OR T WAVE CHANGES)  ........................................................................................ 455
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R – WAVE:......................................................................................................................................................... 455
TALL R – WAVE  .............................................................................................................................................. 455
RIGHT VENTRICULAR HYPERTROPHY: ....................................................................................................................... 455
RBBB: DOMINANT DEFLECTION IN V1 IS UPRIGHT, .................................................................................................... 456
LEFT VENTRICULAR HYPERTROPHY: ......................................................................................................................... 456
LBBB: .............................................................................................................................................................. 456
T-WAVE: ........................................................................................................................................................... 456
U WAVE: ........................................................................................................................................................... 456
P-R SEGMENT: ................................................................................................................................................... 456
PROLONGED P-R INTERVAL: .................................................................................................................................. 457
SHORTENED P-R INTERVAL: .................................................................................................................................. 457
SHORTENED QT INTERVAL: ................................................................................................................................... 457
PROLONGED QT INTERVAL:................................................................................................................................... 457
HYPOCALCEMIA < 4.5 MEQ/L. .............................................................................................................................. 457
HYPERCALCEMIA > 5.3 MEQ/L .............................................................................................................................. 457
HYPOMAGNESAEMIA ≈ HYPOKALEMIA<1.5MEQ/L ................................................................................................... 457
HYPERMAGNESEMIA ≈ HYPERKALEMIA > 2.5 MEQ/L................................................................................................. 457
HYPOKALEMIA: (<3.5 MEQ/L ): ............................................................................................................................ 457
CHAPTER 24 - NON INVASIVE METHODS TO ASSESS VENTRICULAR FUNCTION ............................................ 459
CARDIAC RHYTHM:.............................................................................................................................................. 459

Mechanical Function of the Ventricles and Peripheral Vascular System ................................................... 459
Oscillometry technique:............................................................................................................................. 459
CVP: ........................................................................................................................................................... 460
Cardiac output:.......................................................................................................................................... 460
ECHOCARDIOGRAPHIC ESTIMATION OF LEFT VENTRICULAR SIZE, FUNCTION AND REGIONAL WALL MOTION. ........................ 460
PROBLEMS IN PATIENT WITH COMPLETE HEART BLOCK COMING FOR SURGERY: ................................................................ 462
Anesthetic management of patients with artificial cardiac Pacemakers: ................................................. 465
CHAPTER 25 - PAROXYSMAL NOCTURNAL DYSPNOEA (PND) ....................................................................... 467
I. DEFINITION: .................................................................................................................................................... 467

II. MECHANISM UNDERLYING (PND): ..................................................................................................................... 467
III. Diagnosis: ............................................................................................................................................. 467
Differential diagnosis: ............................................................................................................................... 467
Treatment: ................................................................................................................................................ 467
CHAPTER 26 ENDOCARDIAL VIABILITY RATIO .............................................................................................. 468
FACTORS AFFECTING MYOCARDIAL O2 SUPPLY AND DEMAND BALANCE........................................................................... 469
CHAPTER 27 CARDIAC PULSE GENERATORS, DEFIBRILLATORS AND CIRCULATORY ASSIST DEVICES ............. 471
CARDIAC PULSE GENERATORS: ...................................................................................................................... 471

PACE MAKERS: ............................................................................................................................................... 472
Indications for perioperative temporary pacing: ...................................................................................... 473
Technique of temporary pacing: ............................................................................................................... 473
PACE MAKERS ................................................................................................................................................ 492
Anesthetic management ........................................................................................................................... 493
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CHAPTER 28 NEW RECOMMENDATIONS: DEFIBRILLATION .......................................................................... 495
Classification of defibrillator. .................................................................................................................... 495

SYNCHRONIZED CARDIOVERSION: ........................................................................................................................... 496
 Definition: ........................................................................................................................................ 496
INDICATIONS FOR CARDIAC ELECTROVERSION: ........................................................................................................... 498
PHYSIOLOGY OF HEART FAILURE: ............................................................................................................................ 504
CHAPTER 29 CIRCULATORY ASSIST DEVICES (CAD) ....................................................................................... 507
INTRA AORTIC BALLOON PUMP (IABP): .......................................................................................................... 507

VENTRICULAR ASSIST DEVICE (VADS): ..................................................................................................................... 512
CHAPTER 30 MYOCARDIAL ISCHEMIC PRE-CONDITIONING ......................................................................... 519
WHAT IS ISCHEMIC PRE-CONDITIONING? ................................................................................................................. 519

MECHANISM OF ISCHEMIC PRE-CONDITIONING: ........................................................................................................ 520
CHAPTER 31 PREOPERATIVE ASSESSMENT AND PREPARATION OF A CARDIAC PATIENT FOR SURGERY....... 528
PREVIOUS MI: ................................................................................................................................................... 528

ANGINA: ........................................................................................................................................................... 528
Congestive cardiac failure (CCF): ............................................................................................................... 529
Arrhythmias:.............................................................................................................................................. 529
Hypertension: ............................................................................................................................................ 529
Diabetes mellitus: ...................................................................................................................................... 529
Renal failure: ............................................................................................................................................. 529
Cerebrovascular disease: ........................................................................................................................... 530
Echocardiography: .................................................................................................................................... 532
Guidelines for preoperative testing: .......................................................................................................... 534
CHAPTER 32 - PERIOPERATIVE RECOGNITION AND TREATMENT OF MYOCARDIAL ISCHEMIA ..................... 537
INCIDENCE OF PERIOPERATIVE ISCHEMIA...................................................................................................... 537

PREOPERATIVE ISCHEMIA...................................................................................................................................... 537
Intraoperative Ischemia ............................................................................................................................ 537
DIAGNOSING MYOCARDIAL ISCHEMIA .......................................................................................................... 538
TREATMENT OF ISCHEMIA ........................................................................................................................ 542
CHAPTER 33 - VASOPRESSORS AND INOTROPES IN CLINICAL PRACTICE ....................................................... 546
CLASSIFICATION OF VASOPRESSORS AND INOTROPES .................................................................................. 546

TABLE I: CLASSIFICATION OF COMMONLY USED SYMPATHOMIMETIC AGENTS AND INOTROPES ............................................ 547
Sympathomimetic agents ......................................................................................................................... 547
Inotropes ................................................................................................................................................... 547
PATHOPHYSIOLOGIC RATIONALE FOR USE OF VASOPRESSORS AND INOTROPES IN CLINICAL CONDITIONS . 552
GUIDELINES FOR EASY ADMINISTRATION OF DRUGS ............................................................................... 555
CHAPTER 34 - HYPERTENSION ...................................................................................................................... 557
DEFINITIONS: ..................................................................................................................................................... 557

Classification and pathophysiology: .......................................................................................................... 558
Mechanisms responsible for changes observed in HTN patients: ............................................................. 558
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Preoperative evaluation: ........................................................................................................................... 559
INDICATIONS: ..................................................................................................................................................... 562
PREOPERATIVE MANAGEMENT: .............................................................................................................................. 563
Monitoring: ............................................................................................................................................... 564
Treatment: ................................................................................................................................................ 567
CHAPTER 35 - CONGENITAL HEART DISEASES .............................................................................................. 569
INTRODUCTION: ............................................................................................................................................. 571

INCIDENCE OF COMMON CONGENITAL HEART DEFECTS ACYANOTIC LESIONS: ................................................................... 571
CYANOTIC LESIONS: ............................................................................................................................................. 571
CLASSIFICATION: ................................................................................................................................................. 571
ATRIAL SEPTAL DEFECT: ........................................................................................................................................ 572
PATHOPHYSIOLOGY: ............................................................................................................................................ 572
Clinical manifestations: ............................................................................................................................. 573
PROGNOSIS AND COMPLICATIONS: ......................................................................................................................... 574
TREATMENT:...................................................................................................................................................... 574
VENTRICULAR SEPTAL DEFECT: ............................................................................................................................... 574
PATHOPHYSIOLOGY: ............................................................................................................................................ 574
Clinical manifestations: ............................................................................................................................. 575
TETRALOGY OF FALLOT: ........................................................................................................................................ 575
HYPERCYANOTIC ATTACK / “TET” SPELL: ................................................................................................................. 576
Treatment of hypercyanotic attacks: ........................................................................................................ 577
Congestive cardiac failure: ........................................................................................................................ 578
ACCURACY OF CAPNOGRAPHY AND PULSE OXIMETRY: ................................................................................................ 584
Breathing system: ..................................................................................................................................... 585
CHD AND PREGNANCY: ............................................................................................................................. 587
CHAPTER 36 - JUGULAR VENOUS PRESSURE – WAVES ................................................................................. 590
PULSE ............................................................................................................................................................. 590

VELOCITY OF THE PULSE: ...................................................................................................................................... 590
RECORDING OF RADIAL – PULSE: ........................................................................................................................... 590
CHAPTER 37 BLOOD – PRESSURE ................................................................................................................. 593
CUT OFF VALUES TO DETERMINE HYPER OR HYPOTENSION: .......................................................................................... 593

Height of SBP indicates: ............................................................................................................................ 593
Height of DBP Indicates: ............................................................................................................................ 593
CHAPTER 38 - CORONARY – CIRCULATION ................................................................................................... 595
RIGHT CORONARY ARTERY (RCA) ................................................................................................................... 595

LEFT CORONARY ARTERY: ...................................................................................................................................... 595
CHAPTER 39 - INTRA-AORTIC BALLOON PUMP (IABP) .................................................................................. 601
ADVANTAGES OF IABP: ....................................................................................................................................... 601

CRITERIA FOR MECHANICAL SUPPORT OF CIRCULATION .......................................................................... 601
INDICATIONS FOR IABP: ................................................................................................................................. 602
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PHYSIOLOGICAL CHANGES WITH IABP: ..................................................................................................... 602
Applications:.............................................................................................................................................. 602
CHAPTER 40 - CPCR – CONTROVERSIES ........................................................................................................ 604
CARDIAC PUMP VERSUS THORACIC PUMP - ..................................................................................................... 604

SITE OF COMPRESSION: ................................................................................................................................. 605
CAB OR ABC? .................................................................................................................................................. 605
THE DEMISE OF POLYPHARMACY.............................................................................................................. 605
COLLOID VERSUS CRYSTALLOID: ............................................................................................................... 606
DEFIBRILLATION: ....................................................................................................................................... 606
CHAPTER 41 - CORONARY CIRUCLATION ...................................................................................................... 608
RIGHT CORONARY ARTERY:................................................................................................................................... 608

TOTAL 6 BRANCH ...................................................................................................................................... 608
LEFT CORONARY ARTERY: ..................................................................................................................................... 609
Left Coronary Artery Divide into: ............................................................................................................... 609
LCA SUPPLIER ............................................................................................................................................ 609
MAJOR DETERMINANTS OF CORONARY FLOW .......................................................................................................... 610
FACTOR AFFECTING MYOCARDIAL O2 SUPPLY DEMAND BALANCE................................................................................... 610
CORONARY STEAL: .............................................................................................................................................. 611
CONDITION PRE-DISPOSING TO THE STEAL PHENOMENON AS ....................................................................................... 612
Drugs causing coronary steal .................................................................................................................... 612
TWO KINDS OF STEAL: .......................................................................................................................................... 612
EFFECTS OF ANESTHETIC AGENTS ON CORONARY CIRCULATION: .................................................................................... 613
Relationship of ECG with coronary artery ................................................................................................. 613
CHAPTER 42 - DISCUSS THE ETIOLOGY, C/F INV & ANESTHETIC MANAGEMENT OF PERICARDIAL EFFUSION?
.................................................................................................................................................................... 615
DEFINITION:....................................................................................................................................................... 615
ETIOLOGY .......................................................................................................................................................... 615
 Common causes Less common ...................................................................................................... 615
C/F ............................................................................................................................................................. 615
Investigations ............................................................................................................................................ 615
Chest X-ray ................................................................................................................................................ 615
ECG ............................................................................................................................................................ 615
Echocardiography: To confirm the diagnosis ............................................................................................ 615
MANAGEMENT:.................................................................................................................................................. 616
ANESTHETIC MANAGEMENT PRE-OPERATIVE PREPARATION ........................................................................................ 616
GENERAL ANESTHESIA IS PREFERRED ....................................................................................................................... 616
CHAPTER 43 - WHAT IS CARDIAC TAMPONADE, C/F, INV, RX AND ANESTHETIC MANAGEMENT? ................ 618
DEFINITION:....................................................................................................................................................... 618
ETIOLOGY .......................................................................................................................................................... 618
C/F .................................................................................................................................................................. 618
CHAPTER 44 - PACE MAKERS................................................................................................................... 620
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PRINCIPLES OF PACING:........................................................................................................................................ 620
CAPTURE ........................................................................................................................................................... 620
THRESHOLD FOR CAPTURE .................................................................................................................................... 620
SENSING ........................................................................................................................................................... 620
Threshold for Sensing ................................................................................................................................ 620
TYPES OF PACEMAKERS: ....................................................................................................................................... 621
CHOICE OF PACING MODE .................................................................................................................................... 622
Pathophysiology features .......................................................................................................................... 622
Life of Pace Maker ..................................................................................................................................... 622
INDICATION: .............................................................................................................................................. 623
PERMANENT PACING ................................................................................................................................ 623
POSITIONING ............................................................................................................................................. 623
COMPLICATION OF TEMPORARY PACING ................................................................................................. 623
OTHER TYPES OF PACING .......................................................................................................................... 623
MALFUNCTION OF PACEMAKER................................................................................................................ 624
Surgery in patients with artificial pacemaker Pre-operative valuation .................................................... 624
Management of Anesthesia ...................................................................................................................... 624
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Chapter 1 CARDIOVASCULAR SYSTEM PHYSIOLOGY
Cardiovascular physiology includes the study of

1. Cellular and molecular biology of the cardiomyocyte.
2. The heart as a pump
3. The regulation of cardiac function by neural and humoral factors.
Cellular Cardiac Physiology:

At the cellular level, the heart consists of 3 major components:
 The cardiomyocytes, cardiac muscle tissue.
 The conduction tissue
 The extracellular connective tissue
Approximately 50% of the cell volume in a contracting cardiomyocyte is made up of

myofibrils (the contractile element) and the remainder consists of mitochondria,
nucleus, sarcoplasmic reticulum and the cytosol.
Whereas, the Purkinje cells, the conducting cardiomyocytes have a low content of
myofibrils, a prominent nucleus and abundant gap junctions.
The cardiomyocytes can be functionally separated into:

1. The excitation system
2. Excitation – Contraction – Coupling
3. Contractile system
The Excitation System:

This includes the initiation of the cardiac impulse at the sinoatrial node (SAN) and the
conduction of the action potential.
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CARDIAC ACTION POTENTIAL
 PHASE 0 - RAPID UPSTROKE

PHASE 1 - EARLY REPOLARISATION
PHASE 2 - PLATEAU
PHASE 3 - REPOLARISATION
PHASE 4 - RMP/ DIASTOLIC DEPOLARISATION
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ACTION POTENTIAL IN PACEMAKER CELLS
Initiation and Conduction of the Cardiac Impulse
The cardiac impulse normally originates in the sinoatrial (SA) mode. The impulse is
rapidly conducted through the atrial fibers to the left atrium and to atrioventricular
node (AV). The normally slower rate of depolarization in AV node (40 – 60 times / min)
allows the faster SA node to control the heart rate.
Impulses from the SA node normally reach the AV node within 0.04s, but leave the AV
node only after another 0.11 S. This delay is the result of slowly conducting small
myocardial fibres within AVN, which depend on the slow Ca2+ channels for the
propagation of action potentials. In contrast, the conduction of impulses in the atria and
ventricles is through the fast sodium channels.
From the AVN, the impulses are carried by the bundle of His, which branch into the right
and the left branches and then forming the complex network of Purkinje, fibres that
depolarize the ventricles.
An impulse arising in the SAN normally requires <0.2s to depolarize the entire heart.
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Anesthetic Implications
1. Halothane, enflurane and isoflurane depress SA node automaticity. But it only
modestly prolongs AVN conduction and refractoriness. Therefore, on giving an
anticholinergic, for sinus bradycardia due to inhalational agents, there is
frequent occurrence of junctional tachycardia.
2. Opioids particularly fentanyl slow AVN conduction, prolongs RR interval, AVN
refractory period and purkinje fibers action potential duration. This depression
of cardiac induction by opioids is more pronounced in patients receiving 
blockers and /or Ca2+ channel blocks. In such case, asystole may follow opioids
induced bradycardia and it usually responds to atropine.
3. The electrophysiological effects of local anesthetics on the heart are seen at
blood concentrations associated with systemic toxicity. At high concentrations,
the LA blocks cardiac fast sodium channels. This slows the conduction of cardiac
impulses, manifesting as prolonged P-R interval and QRS complex, also re-entry
ventricular tachyarrhythmia.
Bupivacaine is more cardiotoxic than lignocaine

Reasons:
1. Bupivacaine depresses the rapid phase of depolarization (Vmax) in Purkinje
fibres and ventricular muscle to a greater extent.
2. Both bupivacaine and lignocaine block the Na+ channels during systole (use
dependent block). During diastole, lignocaine dissociates rapidly and hence the
Na channels recover completely. In contrast, bupivacaine dissociates off these
channels at a slow rate, thus causing persistent depression and enhancing
toxicity. The toxicity produced is more in patients on drugs that inhibit
myocardial impulse propagation e.g.  – blockers, digitalis and calcium channel
blockers.
Excitation Contraction Coupling (ECC):

The sequence of intracellular events that begins when an action potential depolarizes
the sarcolemmal membrane and ends with myofilament contraction is classically
defined as ECC.
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Depolarization of sarcolemma of Cardiomyocytes (Systole)


In flux of Ca2+ through Lt-type (Voltage gated)
Ca2+ Channels
(+)  “Ca 2+ induced Ca2+ release
Further release of stored Ca2+ from the sarcoplasmic reticulum (SR), through
Ryanodine receptors

Ca2+ binds to Troponin C subunit

Conformational change in Troponin – Tropomyosin regulatory complex that allows actin
and myosin filaments to interact

ATP dependent action – myosin cross – bridging

Contraction / Shortening of each sarcomere
Relaxation / Diastole:
The cross bridging of action and myosin is turned off by a fall in the cytosolic calcium.
This occurs by
1. The active uptake of calcium into the SR by the ATP dependent pump SERA, i.e.
Sarcoplasmic reticulum ATPase (Ca2+ is stored in SR, bound to calsequestrin and
calreticulin)
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Extrusion of calcium by Na+ - Ca2+ exchanger.

 Cytosolic calcium

Release of calcium bound to Troponin C

Separation of actinmyosin cross bridge

Relaxation
Therefore, the initial rate of
Ca2+influx, the intracellular Ca2+ concentration and then its
uptake determine, respectively, the force of contraction and the rate of relaxation.
Anesthetic Implications:
 Volatile anesthetics depress myocardial contractility by reducing cytosolic Ca 2+
concentration, by
o Inhibition of the L-type and T-type Ca2+ channel, thus reducing Ca2+ influx.
o Stimulation of Ca2+ release from SR through Ryanodine receptors, leading to a
leak and hence reducing stores of Ca2+ in SR.
o Inhibition of Na+-Ca+ exchange. This is more important in neonatal
myocardium.
o Direct depression of the sensitivity of contractile apparatus to activator Ca2+
and decreased myofibrillar ATPase activity (minor role).
 Acidosis causes a depression in cardiac contractility by impairing Ca2+ influx and
/ or decreasing the release of calcium from SR.
The Cardiac Cycle:

Is the sequence of electrical and mechanical events during the course of a single heart
beat.
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Figure 18-1 the electrical and mechanical events during a single cardiac cycle are
depicted. Shown are pressure curves of aortic blood flow, ventricular volume, venous
pulse, and the electrocardiogram.
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Venous return to right and left atria (JVP – v wave)

Increase in atrial pressure > Ventricular pressure

Opening of atrial – ventricular valves

Blood flows passively into ventricular chamber (JVP- y descent)
(75% of ventricular filling)

Atrial systole / kick (20 – 25% of ventricular filling)
(P Wave – ECG, A wave – JVP)

Closure of AV values

Isovolumetric Contraction of Ventricles (JVP – c wave, ECG – QRS)

Ventricular pressure > Aortic / Pulmonary artery pressure

Opening of aortic and pulmonary valve

Ventricular ejection

Progressive fall in ventricular pressure

Opening of aortic and pulmonary valve

Ventricular ejection

Progressive fall in ventricular pressure

Closure of aortic and pulmonary valves

Isovolumetric relaxation (ECG – T wave)

Decreased ventricular pressure < atrial pressure

Opening of AV values
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Length of Systole and Diastole:

Systole : 1/3rd of cardiac cycle
Diastole : 2/3rd of the cardiac cycle
HR = 75 / min
Duration of cardiac cycle : 0.8 Seconds
Systole : 0.27 s
Diastole : 0.53 s
Clinical Importance:
Duration of diastole is important, as it is during diastole that:

1. The cardiac muscle rests
2. Ventricular filling occurs
3. Coronary blood flow to the ventricles
At very high heart rate (> 180-200 bpm), ventricular filling may be compromised, thus
decreasing the cardiac output and also impairing the LV perfusion.
Determinants of Ventricular Systolic Function:

Ventricular systolic function is equated with cardiac output, and is defined as the
amount of blood pumped by the heart per unit time.
Cardiac Output (CO) = Stroke volume x Heart rate
5 L. / min
Cardiac Index = CO/BSA
= 2.5 – 4.2 L/min/m2
It has a wide range and hence is a relatively insensitive measurement of ventricular
function.
Cardiac Reserve = Difference between output at maximum effort and output at rest.
Distribution of CO:
Kidneys : 1300 ml Liver : 1500 ml
Muscles : 800 ml Heart : 250 ml
Brain : 700 ml Others: 500 ml
Measurement of CO: is based in Fick principle which is based on the concept of
‘conservation of mass’.
Accordingly, the amount of oxygen consumed by an individual equal the difference
between arterial and venous (a-v) oxygen content multiplied by cardiac output.
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Therefore VO2 = (CaO2 – CvO2) x CO
or
VO2
CO - ………………...
(CaO2 – CVO2)
CaO2 - From arterial line
CvO2 - From pulmonary artery
VO2 - Difference in oxygen concentration of inspired and expired air
Other methods:
1. Thermodilution method
2. Dye dilution method (Indocyanine green)
3. Trans Oesophageal echocardiography and Doppler
Factors determining cardiac output:

Are the heart rate and stroke volume.
Heart rate
 Cardiac output is directly proportional to heart rate.
 But only upto a certain extent (160 bpm) beyond this there is not much increase
in CO, due to impaired LV diastolic filling.
 Myocardial contractility also increases directly in proportion to HR. This
phenomenon is called Bowditch staircase / treppe / for frequency relationship.
Thus, an increased HR incrementally increases contractility upto a certain extent
(HR = 180 bpm). Beyond which the force of contraction decreases.
Stroke volume
 Is the amount of blood pumped out of each ventricle per beat

SV = 60 – 90 (average 70) ml /beat.
 The major factors affecting stroke volume

Preload
After load
Contractility
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Wall motion abnormalities
Valvular dysfunction
Preload:
Is defined as the volume of blood contained in the LV cavity at end-diastole (EDV). This
volume establishes passive stretch on each LV myofibril immediately before isovolumic
contraction.
 The relationship between CO and LVEDV known as Frank – Starling relationship.
 It states that stretching of sarcomere (LVEDV) results in enhanced myocardial
contractility in the subsequent contractions, until excessive EDV are reached.
Over distension of the ventricle can lead to dilatation and even decrease in CO.
 The frank starling mechanism may remain intact even in a failing heart, however,
ventricular remodeling after injury or in over heart failure it may not hold true.
Cellular Basis:
 LVED

Stretching of Sarcomere

 Interaction between actions

Increased actin – myosin cross bridging which is equivalent to increase
in muscle performance
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Factors affecting ventricular preload:
Venous return
Blood volume
Ventricular compliance
 in Ischemia
Hypertrophy
Pericardial disease
Increased airway pressure e.g. IPPV
HR
Rhythm / atrial contraction  in atrial flutter, fibrillation
Measurement of Preload / LVEDV

1. It is clinically difficult: Transesophageal echocardiography and contrast
ventriculography provides only approximations of the value.
2. Hence clinically the following parameters are used to estimate LVEDV.
a). LVED Pressure: It is a poor reflection EDV, especially in pathologic states

where ventricular compliance is altered.
E.g.  compliance =  LVEDP


This may imply capillary wedge pressure
b). Pulmonary capillary wedge pressure

c). Central venous pressure
After load:
 Is the resistance to LV ejection by arterial vasculature.
 It is the tension against which the cardiac muscle must contract during systole.
 It is equated with ventricular wall tension during systole or arterial impedance
to ejection.
 Ventricular wall tension; Is the pressure the ventricle must overcome to reduce
its cavity. Expressed by Laplace’s law.
PXR
Wall Stress = ………………..
2h
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Where,
P – Intraventricular pressure dependent on
 Force of ventricular contraction
 Aortic compliance (dilatation / stiff)
 Viscosity and density of blood
 Systemic vascular resistance
R – Ventricular radius
 Larger the radius (dilation), greater the tension required to develop the same
pressure.
H – Wall thickness
An increase in wall thickness (as in LVH), decreases the ventricular wall tension.
E.g. LVH due to systemic hypertension and aortic stenosis.
1). LV after load is equated with SVR
Arteriolar tone is the primary determinant Where,
MAP - Mean arterial pressure (mmHg)
CVP - Central venous pressure
CO - Cardiac output
Normal SVR = 900 – 1500 dyne s/cm5
MAP – CVP
SVR = 80 x ………………….
CO
Therefore after load is increased in chronic HTN, AS.
2). Right ventricular after load, is mainly dependent on pulmonary vascular
resistance.
PAP – LAP
PVR = 80 x ………………..
CO
Where,
PAP – Pulmonary artery pressure
LAP – Left atrial pressure / PCWP
Normal PVR – 50 – 150 dyne. s/cm5
CO is inversely related to after load.
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Patients with myocardial dysfunction become increasingly sensitive to after load.
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Measurement of After load:
1. Aortic impedance is an accurate means to gauge after load.
Aortic Pressure
Aortic impedance =….. ………………
Aortic flow
Echocardiography can estimate aortic impedance non-invasively by measuring aortic
blood flow.
2. In clinical practice, systolic BP is used to approximate after load, provided AS is

absent.
Myocardial Contractility (Inotropism)

 Is defined as the work performed by cardiac muscle at any end – diastolic
volume.
 It is the “Intrinsic” ability of the myocardium to pump in the absence of changes
in preload and after load.
 CO  myocardial contractility
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Factors affecting Contractility:
- HR (Bowditch staircase)
- Sympathetic stimulation (1 Receptor)
- Circulating catecholamines
Drugs: E.g. Digitalis – Inhabit Na+ - K + ATPase, thus limiting Na+ influx =  efflux of Ca by
Na+ - Ca2+ pump → Ca2+ availability →contractility
- Hypoxia
- Acidosis
- Loss of functioning muscle mass – ischemia
- Anesthetic drugs – inhalational agents
- Barbiturates (decreased Ca2+ influx)
Measurement of Intrinsic Contractile Activity:

1. Pressure volume loops best method
- Initially described by Frank
- The changes in left ventricular pressure with respect to volume
occurs in counter clock direction.
But this is an invasive procedure requiring placement of cardiac catheter in LV to

measure the volume.
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A - MITRAL VALVLE CLOSURE

B - AORTIC VALVE OPENING
C - AORTIC VALVE CLOSURE
D - MITRAL VALVE OPENING
SYSTOLIC DYSFUNCTION DIASTOLIC DYSFUNCTION

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Ejection Fraction (EF):
Commonly used non-invasive index.
Fraction of the end-diastolic ventricular volume ejected
EDV – ESV
EF = ………………
EDV
 Measurement: Transthoracic or TEE, Cardiac catheterization
Wall Motion Abnormalities

 Due to ischemia, hypertrophy
 Hypokinesia, akinesia, dyskinesis (paradoxic bulging)
 →Contractility →abnormal emptying →CO
 Ventricular relaxation and filling of the ventricle.
 Depends on:
1. Passive chamber stiffness
o IHD
o Scarring
o Hypertrophic obstructive cardiomyopathy
2. Pressure or volume overload hypertrophy
3. Diastolic interaction between the 2 ventricles.
 Isovolumic relaxation is an energy dependent process, requiring ATP for the
clearance of Ca2+ from the myoplasm by sarcolemmal pumps.
Assessment:
 Invasive: Maximal rate of decay of LV pressure (-Dp/df)
 Noninvasively by Doppler echocardiography, to evaluate transmitted blood flow.
E- Early filling Reversal of E/A ratio Pseudo-normalization in

A – Atrial systole end stage heart failure as LV Compliance and
LVEDP 
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Normal  Relaxation  Preload
IVRT 70 – 90 Ms > 100 ms 70 – 90 ms
E/A ratio 0.8 – 1.2 < 0.8 0.8 – 1.2
DTE 150 – 300 ms > 250 ms 150 – 300ms
Neural Regulation of Cardiac Function:

At rest, the major influence on the heart is parasympathetic. During stress, the
sympathetic influence becomes predominant.
Parasympathetic NS has a more direct inhibitory effect in the atria and has a
negative modulatory effect in the ventricles.
Parasympathetic innervations is through vagus nerves.
Effect: SAN activity slows AV conduction,  atrial contractile force.
Sympathetic innervations of the heart is more predominant in the ventricle than the
atrium.
Effect: +ve chronotropic (HR), +ve inotropic (contractility), + ve Lusitropic
(relaxation) effects.
Hormones affecting cardiac function

Angiotensin + Inotropy /+ Chronotropy Cardiac hypertrophy and
Modulator of cardiac growth adverse remodeling of
and function myocardium
Natriuretic peptides Released by cardiomyocytes in Increase in CHF
ANP, BNP response to pressure and
volume overload
Adrenomedullin + Inotropy / Chronotropy
Vasopressin
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Coronary Circulation
 Coronary ostia arise from the sinuses of valsalva above the expanse of aortic
valvular cusps.
 Arterial supply
Right – Coronary Artery

Left Coronary Artery
RA SAN (60%)
RV 70% LCCA LAD
AVN (90%)
His Bundle
PDA 10 to 15%
Lateral wall
of LV
Septum &
Anterior wall of
LV + RT & LT
Inferior wall of the Bundle Branch
LV & postero-superior Inter-
ventricular septum
“Coronary dominance”
Here,
PDA – Posterior descending artery
LCCA – Left circumflex coronary artery
LAD – Left anterior descending artery
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Venous Drainage
Great Cardiac Veins
LV Venous
Middle Cardiac Veins
Return
Small cardiac Veins
Coronary Sinus
Minor
Cardiac
Veins
Thebesian Veins Right Atrium
Directly into right and left ventricles by

passing pulmonary circulation.
Thus accounts of normal
physiologic arterio – venous
shunting
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CORONARY BLOOD FLOW DURING CARDIAC CYCLE
Coronary Blood Flow (CBF)

 CBF = 250 ml /min at rest (5% of CO)
 Coronary perfusion is unique in that it is intermittent rather than continuous as
in other organs.
 The perfusion depends upon the pressure gradient between the chambers of the
heart and aorta.
Pressure in aorta, LV and RV in systole and diastole
Aorta LV RV
Systole 120 121 25
Diastole 80 0 0
 During systolic contraction of the left ventricle, the pressure within the LV is
equal to / exceeds the pressure in aorta. Also, the force of LV contraction almost
completely occludes the intra-myocardial coronary arteries. Thus, during systole
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no BF occurs to LV, especially the subendocardium. Consequently the LV is
perfused only during diastole. (However perfusion of the superficial epicardial
vessels does occur)
 Blood flow to the right ventricle occurs during both systole and diastole, as intra-
myocardial pressure is lower than that in the aorta.
 The coronary BF is determined by coronary perfusion pressure (CPP).
CPP = Aortic Diastolic Pressure – LVEDP
Thus decrease in aortic pressure or increase in LVEDP reduces the coronary
perfusion.
 Tachycardia, by reducing the diastolic time, hampers CBF to the LV.
 The endocardium tends to be most vulnerable to ischemia during decrease in
CPP, as it is subjected to greatest intramural pressures.
Auto-Regulation of CBF
 Coronary perfusion is auto regulated to maintain a constant flow between
perfusion pressures of 50 -1 20 mmHg.
 Beyond this range, blood flow becomes increasingly pressure dependent.
 The principal site of auto regulation is the coronary arteriole (< 150 m
diameter)
Factors affecting the CBF:

Myocardial oxygen consumption (MVO2)
o Most important determinant
o MVO2 = 10 ml / 100g / min at rest
o The myocardium extracts 70 – 75% of the arterial oxygen, compared with 25%
in most other tissues (Coronary venous O2 saturation is usually 30%, PO2 = 18-
20 mmHg)
o Therefore, any increase in myocardial oxygen demand as during exercise must
be met by us increase in CBR as the myocardium cannot extract more O2.
 Factors determining MVO2
 Heart rate
Tachycardia - Myocardial O2 demand
- But decreases diastolic filling
 Tachycardia is dangerous in patients with coronary artery disease, because
increase in O2 demand cannot be matched by increase in supply
 Wall tension
Increase in wall tension  Increased O2 demand
According to Laplace equation
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Wall Tension () p x r / 2h
Therefore wall tension increases during
Increased systolic pressure / after load – as in HTN, AS
Increased diastolic pressure / preload – as in AR, MR
Wall tension decrease with increase in wall thickness (LVH). However,
the increased thickness increases the MVO2, thus raising the risk of ischemia.
 Contractile status
o Increased Contractility  Increased MVO2
o As in – sympathetic nervous system + ionotropes
o Therefore in coronary artery disease,  antagonists and literates decreased
myocardial O2 demand.
Arterial Oxygen content

o Hypoxia releases adenosine, causing coronary
o Vasodilatation thus increased CBF.
Neural control
 Sympathetic stimulation
1 receptors – Located on larger epicardial vessels
Transient vasoconstriction
1 – increased contractility → Increased MVO2 hence increased CBF.
2 - Coronary vasodilation → Increased CBF
 Parasympathetic: effects on coronary vasculature are generally mirror and are
weakly vasodilatory.
 Heart rate: Increased MVO2
But decreased diastolic filing
Therefore tachycardia can alternate autoregulation.
Effects of Anesthetic Agents:

Volatile Agents:
 Involves action on ATP sensitive K+channels and stimulation of adenosine (A1)

receptor.
 Most volatile agents cause coronary vasodilation and reduction in MVO2. Also
they protect against reperfusion injury. Therefore beneficial in settings of
myocardial ischemia.
 Halothane and isoflurane – greatest effect
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 Sevoflurane – Lacks coronary vasodilating properties, Dose dependent abolition
of autoregulation.
Cardiac Reflexes:
Are faster acting reflex loops between the heart and the CNS that contribute to the
regulation of cardiac function an maintenance of physiologic homeostasis.
Baro-receptor Reflex (Carotid Sinus Reflex)

Maintains BP through a negative feedback loop.
Stimulus: Increase in systemic BP > 170 mm Hg.
+
Stretch receptors in the carotid sinus and aortic arch

Gloss pharyngeal and vagus nerves

Nucleus of Tractus Solitarius in Medulla
Inhibits sympathetic discharge Parasympathetic NS
 in vascular tone, Bradycardia,  Myocardial contractility
 BP
 Reverse effects are elicited with onset of hypotension

 It plays an important role during acute blood loss and shock.
 The reflex are loses its functional capacity at a BP < 50 mmHg.
 Volatile anesthetics inhibit the reflex.
 Patients with chronic hypertension also had a decreased Baroreceptor reflex
response.
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Bainbridge Reflex
Increase in right – sided filling pressure (E.g. Hypervolemia)
+
Stretch receptors in the RA wall and cavoatrial junction
Rt. Atrial  Vagal efferent’s
stretch Cardiovascular centre in medulla Centre: Dorsal motor
+  nucleus of vagus
SAN Inhibit parasympathetic system

 HR & Automaticity
Marey’s Law:
“A pulse of low tension is fast”: The baroreceptors in the carotid sinus and aortic
arch normally respond to a fall in blood pressure by producing a compensatory
tachycardia through vagal afferent and efferent pathways.
Most patients under spinal anesthesia exhibit bradycardia. This is due to predominance
of brain bridge effect. In spinal anesthesia, venous pooling in the periphery reduces
stimulation of the volume receptors, thereby diminishing activity of the cardiac
sympathetic nerves. The result is vagal predominance and bradycardia.
Chemoreceptor Reflex:
Decrease in PaO2< 50 mmHg/acidosis
+
Chemoreceptors in the carotid bodies and aortic body

Sinus nerve of Hearing (a branch gloss pharyngeal of IX CN) and Vagus (X)

Chemosensitive area of medulla
Respiratory centers PNS
Bradycardia & decrease Contractility HR & myocardial contractility
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Bezold Jarisch Reflex:
Noxious Ventricular stimuli
 + Vagus Nerve & type C pain receptor
Stimulus Serotonin Mechanoreceptors in ventricle
+
Vagal afferent C-fibres
X nerve – Efferent & Efferent
+
PNS

Bradycardia, Hypotension, Coronary dilation & Apnea
Importance: It is cardio protective in MI, revascularization injury.
Valsalval Maneuver:
Forced expiration against a closed glottis

 Intrathoracic pressure,  CVP & VR
 CO & BP
+
Baroreceptors

 HR & Contractility
The opposite occurs when glottis opens
Cushing’s Reflex:
Intracranial pressure

cerebral ischemia (at medullary vasomotor centre)
+
Sympathetic nervous system

 HR,  BP & Myocardial contractility, in an effort to improve cerebral perfusion

Reflex bradycardia mediated by baroreceptors
Therefore there is hypertension and bradycardia.
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Oculo-cardiac Reflex: (Also called as Aschenr’s reflex or Trigemino-
vagal reflex)
Pressure on the globe or traction on extraocular muscles

+
Stretch receptors on extraocular muscles
+
Short & long ciliary nerves + Ophthalmic division of V CN
+
Gasserian ganglion
 + PNS

Bradycardia
Incidence: 30% - 90% of ocular surgeries. Can be attenuated by administration of an
antimusarmic drug (atropine / glycopyrrolate).
Cardiovascular responses to Anesthetic maneuvers and to surgery
Laryngoscopy and intubation
o Marked rise in heart rate and BP

o Although transient, it is invariable and significant
o Systolic pressure may increase by a around 45 mmHg.
o Due to handling / manipulation of epiglottis, which causes sympathetic
stimulation and release of epinephrine and nor – epinephrine.
o The effect is more pronounced in patients with coronary artery disease and
valvular heart disease.
This pressor response can be decreased by:
1). Maintaining adequate depth of anesthesia.
2). Minimal duration and intensity of airway manipulation for <20 seconds.
3). Spraying of a topical anesthetic agents like Lidocaine 4% or 10%, 1 to 2 minutes
prior.
4). IV Inj. Lidocaine 2%, 1.5 mg / Kg given about 90 seconds prior to laryngoscopy.
5).  Blockers – 3 minutes prior
Propronolol: 0.1 – 0.2 mg / Kg
Esmolol: 500 g / Kg / Min – loading dose
100 g / Kg / min – in fusion for 5 minutes
7). Oral Clonidine 4 g / Kg 1.5 hrs prior
centrally acting antihypertensive
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Positive pressure ventilation
 Causes a rise in mean intra-thoracic pressure.
 This decreases the venous return and can decrease the cardiac output and hence
BP.
 Similar to valsalva response.
 But in normal patients, reflex constriction of venous capacitance vessels,
maintains the venous return and systemic arterial BP.
 Compensatory mechanisms are interfered in
Hypovolemia
Head up tilt
Intrathecal anesthesia
Old age, myocardial disease
Posture
 With anesthetically induced impairment of the autonomic control of CVS,
substantial alterations may occur, when the patient’s position is altered from
horizontal.
 E.g. Steep head-up, will decrease the venous return and hence the cardiac output.
 Conversely the head-down position, lithotomy position, will maintain the BP and
may mask the effects of hypovolemia until the patient is returned to the
horizontal at the end of the surgery, when it may lead to sudden hypotension.
Surgical stimulation
 Leads to sympathetic response – ↑ SBP, ↑ HR and SVR
 It can also lead to vagal stimulation, as a consequence of pulling on the
mesentery, uterus, gall bladder, G-E junction, where bradycardia and
hypotension occur.
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Chapter 2 ADULT, PEDIATRIC AND NEWBORN
RESUSCITATION
Overviews Cardiopulmonary resuscitation (CPR):

In the operating room (OR) is the responsibility of the anesthesiologist, who
knows the location and function of resuscitation equipment, delegates tasks, and instills
calmness in assisting personnel. The protocols described below have been modified as
appropriate for the anesthesiologist in a hospital setting but closely follow the
evidenced-based 2005 American Heart Association Guidelines for Cardiopulmonary
Resuscitation and Emergency Cardiovascular Care.
These guidelines emphasize the importance of the prompt delivery of effective,
uninterrupted chest compressions, even before checking that a defibrillation has been
successful, to deliver oxygen and energy substrates to the myocardium. An additional
major change in the guidelines is the reduction of ventilation that may decrease venous
return to the heart and diminish cardiac output. Table 37.1 lists the classifications for
the quality of evidence used to support most of the protocol interventions presented in
this chapter.
Cardiac arrest
Diagnosis: The absence of a palpable pulse in a major peripheral artery (carotid,
radial, or femoral) in an unconscious, unmonitored patient is diagnostic of a
cardiac arrest. An electrocardiogram (ECG) may reveal asystole, ventricular
fibrillation (VF), ventricular tachycardia (VT), or even an organized rhythm (as in
pulseless electrical activity).
Etiologies:
Common causes of cardiac arrest areas follows:
1. Hypoxemia.
2. Acid-base disturbances.
3. Derangements of potassium, calcium, and magnesium.
4. Hypovolemia.
5. Adverse drug effects.
6. Pericardial tamponade.
7. Tension pneumothorax.
8. Pulmonary embolus.
9. Hypothermia.
10. Myocardial infarction.
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Pathophysiology
With the onset of a cardiac arrest, effective blood flow ceases, and tissue hypoxia,
anaerobic metabolism, and accumulation of cellular wastes result. Organ function is
compromised, and permanent damage ensues unless resuscitation measures are
instituted within minutes. Acidosis from anaerobic metabolism may cause systemic
vasodilation, pulmonary vasoconstriction, and decreased responsiveness to
catecholamines.
Adult resuscitation
Basic life support:
Includes basic techniques taught to the general public but applies equally to OR
situations. A cardiac arrest should be suspected in any person unexpectedly found un-
conscious. If the subject is unarousable, the "ABCDs" (airway, breathing, circulation and
defibrillation) of resuscitation should be followed after first calling for assistance. For
lone rescuers, the lay public is taught the "phone first/phone fast" rule (evidence class
indeterminate). For adults, children beyond the onset of adolescence or puberty (12 to
14 years of age), and all children known to be at high risk for dysrrhythmias, the
emergency medical system (EMS) should be activated (phone 911) or an automatic
external defibrillator (AED) located before CPR is started by a lone rescuer ("phone
first"). An initial resuscitation attempt followed by the activation of EMS ("phone fast")
is indicated for children aged younger than the onset of puberty because cessation of
respiration is the usual etiology of a cardiac arrest in this population. In cases of
submersion, near drowning, arrest secondary to trauma, and drug overdose, the "phone
fast" rule applies. Healthcare providers can tailor the sequence of rescue actions as
deemed appropriate for the likely etiology of the arrest based on any additional infor-
mation or evidence they may be aware of regarding the patient or the nature of the
arrest.
Airway and breathing:

Spontaneous ventilation is evaluated by observation and auscultation and is aided by
repositioning or insertion of an oropharyngeal or nasopharyngeal airway. In the
absence of effective spontaneous ventilation, rescue breathing is begun (or ventilation
by bag-valve-mask with 100% 02). Two slow breaths at loin airway pressures (to limit
gastric distention) are delivered initially, followed by 8 to 10 breaths per minute. If
ventilation is not possible after these maneuvers, efforts to. clear the airway of a
suspected foreign body (e.g., Heimlich maneuver, chest compressions, or manual
removal) should be attempted. Checks but are taught to initiate chest compressions in
the absence of signs
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Circulation:
The circulation is assessed by palpation of the carotid artery pulse for 5 to 10 seconds.
In the absence of a palpable pulse, artificial circulation should be instituted with
external chest compressions. (The presence of a pulse does not necessarily mean that an
adequate mean arterial pressure is present. Lay rescuers no longer perform pulse
checks but are taught to initiate chest compressions in the absence of signs of
circulation such as moving, coughing, and breathing.) The patient should be on a firm
surface (.e.g., backboard) with the head on the same level as the thorax. The rescuer
(surgeon in the OR) should compress the lower half of the sternum by placing the heel
of one hand on the patient's sternum in the center of the chest, between the nipples, and
the heel of the other hand on top of the first so that the hands are overlapped and
parallel (class IIa). The rescuer's shoulders should be positioned directly over the
patient, with the elbows locked for effective compressions. Sternal depression during
CPR is to a depth of 1.5 to 2.0 inches in a normal-sized adult. A 1:1 compression-
relaxation ratio at a rate of 100 compressions per minute is recommended. For a prone
patient in the OR who cannot be quickly turned supine for CPR, one rescuer can place a
clenched fist between the subxiphoid area and the OR table while compressions are
administered over the corresponding region of the back. The chest compression-to
ventilation ratio is 30:2. This ratio is used for the resuscitation of adults and children
when only. One rescuer is present. If an advanced airway (i.e., endotracheal tube or
laryngeal mask airway) is in place during two-person CPR, there is no need to
synchronize breaths between compressions. Ventilations should be given at a rate of 8
to 10 breaths per minute, and chest compressions should be given at a rate of 100 per
minute without pauses for ventilation.
Defibrillation:
Within 3 minutes in the hospital (evidence class I) and 5 minutes after calling the EMS
(along with immediate high-quality CPR) is the major determinant of a successful
resuscitation because VF is the most likely etiology of a cardiac arrest in adults. Public-
access defibrillation programs have now enabled "level I" responders (e.g., fire
personnel, police, security guards, and airline attendants) to employ readily accessible
AEDs. AEDs are small, lightweight defibrillators that use adhesive electrode pads for
sensing and for delivering shocks. The AED, after analysis of the frequency, amplitude,
and slope of the ECG signal, advises either "shock indicated" or "no shock indicated."
The AF.D is manually triggered and does not automatically defibrillate the patient.
Reassessment:
CPR should be resumed immediately after shock delivery without pausing for a pulse or
rhythm check, and it should be continued for five cycles (or about 2 minutes if an
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advanced airway is in place) before the rhythm is rechecked. Healthcare providers
should also check for a pulse if an organized rhythm has established. In the absence of a
pulse or a "no shock indicated" with an AED, CPR should be resumed with rhythm
checks every five cycles.
Advanced cardiac life support:
(ACLS), including endotracheal intubation, electrical defibrillation, and pharmacologic

intervention, is the definitive treatment for cardiac arrest. Specific protocols are found
in Figures 37.1 through 37.3:
Intubation:
Swift control of the airway (with minimal interruptions in chest compressions and no
delay in defibrillation) will optimize oxygenation and removal of carbon dioxide during
resuscitation. Endotracheal intubation (confirmed by
NEW Guidelines:
The 2010 AHA Guidelines for CPR and ECC recommend a change in the BLS sequence of
steps from A-B-C (Airway, Breathing, Chest compressions) to C-A-B (Chest
compressions, Airway, Breathing) for adults, children, and infants (excluding the newly
born; see Neonatal Resuscitation section). This fundamental change in CPR sequence
will require reeducation of everyone who has ever learned CPR, but the consensus of
the authors and experts involved in the creation of the 2010 AHA Guidelines for CPR
and ECC is that the benefit will justify the effort.
Reasons: The vast majority of cardiac arrests occur in adults, and the highest survival
rates from cardiac arrest are reported among patients of all ages who have a witnessed
arrest and an initial rhythm of ventricular fibrillation (VF) or pulseless ventricular
tachycardia (VT). In these patients, the critical initial elements of BLS are chest
compressions and early defibrillation. In the A-B-C sequence, chest compressions are
often delayed while the responder opens the airway to give mouth-to-mouth breaths,
retrieves a barrier device, or gathers and assembles ventilation equipment. By changing
the sequence to C-A-B, chest compressions will be initiated sooner and the delay in
ventilation should be minimal (ie, only the time required to deliver the first cycle of 30
chest compressions, or approximately 18 seconds; when 2 rescuers are present for
resuscitation of the infant or child, the delay will be even shorter).
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Capnography) by the most experienced person present should minimally disrupt the
resuscitative measures. The endotracheal tube may be used to deliver certain drugs if
intravenous (IV) access has not been established. Examples are Naloxone, atropine,
vasopressin, epinephrine, and lidocaine ("NAVEL''). Because peak drug concentrations
are lower with the endotracheal route compared with IV administration, higher doses
(two to three times) diluted in 10 mL of sterile saline should be used.
Defibrillation VT and VF (see Fig. 37.1):

Are the most common arrhythmias associated with a cardiac arrest. As the du-
ration of a VF/VT arrest increases, the cardiac activity deteriorates and becomes
more difficult to convert to a viable rhythm. Therefore, early defibrillation is the
priority and can often be administered by the anesthetist without compromising
the surgical field. It is the responsibility of the person operating the defibrillator
to ensure that members of the resuscitation team are not in contact with the
patient during defibrillation.
a. Biphasic waveform defibrillators are used in virtually all AEDs and manual
defibrillators sold in the United States today. They function by delivering an
energy that flows in a positive direction for specified milliseconds followed by
a reversal in the negative direction. The optimal energy needed to terminate
VF is device specific, depends on the manufacturer and the type of waveform
used, and ranges from 120 to 200 J. If the optimum energy is not indicated on
the front of the defibrillator, 200 J should be used. If VF is at any time
terminated by a shock and then recurs, subsequent shocks should be given at
the previously successful energy level.
b. Monophasic waveform defibrillators, still used in many institutions, deliver

energy in a unidirectional manner. The initial and subsequent defibrillations should be
given at 360 J.
c. Cardioversion for atrial flutter, other supraventricular dysrrhythmias such as
paroxysmal supraventricular tachycardia (PSVT), and hemodynamically stable VT
generally require less energy (50 to 100 J Monophasic) than what is necessary for atrial
fibrillation (AF) (100 to 120 J). The optimal energy for cardioversion with biphasic
waveform has not yet been established, but experience with elective cardioversion of AF
indicates that an initial energy of 100 to 120 J will be efficacious and can be
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extrapolated to other tachyarrhythmia. Cardioversion will not be effective for the
treatment of junctional tachycardia or ectopic or multifocal atrial tachycardia because
these rhythms are caused by an automatic focus rather than reentry. In fact, delivery of
a shock to a heart with a rapid automatic focus may actually increase the rate of the
tachyarrhythmia.
Pacing:
High-grade heart block with profound bradycardia is an etiology of cardiac arrest (see
Fig. 37.3). Temporary pacing should be t.sed when the heart rate does not increase with
pharmacologic therapy. Transcutaneous pacing is the easiest method to increase the
ventricular rate. Transesophageal atrial pacing is efficacious for sinus bradycardia with
maintained atrioventricular WV) conduction and is useful intra-operatively for
bradycardia-related hypotension in otherwise stable patients. Transvenous pacing via a
temporary wire into the right heart is a third option to increase heart (rate , while CPR
continues). Special pacing pulmonary artery catheters are capable of AN pacing.
Intravenous access:
Is imperative for a successful resuscitation. The most desirable route is into the central
circulation. Central lines can be achieved via internal jugular, external jugular,
subclavian, or femoral veins and sometimes via peripheral veins (long lines). Choice of
route is predicated on the anatomy of the patient, experience of the physician, and what
is the least disruptive to the resuscitation. Short (peripheral) catheters in antecubital
veins are adequate when an appropriate volume is used to flush medications toward the
central circulation. Fluid replacement is indicated for patients with known or suspected
intravascular volume depletion.
Drugs.
The drugs described below are used in ACLS protocols for the treatment of
hemodynamic instability, myocardial ischemia or infarction, and arrhythmias. The
doses of drugs used for pediatric advanced life support (PALS) are in parentheses
following discussion of adult doses.
a. Adenosine, an endogenous purine nucleotide with a half-life of 5 seconds,

slows A-V nodal conduction and interrupts A-V node reentry pathways to
convert a PSVT to a sinus rhythm. It also assists in the differential diagnosis
of supraventricular tachycardia (e.g., atrial flutter with a rapid ventricular
response versus RSVT). Dosing is based on peripheral administration and
should be halved if given through central venous access. The initial dose is a
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6-mg rapid IV bolus. A brief asystole ensues that is followed by P waves,
flutter waves, or fibrillation waves that are initially without ventricular
responses. PSVT is sometimes converted to a sinus rhythm by the 6-mg dose
of adenosine. A second injection of 12 mg may terminate PSVT if the first
dose is unsuccessful. Recurrent PSVT AF, and atrial flutter will require
longer-acting drugs for definitive treatment. The dose of adenosine should
be increased in the presence of methylxanthines (competitive inhibition)
and decreased if dipyridamole (potentiation via blockage of nucleoside
transport) has been administered. (PALS: 0.1 mg/kg; repeat dose 0.2 mg/kg;
maximum dose 12 mg.)
Amiodarone:
Is the most versatile drug in the ACLS algorithms. It has the properties of all four classes
of antiarrhythmics (lengthening of action potential, sodium channel blockade at high
frequencies of stimulation, noncompetitive antisynaptic actions, and negative chro-
notropism). Because of its high efficacy and low incidence of incidence of pro-
dysrrhythmias effects, it is the preferred anti-dysryhtmias for patients with severely
impaired cardiac function. The dose for the treatment of unstable VT or VF is 300 mg
diluted in 20 to 30 mL of saline or 5% dextrose in water (D5\V) and administered
rapidly. For the treatment of more stable disorders, the dose is 150 mg administered
over 10 minutes, followed by an infusion of 1 mg/minute for 6 hours and then 0.5
mg/minute. The maximum daily dose is 2 g. immediate side effects can be bradycardia
and hypotension. With chronic use, hypothyroidism, elevation of hepatic enzymes,
alveolar pneumonitis, and pulmonary fibrosis may occur. (PALS: loading dose, 5 mg/kg;
maximum dose, 15 mg/kg/day.) Amiodarone is indicated in the following
dysrrhythmias situations.
1. Unstable VT (evidence class IIb).
2. VF after failed electrical defibrillation and epinephrine treatment (class IIb).
3. Rate control during stable monomorphic VT, polymorphic VT (class IIb), or AT
(class IIa).
4. Ventricular rate control of rapid atrial arrhythmias when digitalis is ineffective -
(class IIb) or when the tachycardia is secondary to accessory pathways (class
IIb).
5. Adjunct to electrical cardioversion of refractory PSVTs (class IIa) or atria]
tachycardia (class IN.
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Atropine is useful in the treatment of hemodynamically:
Significant bradycardia (evidence class I) or AN block occurring at the nodal level
(evidence class IIa). It increases the rate of sinus node discharge and enhances A-V node
conduction by its vagolytic activity. The dose of atropine for bradycardia or A-V block is
0.5 mg repeated every 3 to 5 min to a total dose of 0.04 mg/kg. For asystole, atropine is
given as a 1-mg bolus repeated in 3 to 5 minutes if needed. Full vagal blockade is ob-
tained at a cumulative dose of 2.4 to 3 mg, (PALS: 0.02 mg/kg; minimum dose, 0.1 mg;
maximum single dose, 0.5 mg in child, 1.0 mg in adolescent.)
-Adrenergic blocking drugs:

(Atenolol, metaprolol, and Propranolol) have established utility (evidence class I) for
patients with unstable angina or myocardial infarction. These drugs reduce the rates of
recurrent ischemia, nonfatal reinfarction, and postinfarction VF. In contrast to calcium
channel blockers, O-blockers are not direct negative ionotropes. Esmolol, in addition to
other 8-blockers, is useful for the acute treatment of PSVT, AF, atria] flutter (evidence
class I), and ectopic atrial tachycardia (evidence class IIb). Initial and subsequent IV
doses, if tolerated, are as follows: atenolol, 5 mg over 5 minutes, repeated once at 10
minutes; metaprolol, three doses of 5 mg every 5 minutes; Propranolol, 0.1 mg/kg
divided into three doses given every 2 to 3 minutes; esmolol, 0.5 rig/kg over I minute
followed by an infusion starting at 50 mg/minute and titrated as needed up to 200
mg/minute. Contraindications include second- or third-degree heart block, hypotension,
and severe congestive heart failure. Atenolol and metaprolol, because of their relatively
specific 81-adrenergic blockade, are preferable to Propranolol in patients with a history
of reactive airway disease. A small number of patients will exhibit bronchospasm with
the administration of any beta-blocker. Most patients with chronic obstructive
pulmonary disease, however, are able to tolerate beta -blockers.
Calcium is indicated during cardiac arrest:

Only when hyperkalemia, hypermagnesemia, hypocalcemia, or toxicity from calcium
channel blockers is suspected. Calcium chloride, 5 to 10 mg/kg IV, can be repeated as
necessary. (PALS: 20 mg/kg.)
Calcium-channel blockers:
Verapamil and diltiazem slow conduction and increase refractoriness in the A-V node.
They are used to treat hemodynamically stable, narrow complex PSVTs that are
unresponsive to vagal maneuvers or adenosine. They can also be used to control the
rate of ventricular response in AT or atria] flutter. The initial verapamil dose is 2.5 to
5.0 mg IV, with subsequent doses of 5 to 10 mg IV administered every 15 to 30 minutes.
Diltiazem is given as an initial bolus of 0.25 mg/kg. An additional dose of 0.35 mg/kg
and an in fusion of 5 to 15 mg/hour can be administered if needed. Their vasodilator
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and negative inotropic properties can cause hypotension, exacerbation of congestive
heart failure, bradycardia, and enhancement of accessory conduction in patients with
Wolf Parkinson-White syndrome. The hypotension can often be reversed with calcium
chloride, 0.5 to 1.0 g IV.
Dopamine has dopaminergic:

(Evident at doses less than 2 g/kg/minute), -adrenergic (evident at 2 to 5
g/kg/minute), and a-adrenergic (at 5 to 10 g/kg/minute) activities. Although the
above are "traditional" doses, the adrenergic effects can manifest at the lowest dosage
levels. Therefore, the drug should be started at a low dose (e.g., 150 /-tg/minute) and
titrated up until the de sired effect (e.g., increased urine output, increased heart
rate/Inotropy, or increased blood pressure) is seen or un desired side effects (e.g.,
tachyarrhythmia) occur.
Epinephrine:
Continues to be the mainstay of pharmacologic therapy for cardiac arrest, although
there is little evidence that it improves survival. Its a-adrenergic vasoconstriction of
noncerebral and noncoronary vascular beds produces compensatory shunting of blood
toward the brain and the heart. High doses may contribute to myocardial dysfunction
and are not recommended. However, high doses may be indicated in specific situations,
such as beta-blocker or calcium channel blocker overdose. The recommended dose is
1.0 mg IV, repeated every 3 to 5 minutes, or administration as an infusion of I to 4
g/minute: Epinephrine used for symptomatic bradycardia is evidence class Ilb. (PALS:
bradycardia, 0.01 mg/kg; pulseless arrest, 0.01 mg/kg.)
lbutilide:
Is used for the acute conversion of AF or atrial flutter, either alone or with electrical
cardioversion. It prolongs the duration of the action potential and increases the
refractory period. The dose of 1 mg given over 10 minutes can be repeated in 10
minutes. The dose for patients weighing less than 60 kg is 0.01 mg/kg. Continuous
monitoring of the patient is required during its administration and for at least 6 hours
thereafter because the major side effect of ibutilide is polymorphic VT (including
torsade de pointes).
Isoproterenol:
Is a β I -and β2-adrenergic agonist. It is a second-line drug used to treat
hemodynamically significant bradycardia that is unresponsive to atropine and
dobutamine in the event that a temporary pacemaker is not available (evidence class
IIb). Its 82 activity can cause hypotension. Isoproterenol is administered by IV infusion
at 2 to 10 Ag/minute, titrated to achieve the desired heart rate.
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Lidocaine:
May be useful for the control (not prophylaxis) of ventricular ectopics during an acute
myocardial infarction. The initial dose during a cardiac arrest is 1.0 to 1.5 mg/kg IV, and
this may be repeated as a 0.5- to 0.75-mg/kg bolus every 3 to 5 minutes to a total dose
of 3 mg/kg. A continuous infusion of lidocaine at a rate of 2 to 4 mg/minute is instituted
after successful resuscitation. The lidocaine dose should be decreased for patients with
reduced cardiac output, hepatic dysfunction, or advanced age. (PALS: 1 mg/kg; infusion,
20 to 50 E.tg/kg/minute.)
0H
Magnesium:
Is a cofactor in a variety of enzyme reactions, including Na+, K+-ATPase.
Hypomagnesaemia can precipitate refractory VF as well as exacerbate hypokalemia.
Magnesium replacement is effective for the treatment of drug-induced torsade de
pointes. The dose for emergent administration is 1 to 2 g in 10 mL of D5W over 1 to 2
minutes. Hypotension and bradycardia are side effects of rapid administration. (PALS:
25 to 50 mg/kg; maximum dose, 2 g.)
Oxygen:
(100%) should be administered to all cardiac arrest victims whether or not ventilation
requires assistance.
Procainamide:
May be considered in patients with preserved ventricular function. The loading dose is a
continuous infusion of 20 mg/minute that is terminated when the arrhythmia is
suppressed, hypotension occurs, the QRS complex is widened by 50% of its original size,
or a total dose of 17 mg/kg is reached. When the arrhythmia is suppressed, a
maintenance infusion of 1 to 4 mg/minute should be initiated, with a reduced dose
considered in the presence of renal failure. It should be used with caution if at all in
patients with preexisting QI' prolongation or if used in combination with other drugs
that prolong the QT interval. An ECG should be examined for QRS widening at least
daily. (PALS. 15 mg/kg.) It is indicated in the follow situations:
(1) Treatment of stable monomorphic VT (Class IIa).
(2) Ventricular rate control in AF and atria] flutter
(3) Control of the heart rhythm in AF or atrial flutter in patients with known pre-
excitation (WPW) syndrome.
(4) For reentrant, narrow-complex tachycardiac that are unable to be controlled by
adenosine or vagal maneuvers.
Sodium bicarbonate:
Administration is detrimental in most cardiac arrests because it creates a paradoxical
intracellular acidosis (evidence class 1II). It may be considered when the standard ACLS
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protocol has failed in the presence of severe preexisting metabolic acidosis, and it may
assist in the treatment of hyperkalemia or tricyclic antidepressant overdose. The initial
dose of bicarbonate is 1 mEq/kg IV, with subsequent doses of 0.5 mEq/kg given every
10 minutes (as guided by arterial blood pH and partial pressure of carbon dioxide
[Paeo2]). (PALS: 1 mEq/kg.)
Vasopressin:
An anti-diuretic and pressor produced in the neurohypophysis, may be substituted for
either the first or second dose of epinephrine in the treatment of pulseless arrest (40
units IV, class indeterminate). It constricts vascular smooth muscle when used in high
doses. It is more effective than epinephrine in maintaining the coronary perfusion
pressure and has a longer half-life of 10 to 20 minutes.
Open-chest direct cardiac compression:

Is an intervention used at institutions with appropriate resources to manage
penetrating chest trauma, abdominal trauma with cardiac arrest, pericardial
tamponade, hypothermia, or pulmonary embolism. Direct cardiac compressions also are
indicated for individuals with anatomic deformities of the chest that prevent adequate
closed-chest compression.
Termination of CPR:
There are no absolute guidelines to determine when to stop an unsuccessful
resuscitation, but there is a very low probability of survival after 30 minutes. It is at the
discretion of the physician in charge to determine when the failure of the cardiovascular
system to respond to adequately applied basic life support and ACLS indicates that the
patient has died. There should be a meticulous documentation of the resuscitation,
including the reasons for terminating the effort.
The advanced directive "do not resuscitate" (DNR) places the anesthesiologist in a key
position with respect to intraoperative and postoperative care. It should not be assumed
that a DNR order is suspended in the perioperative period. Institution-specific written
guidelines should be reviewed. In advance of a procedure, physicians and the patient
with the DNR status (or the patient's health care proxy) should clarify what
resuscitative measures would be compatible with the patient's wishes-i.e., goal-directed
care. For example, the use of a pressor to control hypotension after induction of general
anesthesia might be permitted while defibrillation and CPR for spontaneous VF might
be prohibited. When asked to perform an emergent intubation outside of the OR, the
anesthesiologist should ask about the patient's code status and is ethically and legally
bound to a known decision to limit treatment.
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Pediatric resuscitation
Basic life support:
The need for CPR in the pediatric age group is rare after the neonatal period. Pediatric
cardiac arrests usually result from hypoxemia linked to respiratory failure or airway ob-
struction. Initial efforts should be directed toward the establishment of a secure airway
and adequate ventilation. The pediatric guidelines apply to infants (1 month after the
perinatal period to I year) and children (I to 8 years of age. For children greater than 8
years old, resuscitation is the same as for adults including the application of the "phone
first" rule. "Phone fast" applies to resuscitation of infants and children before the start
of puberty and to resuscitation of any child with suspected drowning, traumatic arrest,
or drug overdose. The lone rescuer should perform five cycles (about 2 minute) of CPR
before calling help. Exceptions to this rule include situations when the arrest of a child
is witnessed and sudden (e.g., an athlete who collapses on the playing field) or
situations in which a child is known to be at high risk for a sudden arrhythmia.
Modifications of the rate and magnitude of compressions and ventilations, as well as of
the hand position for compressions, are necessary because of anatomic and physiologic
differences (Table 37.2). Differences between pediatric and adult resuscitation
techniques are detailed below.

Maneuvers to establish an airway are the same as in the adult, with a few caveats. For
children less than 1 year of age, abdominal thrusts are not used because the
gastrointestinal tract can be damaged easily. Hyperextension of an infant's neck for the
head tilt/chin lift may lead to airway obstruction because of the small diameter and ease
of compression of the immature airway. Submental compression while performing the
chin lift can also lead to airway obstruction by pushing the tongue into the pharynx.
Ventilations should be given slowly with low airway pressures to avoid gastric
distention and should be of sufficient volume to cause the chest to rise and fall.
Circulation:
The brachial or femoral artery is used for pulse assessment in infants because the
carotid artery is difficult to palpate. In the absence of a pulse, chest compressions
should be initiated at a compression/relaxation ratio of 1:1. These are delivered to
infants by using two fingertips applied to the sternum or by encircling the chest with
both hands and using the thumbs to depress the sternum one fingerbreadth below the
intermammary line. In older children, the correct hand position is determined as for
adults but with only one hand depressing the sternum to about one-third to one-half of
the anterior-posterior depth of the chest. The compression/ventilation ratio is 30:2 for
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one-rescuer CPR of infants and children and 15:2 when two rescuers are available. Ven-
tilations should be given at a rate of 8 to 10 breaths per minute, and chest compressions
should be given at a rate of 100 per minute. If an advanced airway is in place during
two-rescuer CPR, there is no need to synchronize breaths between compressions.
Table 37.2 Adult and pediatric cardiopulmonary resuscitation

Ventilation:
Ventilations / Compressions
Age Compression Depth of Compressions
min /min
Ratio
Neonate Infant 30 90 3:1a,b 1/3 depth of chest
(<1 yr) 12-20 100 30:2a / 15:2b 1/3-1/2 depth of chest
Child 12-20 100 30:2a / 15:2b 1/3-1/2 depth of chest
(1-8 year)
Adult and child > 10 – 12 100 30:2a, b 1.5 - 2 inches
8 year
a One person rescue
b Two person rescue
Pediatric advanced life support:

Most pediatric cardiac arrests present as asystole or bradycardia rather than
ventricular arrhythmias. In infants less than I year old, respiratory and idiopathic
(sudden infant death syndrome) etiologies predominate. Anatomic and physiologic
differences from the adult require defibrillator settings and drug doses to be weight
based. Specific PALS algorithms are illustrated in Figures 37.4 through 37.6.
Intubation:
The endotracheal tube size is based on the patient's age (un-cuffed tube size [mm inner
diameter] = 4 (age/4) for children over 2 years old. Use one half-size smaller for a
cuffed tube). Atropine, epinephrine, lidocaine, or naloxone can be administered via the
endotracheal tube before establishment of IV access.
Defibrillation:
Defibrillator paddles used for infants are 4.5 cm in diameter, and those used for older
children are 8 cm in diameter. For either Monophasic or biphasic devices, the energy
level is 2 J/kg for the initial shock and 4 J/kg, or the lowest level that was previously
successful, for any subsequent shocks. Hypoxemia, acidosis, and hypothermia should be
considered as treatable causes of an arrest if the defibrillation attempts are
unsuccessful. For cardioversion, the starting energy is 0.2 J/kg, with escalation to 1.0
J/kg if needed. The configuration for pediatric paddles varies among defibrillators.
Intravenous access:
Central venous access is preferred, but existing peripheral IVs should be used without
delay. The femoral vein can be used with a catheter of suitable length. The intraosseous
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route may also be used in children. A bone marrow biopsy needle or spinal needle is
inserted into the tibia] shaft away from the epiphyseal plates to gain access to the large
venous sinuses of the bone marrow. If none of the above is available, the endotracheal
tube may be used to deliver essential medications if they are diluted in 2 to 5 mL of
normal saline to ensure their delivery to the pulmonary vasculature.
Medications:
Most of the drugs described in the adult ACLS section (III.B.6) apply to PALS with doses
adjusted to the child's weight.
Neonatal resuscitation:
The neonatal period extends through the first 28 days of life. Someone who is skilled in
resuscitation of newborns should be present at every delivery. Resuscitation is divided
into four phases: stimulation and suctioning, ventilation, chest compressions, and
delivery of resuscitation drugs and fluids. Resuscitation is often needed during an
emergent cesarean section for fetal distress. In the event that the anesthesiologist is the
only one available to treat the newborn, the neonatal warmer should be brought to the
head of the OR table to facilitate the treatment and monitoring of the mother and child
until the pediatrician arrives.
Assessment:
Immediate neonatal resuscitation is crucial, because profound hypoxemia occurs
rapidly and will be exacerbated by respiratory acidosis, which contributes to the
persistence of fetal circulation and right-to-left shunting. A neonate who requires
resuscitation will likely have a significant right-to-left shunt.
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1. The Apgar score is an objective assessment of the physiologic well-being of the
child and is done 1 and 5 minutes after birth (Table 28.2).
2. An Apgar score of 0 to 2 mandates immediate CPR. Neonates with scores of 3 to 4

will need bag and mask ventilation and may require more extensive resuscitation.
Supplemental oxygen and stimulation are normally sufficient for newborns with
Apgar scores of 5 to 7. Respiratory activity should be evaluated by watching chest
excursions and by auscultation. The heart rate is assessed by auscultation or by
palpation of the umbilical pulse.
Four phases of newborn resuscitation:

Each step is allotted approximately 30 seconds, including reevaluation after the step is
completed. The decision whether to proceed to the next step is determined by
assessment of three vital signs: respiration, heart rate, and color (Fig. 37.7).
Stimulation and suctioning:

The cold-intolerant neonate should be dried thoroughly after birth and placed in a pre-
warmed environment to minimize heat loss and the exacerbation of acidosis. Placement
in the lateral Trendelenberg position with the head in a "sniffing" position to open the
airway will assist with the drainage of secretions. The mouth and nose should be
suctioned with a bulb syringe to remove blood, mucus, and meconium. Suctioning
should be limited to 10 seconds, with oxygen supplied between attempts. During
suctioning, the heart rate should be monitored, because bradycardia cart occur from
hypoxemia or from vagal reflexes to pharyngeal stimulation. Drying and suctioning
usually provide adequate respiratory stimulation. Additional measures include gently
rubbing the newborn's back and slapping the soles of the feet. For infants born to moth-
ers with meconium staining of amniotic fluid, the airway is traditionally suctioned by
the obstetrician after delivery of the head but before delivery of the thorax (intrapartum
suctioning). Routine intrapartum suctioning has not been shown to be effective at
decreasing the risk of aspiration syndrome and is no longer advised (class I). Intubation
for suctioning does not offer any benefit for the infant who is vigorous with strong
respiratory efforts, good muscle tone, and a heart rate >100 beats per minute (class 1).
Endotracheal suctioning should be performed immediately after birth for infants with
meconium and repeated until the trachea is clear. Each period of suctioning is kept brief
to avoid bradycardia.
Ventilation:
After the initial steps of stimulation and stabilization, babies who are breathing and
have a heart rate greater than 100 beats per minute but exhibit central cyanosis (de-
termined by examining the face, trunk, and mucous membranes) should be
administered supplemental free-flow oxygen. Acrocyanosis (blue color of the hands and
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feet alone) is usually normal and is not a reliable indicator of hypoxemia. Positive
pressure ventilation with 100% oxygen is used for apnea, cyanosis, and heart rates
below 100 beats per minute. Bag and mask ventilation should be attempted initially.
The initial breath may require airway pressures as
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high as 30- to 40-cm l-I2Oheld for 2 seconds to permit adequate lung expansion. All
breaths should be at the lowest pressure possible (while ensuring adequate chest
expansion) to prevent gastric distention that may lead to further respiratory
compromise. Assisted ventilation is continued until there are adequate spontaneous
breaths and a heart rate greater than 100 beats per minute. Endotracheal intubation is
used when mask ventilation is ineffective, tracheal suctioning is needed (e.g., meconium
aspiration), or prolonged Ventilatory assistance is anticipated.
Chest compressions:
For initial heart rates less than 100 beats per minute, the heart rate is reassessed after
adequate ventilation with 100% oxygen has been performed for 30 seconds. If the heart
rate is less than 60 beats per minute, chest compressions are required in addition to
continued assisted ventilation. They should be delivered on the lower third of the
sternum, and the chest should be compressed approximately one-third of its anterior-
posterior depth. Compressions and ventilations should be coordinated to avoid
simultaneous delivery and delivered at a 3:1 ratio, with 90 compressions and 30
breaths to achieve approximately 120-events per minute. The compressions are
stopped about every 30 seconds to reassess respirations, heart rate, and color and
should continue until the spontaneous heart rate is greater than 60 beats per minute.
Delivery of resuscitation drugs and fluids:

Resuscitation drugs should be administered when the heart rate remains below 60
beats per minute despite adequate ventilation with 100% oxygen and chest
compressions. The umbilical vein, the largest and thinnest of the three umbilical vessels,
provides the best vascular access for resuscitation of the newborn. It is cannulated with
a 3.5- to 5.0-French umbilical catheter after the umbilical cord stump has been prepped
with an antiseptic and trimmed. Sterile umbilical tape placed at the base of the cord will
prevent bleeding. "The catheter should be placed below the skin level with blood
aspirated freely, and care must be taken not to permit air into the system. If vascular
access is unavailable, the endotracheal tube can be used to administer epinephrine,
atropine, lidocaine, or naloxone. The drugs may be diluted in l to 2 mL of normal saline
to ensure their delivery to the pulmonary vasculature.
Drug and fluid dosages
a. Supplementary oxygen is recommended whenever positive pressure

ventilation is used, and free-flow oxygen should be administered to babies
who are breathing but w have central cyanosis (class indeterminate).
Undiluted oxygen is typically used for assisted ventilation, but some
recent clinical studies have raised new concerns about its potential
adverse effects on respiratory physiology and cerebral circulation. There
is also the concern of potential tissue damage from oxygen free radicals.
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Some clinicians begin resuscitation with an oxygen concentration that is
less than 100%, and the latest recommendations state that it is
"reasonable" to do so.
Epinephrine:
The P-adrenergic effect of epinephrine increases the intrinsic heart rate during neonatal
resuscitation. Epinephrine should be used for asystole and for heart rates less than 60
beats per minute despite adequate oxygenation and chest compressions. The dose is
0.01 to 0.03 mg /kg of a 1:10,000 (1 mg/mL) solution IV While access is being obtained,
a higher dose (up to 0.1 mg/kg) may be administered through the endotracheal tube.
Doses can be repeated every 3 to 5 minutes, as needed.
Naloxone:
Is a specific opiate antagonist used for neonatal respiratory depression secondary to

narcotics administered to the mother. The initial dose is 0.1 mg/kg. The respiratory
status of the child should be monitored for an extended period of time after narcotic
reversal because the duration of action of naloxone is shorter than that of many
narcotics. An acute withdrawal reaction may be precipitated in the child of a narcotic-
addicted mother.
The routine use of sodium bicarbonate is not recommended. The use of bicarbonate
may be considered during prolonged arrests in an attempt to relieve depression of
myocardial function and reduced action of catecholamines induced by marked acidosis.
Intraventricular hemorrhage in premature infants has been associated with the osmolar
load occurring with bicarbonate administration. A neonatal preparation of sodium.
bicarbonate (4.2°10 or 0.5 mEq/mL) should be used to prevent this from occurring. The
initial dose is 1 mEq/kg IV given over 2 minutes. Subsequent doses of 0.5 mEq/kg may
be given every 10 minutes and should be guided by arterial blood pH and Paco2.
Atropine, calcium, and glucose are not recommended for use in neonatal resuscitation
unless specifically indicated.
Fluids. Hypovolemia should be considered in the setting of peripartum hemorrhage or
when hypotension, weak pulses, and persistent pallor are present despite adequate
oxygenation and chest compressions. The fluid of choice for volume expansion in the
delivery room is an isotonic crystalloid rather than albumin (class IIb). The volume
infused should be 10 mL/kg and repeated as necessary. The administration of volume
expanders such as albumin rapidly to premature infants has been associated with
intraventricular hemorrhage.
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Chapter 3 “ANESTHETIC MANAGEMENT OF
HYPERTENSIVE PATIENTS”
HISTORY:
 1700 BC: Description of blood pressure appeared early when Chinese were
aware that “if large amount of salts are taken, the pulse will stiffen or harden”
 1773: Stephen Hales measured blood pressure for the first time. Fredrick
Mahmood incorporated measurement of blood pressure routinely.
INTRODUCTION
An elevated blood pressure is one of the most important public health problems in both
developed and developing countries. Since these patients are generally asymptomatic
they often fail to get medical aid. It is a readily detectable, easily treatable disorder
which leads to lethal complications if neglected.
PREVALENCE
In India prevalence is 10 – 25% in rural and urban population. There is higher
prevalence in non white population and in females after the age of 50 (related to
hormonal change of menopause). The ratio of F:M increases from 0.6 to 0.7 at age 30 to
1.1 to 1.2 at age 65.
DEFINITION
An adult (18 years of age or older) is considered to manifest systemic hypertension
when the systole /diastole blood pressure is 140/90mmHg or more on two separate
occasions measured at least 1-2 weeks apart.
WHITE COAT HYPERTENSION

Individual whose blood pressure is high when measured in the office by a professional
than when done at home or under casual circumstances commonly seen among the
elderly, pregnant and anxious patient’s.
REVERSE WHITE COAT HYPERTENSION

A small proportion of patients especially elderly on treatment may have reverse white
coat hypertension, i.e. normal office, but elevated ambulatory readings.
LABILE HYPERTENSION
Patients with blood pressure readings in the hypertensive range at times and not
always. They are considered to have borderline hypertension.
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PSEUDO HYPERTENSION
Elderly patients having marked sclerotic brachial arteries that are not occluded until
very high pressure are exerted by the balloon. Therefore cuff levels may be
considerably higher than those measured intra arterially.
HYPERTENSIVE EMERGENCY
Blood pressure more than 160/90mmHg with associated end organ damage (like CHF,
arrhythmia, aneurismal rupture) is called hypertensive emergency. They require
immediate IV therapy. BP should be reduced to 25% with in minutes to hours.
HYPERTENSIVE URGERNCIES
Sudden increase in BP more than 169/90mmHg with out any features of end organ
damage. They can be treated by oral Antihypertensives.
HYPERTENSIVE CRISIS
A systolic BP more than 200mmHg and diastolic over 120mmHg.
Classification of blood pressure for adults > 18 years (JNC – Classification)

Systolic pressure mm Diastolic Pressure
Category
Hg mm Hg
Optimal <120 <80
Normal <130 <85
High normal 130 – 139 85 – 89
Hypertension
Stage 1 (mild) 140 – 159 90 – 99
Stage 2 (moderate) 160 – 179 100 – 109
Stage 3 (Severe) 180 – 209 110 – 119
Stage 4 (Very Severe) > 210 > 120
Isolated systolic hypertension > 140 < 90
CLASSIFICATION
 Hypertension can be classified according to th \e its subtype – systolic, diastolic
and pulse pressure.
 Systolic hypertension is a marker of macro vascular disease (large artery
diseases like atherosclerosis) seen in elderly more than 60 years with isolated
systolic hypertension.
 Diastolic hypertension results in micro vascular complication in vessels less than
1 mm size (arteriosclerosis) seen in patients less than 50 years. It is an
important marker of coronary heart disease.
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 Some patients have both systolic and diastolic hypertension categorized as
combined systolic and diastolic hypertension.
ETIOLOGY OF HYPERTENSION
1. Essential hypertension
2. Renal
 Chronic pyelonephritis
 Acute and Chronic GN
 Reno-vascular stenosis or renal infarction
 Rennin producing tumour
3. Endocrine
 Oral contraceptives
 Adrenocortical hyperfunction
Cushing’s disease and syndrome
Primary hyperaldosteronism (Conn’s syndrome)
Congenital or hereditary adrenogenital syndrome
 Pheochromocytoma
 Myxedema
 Acromegaly
 Hyperparathyroidism
4. Neurogenic
 Psychogenic
 Diencephalic syndrome
 Familial dysautonomia (Riley–Day)
 Polyneuritis (acute porphyria lead poison)
 Increased intra cranial pressure
5. Miscellaneous
 Coarctation of aorta
 Increased intravascular volume (excessive transfusion polycythemia vera)
 Polyarteritis nodosa
 Hypercalcemia
 Sudden withdrawal of Antihypertensives
 Obstructive sleep apnea.
6. Unknown etiology
 Toxemia pregnancy
 Acute intermittent porphyria
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MECHANISM OF HYPERTENSION
To provide a frame work of understanding the pathogenesis and treatment option of
hypertensive disorders, it is useful to understand the factors involved in the regulation
of both normal and elevated arterial pressure.
Arterial pressure
Peripheral resistance Cardiac Output
Vascular Vascular Stroke Heart Size of

function Structure Volume Rate Vascular
Compartment
INTRA VASCULAR VOLUME

Vascular volume is a primary determinant of arterial pressure.
INTERSTITIAL SPACE
ECF
VASCULAR SPACE
 Thus alteration in total ECF volume is associated with proportionate change of

blood volume.
 Predominant ion of ECF is sodium. Thus if intake of sodium chloride exceeds the
capacity of kidney to excrete, the vascular volume initially expands and cardiac
output increases.
Many vascular beds (kidney, brain has a capacity to auto regulate blood flow and if
constant blood flow is to be maintained in the face of increased arterial pressure,
resistance within the bed must increase.
Pressure across vascular beds
Blood flow = ……………………………………………
Vascular resistance
GENETIC CONSIDERATION
Hypertension is a polygenic disorder and different patients may carry different subsets
of genes that leads to elevated BP and to different phenotypes associated with
hypertension.
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E.g.: Obesity, dyslipidemia, insulin resistance
AUTONOMIC NERVOUS SYSTEM

 Autonomic nervous system maintains cardiovascular hemostasis. The three
endogenous catecholamines namely epinephrine, nor epinephrine and dopamine
play important role in tonic and phasic cardiovascular regulation.
 They mainly act on adrenergic receptors – alpha 1, alpha 2, beta 1, and beta 2
with varying affinities.
 Alpha receptors are more avidly occupied and activated by NE than by Ep and
the reverse is true for beta receptors.
 Alpha 1 receptors are located in post synaptic cells in the smooth muscle and
elicit vasoconstriction.
 Alpha 2 receptors are located in presynaptic membrane of post ganglionic nerve
terminal that synthesize NE when activated by catecholamines.
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AUTONOMIC NERVOUS SYSTEM
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 Alpha 2 receptors act as a negative feedback by inhibiting further release of NE.
 Different antihypertensive agents either inhibit alpha 1 or act as agonist to alpha
2 receptor and reduce sympathetic outflow.
 Beta 1 receptor stimulates the rate and strength of cardiac contraction and
consequently increase CO.
 Beta 1 receptor stimulation also stimulates rennin release from kidney.
 Another class of anti-hypertensives act by inhibiting beta 1 receptors.
 Activation of beta 2 receptor result in relaxation of vascular smooth muscle and
result in vasodilation.
 Levels of circulating catecholamines may affect the number of adrenoreceptors.
In case of high levels of catecholamines there is down regulation of receptors and
if catecholamine levels are low, there is upregulation of receptors. Example for
this is in case of Pheochromocytoma where the catecholamines concentration is
high and thus there is down regulation of receptors. So when patient assumes an
upright position there is lack of any induced NE vasoconstriction which explains
orthostatic hypertension.
 Chronic administration of agents that block adrenergic receptors may result in
up regulation and the withdrawal of these agents may procedure a condition of
hypersensitivity.
 Once released rennin converts angiotensinogen to angiotensin I Angiotensin I is
to angiotensin II (active octapeptide) by ACE, the same converting enzyme
cleaves a number of other peptides and thereby inactivates the vasodilator
bradykinin.
 Angiotensin 2 releases aldosterone which increases sodium reabsorption via
epithelial sodium channel.
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 Angiotensin 2 play a role in pathogenesis of atherosclerosis, cardiac hypertrophy

and renal failure through a direct cellular action on vessel wall via AT 1 receptor.
And thus treatment with AT 1 blockers prevent end organ damage.
 But AT 2 receptors are beneficial. When activated they cause vasodilation,
sodium excretion and inhibition of cell growth and matrix formation; and they
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improve vascular remodeling. AT I receptor blockade result in increase in AT II
receptor activity and thus gives an additional protection.
 Aldosterone act via mineralocorticoid receptors within the myocardium to
enhance the extracellular matrix and collagen deposition. High circulating
aldosterone levels stimulate cardiac fibrosis and LVH. Drugs like spironolactone
(aldosterone antagonist) prevent aldosterone induced myocardial fibrosis.
VASCULAR MECHANISM
 Vascular radius compliance and elasticity are important determinant of arterial
pressure.
 Resistance to flow varies inversely with fourth power of radius and consequently
small decrease in lumen size significantly increase resistance.
 In hypertensive patients structural, mechanical or functional changes may
reduce lumen diameter of small arteries and arterioles.
 Remodeling refers to geometrical alteration in vessel wall without changing
vessel volume.
 Vascular remodeling results in decreased lumen size and hence contribute to
increased peripheral resistance.
 Lumen diameter is also related to elasticity of the vessel. Vessel with high degree
of elasticity can accommodate an increase of volume with relatively little change
of pressure.
 Hypertensive patients have stiffer arteries and atherosclerotic patients may have
particularly high systolic BP and wide pulse pressure as a consequence of
decreased vascular compliance due to structural change in vascular wall.
PATHOLOGICAL CONSEQUENSE OF HYPERTENSION

HEART:
Heart disease is the most common cause of death in hypertensive patients.
1. LHV
2. Diastolic dysfunction
3. CCF
4. Atherosclerotic coronary artery
5. Cardiac arrhythmias
BRAIN
 Brain infarction (85%)
 Brain hemorrhage
 Impaired cognition in aging population
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 Cerebral blood flow remain unchanged over a wide range of arterial pressure via
autoregulation.
 Cerebral autoregulation curve is shifted to right in patient with chronic arterial
hypertension.
KIDNEY
 Primary renal disease is the most common etiology of secondary hypertension.
Conversely hypertension is a risk factor for renal injury and ESRD.
 Renal risk is more closely related to systolic than diastolic changes.
ANTI HYPERTENSIVE DRUGS
BP = COX PVR
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ANTIHYPERTENSIVE DRUG
 Different types of anti hypertensive agents act at different sites. Because
hypertension is frequently multifactorial in origin it may be difficult to find ideal
drug for a given patient and drug combinations are often used.
 BP = CO x PVR
 All of these drugs act either by decreasing CO or by decreasing peripheral
vascular resistance (PVR).
DIURETICS
 Widely recommended as first line therapy
 Prevent target organ damage
 Inexpensive
 Used as monotherapy or in combination with beta blockers, Ace inhibitors and
ARB (angiogenesis receptor blockers).
 Main MOA of a diuretic is loss of sodium and water thus causing volume
depletion, decrease in plasma volume, ECF volume and CO. Within 6-8 weeks CO
returns to normal, lowered BP now is due to fall in peripheral resistance.
 When diuretics are used there is volume depletion. This will in turn trigger
release of rennin which causes vasoconstriction. So the concurrent use of beta
blocker, ACI, ARB or CCB (calcium channel blockers) oppose diuretic induced
vasoconstriction.
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MECHANISM OF ACTION OF DIURETICS:
Anesthetic consideration:
 Hypokalemia associated with diuretics may lead to cardiac dysrrhythmias.
 Hypovolemia associated with diuretic may exaggerate hypotension during
induction.
BETA BLOCKERS FOR HYPERTENSION

Especially suitable for patients with increased adrenergic drive.
There is an early fall in HR, SV and CO but this does not lead to corresponding fall in BP
because of baroreflex mediated increase in peripheral alpha adrenergic
vasoconstriction, with a rise in systemic vascular resistance. Within a few days beta
blockade of prejunctional receptors occur on the terminal neuron with consequent
inhibition of release of NE, which may explain why the SVR falls to normal. They also
act via adrenergic nerve mediated rennin release from JG cells.
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Anesthetic considerations:
Anesthetic agents that contribute to bradycardia and depressed contractility will
augment the effect of adrenergic agonists.
Combination of vagotonic drugs (narcotics scoline) may cause profound bradycardia so
it may be advisable to first increase heart rate by using atropine or glycopyrrolate.
 Blockers should be continued till the day of surgery in order to have an
antihypertensive effect as well as to prevent rebound hypertension which may occur
due to abrupt withdrawal.
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MECHANISM OF ACTION OF BETA BLOCKERS
 Sympathetic stimuli. E.g. Clonidine in alpha 2 agonist that inhibits sympathetic

outflow result in rebound hypertension with abrupt cessation probably as a
consequence of up regulation of alpha 1 receptors. *
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RENIN – ANGIOTENSIN – ALDOSTERONE MECHANISM
 They contribute to regulation of arterial pressure via the vasoconstrictor
property of angiotensin 2 and the sodium retaining property of aldosterone.
 Most of the rennin is synthesized mainly in JG cells and macula densa. Three
primary stimuli for rennin secretion includes
1. Decrease in sodium chloride transport in the ascending limb of LH.
2. Decrease pressure or stretch with the renal afferent arteriole (baroreceptor
mechanism)
3. Sympathetic nervous system stimulation of rennin secreting cells via beta 1
receptors.
 Conversely rennin secretion is inhibited by increased sodium chloride transport
in ascending limb of loop of Henle, by increase stretch in afferent arteriole and by
beta 1 receptor blockade.
 In addition rennin secretion is influenced by number of humoral factors
including angiotensin 2.
 Angiotensin 2 directly inhibit rennin secretion via angiotensin 2 type 1 receptors.
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MECHANISM OF ACTION OF ACE INHIBITORS
ANGIOTENSIN RECEPTOR ANTAGONIST

Losartan, valsartan, telmisartan: They inhibit binding of angiotensin II to AT-II
receptors.
ALPHA ADRENERGIC BLOCKERS

 Alpha blocker – prazosin, terazocin
 Alpha 1 and alpha 2 receptor blockade – phentolamine and Phenoxybenzamine
 First dose hypotension is a common side effect.
 Especially useful in elderly male with BPH and hypertension.
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DIRECT VASODILATORS
 Veno-dilators – reduces preload.
Nitroglycerin
Isosorbide Di nitrate
 Anterior dilators – reduces After load.
Hydralazine
Minoxidil
 Balanced dilators – reduces both preload and after-load
Sodium nitroprusside. Prazosin
CENTRAL ADRENERGIC INHIBITORS

1. Reserpine
2. Clonidine
3. Methyl dopa
4. Guanabenz
Recent Advances:
Recent advance in treatment of perioperative hypertension. ECLIPS TRIAL 2007.
Which compared clevidipine an IV ultra short acting (~ 1 min) dihydropyridine calcium
channel blocker with nitroglycerine, SNP or nicaridipine in the treatment of
perioperative hypertension found clevidipine to be superior safer alternative over
routinely used antihypertensive agent.
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GUIDELINES FOR SELECTING INITIAL DRUG TREATMENT FOR HYPERTENSION
Class of Drug Compelling Possible Compelling Possible
indications indications contraindications contraindications
Diuretics Heart failure Elderly Diabetes Gout Dyslipidemia
patients systolic
hypertension
-Blockers Angina After Heart failure Asthma and COPD Dyslipidemia
myocardial infarct Pregnancy Heart Block Athletes and
Tachyarrhythmia Diabetes physically active
patients
ACE inhibitors Heart failure Left Pregnancy
ventricular Hyperkalemia
dysfunction after bilateral renal
myocardial infarct artery stenosis
diabetic nephropathy
Calcium Angina Elderly Peripheral Heart bock Congestive heart
antagonists patients systolic vascular failure
hypertension disease
Angiotensin II ACE inhibitor cough Heart failure Pregnancy
antagonists bilateral renal
artery stenosis
hyperkalemia
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MECHANISM OF ACTION OF CALCIUM CHANNEL BLOCKERS
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RECOMMENDED COMBINATIONS IN VARIOUS EMERGENCIES
Disorder Drugs
Acute pulmonary embolism Nitroprusside or fenoldopam in combination with
nitroglycerine and loop diuretics
Acute myocardial infarction Labetalol, esmolol with nitroglycerine
Hypertensive encephalopathy Labetalol, nicardipine or fenoldopam
Acute aortic dissection Labetalol, nicardipine or fenoldopam
Acute aortic dissection Labetalol, nitroprusside with esmolol
Eclampsia Hydralazine, labetalol, nicardipine
Acute renal failure Fenoldopam or nicardipine
PRE-ANESTHETIC EVALUATION:
History:
Good rapport with the patient will allay all fears anxiety and apprehension.
 Risk factors for adverse prognosis of hypertension should be searched for like
 Black race
 Youth
 Male sex
 Smoking
 Diabetes mellitus
 Hypercholesterolemia
 Obesity
Treatment history to be taken to know

o Adequacy of BP control
o Review pharmacology of drug being used and to predict and take measure to
prevent adverse drug interaction.
o History regarding palpitation syncope angina, chest pain, exercise tolerance
dyspnoea due to cardiac failure.
o Symptoms related to underlying disease in secondary hypertension.
On Examination
 Prominent left ventricular impulse.
 Faint murmur of aortic regurgitation
 Presyotolic (Atrial, 4th) heart sound in CVH.
 Protodiastolic (Ventricular 3rd) heart sound or summation gallop rhythm with
pulmonary rales indicates CHF.
 Focal neurological signs indicative of TIA.
 Fundoscopic finding.
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LAB INVESTIGATIONS
Laboratory tests for evaluation of hypertension
BASIC TESTS FOR INITIAL EVALUATION
 Always included
Urine for protein, blood and glucose
Microscopic urinalysis – renal status
Hematocrit
Serum potassium (baseline for treatment with diuretics
mineralocorticoid – induced HTN)
Serum creatinine and / or blood urea nitrogen
Fasting glucose (DM associated with arteriosclerosis and endocrine
disorders.
Total cholesterol
Electrocardiogram echocardiography & CXR
 Usually included depending on cost and other factors
a. Thyroid – stimulating hormone
b. White blood cell count
c. HDL and LDL cholesterol and triglycerides
d. Serum calcium and phosphate
e. Chest x-ray, limited echocardiogram
(Aortic dilation and rib making in coarctation of aorta)
PRE OPERATIVE MANAGEMENT

 Elective surgery should be delayed for patients with severe hypertension
(diastolic Bp > 115 mmHg) or with severe isolated systolic hypertension (systolic
Bp > 200mmHg) until the Bp falls to or below 180 / 110 mmHg. If time permits
Bp should be lowered over 6-8 week to less than 140/90 mmHg. Acute control
within several hours is inadvisable before elective surgery because this practice
may put the cerebral or other circulation at risk for ischemia.
 Current opinion favors continuation of anti hypertensive medications, especially
 blockers up to the time of surgery, acute withdrawal may result in precipitation
of ischemic or myocardial events.
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 ACE inhibitors therapy until the day of surgery might increase the probability of
hypotension at induction, this hypotensive response readily respond to
crystalloid fluid infusion and administration of sympathomimetic drugs such as
ephedrine. In patients considered to be at high risk for intra operative
hypovolemia and subsequent hypotension it is advised to discontinue the drug
24-48 prior to surgery (drug induced impairment of sympathetic nervous
system).
 In patients without rise of cardiac complication of surgery and anesthesia
modest reduction in K+ level (3-3.5 mEq/L) should not prompt postponement of
surgery but patients with more severe K depletion < 2.9 mEq/L should be started
1 week before surgery if renal function is not impaired. In surgical emergencies
K+ may be given at a rate not exceeding 0.5 mEq/Kg of body weight per hour.
Administration should be discontinued during surgery and continue post
operatively depending on serial K+ determination.
 Mild to moderate Hypertension can be resolved prior to administration of
anxiolytic. E.g.: Midazolam.
 Centrally acting drugs like clonidine may cause sedation by itself and act as a
premedication. Clonidine 1-3 g /kg body weight IV or 50 g IV bolus or 5g/kg,
orally 2 hours before surgery.
 A small oral dose of a  adrenergic blocking agent given pre operatively to
untreated asymptomatic, mildly hypertensive patients effectively attenuate
tachycardia with tracheal intubation.
 Hydration of hypertensive patients prior to induction of anesthesia is indicated
because these patients may be vasoconstricted and volume depleted. Adequate
hydration attenuates the fluctuation of Bp often seen during anesthesia.
 Combined regional technique like epidural and light general anesthesia may
effectively block the sensory input from the surgical site and are well tolerated
hemodynamically and contribute to the suppression of excess sympathoadrenal
activity.
 Main anesthetic goal is to minimize wide fluctuation of Bp in response to
anesthetic and surgical stimulus to prevent the following.
o MI from tachycardia or less commonly from either hypertension or
hypotension.
o Cerebral hypoperfusion from hypotension.
o Cerebral hemorrhage and hypertensive or embolic stroke from rupture of
plaques either locally or from the aorta and neck vessels.
o Renal failure & hypoperfusion.
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MONITORING
 Selection of monitors for patients with essential hypertension depends on
complexity of the surgery and pre-operative status of the patient.
 ECG is useful in detecting MI events during sympathetic over activity.
 ECG multiple lead ST analysis is essential because hypertensive patients are at
increased risk of MI regardless of presence or absence of CAD.
 Continuous monitoring of NIBP.
 Pulse oximetry for peripheral blood flow and oxygenation
 ET CO2 to maintain normocarbia.
 In case of renal impairment or any surgeries lasting for more than 2 hours urine
output should be closely monitored by placing an indwelling catheter.
 Invasive monitors like intra arterial catheter, pulmonary arterial catheter are
reserved for extensive surgery or in LV dysfunction.
 Transesophageal echo is used in LVF for adequate IV fluid volume replacement.
PREMEDICATION
 To relieve anxiety and induce sedation
- Assure the patient
- Explain to him about Anesthesia
- Diazepam 10 mg OR lorazepam (2-4 mg) are associated with lesser
increase in plasma CA.
 To provide Hemodynamic Stability

- Clonidine 5 mg / kg orally
 To provide Analgesia
- Premedication with parenteral narcotics will lower the dose required
for IV induction.
- Drugs like morphine can be used as both pre OR intra operatively
because they decrease sympathetic tone.
 To control secretion & prevent reflex bradycardia – glycopyrrolate or Atropine is
used respectively.
 To prevent Nausea & vomiting
Ondansetron
Metoclopramide
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INDUCTION OF ANESTHESIA
 Induction of anesthesia and endotracheal intubation are often a period of
instability for hypertensive patient.
 Regardless of level of pre-operative blood pressure control, many patients with
hypertension display an accentuated hypotensive response to induction of
anesthesia followed by exaggerated hypertensive response to intubation.
 The hypotensive response at induction may reflect the additive circulatory
depressant effect of anesthetic agent and hypertensive agents. Many
antihypertensive agents and general anesthetic are vasodilators, cardiac
depressants or both. In addition many hypertensives are already volume
depleted.
 In tracheal intubation stimulation of tracheal and laryngeal receptors result in
marked increase in the elaboration of sympathetic amines. This sympathetic
stimulation results in tachycardia and increase in Bp. In normotensive patients
the rise is approximately 20 – 25 mmHg. It is much higher in hypertensive
patients. The increase in Bp results from vasoconstriction because of unopposed
stimulation in hypertensive patients taking  blocking drugs.
MEASURES TO BLUNT THIS RESPONSE INCLUDE

 The rising BP and Hr occur about 15 seconds after the start of laryngoscopy and
becomes maximal after 30 to 40 seconds. Thus limiting laryngoscopy to 15
seconds or less can minimize blood pressure elevation.
 Intubation should be performed under deep anesthesia (provided hypotension
can be avoided)
 Depending anesthesia with a potent volatile agent for 5 to 10 minutes.
 Administration of opioid
Fentanyl 2.5 – 5 g/kg
Alfentanyl 15 – 25 g/kg
Remifentanyl 0.5 – 1 g/kg
 Administration of lidocaine 1.5 mg / kg IV
 Using topical airway anesthesia
 Achieving beta adrenergic blockade with esmolol 0.3 to 0.5 mg/kg,
Propranolol 1-3 mg or labetalol 5-20 mg.
INDUCTION AGENT
 Propofol, barbiturates Benzodiazepines and etomidate are equally safe as
inducing agents.
 Ketamine by itself is contraindicated because its sympathetic stimulation can
precipitate marked hypertension.
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MAINTENANCE
 A balanced technique of opioid + nitrous oxide + muscle relaxant is proved to be
ideal. Sometimes this may not be effective in blocking the sensory input from the
surgical field which may result in elevation of BP. In that case higher conc. Of
inhalation agent may be required.
 Potent inhalational agents provide greater control of hypertension but les
stability. Isoflurane, desflurane and sevoflurane possess the advantage of more
peripheral vasodilation and are less cardiac depressant. The combination of
nitrous oxide and low to moderate dose of narcotics and potent inhalation agent
may provide the most stable intraoperative course.
MUSCLE RELAXANT
With possible exception of a large bolus dose of pancuronium any muscle relaxant can
be routinely used. Hypotension following histamine releasing muscle relaxant like
atracurium (large intubating dose) may be exaggerated in hypertensive patients.
INTRA OPERATIVE MANAGEMENT

Objective: overall anesthetic plan of management is to maintain an appropriate stable
Bp range.
 Long standing or poorly controlled hypertension have altered auto regulation of
CBF, higher than normal mean blood pressure may be required to maintain
adequate CBF.
 Arterial Bp should generally be kept within 10-20% of pre-operative level if
marked hypertension is present (>180/120). Preoperative Bp should be
maintained in the high normal range (150 – 140/90-80 mmHg).
INTRAOPERATIVE HYPERTENSION
 Main cause of intraoperative hypertension is because of sympathetic stimulation
due to painful stimuli as a result of inadequate depth of anesthesia.
 Hypertension may also be due to hypoxemia and hypercapnia.
 Before treatment of intraoperative hypertension other causes should be ruled
out.
 Parenteral agents for acute treatment include.
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Agent Dosage Range Onset Duration
Nitroprusside 0.5 – 10 g/kg/min 30-60 1-5 min
Nitroglycerin 0.5-10g/kg/min 1 min 3-5 min
Esmolol 0.5 mg / kg over 1 min ; 1 min 12 – 20 min
50 – 300 g/kg/min
Labetalol 5-20 mg 1-2 min 4-8 h
Propranolol 1-3 mg 1-2 min 4-6 h
Trimethaphan 1-6mg/min 1-3min 10-30 min
Phentolamine 1-5 mg 1-10 min 20-40 mm
Diazoxide 1-3mg/kg slowly 2-10 min 4-6 h
Hydralazine 5-20 mg 5-20 min 4-8 h
Nifedipine 10 mg 5-10 min 4-8 h
Methyldopa 250 – 1000 mg 2-3 h 6- 12 h
Nicardipine 0.25 – 0.5 mg 1-5 min 3-4 h
5.15 mg / h
Enalapril 0.625 – 1.25 mg 6-15 min 4-6 h
Fenoldopam 0.1 – 1.6 mg / kg / min 5 min 5 min
 Nitroprusside remains the most rapid and effective agent for the intraoperative
treatment of moderate to severe hypertension.
 Nitroglycerine may also be used but less effective. But it is effective in treating
and preventing MI.
 Nifedipine can also be used, but reflex tachycardia associated with sublingual
nifedipine has been associated with MI and delayed onset in antihypertensive
action.
 Hydralazine 5mg increments may be titrated to decrease Bp safely with little
chance of excessive reduction. The onset of action is 10 – 15 min with 1-2 hours
duration.
 Labetalol 5-10 mg increments are very useful in controlling hypertension and
tachycardia. Beta blockers can be used after significant rise in BP because these
agents act directly to antagonize the effect catecholamines.
POST OPERATIVE MANAGEMENT

 Post operative hyper/hypo tension should be carefully monitored.
 The cause of post operative hypertension include pain, emergency excitement,
hypoxemia, hypercarbia, reaction to ET tube, full bladder, hypothermia, relative
hypervolemia from intra operative administration of excessive fluid.
 The most common cause of post operative hypertension is incisional pain.
 Depending on the cause of hypertension IV analgesic and anti-hypertensives or
diuretics should be titrated to control hypertension.
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 If both tachycardia and hypertension occurred post operatively calcium channel
blocker such as verapamil, diltiazem or nicardipine and beta blocking agents
such as propranolol, metaprolol, esmolol, labetalol are preferred agents.
 Hypertension resulting from pain can be preventable or attenuated by asking the
surgeon to inject a long lasting local anesthetic along the incision or to perform a
local nerve block.
CONCLUSION
Knowledge of etiology nature of hypertension and medication used to treat these
disease will certainly provide for a safer and better anesthetic care for a larger segment
of population.
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Acute treatment of hypertensive crisis
(Diastolic Pressure > 120mm Hg)
Consult ER or Critical care physician
Examine patient for evidence of end-organ damage
Yes No
Hypertensive emergency Hypertensive Urgency
Admit to Intensive Care Unit
Assess for etiology / Treatment with oral agents

associated conditions Beta –blocker
MI, CHF Eclampsia ACE inhibitor
Thyrotoxicosis Alpha Blocker
Connective tissue / Vasculitis Calcium channel blocker
Acute renal failure / GN Central sympathetic blocker
Drug over dose
Intracranial haemorrhage Observe patient for 2-4 hours
Encephalopathy to ensure BP - < 110 mm Hg
Acute aortic dissection
Treat with parenteral agents Follow-up

Nitroprusside, Nitroglycerine Ensure the patient
Nicardipine, Fenoldopam has follow up with a
Labetalol, Esmolol
primary physician
Enalaprilat
within 48 hours for
Avoid decreasing BP > 25%
in first 2 hours. Goal: Gradually decrease further
diastolic BP to 100-105 mm Hg over management
(6 hours)
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Chapter 4 ANESTHESIA FOR PATIENT WITH MS AND MR
INTRODUCTION
Anesthetic management of surgery in a patient with valvular heart disease (VHD) poses
an unusual challenge to the anesthesiologist, VHD alters the normal functioning of the
heart, but the heart possesses considerable capacity to adapt and compensate for the
abnormal stress imposed upon it. These hemodynamic changes eventually lead to
cardiac muscle dysfunction and CCF.
The role of the anesthesiologist is to protect and preserve the physiologic function.
Successful management of these patients require a clear understanding of the
Pathophysiology and hemodynamic consequences of the individual lesions, so that
anesthetic techniques and drugs can be chosen with a view to maintain optimal cardiac
performance.
Mitral Stenosis
Mitral stenosis is defined as the narrowing of the mitral valve opening, mostly by the
scar formation, which hinder left ventricular filling.
Anatomy
The mitral valve complex, components:
 The mitral atrioventricular orifice
 Valvular annulus
 Leaflets (Valve) / (cusps)
 Chordae tendineae
 Papillary muscles
The anterior and posterior leaflets are separated by anterolateral and posteriomedial
commisures. Two leaflets are attached by about 120 chordae tendineae to two papillary
muscles.
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In normal adults the normal cross sectional area of the mitral valve orifice is 4 to 6 cm 2.
Etiology and pathology:

The predominant cause of mitral stenosis is rheumatic fever (99% of cases). Rheumatic
fever results in four form of fusion of the mitral valve apparatus leading to stenosis:
 Commissural (30%)
 Cuspal (15%)
 Chordal (10%)
 Combined
Rheumatic fever produces varying degree of commissural fusion.
 Small fish mouth type of stenosis
 Marked fusion resulting in button hole valves,
 Thickening and calcification of cusps contributes to varying degree of stenosis
through resultant immobility
 Chordal fibrosis and fusion may restrict valve leaflet movement and reduction in
orifice area
 Chordal calcification with shortening may also create subvalvular stenosis.
In patients with RHD, the mitral valve alone is involved in 65% to 70% of cases (25%
pure MS & 40% combined MS and MR), and mitral and aortic in about 25%
Other causes
 Congenital
 Malignant carcinoid
 Systemic lupus erythematous
 Rheumatoid arthritis
 Mucopolysaccharidoses (Hunter – hurler phenotype)
 Fabry’s disease
 Amyloidosis
 Methysergide therapy
 Atherosclerotic in elderly
 Coxsackie B virus
Simulating Conditions
 Left atrial tumor (atrial myxoma)
 Ball – valve thrombus in LA
 Infective endocarditis with large vegetations
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Pathophysiology
 Characteristics of a normal mitral valve:
 Mitral valve orifice area (MVA) greater than 4.0 cm 2
 Mitral valve flow (MVF) of 150 to 200ml / sec / diastole
Cardiac output
MVF = …….………………………………………….
Diastolic filling period x heart rate
Transvalvular gradient of less than 2mm Hg.

 TVG = Left atrial pressure {LAP} – Left ventricular diastolic pressure {LVDP}
 Normal, LAP = 2 – 10 mm Hg {mean}
 LVDP = 3 – 12mm Hg.
 The relationship between MVA, MVF and Transvalvular gradient can be
expressed by the Gorlin’s equation.
MVF
MVA = ……………………………………….
K Transvalvular gradient
Where K, is a hydraulic constant ; K = 38.
If, we consider a constant MVA, rearrange terms, and eliminate the constant, we have a
more useful expression of clinical variables determining atrial and ventricular pressure
Transvalvular gradient = (MVF)2 ; or
LAP – LVDP = {Cardiac output / diastolic time } 2
Therefore, when cardiac output increases or the diastolic filling period decreases, the
gradient across the MV is altered by the square of the original changes.
Conditions that increase Transvalvular gradient

Cardiac output Diastolic time
Exercise, Emotional stress, Infection, Pregnancy, Tachycardia
Hypervolemia, Hyperthyroidism Atrial fibrillations
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MITRAL STENOSIS
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The combination of mitral valvular disease atrial inflammation lead to
1. Atrial dilation
2. Fibrosis atrial wall
3. Disorganization atrial conduction bundles
Pulmonary. Artery (18-25) = >30

Mean (6 – 10) = >20
Protection against POI Edema
Thickening at capillary basement membrane, collagen deposition, fibrosis
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Mitral valve Stenosis:

Grades MVA
Mild 1.5 – 2.5 cm2
Moderate 1.1 – 1.5 cm2
Severe 0.6 – 1 cm 2
Critical Less than 0.6 cm 2
Abnormal elevated transvalvular pressure gradient is the hemodynamic hall mark of
mitral stenosis.
Pressure Gradient across stenotic Mitral valve:

Grade Gradient
Normal, Moderate, Severe, Critical 2mm Hg
Mild 2-6 mm Hg
Moderate 6 – 12mm Hg
Severe More than 12
Although elevation is a mechanism to maintain normal cardiac output, elevated left
atrial pressure, in turn raises pulmonary venous and capillary pressure and may
actually decrease left ventricular filling volume and pressure, thus producing
hemodynamic abnormalities both proximal and distal to stenosis.
Hemodynamic alterations in rest and exercise

Mild Moderate Severe
Grade
Rest Exercise Rest Exercise Rest Exercise
LAP N     
PAP N  N/   
CO N  N  N/ 
Any condition that elevates transvalvular gradient worsens hemodynamic and can
precipitate symptoms
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History
(DISEASE PROGRESSION)
Pressure volume loop in mitral stenosis.
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Distal: Distal to obstructed MV, the LV is not subjected to either pressure or volume
overload. LVDP is essentially normal and LVEDV is within normal range in most
patients.
Indices of overall systolic function indicate that systolic function is compromised in up
to 25% of patients most likely resulting from chronic reduction in preload.
The hemodynamic response to mitral obstruction ranges from a normal CO and high
transvalvular gradient (moderate MS) to a marked reduced CO and low transvalvular
gradient (severe MS)
Proximal: Left atrial function gradually changes as a disease progress. As the
stenosis become more severe, the left atrial pressure progressively increases. This
increase pressure is reflected into pulmonary circulation, where it elevates pulmonary
venous pressure and cause perivascular edema. This will leads to decrease lung
compliance and increase work of breathing. The combination of mitral valve disease
and atrial inflammation secondary to rheumatic carditis cause left atrial dilation and
disorganization of atrial muscle bundles. This leads to disparate conduction velocities
and in homogenous refractory period, eventually precipitating atrial fibrillation.
Thrombi may form in the enlarged left atrial appendage, these emboli transmitted to
brain, liver, spleen. Kidney and extremities.
Pulmonary Hypertension results from: Passive backward transmission of the elevated
left atrial pressure.
Pulmonary arteriolar constriction, triggered by left atrial and pulmonary venous
hypertension. {reactive pulmonary hypertension}
Organic obliterative changes in pulmonary vascular bed due to chronically elevated
pressures. (Hypertrophy of pulmonary artery muscular layer as a result of ed
pressure).
In time severe pulmonary hypertension results in right sided heart failure, with dilation
of right ventricle and its annulus and secondary tricuspid and sometime pulmonary
regurgitation.
Clinical Assessment:
History
Ms is characterized by slow progressive course there is a long a symptomatic period of
10 to 30 years following initial attack of rheumatic fever until the development of class
1 to 11 symptoms.
Patient initially may present with auscultatory signs of mitral stenosis. The onset of
atrial fibrillation can cause abrupt deterioration. Disabling symptoms occur in the late
stage of disease.
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In tropical climates disease tends to progress more rapidly and frequently causing
severe symptoms in patients less than the age of 20 years.
Symptoms:
Dyspnea: The principle symptom of MS is exertional dyspnea, largely the results of
reduced pulmonary compliance.
NEW YORK HEART ASSOCIATION

 Class 1 -No symptom with ordinary physical activity.
 Class 2 -Symptoms with ordinary activity, slight limitation of physical activity,
comfortable at rest.
 Class 3 -Symptoms with less than ordinary activity. Marked limitation of activity,
and comfortable at rest.
 Class 4 -Symptoms with any physical activity or even at rest.
Cough
Wheeze
Orthopnea and PND – last stage
Frank pulmonary edema. The latter may precipitated by any condition that increases
flow across the stenotic mitral valve.
Hemoptysis: This may be due to rupture of thin walled bronchial veins usually as a
consequence of sudden rise in LAP.
Chest Pain
Palpitation
Systemic embolism; This may be first symptom and may occur even before
development of dyspnea. Symptom depends on vessel involved:
Altered consciousness (cerebral vessels)
Myocardial ischemia and angina pectoris (coronary)
Systemic hypertension (renal)
Pulmonary infection
Fatigue
Abdominal discomfort due to hepatic congestion
Edema
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Other symptoms:
Ortners syndrome: compression of the left recurrent laryngeal nerve by greatly dilated
left atrium, enlarged tracheobronchial lymph nodes, and a dilated pulmonary artery
may cause hoarseness of voice. A history of one or more attacks of acute Rheumatic
fever can be elicited in 30% of adult pt. The diagnosis of ARF is made by applying the
modified Jones Criteria.
Major criteria Minor criteria Laboratory Essential criteria

Carditis Fever Acute phase reactants Increase in ASO titer,
Arthritis Arthralgia leukocytosis raised positive throat culture for
Subcutaneous Previous h/o ESR, C-reactive streptococcal infection,
Nodules rheumatic protein Recent h/o scarlet fever.
Erythema fever
marginatum
Chorea
Two major or one major and two minor criteria, in the presence of essential criteria, is
required to diagnose Acute Rheumatic fever.
Mild Moderate Severe
Dyspnoea Dyspnoea Dyspnoea
Fatigue Cough Leg Edema
Cough + Hemoptysis Rt. Hypochondriac Pain
Orthopnea Ascites
Syncope
Cough chest infection
Physical examination
 Mitral facies: Characterized by pinkish – purple patches on cheeks. These are
seen in patients with severe MS producing low cardiac output, and systemic
vasoconstriction.
 Pulse: Normal or low volume
 Bp – narrow pulse pressure
– Jugular venous pulse
Prominent a wave = pulmonary hypertension
Rapid deep y descent – tricuspid regurgitation
Absent a wave = atrial fibrillation
 Inspection and Palpation:
apex beat = normal in isolated MS, it may be shifted in Rt. Ventricular hypertrophy.
Tapping apex beat = pliable mitral valve leaflet.
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Diastolic thrill
Loud P2 in second left ICS = Pulmonary hypertension
Parasternal Heave = pulmonary hypertension.
Auscultation
Mild to moderate MS
Accentuated S1
Opening Snap (OS)
Diastolic murmur: Low pitched, rough, rumbling, diastolic murmur, starts

immediately after OS, the murmur is brief (early diastolic) and resumes in presystole
(presystolic accentuation). Murmur is best heard at the apex, bell of the stethoscope
and with the patient in the left lateral position. On expiration.
Severe MS:
Short A2 – OS interval
Increased length of mid diastolic murmur.
Severe MS with pulmonary hypertension

Accentuated P2
Systolic murmur of TR
Graham steel murmur of PR
S4 originating from right ventricle
MS, rigid valve No. S1 accentuation, Absent OS.
Signs of Right heart failure

Hepatomegaly, raised JVP, Ascites, Ankle edema, Pleural effusion (right side)
Signs of atrial fibrillation

Ventricular rate (heart rate) more than 100 – 150 / min.
Irregularly irregular pulse with pulse deficit more than 10.
Low volume pulse, BP decreased with narrow pulse pressure
Varying intensity S1.
Loss of presystolic accentuation of diastolic murmur.
P2 very loud (Varying intensity)
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Laboratory finding
Electrocardiogram: It is relatively insensitivity for detecting Mild MS, but it show
characteristic changes in moderate to severe obstruction.
 Left atrial enlargement (P mitral)
 Broad 93 mm or more) component of P waves in leads V1 through V2, with a
depth and with of 1mm or more.
 Right ventricular hypertrophy
 Tall (or relatively tall) R wave in lead V1
 R:S ratio more than 1 in lead V1
 Deep S wave in leads 1, avL, and V4 through V6
 RAD of QRS complexes
Asymptomatic - Normal ECG

Mild - P mitrale (LAE)
Moderate - P mitrale with RVH, right axis deviation
Severe - Bilateral atrial enlargement, RVH, right axis Deviation
Atrial fibrillation
Fibrillation waves in leads V1 or V2 of 1 mm or more.
Chest Cardiograph
 Straightening of left heart border
 Prominence of main pulmonary artery
 Dilation of upper lobe pulmonary veins
 Kerley B lines
 Calcification of mitral valves
 Double shadow
 Backward displacement of esophagus by enlarged LA.
 Elevation of left main bronchus.
 Calcification of mitral valve, best seen on fluoroscopy
Echocardiogram: This is the most sensitive and specific non invasive method for
diagnosing and quantifying severity of MS.
 Mitral valve severity
 Mitral valve morphology
 Presence of severity of coexisting mitral regurgitation
 Left atrial size and function
 Pulmonary systolic pressure s
 Left atrial size and function
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 Pulmonary systolic pressures
 Left ventricular size and function
 Right ventricular size and function
 Evaluation for rheumatic involvement of aortic or tricuspid valves.
Cardiac catheterization
Catheterization is indicated to assess hemodynamics, when there is discrepancy
between Doppler derived hemodynamic and clinical status of a symptomatic patient.
Blood examination:
Raised ESR
increasing titers of antistreptolysin O
Anti DNA ase B.
Treatment
American college of cardiology (ACC) and American Heart association (AHA) guidelines
for treatment of patients with mitral Stenosis.
Medical treatment
Prophylaxis of  hemolytic streptococcus:
AHA and WHO recommendation for anti-streptococcal prophylaxis:
 Inj Benzathine Pencilline 1.2 million units IM every 3 weeks
 Tab Pencillin 250 mg BD, Po
 Tab Sulfadiazine 1.0 OD
Guideline recommends lifelong prophylaxis.

 Prophylaxis for ineffective endocarditis
 In symptomatic patients
Restriction of salt intake
Maintenance doses of oral diuretics
Surgical Correction
Anesthetic management:
Pre – operative Evaluation
 Assessment of severity of lesion.
 Recognition of its hemodynamic significance.
 Assessment of left ventricular function
 Assessment of secondary effect on pulmonary, renal and hepatic function
 Assessment of associated major organ system disease.
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 Consideration of drug therapy (Digitalis, Diuretics,  blockers, anticoagulants,
antibiotics).
 Assessment of need for further investigation and treatment.
History:
 Dyspnea, orthopnea and PND – grade severity
 Palpitation (initially paroxysmal later persistent) atrial fibrillation
 Neurological symptoms – thromboembolism.
 A review of medications should evaluate efficacy and exclude serious side effects.
Physical Examination
 S3 Gallop, Pulmonary rales – left heart failure.
Jugular venous distension, Hepato – jugular reflux,
Hepatosplenomegaly, Pedal edema – right heart failure
 Auscultatory findings – confirm valvular dysfunction
 Neurologic deficits – usually secondary to embolic phenomenon should be
documented.
Laboratory Evaluation
Routine investigations:
Cardiologic Radiologic Hematologic Biochemical
Twelve Posterio – anterior Full blood Arterial blood gas Urea,
Leads Chest radiograph count Creatinine, Electrolytes, LFT,
ECG coagulation Blood Glucose.
 Electrographic findings are generally non-specific. A prolonged P-R interval may
suggest digoxin toxicity.
 A chest film is invaluable in assessing left atrial enlargement and pulmonary
vascular congestion.
 Reversal of anticoagulation should be documented with a prothrombine time
and partial thromboplastin time.
 Arterial blood gases should be measured in patients with significant pulmonary
symptoms.
 Liver function tests are useful in assessing hepatic dysfunction caused by passive
hepatic congestion in patients with chronic right sided failure.
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Drugs
Classes and uses of drugs

Classes of drugs Principal uses
Diuretics Preload reduction in heart failure
Beta – blockers Control of ventricular rate in AF
Calcium antagonists Control ventricular rate in AF
Digoxin Increase contractility in heart failure control of ventricular
rate in AF
Coumarin anticoagulants Prevention of atrial thrombus formation in AF
Antiarrythmatic drugs Atrial and Ventricular Tachyarrhythmia
Interaction with anesthesia: discontinuing drugs

There are no interaction between drugs used to treat heart disease and anesthesia of
such severity that the drugs must be stopped before surgery.
Drugs Interaction Solution
Diuretic Hypokalemia leading to Potassium administration
arrhythmias
Beta blockers Extreme bradycardia in Anticholinergic drugs
combination with opioids
Digoxin Hypokalemia leading to Potassium administration
arrhythmias
Coumarin Increased bleeding Fresh frozen plasma
anticoagulants
 It is generally recommended that drugs be continued up to surgery.
 To avoid embarrassing the patient, diuretics are best avoided with sedative
premedication.
 Beta blockers should always be continued.
 No data support discontinuing digoxin in any patient preoperatively,
 It is particularly important to continue digitalis therapy throughout the
perioperative period in patients who are receiving the drug for heart rate
control.
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Anticoagulation management
Access thromboemobolic risk
High ?
Prior h/o embolism ?
Presence of a thrombus ?
Atrial fibrillation ?
A prosthetic mechanical valve ?
Yes No
Stop anticoagulation the day before Stop anticoagulation three days

surgery ; reverse with vitamin K or Prior to surgery
fresh frozen plasma
Initiate intra venous Restart two three days

Heparin postoperatively 12-24 hrs post operatively
Table 20 – 15. Prophylactic regimens for various procedures
For dental, oral, respiratory tract, or esophageal procedures
I. Standard general prophylaxis for patients at risk: Amoxicillin: adults, 2.0 g

(children, 50 mg / kg) given orally 1 h before procedure.
II. Unable to take oral medications: Ampicillin: Adults, 2.0 g (children, 50 mg /
kg) given IM or IV within 30 min before procedure.
III. Amoxicillin / Ampicillin / penicillin allergic patients: Clindamycin: adults,
600mg (children, 20 mg / kg) given orally 1 h before procedure or Cephalexin or
Cefadroxil, adults, 2.0 g (children, 50 mg/kg) orally 1 h before procedure or
Azithromycin or Clarithromycin: adults 500 mg (children, 15 mg / kg) orally 1 h
before procedure.
IV. Amoxicillin / Ampicillin / penicillin allergic patients unable to take oral
medication: Clindamycin: adults, 600mg (children, 20 mg/kg) IV within 30 min
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before procedure or Cefazolin: adults, 1.0 g (children, 25 mg / kg) IM or IV within
30 min before procedure.
For genitourinary / gastrointestinal procedures

I. High risk patients: Ampicillin plus gentamicin: Ampicillin (adults, 2.0 g:
children, 50 mg / kg) plus gentamicin 1.5 mg / kg (for both adults and children.
Not to exceed 120mg) IM or IV within 30 min before starting procedure; 6 h
later, ampicillin (adults, 1.0 g ; children, 25 mg / kg) IM or IV, or amoxicillin
(adults 1.0 g, children, 25 mg / kg) orally.
II. High risk patients allergic to Ampicillin / amoxicillin: Vancomycin plus
gentamicin: vancomycin (adults, 1.0 g ; children, 20 mg / kg) IV over 1 -2 hr plus
gentamicin 1.5 mg / kg (for both adults and children, not to exceed 120 mg) IM
or IV: complete injection / infusion within 30 min before starting procedure.
III. Moderate risk patients: Amoxicillin: adults, 2.0 g (children, 50 mg / kg) orally
1 h before procedure or Ampicillin: Adults, 2.0 g (children, 50 mg / kg) IM or IV
within 30 min before starting procedure.
IV. Moderate risk patients allergic to ampicillin / amoxicillin: Vancomycin ;
adults, 1.0 g (children 20 mg / kg) IV over 1-2 h ; complete infusion within 30
min of starting the procedure.
 Antibiotic prophylaxis: The risk of infective endocarditis in patients with
valvular heart disease following bacteremic events is well established.
 Prophylaxis should generally follow the general guidelines recommended by the
American Heart Association (AHA).
Premedication
 Antianxiety: Midazolam is the benzodiazepine most commonly used for
anxiolytic. The usual intra muscular dose is 0.05 to 0.1 mg / kg. it is common to
administer titrated doses of 1.0 to 2.5 mg at a time intravenously. Heavy
premedication, produces significant hypoxemia and oxygen should be
administered.
 Hypoxemia and hypercarbia can aggravate pre-existing pulmonary hypertension.
 Antisialagogue: with less likelihood of increasing heart rate, glycopyrrolate is the
drug of choice.
 Scopolamine can also be used but it is more likely to produce sedation and
amnesia (0.06 mg/ kg).
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Mitral Stenosis – hemodynamic goals:
Preload Maintain, preload, avoid hypovolemia
After load Prevent pulmonary vasoconstriction (hypoxia, hypercarbia)
ionotropes may be required for systemic hypotension.
Contractility RV dysfunction may be a problem with long standing pulmonary
hypertension.
Rate Low end of normal. Avoid tachycardia
Rhythm Maintained
Monitoring
ASA recommended monitors

 Oxygen analyzer
 Pulse oximetry
 End tidal CO2
 ECG
 NIBP, Heart rate, Temperature
Direct intra arterial BP Major surgical procedure where
Central venous pressure Large fluid shifts and in pt with
severe MS.
Pulmonary artery catheters– Poor ventricular function, Left ventricular ejection

fraction less than 40%, Elevated pulmonary vascular pressures. TEE – Long complex
procedures.
CHOICE OF TECHNIQUE:
Patient coming for Non Cardiac Surgery

General Anesthesia
 No data suggest one best technique. Familiarity with all anesthetics and their
physiologic and pharmacologic effects in these patients allow great flexibility in
anesthetic solution.
 Induction
 Preoxygenation is mandatory
 It should be emphasized that anesthetic requirements are extremely variable
and generally are inversely related to ventricle function.
 Inj. Thiopentone 3-5 mg / kg
Inj Propofol 1.5 – 2.5 mg / kg
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Inj. Etomidate 0.3 mg / kg
Inj Midazolam 0.1 – 0.2 mg / kg
Are excellent as sole induction drugs in cardiac patients, agents should be given in small
doses, slowly and in increments. High dose narcotics techniques may be useful when
postoperative mechanical ventilation is planned inj. Midazolam 0.15 mg / kg +
Inj Fentanyl 3- 5 µ / kg.
INTUBATION
Cardio stable non depolarizing muscle relaxants are preferred
Inj. Rocuronium 0.6 – 1.2 mg / kg iv
Inj vecuronium 0.08 – 0.12 mg / kg iv
In an anticipated difficult intubation
Inj. Scoline 1-2 mg / kg IV
Hemodynamic stability during intubation is achieved by ensuring that all drugs have
time to be effective
Hypertensive response to intubation can be attenuated by
Inj lidocaine 1.5 mg / kg (1-2min)
Beta adrenergic blockade: Inj esmolol 0.2 – 0.5 mg / kg
Inj Propranolol 1 -3 mg
Inj labetalol 5 – 20 mg
Topical airway anesthesia
Analgesia
Inj Fentanyl 2 – 3 µ / kg
Inj sufentanyl 0.1 – 0.4 µ / kg
Inj Alfentanyl 5- 10 µ / kg
Inj Remifentanyl 0.25 – 1.0 µ / kg, pr 0.05 – 0.1 µ/ kg / min infusion
Maintenance
Volatile agents may be used all agents have been used safely, nitrous oxide should be
used cautiously, as it acutely increase PVR in some patients.
Muscle relaxants
Pancuronium is avoided (as it generally causes tachycardia)
Vecuronium 0.04 – 0.06 mg / kg.
Controlled ventilation
Maintain normocapnia
Avoid hypoxemia
Fluid: Replacements titrated to maintain CVP > 6mm hg
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Reversal
There is no contraindication for pharmacologic reversal of non depolarizing muscle
relaxants.
Inj neostiogmine 0.05 mg / kg +Inj glycopyrrolate 0.01 mg / kg
Extubation
after attenuating pressor response
Intraoperative complications
Tachycardia controlled by deepening anesthesia with an opioid

Beta blocker: Inj esmolol 0.2 – 0.5 mg / kg
Pulmonary edema
It may occur because of tachycardia associated with lighter plane of anesthesia or
during laryngoscopy and intubation or because of injudicious use of I.V. fluids.
Rx-100% oxygen, head up position, Inj Furosemide 40 -80 mg, Inj Aminophylline, PEEP
is of beneficial if the patient is hemodynamically stable. Inotropic support with
Dobutamine or dopamine may be needed in some patients.
Systemic Embolization
Can occur intraoperatively which should be organized and treated. Post operatively all
peripheral pulses should be felt.
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Atrial fibrillation
Acute hypertension – Inj. Nitroprusside 0.5 – 10 micro gram / kg per min with
monitoring.
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Hypotension – Inj phenylephrine 0.2 mg increments.
Category Recommended Not recommended

Inducing agents Etomidate, Opioids, Ketamine
Benzodiazepines
Maintenance Opioids Potent inhalation agents in
agents high concentrations
Muscle relaxants Succinylcholine, Rocuronium, Pancuronium
Cisatracurium
Hypotension Phenylephrine B-Adrenergic against,
Ephedrine, Epinephrine,
Dopamine, Dobutamine
Right heart failure Reverse pulmonary
vasoconstriction, Dilate
pulmonary. Vasculature
Postoperative management
Plain relief:
epidural analgesia >>>> systemic opioids
bupivacaine 0.25% - 0.0625% + fentanyl 4-5 µg / ml
Regional anesthesia in conjunction with other modalities tailored to each patients need
may prove to offer best outcome for patients. Patients with decreased pulmonary
compliance, increased oxygen cost of breathing, and deteriorating hemodynamics may
require Ventilatory support.
REGIONAL ANESTHESIA
 To maintain blood pressure in the presence of a limited cardiac output, patients
with mitral stenosis normally develop increased systemic vascular resistance.
Hence, very sensitive to the vasodilating effects of spinal and epidural anesthesia.
 The sympathetic blockade from an epidural or spinal anesthesia is characterized
by dilation of systemic arteries and veins and an increase in venous capacitance.
The latter effect, decreases the preload with the former can result in
cardiovascular collapse, this is especially significant in patients in severe stenosis
(relatively fixed cardiac output)
 Bradycardia (unopposed vagal activity) becomes an added factor for sudden
hemodynamic deterioration.
 With careful attention to fluid loading patients with mild to moderate stenosis
can be safely managed with neuraxial blockade.
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EPIDURAL / SPINAL
An epidural anesthesia is preferred, as it causes graded hypotension, body homeostatic
mechanisms can react to fall in blood pressure and there will be time for pharmacologic
correction as well.
 Subarachnoid block is preferably avoided, due to unpredictable fall in blood
pressure and failure of hemostasis mechanisms to react fast enough to
compensate for fall in pressure.
 In severe stenosis, general anesthesia with controlled ventilation is the preferred
technique.
Peripheral nerve block

With appropriate sedation and supplemental oxygen this can be a useful approach.
Minimal mandatory monitoring is essential
Epinephrine in local anesthetic tachycardia
Pregnancy with mitral stenosis

Mitral stenosis is the common valvular disease in pregnant women accounting for 75%
to 90% of the significant cardiac lesion.
Clinical presentation
Previously asymptomatic
Dyspnea
Hemoptysis
Fatigue
Symptoms of right heart failure
Thromboembolism
Physical examination
Accentuated S1
Diastolic murmur
Opening snap
Prestolic accentuation
The physician must be able to recognize subtle differences from findings in normal
pregnancy and suggested pathology.
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Laboratory examination
ECG-LAW, AF, RVH
Echocardiography
Invasive test – rarely indicated
Treatment
Medical management
Restriction of physical intake
Restriction of salt intake
Cautious use of oral diuretics
Beta blocker to reduce heart rate
Aggressive treatment of AF
When sever mitral stenosis is unresponsive to medical therapy valve should be replaced
or repaired by second trimester
Surgical management
PMBV under echocardiograph guidance is preferred
Open heart surgery is well tolerated by the mother but increases the risk of fetal loss.
Obstetric Management
Labor and vaginal delivery are standard in these woman with cesarean reserved for
obstetric indications.
Invasive monitoring with an arterial catheter, CVP, or PA catheter is advisable for
women with severe MS and for those who have symptomatic during pregnancy.
Drug commonly used for epidural labor analgesia:
Bupivacaine 0.125% - 0.0625% + Fentanyl 1-2 g / ml.
Anesthesia for caesarean section
Hemodynamic goals
Regional anesthesia
Epidural anesthesia is an excellent choice; the induced sympathectomy reduces both

preload and after load, relieves pulmonary congestion, and in some cases increases the
forward flow.
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Suggested Schedule:
General Anesthesia
Similar guidelines as for MS with non cardiac surgery are followed. Anesthesia is
preferably maintained with volatile agents (halothane or sevoflurane) to avoid narcotic
induced neonatal depression.
The neonatal resuscitation team should be informed about high doses of narcotic being
used.
Patients with severe MS may need elective postoperative ventilation. Intravenous
opioids and NSAIDs are used for post operative analgesia. Postoperative care should
occur in an ICU because the risk of major morbidity and mortality is greatest in
postpartum period.
Mitral Stenosis: Anesthetic Management in Labor

Oxygen administration, left lateral position
Antibiotic prophylaxis
Fluid restriction (with monitoring to maintain preload)
Slow heart rate
-blockade, analgesia, phenylephrine (not ephedrine) for hypotension
Prevention / treatment of a trial fibrillation
Digoxin, Verapamil, --blockade
DC Cardioversion
Monitoring
ECG, Pulse oximetry
Pulmonary artery catheter filling pressure high, follow trends
Peripheral arterial line
Regional analgesia
Epidural or CSE, avoid abrupt SVR
Dose in Second stage, elective forceps delivery likely
Cesarean section
Epidural probably preferred
Maintain filling pressures
Post partum high risk period
First 1-2 hours critical
Possible use of epidural postoperative / postpartum
* CSE = Combined spinal epidural technique.
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Emergency:
Decision immediate threat to the life of woman / fetus delivery interval should be < 30
min.
 Grade 1 mitral stenosis – Lumbar subarachnoid Block.
 Grade 2 & 3 mitral stenosis segmental epidural
 Grade 4 green hill technique – infiltration block following delivery of the baby,
TIVA.
 Urgent: Maternal / fetal compromise which in not immediately life threatening
baby should be delivered within 2 hrs.
 Grade 1 mitral stenosis – Lumbar subarachnoid Block
 Grade 2, 3 & 4 mitral stenosis selective segmental epidural
 Scheduled: Needing early delivery but no maternal / fetal compromise
 Grade 1 mitral stenosis – lumbar subarachnoid block
 Grade 2, 3 & 4 mitral stenosis selective segmental epidural with post op
analgesia
 Elective: at a time of suit the woman and maternity team.
 Grade 2, 3 & 4 mitral stenosis selective segmental epidural
 Scheduled: Needing early delivery but no maternal / fetal compromise
 Grade 2, 3 & 4 mitral stenosis selective segmental epidural with post op
analgesia.
 Elective: At a time of suit the woman and maternity team.
 Grade 1 mitral stenosis – Lumbar subarachnoid Block.
 Grade 2, 3 & 4 mitral stenosis Selective segmental epidural with post op
analgesia – Patient controlled Analgesia with EPIDURAL drug delivering systems.
Patient coming for Cardiac surgery:
Percutaneous Balloon Valvuloplasty
Indication
 Children, Adolescents, Very elderly
 MS after surgical valvotomy
 Pregnant women with MS
Criteria for Valvuloplasty

Significant symptom
Isolated MS
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No (or trivial) MR
Mobile, non calcified valve
LA free of thrombosis
Contraindication
 Severe MR / AR
 Thrombosis in Left atrium
 Stenotic prosthetic valves
 Dense calcification of valve
Procedure
 Consists of advancing a small balloon floatation catheter across the interatrial
septum, Enlarging the opening, then advancing a large (23 – 25 mm) Hour glass
shaped balloon and inflating it within the orifice. Alternatively, two smaller (15 –
20mm) side by side balloons across the mitral orifice may be employed, a third
technique involve retrograde, non-trans septal dilation of the mitral valve using a
steerable guide wire.
 Procedure is performed under light sedation, so anesthesiologist has a limited
role
 If patient suddenly develops acute MR (serious complication of BMV) and
necessitates MVR.
 Emergency BMV performed on very sick patient (valve area less than 0.6 cm 2).
These patients are in pulmonary edema needing Ventilatory support.
Advantages
 Percutaneous approach
 LA / Sedation
 Good hemodynamic results
 Good long term outcome
Disadvantages
 No direct visualization of valve
CLOSED MITRAL VALVOTOMY / OMV / MVR
Closed mitral valvotomy
Indication
 Pure isolated MS, without calcification
 Mitral stenosis with pulmonary Hypertension or AF
 Mitral stenosis with pregnancy, early 11nd trimester, as first time surgery.
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 Emergency CMV, if signs of early CCF.
 It is performed through an incision in the side of the chest (a anterior lateral
thoracotomy). The surgeon places a finger inside the left atrium. Using this
finger as guide, then passes an instrument called a Tubb’s dilator into the left
ventricle through a small opening in its wall, and then across the orifice of the
mitral valve. When the Tubb’s dilator is opened by pressing on a handle, its
blades widen, and tear or split open the narrow mitral valve, thus relieving
mitral stenosis.
 The operation has its limitations. It cannot be used when the valve is calcified,
when there is a blood clot in the left atrium or in very severe disease where the
mitral valve is badly scarred and distorted. But in developing nations like India,
the operation is still the one of first choice for mitral stenosis.
Position – right semi lateral / thoracotomy
INTRA OPERATIVE PRECAUTION:

 Deflation of lung while opening pleura
 During valvotomy 100% oxygenation
 Valvotomy time not more than 3 beats / 3 stroke volume
 Monitor bradycardia, arrest during handling of heart.
 Avoid hypoxia, hypercarbia and hypotension, avoid excessive tachycardia,
bradycardia, arrhythmias.
 Assess blood loss
 Full expansion of lungs before closure, to prevent atelectasis compress carotids
with fingers or innominate at the base of aorta to prevent emboli going into brain
if AF suspected
 Should check all peripheral pulsation, level of consciousness, urine output. Drain
into thorax, connected to underwater seal, oxygen via (venturi mask).
 Post operative complication: Hypotension, Arrhythmias, Oliguria, Pulmonary
edema, Embolism, MR.
Open mitral commissurotomy and replacement

 Indicated in patients of NYHA functional class 111 or 1v with moderate or severe
mitral stenosis, if percutaneous mitral balloon valvoplasty not available.
 Significant calcification, fibrosis and subvalvular fusion will require mitral valve
replacement then repair.
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ANESTHETIC MANAGEMENT
Current drug therapy is usually continued until the time of surgery
Premedication:
Benzodiazepine (diazepam 0.05 – 01. mg / kg or lorazepam 0.05 – 0.07 mg / kg orally
night before surgery, 0
MORPHINE 0.2 – 0.3 mg / kg IM 1-2 hrs before
Promethazine 25 mg surgery
With scopolamine 0.006 mg / kg.
Anesthesia of choice:
Surgery is done with the help of Cardio pulmonary bypass, General anesthesia with ET
intubation is obvious choice, and epidural for post operative analgesia.
Induction
If post operative ventilation is anticipated
Narcotic
Opioids may be favored
Inj fentanyl 10 – 50 µg / kg
Inj sufentanyl 10 – 20 µg / kg
Inj Alfentanyl 100 – 300 µg / kg (loading dose)
25 – 150 µg / kg (maintenance dose)
Inj. Remifentanyl 1.0 µg / kg (loading dose)
0.5 – 2.0 µg / kg (maintenance)
Recent anesthetic technique – permitting early extubation (fast tracking)
Inj Thiopentone 3.5 mg / kg
Inj. Propofol 1.5 – 2.5 mg / kg
Inj. Etomidate 0.3 mg / kg
Inj. Midazolam 0.1 – 0.2 mg / kg
Are excellent as sole induction drugs in cardiac patients, agents should be given in small
doses, slowly and in increments.
Muscle relaxation:
Cardio stable non depolarizing muscle relaxants are preferred.
Inj Rocuronium 0.6 – 1.2 mg / kg iv
Inj vecuronium 0.08 – 0.12 mg / kg iv
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Inj Rocuronium 0.6 – 1.2 mg / kg IV
Inj vecuronium 0.08 – 0.12 mg / kg IV
Inj. Scoline 1-2 mg / kg IV
Hemodynamic stability during intubation is achieved by ensuring that all drugs have
time to be effective
Hypertensive response to intubation can be attenuated by
Inj. Lidocaine 1.5 mg / kg (1-2 min)
Intubation is facilitated with pancuronium bromide 0.1 mg / kg. may be useful in
balancing the vagolytic effect of narcotics.
Analgesia
Inj fentanyl 2 – 3 µg / kg
Inj sufentanil 0.5 – 2 µg / kg
Inj Alfentanil 5- 10 µg / kg
Inj Remifentanyl 0.25 – 1.0 µg / kg, 0r 0.05 – 2.0 µg / kg / min infusion.
Maintenances
Can be accomplished with N2O and an inhalation agent such as Halothane or Isoflurane.
With increments of narcotic agent and controlled ventilation patient with MS has low
CO and gets easily depressed during intracardiac manipulation of heart – so severe
decrease in BP and HR during the procedure are common – 100% oxygen and use of
ionotropes and atropine may be necessary.
Following replacement, the chronically under filled, under worked LV may be unable to
handle the new work load. Inotropic support is usually required, post operative elective
ventilation should be done, post operative epidural administration of opioids may be
alternative to IV opioids. NSAIDS may play an increasing role in management of post
operative pain.
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Approach Advantages Disadvantages

Closed surgical Inexpensive, Relatively No direct visualization of
valvotomy simple, good valve, only feasible with
hemodynamic results in flexible, non calcified valves,
selected patients. Good contraindicated if MR>2+,
long term outcome. Surgical procedure with
general anesthesia
Open Surgical valvotomy Visualization of valve Best results with flexible, non
allows direct valvotomy, calcified valves, surgical
concurrent annuloplasty procedures with general
for MR is feasible anesthesia.
Valve replacement Feasible in all patients Surgical procedure with
regardless of extent of general anesthesia, Effect of
valve calcification or loss of annular papillary
severity of MR. muscle continuity on LV
function, prosthetic valve,
chronic anticoagulation.
Balloon mitral Percutaneous approach, No direct visualization of
valvotomy Local anesthesia, good valve, only feasible with
hemodynamic results in flexible, non calcified valves,
selected patients, good contraindicated if MR >2+.
long term outcome
Mitral regurgitation
Mitral regurgitation is sometimes called mitral insufficiency or mitral incompetence. In
mitral regurgitation the valve does not close properly. This causes blood to leak back
(regurgitate) into the left atrium when the left ventricle contracts. Basically, the more
‘open’ the valve remains, the more blood ‘regurgitates’, the more severe the problem.
Causes
 Acute rheumatic heart disease remains a significant consideration in those with
mitral regurgitation who are younger than 40 years.
 MVP (i.e. myxomatous degeneration is usually a slow process, with a major
complication being the rupture of the chordae tendineae. (Acute regurgitation,
as mentioned earlier, can be caused by chordae tendineae rupture or papillary
muscle dysfunction).
 The literature now seems to suggest that MVP has become the most common
cause of mitral regurgitation in the adult population.
 In addition, MVP and CAD have become major mechanisms for incompetence of
the mitral valve.
 Ischemia is responsible for 3-25% of mitral regurgitation.
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 The severity of regurgitation is directly proportional to the degree of left
ventricular Hypokinesia.
 Mitral annular calcification can contribute to regurgitation. Impaired
constriction of the annulus results in poor valve closure.
 Left ventricular dilatation and heart failure can produce annular dilation and
poor valve closure resulting in mitral regurgitation.
 Tendineae rupture can be due to endocarditis, myocardial infarction, or trauma.
 Papillary muscle dysfunction usually is increased by infarction.
 Other causes include the following
Ehlers – Danlos syndrome
Marfan’s syndrome
Osteogenesis imperfecta
Systemic lupus erythematous (SLE)
Pathophysiology
Acute phase
Acute mitral regurgitation (as may occur due to the sudden rupture of a chordae
tendineae or papillary muscle) causes a sudden volume overload of both the left atrium
and the left ventricle. The left ventricle develops volume overload because with every
contraction it now has to pump out not only the volume of blood that goes into the aorta
(the forward cardiac output or forward stroke volume), but also the blood that
regurgitates into the left atrium (the regurgitate volume). The combination of the
forward stroke volume and the regurgitate volume is known as the total stroke volume
of the left ventricle.
In the acute setting, the stroke volume of the left ventricle is increased (increased
ejection fraction), but the forward cardiac output is decreased. The mechanism by
which the total stroke volume is increased is known as the Frank – Starling mechanism.
The regurgitant volume causes a volume overload and a pressure overload of the left
atrium. The increased pressures in the left atrium inhibit drainage of blood from the
lungs via the pulmonary veins. This causes pulmonary congestion.
Chronic compensated phase

If the mitral regurgitation develops slowly over months to years or if the acute phase
can be managed with medical therapy, the individual will enter the chronic
compensated phase of the disease. In this phase, the left ventricle develops eccentric
hypertrophy in order to better manage the larger than normal stroke volume. The
eccentric hypertrophy and the increased diastolic volume combine to increase the
stroke volume (to levels well above normal) so that the forward stroke volume (forward
cardiac output) approaches the normal levels.
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In the left atrium, the volume overload causes enlargement of the chamber of the
atrium, allowing the filling pressure in the left atrium to decrease.
This improves the drainage from the pulmonary veins, and signs and symptoms of
pulmonary congestion will decrease.
These changes in the left ventricle and left atrium improve the low forward cardiac
output state and the pulmonary congestion that occur in the acute phase of the disease.
Individuals in the chronic compensated phase may be asymptomatic and have normal
exercise tolerances.
Chronic de-compensated phase

An individual may be in the compensated phase of mitral regurgitation for years, but
will eventually develop left ventricular dysfunction, the hallmark for the chronic
decompensated phase of mitral regurgitation. It is currently unclear what causes an
individual to enter the decompensate phase of this disease. However, the
decompensated phase is characterized by calcium overload within the cardiac
myocytes.
In this phase, the ventricular myocardium is no longer able to contract adequately to
compensate for the volume overload of mitral regurgitation, and the stroke volume of
the left ventricle will decrease. The decreased stroke volume causes a decreased
forward cardiac output and an increase in the end systolic volume. The increased end
systolic volume translates to increased filling pressures of the ventricular and increased
pulmonary venous congestion. The individual may again have symptoms of congestive
heart failure.
The left ventricle begins to dilate during this phase. This causes a dilatation of the
mitral valve annulus, which may worsen the degree of mitral regurgitation. The dilated
left ventricle causes an increase in the wall stress of the cardiac chamber as well.
While the ejection fraction is less in the chronic decompensated phase than in the acute
phase or the chronic compensated phase of mitral regurgitation, it may still be in the
normal range (i.e. > 50 percent), and may not decrease until late in the disease course.
A decreased ejection fraction in an individual with mitral regurgitation and no other
cardiac abnormality should alert the physician that the disease may be in its
decompensated phase.
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Comparison of acute and chronic mitral regurgitation

Acute mitral regurgitation Chronic mitral regurgitation
Electrocardiogram Normal P. mitrale, atrial fibrillation, left
ventricular hypertrophy
Hear size Normal Cardiomegaly, left atrial
enlargement
Systolic murmur Heard at the base, radiates to Heard at the apex, radiates to
the neck, spine, or top of head the axilla
Apical thrill May be absent Present
Jugular venous Present Absent
distension
History
Mitral regurgitation can be tolerated for many years.
 The initial symptoms of dyspnea and fatigue can rapidly progress to orthopnea
and paroxysmal nocturnal dyspnea.
 Patients with angina type pain may have underlying ischemia.
 Atypical chest pain can be associated with MVP syndrome.
 In those with MVP, palpitations and atypical chest pain are the most frequent
complaints. Two thirds of these patients are female, often with an underlying
panic disorder.
 With underlying coronary artery disease (CAD), regurgitation usually is
associated with symptoms of angina pectoris.
 Regurgitation also can develop acutely with myocardial infarction, secondary to
papillary muscle rupture.
 CAD often is accompanied by dyspnea, fatigue, orthopnea, and fluid retention.
Chest pain is usually minimal in these patients.
 When mitral regurgitation is due to left ventricular dilation and altered valve
function, patients often have chronic left sided heart failure. In acute mitrla
regurgitation from sudden disruption of the mitral valve, the symptoms are due
to acute pulmonary edema.
Physical
 The Classic murmur of mitral regurgitation is a high pitched holosystolic
murmur beginning with the first heart sound and extending to the second heart
sound.
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 The intensity usually is constant throughout systolic ejection, often radiating to
the axilla. The harshness of the murmur does not correlate with the magnitude
of the valvular defect.
 Patients with severe disease often have a third heart sound, a consequence of the
increased ventricular filling volume that is ejected into the left ventricle under
higher than normal pressure.
 Patients with MVP often have a mid to late systolic click and a late systolic
murmur. These patients are usually female and often have orthostatic
hypotension.
 Patients with CAD can have the above mentioned murmur any time during
systole, accompanied by an atrial gallop.
 In acute mitral regurgitation, the examination usually is consistent with acute
pulmonary edema and left ventricular failure.
 The heart size usually is normal, but an audible systolic thrill is often present.
 The murmur often is harsh. It may be heard over the back of the neck, vertebra,
and / or sacrum and may radiate to the axilla, back, and left Sternal border.
Imaging Studies
Chest radiography
 The cardiac silhouette often is normal in patients with MVP.
 With chronic mitral regurgitation, left ventricular and left atrial enlargement are
present.
 The left atrium can be large enough that it produces elevation of the left
mainstem bronchus.
 Occasionally, the double density sign can be seen along the right heart border,
which is produced by the shadow of the wall of the dilated left atrium.
 The heart size of patients with CAD can range from normal to significant dilation
of the left ventricle and left atrium.
 Mitral regurgitation presents with acute pulmonary edema and a normal cardiac
silhouette with acute mitral regurgitation that is secondary to a rupture of a
valve apparatus.
Two dimensional echocardiography

 Evidence of posterior motion of valve leaflets during mid-systole is present in
patients with MVP.
 Annular calcifications may be seen in patients with CAD. In addition, evidence of
posterior or inferior wall motion abnormalities may be observed.
 With acute mitral regurgitation, the ruptured chordae tendineae or papillary
muscle, as well as perforated intraventricular septum, can be visualized.
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 The left atrium and ventricle is of normal size.
 Transoesophageal echocardiography provides a better estimate of the severity of
damage.
Other Tests
Electrocardiography
Chronic mitral regurgitation
Atrial fibrillation often is present secondary to a dilated left atrium.
The ECG shows evidence of left ventricular hypertrophy and left atrial enlargement.
CAD: Evidence of inferior and posterior Q waves may be present, indicating prior
infarction.
MVP
Patients most commonly have ST – and T- wave changes, with T-Wave inversions in the
inferior leads.
ECG may reveal an underlying arrhythmia (e.g. Sinus arrhythmia, sinus arrest, atrial
fibrillation, premature ventricular contractions [PVCs]).
Acute mitral regurgitation: ECG may reveal evidence of an acute myocardial infarction,
more commonly inferior or posterior.
Procedures
Cardiac catheterization
Angiography is considered to be the criterion standard in the assessment of the severity
of the disease.
Mitral regurgitation is graded on a scale from 0 (none), 1 (mild), 2 (moderate), 3 (The
severity is based on the opacity of the left atrium.
The regurgitant volume can be calculated based on information from the
catheterization.
In addition, this test will identify those with underlying CAD.
Complications
Patients with acute mitral regurgitation secondary to infarction emergently requiring
valve replacement have a 60 – 80% mortality rate if they present with severe
pulmonary edema.
Major complications from chronic regurgitation include the following:
Severe LV dysfunction
Chronic congestive heart failure
Atrial fibrillation and its complications (e.g., left atrial thrombus with embolization and
stroke)
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Sudden death, ruptured chordae tendineae, and endocarditis remain infrequent
complications of regurgitation secondary to long standing mitral prolapse.
Indications for surgery for chronic mitral regurgitation

Indications for surgery for chronic mitral regurgitation include signs of left ventricular
dysfunction. These include an ejection fraction of less than 60 percent and a left
ventricular and systolic dimension (LVESD) of greater than 45mm.
Symptoms LV EF LVESD
NYHA II – IV > 60 Percent < 45mm
Asymptomatic or symptomatic 50 – 60 percent ≥ 45 mm
Asymptomatic or symptomatic <50 percent or ≥ 45mm
Pulmonary artery systolic pressure ≥ 5- mm Hg
Quantification of mitral regurgitation

The degree of severity of mitral regurgitation can be quantified by the percentage of the
left ventricular stroke volume that regurgitates into the left atrium (the regurgitant
fraction).
Methods that have been used to assess the regurgitant fraction in mitral regurgitation
include echocardiography, cardiac catheterization, fast CT scan, and cardiac MRI.
The echocardiography technique to measure the regurgitant fraction is to determine the
forward flow thought to be mitral valve (from the left atrium to the left ventricle) during
ventricular diastole, and comparing it with the flow out of the left ventricle through the
aortic valve in ventricular systole. This method assumes that the aortic valve does not
suffer from aortic insufficiency. The regurgitant fraction would be described as:
Another way to quantify the degree of mitral regurgitation is to determine the area of
the regurgitant flow at the level of the valve. This is known as the regurgitant orifice
area, ad correlates with the size of the defect in the mitral valve. One particular
echocardiography technique used to measure the orifice area is measurement of the
proximal isovelocity surface area (PISA). The flaw of using PISA to determine the mitral
valve regurgitant orifice area is that it measures the flow at one moment in time in the
cardiac cycle, which may not reflect the average performance of the regurgitant jet.
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Determination of the degree of mitral regurgitation

Degree of mitral regurgitation Regurgitant fraction Regurgitant
Orifice area
Mild mitral regurgitation < 20 percent
Moderate mitral regurgitation 20 – 40 percent
Moderate to severe mitral regurgitation 40 – 60 percent
Severe mitral regurgitation > 60 percent > 0.3 cm2
Treatment
Treatment also includes preventing infection and treating symptoms as they develop,
including.
Vasodilators, usually ACE inhibitors, to help widen blood vessels and help the heart
work better.
Diuretics to treat symptoms of heart failure and reduce the workload on your heart.
Anticoagulants, such as warfarin (Coumadin), to prevent blood clots if you also have a
heart rhythm problem called atrial fibrillation.
Beta blockers, calcium channel blockers, or antiarrhythmics, to control heart rate.
In acute mitral regurgitation secondary to a mechanical defect in the heart (i.e.: rupture
of papillary muscle or chordae tendineae), the treatment of choice is urgent mitral valve
replacement. If the patient is hypotensive prior to the surgical procedure, as intra-
aortic balloon pump may be placed in order to improve perfusion of the organs and to
decrease the degree of mitral regurgitation.
You may need surgery to repair or replace your metal valve if you get symptoms of
heart failure, if the size of your left ventricle pumping increases or if your heart
weakens.
Main anesthetic Goals:

 Avoid sudden bradycardia.
 Avoid sudden increase in systemic vascular resistance
 Avoid drug related myocardial impression.
 Regurgitant flow indicates V wave present on the recording of pulmonary artery
occlusion pressure. Size of V wave should be monitored as it correlates the
magnitude of regurgitation.
Monitoring during anesthesia is most important

 ECG for rate, rhythm and evidence of ischemia
 Arterial blood pressure.
 Blood gas analysis
 Temperature
 Central venous pressure
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 Pulmonary artery catheter is useful to note the change in V wave amplitude.
 Urinary output
Anesthetic management
Goals
Heart rate Maintain HR > 90/min
Avoid Bradycardia
HR kept in normal to elevated range
Preload Augmentation & Maintenance of preload is helpful
Contractile state Maintained
Minimize drug induce myocardial depression
Systemic vascular resistance Avoid sudden in SVR. Avoid alpha adrenergic agents
Pulmonary vascular Avoid in PVR
resistance Avoid hypoxemia, hypercapnia, acidosis
General Anesthesia – Anesthetic Technique of Choice
Induction: Avoid Bradycardia & abrupt changes in SVR

No LV Dysfunction – inj. Thiopentone 3-5 mg / kg
LV Dysfunction – inj. Midazolam 0.2 – 0.3 mg / kg
+ Inj Fentanyl 0.01 mg / kg
Bradycardia that may accompany Scoline 1-2 mg / kg is not desirable
Vecuronium 0.1 mg / kg or Rocuronium 1-2 mg / kg
Maintenance
No LV Dysfunction – NO + Volatile anesthetics
LV Dysfunction – Opioid Anesthetic Fentanyl 1-2 g / kg
Volatile Anesthetics attenuate undesirable increase in BP & SVR associated with surgical
stimulation.
Muscle relaxant– Pancuronium is used as it causes tachycardia. Controlled Ventilation

– Normocapnia, Avoid Hypoxia Intra Operative fluids – Maintenance of Intravascular
volume with prompt replacement of blood loss to maintain cardiac filling volumes
ejection of optimal LV stroke volume.
Reversal
Neostiogmine + Atropine or Glycopyrrolate
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Chapter 5 ANESTHESIA FOR PATIENTS WITH AS AND AR
(NON CARDIAC SURGERIES)
AORTIC STENOSIS
INTRODUCTION
Cardiovascular disease – particularly hypertensive, ischemic, and valvular heart disease
– are the medical illness most frequently encountered in anesthetic practice and a major
cause of perioperative morbidity and mortality. Management of patients with these
diseases continues to challenge the ingenuity and resources of the anesthesiologist.
ANATOMY
1). The aortic and pulmonary valves are called semi-lunar valves because their
cusps are semi-lunar in shape.
2). Each valve has 3 cusps which are attached directly to the vessel wall there being
no fibrous ring. The cusps from small pockets with their mouths directed away from
the ventricular cavity. The free margin of each cusp contains a central fibrous nodule
from each side of which a thin smooth margin (lunule) extends up to the base of the
cusp. These valves are closed during ventricular diastole when each cusp bulges
towards the ventricular cavity.
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CLASSIFICATION
Valvular aortic Subvalvular Supra valvular

stenosis aortic stenosis aortic stenosis
AETIOLOGY
Valvular aortic stenosis
Acquired
 Rheumatic fever
 Fibro-calcify deformity of a bicuspid valve
 SLE
 Infective endocarditis
Congenital
 Unicuspid unicommissural valve
 Three cusped valve with fusion of commisures
 Hypoplastic annulus
 Subvalvular aortic stenosis
 Membranous diaphragm
 Hypertrophic cardiomyopathy
 Supravalvular aortic stenosis
 Hourglass constriction of aorta
 Hypoplasia of aorta
 Fibro membranous lesion of aorta
CLINICAL FEATURES
Symptoms: Patients with rheumatic aortic stenosis may be asymptomatic for 30 – 40
years or more. The onset of any one of the triad of symptoms is an ominous sign and
indicates a life expectancy of less than 5 years.
1. Angina Pectoris: Angina is the initial symptom in 50 -70% of patients with severe
aortic stenosis. Once angina develops the average life expectancy is about 5
years.
2. Syncope: Syncope is the first symptom in 15 – 30% of patients. Once syncope
appears the average life expectancy is 3-4 years.
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3. Congestive heart failure: Once the signs of LVF occur, the average life expectancy
is only 1-2 years (exertional breathlessness, orthopnea, PND, Angina and cough).
Incidence of sudden death > 10%. Longevity increase after valve replacement.
Signs
 Pulses parvus et tardus is a slow rising pulse felt in carotids (delayed carotid
upstroke) due to prolongation of ejection phase. Classic anacortic pulse is seen
in severe aortic stenosis.
 Systolic thrill in carotids.
 Systolic thrill at aortic area radiating to carotids and lower left Sternal border.
 Heaving apical impulse.
Auscultation
The murmur of aortic stenosis is an ejection systolic murmur best heard at the aortic
area, conducted to carotids. It is best heard with the patient sitting up, leaning forwards
and breath held in expiration.
 Soft, short ESM with early peaking suggests mild stenosis.
 Harsh, loud, long ESM with late peaking suggests severe stenosis.
 Early ejection systolic murmur with opening snap.
 Paradoxical split of S2
 S4 at apex indicates LVH
 S3 indicates LV dilation
PATHOPHYSIOLOGY
Normal : Aortic valve area 2.5 – 3.5 cm2
Calculation of Stenosis:
Gorlin’s modification of standard hydraulic formula
(Cardiac output / systolic ejection period) x H.R.
Aortic valve orifice (cm2) = 1 x 44.5 x mean aortic pressure gradient
Where 1 = Aortic orifice constant

44.5 – hydraulic constant Simplified version of Gorlin’s formula
Cardiac output (lt/min)

=
Aortic valve area (cm2) Mean aortic pressure gradient
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Aortic valve area reduction
Normal - 2.6 – 3.5 cm2
Mild - 1.2 – 1.8 cm2
Mod - 0.8 – 1.2 cm2
Significant - 0.6 – 0.8 cm2
Critical - < 0.6 cm2
Left ventricle Aortic pressure gradient

Mild - 12 – 15 mm of Hg
Mod - 25 – 40 mm of Hg
Significant - 40 – 50 mm of Hg
Critical - 50mmhg
In AS the increased systolic pressure gradient elevates left ventricular wall tension in
accordance with the Laplace’s law for wall tension developed in a spherical chamber
Wall tension = P X R/2h

P = Intraventricular pressure, R – Radius & h = wall thickness
Primary stimulus:
Pressures overload increased peak parallel Wall

Systolic gradient replication of thickening
Sarcomere
Concentric
Hypertrophy
While on increase in wall thickness minimizes the systolic wall tension it also decreases
diastolic chamber compliance. Thus in the concentrically hypertrophied ventricle small
changes in diastolic volume are associated with large change in ventricular filling
pressure.
Mild aortic stenosis – Asymptomatic with physiologic compensation

As the stenosis progresses, the maintenance of normal stroke volume is associated with
an increasing LV systolic pressure to as much as 300 mmHg whereas the aortic systolic
pressure and stroke volume remain relatively normal. This results in a compensatory
L.V. hypertrophy.
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Moderate to severe aortic stenosis – Symptomatic impairment
As the stenosis progresses to the critical orifice size, dilation as well as hypertrophy of
LV may occur, leading to increase in LVEDP. The increase in LVEDP leads to increase in
myocardial O2 demand. Supply is impeded owing to an elevated LVEDP causing a
decrease in coronary perfusion pressure.
Continuation of the disease process with reduction of the aortic valve index to less than
0.6 cm2 / m2 leads to further decrease in ejection fraction and an increase in LVEDP.
Left atrial pressure increases to more than 25 – 30 mmHg leading to increase in
pressure in the pulmonary venous circuit and pulmonary edema develops. Normally
sudden death will intervene, but if patient is able to survive, the increasing pulmonary
arterial HTN eventually will produce RV failure.
Aortic stenosis

Obstruction to ejection of blood into the aorta

in L.V. pressure

L.V. Hypertrophy

L.V. Dilatation

LA Pressure

Pulmonary hypertension

Pulmonary edema

RV failure

LVEDP

Myocardial O2 Demand

Angina Pectoris

Sudden death
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PRESSURE VOLUME RELATIONSHIP
Normal In Aortic Stenosis
Goals of Preoperative Management
1. Heart Rate: Extremes of heart rate are not tolerated well. Because of the
importance of atrial contraction for LV filling, it is essential to maintain a sinus
rhythm. A high heart rate can lead to decreased coronary perfusion and a low
heart rate can limit cardiac output. Low heart rates (50-70 bpm) are preferred to
allow time for systolic ejection across a stenotic aortic valve.
2. Left ventricular preload: Due to the decreased compliance and increase in
LVEDP and LVEDV, preload augmentation is necessary to maintain a normal
stroke volume.
3. Contractility: Stroke volume is maintained through preservation of a heightened
contractile state.
4. Systemic vascular resistance: Avoid sudden increase or decrease in systemic
vascular resistance. Decrease in SVR can lead to decrease in coronary perfusion
and an increase in SVR can lead to decrease in stroke volume.
5. Pulmonary vascular resistance: Except for end stage AS pulmonary artery
pressures remain relatively normal. Special intervention for stabilizing
pulmonary vascular resistance is not necessary.
Assessment of severity:
 Symptomatic patients
 Narrow pulse pressure
 Systolic thrill
 S3, S4
 ST and T wave changes
 Cardiac enlargement in X – ray
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Risk factors for adverse reactions in non cardiac surgery:
Patient related
 Unstable coronary syndromes
 Chronic heart failure
 Severe or symptomatic valvular heart disease
 IDDM
 Renal insufficiency
 Arrhythmias
 Poor functional status MET 4
 Uncontrolled systemic hypertension
 Obstructive and restrictive pulmonary disease
Procedure related
 High risk surgery (cardiac risk >5%)
o Aortic and other, major vascular surgery
o Peripheral vascular surgery
o Anticipated prolonged surgery associated with large fluid shifts and blood
loss
o Surgical emergencies
 Intermediate (Reported cardiac risk <5%)
o Carotid Endarterectomy
o Head and neck
o Intraperitoneal and Intrathoracic
o Prostate
 Low (Reported cardiac risk < 1%)
o Endoscopic procedures
o Superficial Procedures
o Cataract
o Brest
Objectives:
 Maintain Sinus Rhythm
 Avoid Bradycardia
 Avoid sudden  or  in SVR
 Optimize iv fluid volume to maintain venous return & LV filling
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Preoperative evaluation
History taking:
History should focus on symptoms related to ventricular function and should be
correlated with lab data. Questions should concern regarding exercise tolerance,
fatigability, pedal edema, chest pain and shortness of breath in general dyspnoea,
orthopnea and PND. And should be graded according to New York Heart Association
functional classification of heart disease. A review of medications should evaluate
efficacy and exclude serious side effects.
Lab investigation
1. Routine blood investigation
2. ASO Titer
3. ECG
a. LVH
b. T-inversion
c. ST – depression
4. Chest X- Ray
a. Calcification of aortic valve
b. Rounding of LV apex
c. Atrial enlargement
d. Pulmonary edema
e. Post stenotic dilation of aorta.
5. ECHO
a. Type of valve pathology
b. Valve area
c. Pressure gradient
d. Extent of LVH
e. Ventricular function
6. TEE
a. Confirm intra operative diagnosis
b. Detection of ischemia
c. assessing ventricular preload and contraction
d. Detection of atherosclerotic
Pre op scoring of the patient depending on type of the surgery and physical exercise
capacity,
Class I – Good physical status enables the patient to undergo any surgical procedure
with low risk despite severe AS.
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Class II – Patient with mean transvalvular pressure gradient of less than 50 mm Hg and
a fair physical status are at intermediate risk and usually show no problems during low
to medium risk procedures.
Class III - Patients with severe cardiac symptoms/ decompensation, aortic valve
replacement may be advisable before non cardiac surgery.
Pre medication
1. H2 blockers – Ranitidine 0.5-1mg/kg
2. Anti emetics – Ondansetron 0.1mg/kg.
3. Anti cholinergic – Glycopyrrolate 0.005-0.01 mg/kg, dose should be reduced in
proportionate to severity of ventricular impairment.
4. Prophylaxis for bacterial endocarditis
MONITORS
Non invasive
1. Pulse oximetry
2. ECG
3. BP monitoring
Invasive
1. IBP
2. CVP
3. PCWP
4. TEE
5. Urine output
Choice of anesthetic technique

1. Regional
2. General anesthesia.
1. Regional
Patients with mild to moderate AS may tolerate Spinal or Epidural anesthesia.

Epidural anesthesia is preferable to spinal anesthesia because of it slower onset of
hypotension which allows more aggressive correction. These are contraindicated in
severe AS.
2. General Anesthesia:
Selection of anesthetic agents is generally less important than the way they are used. It
should be emphasized that anesthetic dose requirement are extremely variable and
generally are inversely related to ventricular function.
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Mild AS: Induction of anesthesia can be achieved with available iv induction drugs.
 Inj Thiopentone 3-5 mg/kg

 Inj Propofol 1.25-2.25mg/kg
 Inj Etomidate 0.2-0.5 mg/kg
 Inj Lignocaine 1-2 mg/kg prior to induction
Maintenance of anesthesia
Mild AS
N2O + opioid agents like fentanyl 1 1-2µg/kg or sufentanyl 10.1-0.4 µg/kg
N2 O + inhalational agents like desflurane, sevoflurane
Moderate to severe AS
Choice of anesthetic agents
High does opioid anesthesia

 Fentanyl 150-100 µg/kg or
Sufentanyl 1 15-25 µg/kg
 Developed to overcome the myocardial depression associated with volatile
anesthetic agents like Halothane and Enflurane.
Disadvantages:
 Prolonged postoperative respiratory depression
 High incidence of patient awareness during surgery
 Fails to control hypertensive reflex to surgical stimulus
 Rigidity during induction
 Postoperative ileus
 Possible impairment of immunity.
Total intravenous anesthesia
Propofol 0.5-1.5 mg/kg infusion
Followed by 25-100 µg/kg/min
Remifentanyl 1 0 -1 µg/kg bolus
Followed by 0.25 – 1 µg/kg/min
Mixed intravenous / inhalation anesthesia

Recent studies show protective effects on ischemic myocardium.
Desflurane, sevoflurane
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Induction:
Propofol 0.5-1.5 mg/kg
Etomidate 0.1 -0.3 mg/kg
Thiopentone 3-5 mg/kg and Midazolam 0.05 mg/kg
Maintenance:
Opioids in small dose with volatile anesthetics like desflurane and sevoflurane at 0.5 –
1.5 MAC
Opioid should not exceed fentanyl and sufentanyl 1 15 and 5 µg/kg respectively for
early extubation.
Or propofol 25-50 µg/kg/min
Advantages:
 Hemodynamic stability
 Ability to change the anesthetic concentration and depth rapidly
Other techniques:
Ketamine 1-2 mg/kg with
Midazolam 0.05 - 0.1 mg/kg
Maintained with
Ketamine 1.3 - 1.6 mg/kg/hr infusion
Midazolam 0.065 - 0.075 mg/kg/hr
Advantages
 Useful technique in frail patients with hemodynamic compromise.
 It is associated with relatively stable hemodynamics, good amnesia analgesia,
minimal postoperative respiratory depression.
Muscle relaxants
Vecuronium: 0.08-0.12 mg/kg intubating dose
0.04 mg/kg maintenance dose
Rocuronium: 0.6-1.2mg/kg/ for rapid sequence intubation
0.15 mg/kg maintenance dose
Scoline is avoided since it can produce negative inotropic and chronotropic effect
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Mod to severe AS
Opioids alone can be used
 Fentanyl 50-100 µgm/kg
 Intravascular fluid volume is maintained by prompt replacement of blood loss
and administration of IV fluids.
 Ensure minimal changes in HR, SVR, PVR and avoid myocardial Depression.
 N2O should be cautiously used as it can acutely increase pulm6n vascular
resistance.
 Muscle relaxants with minimal effects on HR, SVR and BP are used.
 Pancuronium is avoided (as it causes tachycardia).
 Controlled ventilation - maintain normocapnia and avoid hypoxemia.
Reversal agents
 Neostiogmine 0.05mg/kg with
 Glycopyrrolate 0.005-0.01 mg/kg
 Inj xylocard 1-2 mg/kg
Perioperative complications:
 Bradycardia or junctional rhythm - Treated with atropine 0,6 mg IV.

 Tachycardia - Controlled by deepening anesthesia or  blocker Esmolol 0.2-0.5
mg/kg.
 SVT/AF
 Verapamil 10-20 mg over 2-20 min maintenance 5 mg/kg/min.
 Diltiazem 0.25 mg/kg followed by second dose 0.35 mg/kg maintain 515mg/hr
cam`
 Digoxin 0.5 mg over 20 minutes followed by increment of 0.25 or 0.125 to 1-1.5
mg over 25 hours. Or cardioversion .
Hypotension –
Ephedrine 2.5 - 10 mg
0.1 mg /kg in children
Phenylephrine 50-100 µg (0.5-1 µg/kg) bolus infusion 100 fig/µg/ml at the rate of 0.25
- 1 mg/kg/min.
Post-Operative Management
Cardiac monitoring is continued post-operatively as pain, hypoxemia and
hypoventilation may increase HR.
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Preemptive analgesia
- Opioid premedication
- Intraoperative opioids
Fentanyl 2-150 µg/kg
Sufentanyl 1 0.25-30 µg/kg
Alfentanyl 1 8 – 100 µg/kg
- Low dose Ketamine 0.2 – 0.5 mg/kg
- Regional nerve block
- Wound infiltration with LA
- Subarachnoid opioids or LA
Patient controlled analgesia
Basal and bolus infusion Dosages and Lockout Intervals for analgesics*
Basal Dose Bolus Dose Lockout Interval
Agonist
Morphine 1.0-2.0 mg/hr 0.5-3.0 mg 5-20 min
Meperidine 10-20 mg/hr 5-30mg 5-15 min
Methadone 1.10 mg/hr 0.5-3.0 mg 5-15 min
Hydromorphone 0.2 mg/hr 0.1-0.5 mg 5-15 min
Fentanyl 50-75µg/hr 15-75µg 3-10 min
Sufentanil 2-7µg/hr 2-10µg 3-10 min
Agonist/antagonist
Pentazocine 5 mg/hr 5-30 mg 5-15 min
Nalbuphine 1 mg/hr 1-5 mg 5-15 min
Bupremorphine Non given 0.03-0.2 mg 5-20 min
Postoperative nausea vomiting:

 Ondansetron 4 mg (0.1 mg/kg in children)
 Granisetron 0.01 -0.4 mg/kg
 Metoclopramide 0.15 mg/kg
 Dexamethasone 4-10 mg (0.1 mg/kg in children) combined with anti-emetics.
Postoperative shivering:
 Supplement O2 and warm IV fluids
 Heating blankets
 Meperidine 10-50 mg
 Forced air warming
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Aortic Regurgitation
Etiology
 Acute aortic regurgitation

o Trauma, Rheumatic fever, infective endocarditis, dissecting aneurysm.
 Chronic aortic regurgitation
o Common causes - Rheumatic, syphilis, bicuspid aortic valve and
atherosclerotic aortic valve.
 Uncommon causes - Infective endocarditis, Marfan's syndrome. Rheumatoid
arthritis, SLE, Ankylosing spondylitis, Reiter's disease. Takayasu's disease,
Aneurysm of aorta.
Common Features
Symptoms:
 Patients with chronic AR remain asymptomatic for years or decades but once
decompensated they deteriorate rapidly.
 Palpitations, exertional breathlessness, orthopnea, dyspnea, PND.
 Angina and syncope.
Peripheral Signs of Aortic Regurgitation

 Collapsing pulse (water-hammer pulse). Best appreciated on the radial artery
when the arm is elevated. This is characterized by a rapid upstroke rapid down
stroke and high volume.
 Pulsus bisferiens - Best felt in the carotids. This is a pulse with double peak, both
being felt in systole. It is seen in severe aortic regurgitation.
 Wide pulse pressure
 Hill's sign: Popliteal cuff systolic blood pressure exceeding brachial cuff systolic
pressure by more than 20 mmHg.
o A difference of 20-39 mmHg - Mild AR
o A difference of 40-59 mmHg - Moderate AR
o A difference of 60 mmHg or more -Severe AR
 Corrigan's neck sign -'Prominent carotid pulsation visible in the neck.
 De-Musset's sign: to and f4r motion of the head synchronous with cardiac cycle.
 Landolfi's sign: change in` size of pupil synchronous with cardiac cycle.
 Muller's sign: Pulsations of uvula.
 Light house sign: capillary pulsations on the forehead arid` face resulting in
alternate blanching and flushing.
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 Quincke's sign: alternate paling and flushing of lightly compressed nail bed or
mucous membrane of mouth.
 Pistol shot femorals - Booming sound synchronous with systole heard over the
femoral arteries.
 Traube's sign: Booming systolic and diastolic sounds heard over the femoral
artery.
Inspection and Palpation:

 Prominent neck pulsations
 Thrill in the carotids
 Hyperdynamic pericardium
 Hyperdynamic apex which is shifted down and out
 Suprasternal pulsations
Auscultation:
 Early diastolic murmur - A high pitched, early diastolic, decrescendo murmur

best heard to Erb's area in rheumatic AR and at aortic area syphilitic AR.. The
murmur is best heard with the diaphragm of the stethoscope, with the patient
sitting up, leaning forwards, breath held in deep expiration and hands clenched.
Pathophysiology:
Primary stimulus
Volume → Increased end → Series replication → Chamber → Eccentric

Overload Diastolic gradient of sarcomere enlargement
hypertrophy
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Acute AR
Sudden → volume overload →Immediate compensatory → Tachycardia and
occurrence on LV sympathetic tone increased contractile state
Acute AR:
Acute AR: The sudden occurrence of AR places a major volume load on the LV. An
immediate compensatory mechanism is increased sympathetic tone that leads to
tachycardia and increased contractile state. The combination of increased LVEDV and
increased stroke volume and heart rate may not be sufficient to maintain a normal
cardiac output leading to rapid deterioration of LV function.
Chronic AR
Stage I: Mild AR – asymptomatic with physiologic compensation:
The onset of AR leads to LV systolic and diastolic volume overload. The increased
volume load leads to LV hypertrophy and dilation. Because. The LVEDV increases
slowly, the LVEDP remains relatively normal. There is no major increase in myocardial
O2 demand.
Stage II: Moderate AR - symptomatic impairment

Occurs as AR progresses to more than 60% of SV, finally leading to irreversible LV
myocardial tissue damage.. An LVEDP ≥20 mmHg suggests LV dysfunction. The onset of
LV dysfunction is followed by increase in pulmonary arterial pressure.
Stage III: Severe AR - Terminal failure

LV dysfunction. Continues to progress and eventually becomes irreversible. Angina
pectoris due to decrease in aortic diastolic pressure may occur. As a compensatory
mechanism for poor cardiac output and poor coronary perfusion, sympathetic
vasoconstriction of the periphery occurs; leading to further decrease in cardiac output.
Aortic Regurgitation
↓
LV systolic and diastolic volume overload
↓
LV hypertrophy and Dilation → angina Pectoris
↓
LVEDP ↑ ≥ 20 mg HG → LVF
↓
↑ Pulmonary artery pressure
↓
RHF
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ANESTHETIC MANAGEMENT:
Preoperative Evaluation:
History taking
Objectives:
 Hr to be maintained 80-100 bts/min
 Excessive myocardial depression is avoided.
 Compensatory increase in cardiac preload to be maintained
Relevant investigations
ASO titer
VDRL (kahn test)
ECG
ECHO
X-ray
angiography
color Doppler
Premedication
 H2 blockers – Ranitidine – 50 mg iv
 Anti emetics – Ondansetron 4 mg iv
1. Anti-cholinergics – Glycopyrrolate 0.005-0.01 mg/kg, dose should be reduced in
proportionate to severity of ventricular impairment.
o Prophylaxis for bacterial endocarditis
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Monitors
Non invasive
I. Pulse oximeter
II. ECG
III. BP monitoring
Invasive
I. IBP
II. CVP
III. PCWP
IV. TEE
V. Urine Output
Choice of anesthetic technique

I. Regional
II. General anesthesia.
Regional
Most patients tolerate spinal and epidural anesthesia provided intra vascular volume is
maintained.
GA
Induction of anesthesia can be achieved with available iv induction drugs.
 Inj Thiopentone 3-5 mg/kg
 Inj Propofol 1.25-2.25mg/kg
 Ink Etomidate 0.2-0.5 mg/kg
 Inj Ketamine 1-2 mg/kg
Ketamine is advantageous when IV fluid volume is judged to be decreased.
Opioids as sole anesthetic agent can be used when LV function is severely compromised.
Fentanyl 150-100 µgm/kg
Alfentanyl 1150-300 µgm/kg
Relaxants
Vecuronium: 0.08-0.12 mg/kg intubating dose, 0.04 mg/kg maintenance dose
Pancuronium is preferable. 0.08-0.12 mg/kg intubating dose
Intra op initially 0.04 mg/kg, followed by 0.01 mg/kg every 20-40 min maintenance
dose
Rocuronium: 0.6-1.2 mg/kg for rapid sequence induction, 0.15 mg/kg maintenance
dose
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Maintenance of anesthesia
N2O + opioid agents or
N2O + inhalational agents
Opioids alone can be used
- Isoflurane and desflurane are preferred because of associated vasodilatation.
Reversal agents
Neostiogmine 0.05 mg/kg with
Glycopyrrolate 0.005-0.01 mg/kg
Post –Operative Management:

Cardiac monitoring is continued post-operatively pain, hypoxemia and hyperventilation
may increase HR.
Preemptive analgesia:
- Opioid premedication
- Intraoperative opioids
o Fentanyl 12-150 µg/kg
o Sufentanyl 10.25-30 µg/kg
o Alfentanyl 18-100 µg/kg
- Low dose Ketamine 0.2 -0.5 mg/kg
- Regional nerve block
- Wound infiltration with LA
- Subarachnoid opioids or LA
Patient control analgesia

Pos-top nausea vomiting:
 Ondansetron 4 mg (0.1 mg/kg in children)
 Granisetron 0.01-0.4 mg/kg
 Metoclopramide 0.15 mg/kg
 Dexamethasone 4-10 mg (0.1, mg/kg in children) combined with antiemetics.
Postoperative shivering:
 Supplement O2 and warm IV fluids
 Heating blankets
 Meperidine 10-50 mg
 Forced air warming
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SUMMARY AND CONCLUSION:
The management of the patient with significant valvular disease is very challenging.
Anesthetic depth is normally titrated to maintain heart rate and BP within acceptable
parameters; however, in the presence of valve dysfunction, the heart is itself decreased
and may have little reserve. When pulmonary hypertension and right heart failure
ensure, it is critical to blunt noxious stimuli, which exacerbate pulmonary hypertension,
without depressing ventricular function. Knowledge of the Pathophysiology of each
lesion is a prerequisite to understanding the hemodynamic goals in these patients.
These aims can then be combined with knowledge of the effects of anesthetic agents to
choose the safest anesthetic course.
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Chapter 6 Prophylactic regiments for various Procedures. For dental,
cardiac, respiratory tract, or esophageal procedures.
Standard general prophylaxis for patients at risk:

Amoxicillin: adults, 2.0 g (children, 50mg/kg) given orally 1h before procedure.
Unable to take oral medications:

Ampicillin: Adults, 2.0g (Children, 50mg/kg) given IM or IV within 30min before
procedure.
Amoxicillin/ampicillin/penicillin allergic patients:

Clindamycin: adults, 600mg (children, 20mg/kg/ given orally 1h before procedure or
Cephalexin 3 or Cefadroxil3: adults, 2.0 g (Children, 50mg/kg) orally 1 h before
procedure or
Azithromycin or Clarithromycin: adults, 500 mg (children, 15mg/kg) orally 1 h before
procedure.
Amoxicillin/ampicillin/penicillin allergic patients unable to take oral medications:

Clindamycin: adults, 600mg (children, 20 mg/kg/) IV within 30min before procedure or
Cefazolin3: adults, 1:0 g (children, 25 mg/kg) IM or IV within 30 min before procedure
For genitourinary/gastrointestinal procedures:
i. High – risk
Ampicillin plus gentamicin: ampicillin (adults, 2.0g: children, 50mg/kg) plus

gentamicin 1.5 mg/kg (for both adults and children, not to exceed 120 mg ) IM or Iv
within 30min before starting procedure ; 6h later, ampicillin (adults, 1.0 g; children, 25
mg/kg) IM or IV, or amoxicillin (adults, 1.0 g; children, 25mg/kg orally
ii. High – risk patients allergic to ampicillin / amoxicillin:
Vancomycin plus gentamicin: Vancomycin (adults, 1.0g: children, 20mg/kg) IV

over 1-2 h plus gentamicin 1.5 mg/kg (for both adults and children, not to exceed 120-
mg) IM or Iv ; complete injection/infusion within 30min before starting procedure.
iii. Moderate – risk patients:
Amoxicillin: adults, 2.0g (children, 50mg/kg) orally 1 h before procedure or

Ampicillin: adults, 2.0g (children, 50mg/kg) IM or IV within 30min before starting
procedure
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iv. Moderate – risk patients allergic to ampicillin/amoxicillin:
Vancomycin: adults, 1.0g (children 20mg/kg) IV over 1-2h; complete infusion

within 30min of starting the procedure.
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Chapter 7 MANAGEMENT OF PERIOPERATIVE ARRYTHMIAS
MANAGEMENT OF PERIOPERATIVE ARRYTHMIAS

A dysrrhythmias is defined as an abnormality of rate, regularity or site of origin of
cardiac impulse or disorder of conduction of impulses.
NORMAL CARDIAC ELECTROPHYSIOLOGY:

For practical purposes, the myocardium can be considered by being comprised of two
cell types; “The working myocardial cells” and “the conductive cells”. The working
myocardial cells have the specialized ability to shorten against a load when electrically
stimulated. The contractile efforts of the working myocardial cells must be co-ordinate
to effect the chamber contraction. It is this coordination which is performed by the cells
of the conduction system.
ANATOMY OF THE CONDUCTION SYSTEM:

Sino-atrial node: (SA node):
The SA node is a bundle of specialized neuromuscular tissue that lies under the
endocardium of the right atrium at the junction of the superior vena cava with right
atrial appendage. Normally it is the dominant pace maker, discharging spontaneously
between 60-100 times a minute.
Atrioventricular node (AV node):

This is a specialized neuro muscular tissue located under the endocardium on the right
side of the interatrial septum, just inferior to the opening of the coronary sinus.
The impulses reach the AV node from SA node through 3 Specialized pathways - the
anterior, middle; the posterior internodal pathways. The impulse arriving from the SA
node is delayed at the AV node for 70-100 ms, before being conducted down the bundle
of his. In the absence of impulse from the SA node, the automaticity of AV node is 40-50
times/ min.
The bundle of His:

This is a continuation of the AV node, located on the right side of the interatrial septum.
It divides into the right and the left bundle branches immediately above the
interventricualr septum. These branches course down on either side of the
interventricualr septum.
The bundle and its branches have the highest conducting velocities among the
conducting tissues of the heart.
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The Lt. Bundle branch soon alters its origin divides into anterior and posterior divisions.
Finally the bundle branch continues on the Purkinje system under the endocardium of
both ventricles. The electrical impulses travel from the endocardium to epicardial
surface of the ventricles.
In the absence of impulse from above, the His purkinje system can spontaneously
discharge electrical impulses at a rate of 20-40 times/ min,
PHYSIOLOGY OF CONDUCTION SYSTEM

In either type of myocardial cell - "the working myocardial cell or the cell of the
conduction system", at rest, the cell interior is electrically negative relative to the
exterior; by approximately 90 mv, called "resting membrane potential''; and is due to
the selective distribution of electrolytes, mainly sodium and Ca2+ outside the cell and
K+ inside the cell. When an electric current is applied to such a cell, the cell membrane
becomes highly permeable to Na+ and later to Ca2+. These ions enter the cell and make
the interior positive in ;.elation to exterior by approximately 20 mv. This process is
called "depolarization". Soon after this, potassium ions leave the cell and bring the cell
interior to -90 mv potential. This process is called "repolarisation". This process of
repolarisation continues with the exchange of Na+, Ca {and K-} ions and ultimately
sodium and calcium ions are predominantly concentrated outside the cells and K+
inside the cells.
The electrical events:

Depolarization and repolarisation, sensed by the intracellular microelectrodes and
displayed on an oscilloscope, is called the `action potential'.
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The action potential (AP) itself can be subdivided into five phases designated 0-4. The
resting phase designated as phase 4, and corresponds to an abundance of Na -` and Cat+
outside the cell and potassium inside.
phase 0 - (Na+ influx) – Depolarization

phase 1- Stoppage of Na+ influx
phase 2- Calcium influx
phase 3- K+ efflux
phase 4- Ions are restored to their original concentration.
The action potential of the cell of the conduction system differs from that of working
myocardial cell. In the cell of the SA node, the phase 4 is not isoelectric, but sloping
upwards. This is due to the gradual spontaneous depolarization of the cell membrane, a
property called automaticity.
This automaticity is due to the higher resting permeability of the cell membrane to Ca2+
and a low permeability to K+.
The slope of phase 0 is less than that of working myocardial cell.
The auto reactivity of SA nodal cell is influenced by various factors like – vagal tone,
sympathetic / catecholamine activity, -adrenergic antagonists / agonists, halothane,
digoxin and Ca2+ channel blockers.
Two important concepts for understanding the development of dysrrhythmias are
excitability and refractoriness.
Excitability is the property of cardiac tissue to depolarize to a given impulse. Increased
excitability which indicates the responsiveness to a lesser stimulus or a greater
response to given stimulus, is an important cause of dysrrhythmias.
During phase 0, 1 and 2 of the AP the myocardial cell does not respond to another
impulse. This time interval is called `absolute refractory period'.
During the latter portion of phase 3, the stronger than usual impulse can produce
another AP and this interval is called `relative refractory period'
The sum of these 2 refractory periods – “effective refractory period’
MECHANISM OF CARDIAC DYSRHYTHMIAS

Cardiac dysrrhythmias can be explained mainly on the basis of:
 Abnormalities of cardiac impulse conduction; (Reentry) and
 Abnormalities of impulse formation (automatic or ectopic)
 Atrioventricular dissociation.
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l. Abnormal impulse conduction (Re-entry)
Re-entry accounts for the most premature beats and tachydysrhythmia.

Conditions necessary for reentry include two pathways over which cardiac impulses are
conducted at different velocities as shown in figure.
One pathway conducts the cardiac impulse forward (antegrade), whereas other
pathway conducts the reentering cardiac impulse backward (retrograde).
In the retrograde pathway, the antegrade conduction is usually blocked or delayed, but
retrograde conduction remains intact. E.g. In myocardial ischemia.
2. Abnormal impulse formation: (Automaticity)
Automatic cardiac dysrrhythmias are due to enhanced automaticity of a focus in the

heart capable of undergoing spontaneous depolarization (repetitive firing) analogues to
that of the sinus node e.g., specialized atrial fibres, fibres of AV junction and purkinje
fibres.
3. Atrioventricular dissociation:
When the atria and ventricles contract independently of each other as in conduction
blocks.
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HAEMODYNAMIC EFFECTS OF DYSRHYTHMIIAS
 Decreased cardiac output
 Change in the delicately balanced myocardial oxygen demand/ supply ratio.
 Depressed myocardial contractility.
 Threat of developing VF by R on T phenomenon.
Lead systems:
Bipolar leads are more useful in the perioperative period than the unipolar leads. Any
location of the electrodes anal any selection of the lead which ensures that a good P
wave and QRS complex are displayed can be used for the peri-operative detection of
dysryhtmias. However, the following leads are recommended.
Lead II: It is standard, bipolar limb lead. The -ve electrode is placed near the right
shoulder, the +ve electrode near the left loin and 3rd. one anywhere (serves as a
ground). It's used because its electrical axis parallels the electrical axis of the heart and
the P-wave is usually observed.
MCL1 (modified chest lead): This lead is obtained by placing the -ve electrode under
the outer third of the left clavicle, the +ve electrode over the 4th intercostal space of
right mid clavicular line.
CBS (central back lead):-ve electrode is placed over the centre of the right scapula, the
+ve electrode over the V5 position and ground electrode anywhere else. Adv.: Larger P-
waves than V5 (>90%) and therefore detection of supraventricular arrhythmias.
PERI-OPERATIVE CAUSES OF DYSRHYTHMIAS:
Tracheal intubation:
It is the most common cause in perioperative period.
The combination of the stimulation of sensitive pharyngeal, laryngeal mucosa, and
action of halothane, Succinylcholine and the development of early hypoxemia is
probably responsible for occurrence of dysrrhythmias.
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Anesthetic agents:
Halogenated hydrocarbons especially halothane, by i) re-entry mechanism ii) sensitizes
the myocardium to both endogenous and exogenous adrenaline.
Ketamine and cocaine – by blocking re-uptake of nor-adrenaline.
Local anesthetics – Spinal or epidural anesthesia may cause parasympathetic
dominance leading to bready – arrhythmias (mild-severe). It’s associated when the
blockade extends to high thoracic levels.
Muscle relaxants:
Succinylcholine – can produce any type of dysrhythmias. Most common ones are sinus
bradycardia, transient sinoatrial arrest and ventricular bigeminy.
Gallamine and pancuronium-produce sinus tachycardia by a vagolytic action.
Reflexes
Vagal stimulation produces sinus bradycardia.
Oculo-cardiac and naso cardiac reflexes produce similar effects.
Pre-existing cardiac disease:

Patients with known cardiac disease are more likely to have dysrrhythmias than those
without.
Injected adrenaline:
Exogenously administered adrenaline can cause dysrrhythmias at a dose of –

2 µg/kg (with the concurrent use of halothane)
4µg/kg mixed with 1% lignocaine (with halothane)
7µg/kg (with isoflurane)
10µg/kg (with enflurane)
Serum electrolytes and ABG

Hypocapnia leads to respiratory alkalosis and hypokalemia which can precipitate
variety of dysrrhythmias. The mechanism is believed to be either altering phase - 4 of
the AP and re-entry mechanism.
Hypercapnia results in sinus tachycardia and VPBs.
Site of injury:
Oral surgery, extraocular ophthalmic surgery, neck surgery and intrathoracic surgery
are common examples of surgical sites producing dysrrhythmias.
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Insertion of catheters:
Passage of central venous catheters or pulmonary artery catheters is a common cause of
dysrrhythmias.
CNS Stimulation and dysfunction of the autonomic nervous system:

Many ECG abnormalities can occur in patients with intracranial disease, especially
subarachnoid haemorrhage. The mechanisms of these arrhythmias appear to be related
to changes in autonomic nervous system.
Diagnosis and management of dysrrhythmias:

For Quick and easy diagnosis of the specific dysrrhythmias, it is worthwhile to have the
following questions in mind.
What is the heart rate?
It the rhythm regular?
Is there a P wave?
Is each QRS complex preceded by a P wave? (P: QRS)
Is QRS complex normal?
What is its significance?
What is the management?
Following are some common intra-operative arrhythmias to which the six questions
should be applied.
Sinus Dysrhythmia:
This is a common dysrrhythmias seen in young awake individual who have slow heart
rates.
The heart rate increases during inspiration and slows during expiration.
Heart rate : 60-100 bpm
Rhythm : Irregular
P-wave : Present, normal looking
P: QRS : each QRS complex is preceded by P wave
QRS complex : Normal
Significance : Normal finding
Treatment : No treatment required
Sinus Bradycardia:
The SA node is the dominant pacemaker, but it discharges at a rate slower than normal.
Causes: Drug effects, actute inferior MI, hypoxia, vagal stimulation and high sympathetic
blockade.
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Rhythm : Regular
P: QRS : each QRS complex is preceded by P wave
Significance:
Not dangerous as long as cardiac output is reasonably well maintained. But heart rates
lower than 40 beats/min are poorly tolerated evening healthy patients and should be
evaluated.
Treatment:
 Initial treatment is with atropine 0.5-1.0 mg IV and repeated as needed at 3 to 5
min intervals up to 0.04 mg/kg. (or 3mg total dose).
 Alternatives include ephedrine (5 to 25 mg IV bolus) or Epinephrine (1-
10µg/min. IV infusions)
 Transcutaneous pacing or transvenous pacing or transvenous pacemakers’
insertion may be needed for severe / refractory sinus bradycardia.
Sinus tachycardia.
The pacemaker site is in the SA node, but the rate is faster than normal.
It is the most commonly occurring arrhythmia in peri-operative period.
Causes:
Plain, inadequate anesthesia, hypovolemia, fever, hypoxia, hypercarbia, heart failure
and drug effects.
Rhythm : Regular
P: QRS : Each QRS complex is preceded by P wave
Significance:
Acceptable over a limited period of time, prolonged tachycardia in patients with
underlying heart diseases can precipitate congestive heart failure, due to increased
myocardial work. Tachycardia decreases coronary perfusion time and can precipitate
angina in patients with coronary artery disease.
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Treatment:
The underlying disorder should be treated, since it is physiological response to stress
placed on heart. Esmolol, propranolol should be used in IHD patients who develops ST
segment changes to prevent further MI.
Atrial Premature beats:

An ectopic pacemaker site, either in the left or the right atrium initiates the the atrial
premature beat (APB). The depolarization occurs before the next SA nodal impulse is
due and hence premature. This ‘ectopics’ depolarization generally resets the SA node
and thus there is no compensatory pause.
Heart rate : Variable, depending on frequency of APB
Rhythm : Irregular
P-wave : Present unless eclipsed by the QRS complex can have an abnormal
shape.
P: QRS : Usually each QRS is preceded by P wave.
QRS complex : usually normal, unless there is ventricular aberration.
Significance:
Usually benign but frequent APB can lead to other more serious supraventricular
arrhythmias or may be a sign of digitalis intoxication.
Treatment:
Since APC are asymptomatic treatment is not required. Rarely b blockers may be used,
if hemodynamic function is impaired.
Paroxysmal Supraventricular tachycardia (PSVT)

This is due to rapidly firing atrial focus other than the SA node, characterized by rapid
regular rhythm usually with narrow QRS complex and lacking the normal SA node P
wave.
MC mechanism is, it’s often initiated by a premature beat and perpetuated by a reentry
cycle, usually in the AV node which begins and ends suddenly.
Classification of SVT:
Reentry
- SA node, Atrial, AV junction, AV junction bypass, WPW syndrome.
Ectopic
- Atrial, AV junction
There can be a block of varying degrees at AV node.
Heart rate : 150-250 bpm.
Rhythm : Regular, unless the impulse originates from multiple atrial foci.
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P-wave : Present can be abnormal.
P: QRS : There is 1:1 relationship, although the ‘P’ wave often may be
hidden in the QRS complex or T wave
QRS complex : usually normal, but St-T changes indicative of ischemia may be
noted.
Significance:
Associated with intrinsic heart disease, systemic illness, thyrotoxicosis, digitalis toxicity,
pulmonary embolism.
Usually produces hemodynamic disturbance. Needs to be treated quickly, can produce
dizziness/syncope due to decrease CO. in patients with cardiac disease it may
precipitate angina, dyspnea and cardiac failure.
Management:
If hemodynamic deterioration is there, cardioversion is the treatment of choice,
beginning at 50 J and progressing to 100, 200, 300, 360 J if needed.
If patient is hemodynamically stable, vagal maneuvers can be tried (e.g.: Valsalva
maneuver in awake patients), carotid massage which should be applied only to one side
in anesthetized patient.
Pharmacological treatment: Adenosine is the drug of choice. It can be given initially

6mg, given rapidly through an antecubital venous catheter. If needed, second dose of 12
mg given in 1-2 min. If central venous catheter is used those doses can be reduced to 3
and 6 mg respectively.
A suggested scheme for use of adenosine including dosage ‘adjustments are as shown
below.
 Peripheral (antecubital): 6mg, then 12 mg if needed and if central: 3mg, then
6mg if needed.
 If taking theophylline containing drugs: 9mg peripherally, 6mg centrally.
 If taking dipyridamole: 2mg peripherally 1 mg centrally.
 Use with caution in asthmatic patient.
If PSVT does not respond to adenosine, Verapamil is the drug of choice, close 5mg IV,
then 7.5 to 10mg in 15-30 min. if needed.
Other drugs which can be used are:
a) Esmolol 0.5 – 1 mg/kg bolus and 50-200 hg/kg/ min infusion.
b) Propranolol - 0.5mg IV bolus doses.
c) Edrophonium 5-10 mg IV bolus
d) Phenylephrine 100pg IV bolus if patient is hypotensive.
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e) ICI digitalization with one of the short acting digitalis preparation digoxin (0.5-1
mg IV).
Radiofrequency ablation is the preferred approach to patients with recurrent
symptomatic reentry SV'I', whether it is due to dual pathway within the AV node or
accessory pathway.
ATRIAL FLUTTER
A very rapid discharge from a focus in the atrium other than the SA node. It is usually
associated with some block at the SA node, this results in saw toothed appearance of the
flutter waves (`F' waves) on the ECG trace. The characteristics of atrial flutter as follows.
Heart rate : Atrial rate 250-350 bpm; with ventricular rate 150 bpm (2:1 or 3:1
AV conduction block).
 Rhythm: Atrial rhythm is regular. The ventricular rhythm may be regular if a
fixed AV block is present or irregular if a variable block exists.
 P-wave: P waves are replaced by ‘F’ waves.
 P: QRS : usually there is 2:1 block, with an atrial rate of 300 bpm and ventricular
rate of 150 bpm, but may vary between 2:1 and 8:1.
 QRS complex : Normal T waves are lost in F waves.
Significance:
It usually indicates the presence of severe heart disease. Like-coronary artery disease,
mitral valve disease, pulmonary embolism, hyperthyroidism, cardiac trauma, cancers of
the heart and myocarditis. Hence needs immediate treatment.
Treatment ;
If hemodynamic deterioration is present because of rapid ventricular response,
cardioversion is the treatment of choice.
Recent onset atrial flutter is typically very sensitive to low energy shocks
(25-50 J).
If hemodynamically stable, patients with rapid ventricular rate, secondary to atrial
flutter, treatment is pharmacologic.
Ibutilide (class III antiarrhythmics drug) – does of 1 mg infused over 10 min. A 2nd dose
can be given 10min after the first, if necessary.
Alternative drugs include;

Diltiazem ;
Loading dose of 0.25mg/kg over 2 min. followed if needed in 10-15 min by 0.35mg/kg.
infusion at a rate of 10mg/hr. Verapamil: 5mg IV initially, then 7.5 to 10mg in 15-30
min if needed. Esmolol (1mg/kg) IV bolus.
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Multifocal (Multiform) atrial tachycardia:
Occur in patient with COPD, hypokalemia, catecholamine administration and acute MI.
Diagnosed by observing the presence of at least 3 morphologically different ‘P’ waves in
the same lead with rate > 100 bpm.
Treatment:
Verapamil – 5 mg initially then 7.5 to 10mg in 15-20 min. correct the underlying cause.
Atrial fibrillation:
AF is an excessively rapid and irregular atrial focus with no P waves appearing on ECG,
but, instead, a fine fibrillatory activity called ‘f’ waves is seen.
This is most irregular rhythm; it is called irregularly irregular and may be associated
with pulse deficit.
The characteristics are as follows;

Heart rate : the atrial rate is 350-500 bpm and the ventricular rate is 60-170
bpm.
Rhythm : Irregularly irregular
P-wave : May or may not be seen, when seen abnormal in shape.
P:QRS : 1:1, but there are three varieties.
Significance:
Usually signifies severe heart disease. Intraoperative causes include hypovolemia,
hypoxia, hypokalemia, hypomagnesaemia, etc., The loss of atrial contraction leads to
reduction of CO by 20-25%. After 24 hours, atrial fibrillation may be associated with the
development of atrial thrombi, with resultant pulmonary and systemic embolization.
Treatment;
If hemodynamic deterioration is present, cardioversion at a initial dose of 100 J and
increased to 200, 300, 360 J if needed.
If this fails, cardioversion may be successful after loading with ibutilide (1 mg infused
over 10min.) success rate is 40-50%.
If hemodynamic deterioration is not present, treatment is pharmacologic –
 Correct precipitating factors, especially electrolyte disturbances.
 Digoxin - 500ug in 100ml NS over 20 min. and repeated at 4-8 hours intervals if
needed. (if K+ concentration is normal) Alternatives are,
 Esmolol (1 mg /kg) IV arid (50-200 pg/'kg)IV infusion,
 Verapamil Sing IV initially and then 7.5 to 10mg in 15min.
 Amiodarone - used where B-blockers and digoxin cannot be used.
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When control of ventricular response is difficult with standard agents - electrode
catheter ablation of AV junction and permanent pace maker insertion can be done.
However if the Fibrillation is present for longer than 4.8 hrs, adequate anticoagulation
for 3-4 weeks should be considered prior to attempting to restore sinus rhythms as
there is heightened risk of embolization when attempts are made to restore sinus
rhythm.
Junction rhythm
The dominant pacemaker is in the region of AV node.
The impulse spreads to atria retrograde at the same time that it spreads antegrade to
the ventricles.
Thus the atria and ventricles may contract at the same time.
Heart rate : Variable 40-180 bpm (nodal bradycardia to junctional tachycardia.
Rhythm : Regular
P-wave : may or may not be seen, when seen abnormal in shape.
P: QRS : 1:1, but there are three varieties.
High nodal rhythm:

The impulse reaches the atrium before the ventricles. Therefore the P ' wave precede
the ORS, but has shortened PR interval (0.1s).
Mid nodal rhythm: The impulse reaches the atrium and the ventricles at the same time.
The `P' wave is lost in the QRS.
Low nodal rhythm: The impulse reaches the ventricle first, then the atrium, so that the
`P' wave follows QRS complex.
QRS complex : Normal unless altered by the `P' wave.
Significance:
Probably the commonest dysrrhythmias under GA especially with the. use of halothane.
The CO may drop by 20-25%.
Treatment
Usually no treatment is required and then rhythm reverts spontaneously. It cardiac
output is significantly decreased, and then atropine, ephedrine, isoprenaline or
temporary pacing are required.
During halothane anesthesia, the cardiac: rhythm may periodically alternate between
sinus rhythm and functional rhythm - called the wandering pacemaker". if this affects
the cardiac output, the concentration of halothane may be decreased and intravenous
anesthetics may be substituted.
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VENTRICULAR PREMATURE BEATS (VPB)
The dominant pacemaker is the SA node. But an occasional impulse arises from a focus
in the myocardium below the AV node and progress through the purkinje system. The
impulse formation may be due to intrinsic heart disease or due to iatrogenic causes like
hypokalemia, hypothermia, acidosis/alkalosis, exogenous adrenaline, hypercapnia and
very commonly direct laryngoscopy and tracheal intubation. VPB are one of the most
common dysrrhythmias seen in the perioperative period.
Heart rate : Depends on underlying sinus rare and frequency of VPBS.
Rhythm : Irregular
P-wave : No ‘P’ wave before the ectopic impulses. It can have an abnormal
shape.
P: QRS : as the p wave is absent, the ectopic QRS complex stands out in
contrast to the regular complexes.
QRS complex : wide and bizarre with a width of more than 0.12 sec. the ST
segment and the T-wave are opposite in configuration to the main deflection of the QRS
complex.
Rhythm : usually regular. Irregular if the VT is paroxysmal.
P-wave : Not generally seen.
P: QRS : No fixed relationship
QRS complex : Wide, bizarre, more than 0.12 sec. in width.
Significance:
The cardiac output is dangerously compromised and requires immediate treatment.
Treatment:
VT can be with pulse (carotid) or without pulse. Treatment for VT without pulse and
ventricular fibrillation is same.
Treatment for VT with pulse:

Correct the underlying causes like hypoxemia, hypercarbia, hypokalemia and/or
hypomagnesaemia.
Treatment of VT depends on the degree of hemodynamic compromise induced by the
tachycardia.
Stable patient:
 If patient is stable, Lidocaine is drug of choice initially in a does of 1.0 to 1.5
mg/kg and repeated in a dose of 0.5 to 0.75 mg/kg every 5-10 min. until
arrhythmia is suppressed or a total of 3 mg/kg has been given.
 If this treatment is ineffective, Procainamide 100mg IV over 5 min. followed by a
infusion of 20-80 µg/kg/min.
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 If these measures fail, bretylium can be administered in a dose of 5-10mg/kg IV
over 8-10 min. If conversion is effective with this drug, an infusion at a rate of 1-
2 mg/min can be started.
 If VT is refractory to this approach, intravenous amiodarone may be effective.
 It exerts antiarrhythmics action. Within a hour of IV administration.
 Initial dose is 150mg in 100m] dextrose in water given over 10mirl. Followed by
a loading infusion of 1mg /min for 6 hours. If break through VT/ VF occurs,
supplemental 150ing infusion, over 10min. can be given.
Unstable patient
In unstable patient (e.g.: iii the presence of systemic hypotension, pulmonary edema, or
clinical or ECG signs of acute ischemia or infarction), cardioversion is the treatment of
choice, with energy doses of 100, 200, 300 and 360 J in progressive increments as
needed.
Management of pulseless ventricular tachycardia or ventricular

fibrillation
For therapeutic purposes, it is reasonable to consider pulseless VT and VF as the same
entity in need of the same interventions. It is the most common type of cardiac arrest
and most treatable; one. 'Flat-, definitive intervention is rapid defibrillation. A 200 J
shock should be delivered immediately. If this shock is unsuccessful, a second shock of
200 to 300 J and if necessary a third shock of 36U J should be administered.
 If cardiac arrest is witnessed but not monitored and a defibrillator is not
available a single precordial thump can be applied before beginning CPR and
while awaiting the arrival of the monitor- defibrillator.
 If at any time VF recurs following successful conversion, the series of upto 3
shocks should be repeated.
 If VT persists despite this initial treatment, pharmacologic therapy becomes
necessary, assuming that airway and ventilation are already controlled by the
anesthesiologist with endotracheal intubation and ventilation with 100%
oxygen.
 Drug therapy begins with epinephrine, assuming that peripheral IV line is
present.
 Initial drag injection can be given by this route, but if cardiac arrest persists, a
central venous catheter should be inserted to ensure more rapid drug delivery
and attainment higher peak arterial concentrations more quickly than peripheral
line.
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 If IV line is not present or cannot be inserted promptly, epinephrine can be
injected into tracheobronchial tree. Here a dose of 2 to 2.5 times the IV dose, is
recommended. (The drug increase both cerebral and myocardial blood flow).
 The recommended dope of epinephrine is 1.0mg (l0ml of 1: 10,000 dilutions).
This dose should be repeated every 3 to 5 min as long as car chic arrest persists.
 Following the initial injection of epinephrine after the 3rd stock, defibrillation
should be attempted against using 360 J. If VF persists, it is necessary to use a
drug with antifibrillatory actions. Lidocaine is the drug of choice.
 Lidocaine is given initially is a dose of 1.5rng/kg followed by 360 J shock. If VF
persists, lidocaine can be repeated in a dose of 1.5mg/ kg in 3 to 5min. with total
loading dose of 3mg, /'kg.
 If lidocaine is ineffective, bretylium can be used. Given in a dose of 5mg/kg,
followed by 360 J shock, If VF remains, a 2nd close of 10mg/kg can be given in 5
min followed by another shock. If necessary a. third dose of 10mg/kg can be
given.
 If still VF or pulseless VT remain refractory think of any electrolytic disorder like
hypokalemia, hyperkalemia, hypomagnesaemia treat them promptly.
 Procainamide and amiodarone can be used in refractory cases.
TORSADES DE POINTS: (TWISTING OF THE POINTS)

It is an atypical form of VT characterized by a twisting of a QRS axis around the baseline
and polymorphic appearance.
 Underlying electrophysiological derangement is non uniform delay in
repolarisation, manifested as a prolonged QT interval on ECG.
 Induced by drugs like quinidine, Procainamide, disopyramide and
phenothiazines and by bradycardia, hypokalemia, hypomagnesaemia or actute
ischemic and infarction.
 Definitive short term therapy is overdrive ventricular or atrial pacing, preferably
latter if AV Conduction is intact.
 Magnesium sulfate can also be used.
 For PVT (without QT prolongation) standard antiarrhythmics therapy as for VT
can be tried.
 If hemodynamic deterioration occurs with PVT, defibrillation should be used.
VENTRICULAR FIBRILLATION
 Ventricular fibrillation is an irregular rhythm resulting either from rapid
discharge of impulses from one or more ventricular foci or from multiple
wandering reentrant circuits in the ventricles.
 No clear cut ventricular complexes are seen.
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 As cardiac output is not generated, VP is synonymous with cardiac arrest.
 The common causes: Myocardial ischemia, hypoxia, hypothermia, c1cctric shock,
electrolyte imbalance and drug effects.
The characteristic are:

Heart rate : Rapid and grossly disorganized.
Rhythm : Totally irregular
P-wave : Not seen.
QRS complex : Not seen.
Significance:
As there is no effective cardiac output, life must be sustained by artificial means, such as
external cardiac massage.
Treatment:
Same as pulseless VT.
VENTRICULAR ASYSTOLE:
The complete and sustained absence of electrical activity, JS most often an irreversible
and therefore terminal event, caused by such derangements as uncorrected persistent
hypoxia, severe hyperkalemia, massive drug over dose, myocardial infarction or
hypothermia.
No ventricular electrical activity is seen. No ventricular output at all cardiac arrest.
Heart rate : Zero
Rhythm : Absent
P-Wave : Absent
QRS complex : Absent
Significance:
The 2nd most common type of cardiac arrest and most resistant to treatment.
Management:
CPR to be started immediately as for VF. Pacing has not been shown to improve survival
from asystole cardiac arrest.
DIAGNOSIS AND MANAGEMENT OF CONDUCTION DEFECTS:

Impairment or abnormalities of conduction of impulses through the conducting system
of the heart results in conduction defects.
The causes of conduction defects during surgery are
 Passage of pulmonary artery. Catheter through the right ventricle.
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 Manifestation of myocardial ischemia.
Three types of conduction system block are possible: SA block, AV block, and
intraventricular conduction block as shown below.
CONDUCTION DEFECTS:
1. Sinus node block
2. AV conduction defects
 First degree AV block
 Second degree AV block
Mobitz type 1
Mobitz type 2
 Third – degree (complete heart block)
3. Intraventricular conduction defects
 RBBB
 Incomplete and complete
 LBBB
 Incomplete and complete
 Left fascicular block (Hemi-block)
 LAHB
 LPHB
 Bifascicular block
 RBBB + LAHB
 RBBB +LPHB
 Alternating LBBB / RBBB
 AV conduction defect + LBBB or RBBB
4. Tri-fascicular block (bilateral bundle branch block + AV conduction defect).
SA node block:
 The block occurs at the sinus node.
 Because atrial excitation is not initiated, P waves are not found on ECG.
 The next beat can be a normal sinus beat, a nodal escape beat or a ventricular
escape beat.
 Permanent pace makers are the mainstay of therapy.
AV conduction block:
 May be complete or incomplete.
 First and second degree AV blocks are incomplete, 3rd degree AV block is
complete.
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First degree AV block:
 Found often in healthy hearts. Associated with coronary artery disease or
digitalis administration.
 Characterized by prolonged P-R interval i.e., P.R interval longer than 0.20 sec.
 All atrial impulses progress though the AV node to the purkinje system. Requires
no treatment.
Second degree AV block:

Associated with the conduction of some, but not all the atrial impulses to the AV node
and into the purkinje system.
It is further subdivided into two specific types.
1. Mobitz type 1 or Wenckebach

It is characterized by progressive lengthening of the P – r interval, until an
impulse is not conducted and the beat is dropped.
 Cause: Digitalis toxicity or MI, reflect disease of the AV node.
Treatment: it is relatively benign and does not require pace maker.
2. Mobitz type 2 block:
 It reflects disease of the bundle of his and purkinje tissues. It is less common,
more serious form of the 2nd degree heart block, since it frequently progress to
complete heart block. Dropped beats occur without any progressive lengthening
of the P-R interval. May require pace maker insertion.
Acute treatment with atropine 0.5 - 2mg IV or Isoprenaline 1 to 4µg/min IV.
Third degree AV block:
Also called complete heart block.

Occur when all electrical activity from the atria fails to progress into the purkinje
system.
The atrial and ventricular contractions have no relationship with each other, although
each chamber contracts regularly.
Ventricular rate - 40 beats/min.
QRS Complex: Normal if the pacemaker site is in the AV node, widened to longer than
0.12 sec when the pace maker site is located in the ventricle.
Significance: Heart rate is usually too slow to maintain adequate cardiac output.
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Treatment: Transvenous pace maker insertion.
INTRAVENTRICULAR CONDUCTION DEFECTS

Which is usually classified as LBBB, RBBB or Hemiblock
LBBB:
It is more serious of conduction disturbances.

QRS complex; wide, more than 0.12 sec. R wave is wide, notched in leads 1, AVL and V6.
Always associated with significant heart disease. Treatment is transvenous pacing.
RBBB
May be associated with chronic lung disease or ASD.
QRS complex: Exceeds 0. II sec. leads VI to V3 have broad rSR1 complex, whereas lead I
and V6 have wide S waves.
It may be of no clinical significance. It's quite common in healthy people.
Hemiblock: Is term used when one of two division of the left r -idle is blocked.
Marriott’s criteria for Left anterior Hemiblock are:

Left axis deviation (usually - 60°)
Small Q in lead I and AVL (0.045 sec) and small R in leads II, III and
AVF
A normal QRS duration. A late intrinsicoid deflection in lead aVF (>0.045 s) An
increased QRS voltage in limb leads.
The criteria for a left posterior hemiblock are as follows:

 Right axis deviation (usually -1200). Small R in lead I and avL and small Q in
leads, II, III and aVF, A Normal QRS duration.
 A late intrinsicoid deflection in lead aVF (>0.045 S). An increased QRS voltage in
limb leads and no evidence of right ventricular hypertrophy.
Bifascicular Block:
 RBBB in combination with block of one of the fascicles of' left bundle branch.
 Commonest cause is advanced coronary artery disease.
 If the anterior fascicle of the left bundle is blocked, ECG shows RBBB and left axis
deviation. If posterior fascicle of the left bundle is blocked, ECG shows RBBB and
right axis deviation.
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 Placement of temporary pacemaker is indicated, if' there is massive fluid shifts or
physiologic derangements are expected or there is any suggestion of syncope.
Trifascicular block:
Trifascicular block is diagnosed, when bifascicular block exists in addition to prolonged
PR interval. High incidence of progression to complete heart block. Perioperative
temporary Pacemaker insertion is indicated.
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Chapter 8 - ANESTHESIA FOR PATIENTS WITH IHD
(Non cardiac surgery)
INTRODUCTION
The increased life expectancy of Indians, coupled with increased incidence of coronary
artery disease among Indians has resulted in increased number of patients coming for
non cardiac elective or emergency surgery.
It is predicted that the percentage of patients older than 65 years of age presenting for
surgery is expected to increase from 25-35% over next 30 years and the number of
cardiac patient having non-cardiac surgery will double.
RISK FACTORS FOR DEVLEOPMENT OF IHD:

1. Cigarette smoking
2. Hypertension
3. Low HDL cholesterol (<40 mg/dl)
4. Diabetes mellitus
5. Family history of CHD
6. Age (men ≥45 yrs, women ≥ 55 yrs)
7. Life style faction
 Obesity (BMI ≥ 30 kg/M2)
 Physical inactivity
 Atherogenic diet.
8. Peripheral vascular disease - these may be associated with coronary artery
disease, limited activity because of claudication may mask clinical features of coronary
artery disease.
9. Chronic pulmonary disease - Hyperoxemia, hypercapnia, acidosis, and increased
work of breathing in an obstructive and restrictive pulmonary disease can lead to
further deterioration of already compromised cardiovascular system.
Myocardial stunning:
After a brief episode of severe ischemia, prolonged myocardial dysfunction with gradual
return of contractile activity occurred. This is termed myocardial stunning.
Myocardial hibernation: Severe chronic ischemia can result in diminished contractile
performance such as chronic regional wall motion abnormalities (RWMAs).
Imbalance between supply and demand can lead to ischemic heart disease.
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RPP (Rate Pressure Product): HR x SBP
Keep RPP less than 12,000
Triple index - HR x SBP x PCWP.
Keep less than 1,50,000
PRQ (Pressure rate quotient): MAP x HP
Quotient < 1.0 (ischemia)
Myocardial supply: Demand ratio (endocardial inability ratio)
Supply - Diastolic pressure time index (DPTI)
= (mean diastolic pressure - LVEDP) x duration of diastole
Demand - Systolic pressure time index (SPTI)
= mean arterial pressure x duration of systole.
DPTI: SPTI < 0.5 => subendocardial ischemia.
Myocardial oxygen supply
= Coronary blood flow X arterial oxygen content
Coronary blood flow
= Coronary perfusion pressure / resistance
Arterial oxygen content
CaO2 = 1.34 X Hb x O2 saturation + 0.0031 x PaO2.
Causes of IHD:
1. Atherosclerosis
2. Coronary spasm
3. Coronary arterial emboli
4. Congenital causes - LAD arising from pulmonary artery
5. Severe anemia
6. Aortic stenosis
7. HOCM.
CLINICAL PRESENTATION OF IHD:

Patients with IHD fall into 2 groups.
1. Patients with stable angina secondary to CAD.
2. Patients with acute coronary syndromes - composed of
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Actute coronary syndrome
No St elevation St Elevation
(minority)
UA NQMI Q-wave MI (majority Develop Q-wave MI)
SYMPTOMS, SIGNS, DIAGNOSIS, TREATMENT FOR SA, UA,

NSTEMIS STEMI
Stable angina Unstable angina & NSTEMI STEMI
DEF & patho-  Episodic clinical syndrome due Defined as angina pectoris or Abrupt decreases in coronary blood
pathyiology to transient myocardial equivalent ischemic discomfort with flow after a thrombotic occlusion of
ischemia one of 3 features. a coronary artery affected by mostly
1. Pain occurs at rest > 10m atherosclerosis. Infarction occurs
2. Severe, new onset plain when an atherosclerotic plaque

fissures, ruptures and leads to
3. Crescendo pattern
thrombus formation with occlusion
NSTEMI-C/F of UA with evidence of
of coronary artery and subsequent
myocardial necrosis, are reflected by
myocardial necrosis.
elevated cardiac markers caused by
imbalance in myocardial O2
supply/demand superimposed on a
coronary obstruction.
Symptoms  Chest discomfort, crescendo-  Chest pain Substernal,  Heavy deep squeezing chest
decrescendo pattern, 2-5 min, epigastrium, radiating at times plain with nausea, vomiting,
caused by exertion, relieved on with pale cool skin, tachycardia. anxiety, impending sense of
rest on NIG tablets grading of doom, radiation + pallor
angina.
Signs  Normal patient  Diaphoresis  Anterior MI-tachycardia,
 Look for evidence of  Cool skin hypertension.
atherosclerosis viz carotid bruit,  Inf. MI-bradycardia,
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abdominal aortic aneurysm,  S3 S4 hypotension.
xanthalesma, Fundoscopic  Rales –basal  Abnormal systolic precordial
changes, nicotine stains pulsation.
 S3 S4
 Splitting of S2
 Transient systolic murmur
 Pericardial friction rales
 ↓ Carotid pulse, ↓ SV
 ↑ Temperature
 ↓SBP by 10-15 mm of hg
Lab findings Stable angina Unstable angina & NSTEMI STEMI
a. ECG  ST segment, T wave changes  ST segment depression of
 LVH Signs transient ST elevation with/or

and T wave inversion.
 Conduction disturbance
(nonspecific)
 Stress ECG (later)
b. Serum cardiac  None  UA-No elevated enzymes  Rise in C Trop I & T

biomarkers  NSTEMI - ↑ in C Trop I & T  Rise in CK –MB
 CKMB  ↑ in myoglobin
c. Cardiac  Stress myocardial perfusion  Stress testing to detect ECHO

imaging imaging may shows areas of significant CAD  Wall motion abnormalities on 2
ischemia D ECHO.
 Stress ECHO more useful  RV infarction, ventricular
aneurysm, LV thrombus,
pericardial effusion.
 Radionuclide imaging
 Defects in perfusion (cold spot)

not specific
d. Non specific  -  - PMN

index tissue Leukocytosis
necrosis ESR ↑
Treatment 1. diagnostic coronary  A. Medical treatment a. Emergency management

arteriography 1. Anti ischemic treatment 1. Control of pain
2. Reassurance  Sublingual nitrates  100% O2
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3. Treatment of risk factor  IV NTG  Aspirin
4. Drug therapy   - blockers  Sublingual nitroglycerin
 Nitrates  Morphine  IV nitrates / NTG
 -blockers 2. Anti thrombotic therapy  Morphine
 Ca ++ blockers  Oral antiplatelets  -blockers
 Antiplatelets drugs  Subcutaneous heparin therapy 2. Reperfusion therapy
 Enhanced external counter  IV heparin therapy a. Pharmacological
pulsation 3. Surgical treatment - Streptokinase
 Surgical revascularization  Diagnostic coronary - Tpa, Rpa, surgical
1. PCI arteriography - PCi – Primary
2. CABG  PCI/CABG 3. CCU management
 Rest, diet, bowels, sedation
 Anti thrombotic
  - blockers
 ACE inhibitors
PREOPERATIVE CARDIAC RISK ASSESSMENT:

A risk factor is defined as any particular feature that may be discovered from the
patient’s clinical history, physical examination or special investigations that is
associated with an increased adverse event when compared to control population
without risk factor.
Various risk assessment systems have been used they include –
ASA status - 1963 revised

Advantages: Stratification of patients based on simple physical assessment. No
expensive tests, resources needed.
Disadvantages: No extra grade for age ≥ 75 years. Complexity and duration of surgery
not considered.
ASA status is a crude index.
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Goldman's CRI - 1977.
i. Age > years 5
ii. MI in previous 6 months 10
iii. S3 gallop or ↑ JVP (0-3 cm) 11
iv. Important aortic stenosis 3
v. Rhythm other than sinus, Pac on last preoperative 7
vi. >5 PVC/min at any time before 7
vii. PaO2, < 60 or PaCO2 > 50mm Hg, 3
K<3.00 mEq/L or HCO3 < 20 mEq/l
BUN > 50 or Cr> 3 mg/dl. Abnormal SGOT, signs of chronic liver disease, bed
ridden from non-cardiac cause
viii. Intraperitoneal, Intrathoracic, aortic surgery 3
ix. Emergency operation 4
Total 53
Class I 0-5 points (low risk)
Class II 6-12 points (intermediate risk)
Class III 13-25 points (high risk)
Class IV ≥ 26 points (very high)
Limitations are:
Index overestimated cardiac risk in class IV patients undergoing non cardiac surgery.
Index under estimated cardiac risk in class I patients undergoing cardiac/aortic surgery.
Study group included only elective non emergent cases.
Detsky’s Modified CRI - 1986

i. Age > 70 years 5
ii. MI < 6 months 10
iii. MI > 6 months 5
iv. Unstable angina 10
v. Pulmonary edema < 1 week 10
vi. Pulmonary edema in the past 5
vii. Non sinus rhythm PAC 5
viii. CCVSA class III 10
ix. CCVSA class IV 20
x. Critical As 20
xi. Emergency operation 5
xii. Poor general status 5
Total 120
(CCVSA Canadian cardiovascular society angina)
These indices may be useful in allocation of patient to a risk group but are not
necessarily useful in predicting individual risk.
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Lee’s revised CRI- 1999.
(Assign one point to each of the following variables)
i. High risk type of surgery (intra-peritoneal, intra-thoracic
or suprainguinal vascular procedures.
ii. History of IHD (history of MI, positive exercise test, current
complaint of ischemic chest pain or use of nitrate therapy
of ECG with Q waves)
iii. History of CHF
iv. History of cerebro-vascular disease
v. Insulin therapy for diabetes
vi. Preoperative serum creatinine > 2.0 mg/gl
Class I = 0 factors,
Class II = 1 factor
Class III = 2 factors
Class IV = >2 factors
Advantages:
Only 6 prognostic factors
Simple variables
Dependant on presence! absence of variable than estimating disease severity.
Can be easily used in PAE form.
Disadvantages:
Not applicable to emergency surgeries.
Not applicable to low risk population.
ACC, AHA guidelines: According to 2002 American College of Cardiology (ACC) and
American Heart Association (AHA) guidelines update on perioperative cardiovascular
evaluation clinical predictors are categorized into major, intermediate, and minor
factors as follows:
Major predictors
 Unstable coronary syndromes
o Acute or recent MI with evidence of important ischemic risk by clinical
symptoms or noninvasive study
o Unstable or severe angina (Canadian class III or IV).
 Decompensated heart failure
 Significant arrhythmias
o High-grade atrioventricular block
o Symptomatic ventricular arrhythmias in the presence of underlying heart
disease
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o Supraventricular arrhythmias with uncontrolled ventricular rate.
 Severe valvular disease
Intermediate predictors
 Mild angina pectoris (Canadian class I or II)
 Previous MI by history or pathologic Q waves
 Compensated or prior heart failure
 Diabetes mellitus (particularly insulin-dependent)
 Renal insufficiency.
Minor predictors:
 Advanced age
 Abnormal ECG (LV hypertrophy, LBBB, ST-T abnormalities)
 Rhythm other than sinus (e.g., atria! fibrillation)
 Low functional capacity (e.g., inability to climb one flight of stairs with a bag of
groceries)
 History of stroke
 Uncontrolled systemic hypertension.
NYHA Classification of heart failure

The New York Heart Association (NYHA) classification of heart failure is determined by
severity of symptoms including dyspnoea and fatigue.
 Class I : No symptoms
 Class II : symptoms with ordinary activity
 Class III : Symptoms with less than ordinary activity
 Class IV : Symptoms at rest
Specific activity scale of cardiac function

 Class I: Can carry at least 24 Ib up eight steps; carry objects that are at least 80
lb; jog/walk 5 mph; ski; or play basketball, football, squash, or handball.
 Class 11: can carry anything up a flight of eight steps without stopping, have
sexual intercourse without stopping, garden, roller skate, dance, or walk at a 4-
mph rate on level ground.
 Class III: Can shower without stopping, strip and make bed, mop floor, hang
washed clothes, clean windows, walks 2.5 mph, bowl, play golf (walk and carry
clubs), push power lawn mower, or dress without stopping because of
symptoms.
 Class IV: Can do none of the previous or have symptoms at rest.
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Surgery specific approach
Type of surgery may identify with likelihood of underlying heart disease e.g. vascular
surgery. Degree of hemodynamic cardiac stress varies with surgery specific techniques.
Higher risk is associated with profound alterations in HR, BP, vascular volume, pain,
bleeding, clotting tendencies, oxygenation and neuro humoral activation. Intensity of
these coronary and myocardial stressors determines likelihood of peri-op cardiac
events, particularly in emergency. Cardiac complications are 2-5 times higher with
emergency than with elective operations.
High (reported cardiac risk often >5%)

o Emergent major operations, particularly in the elderly.
o Aortic and other major vascular
o Peripheral vascular
o Anticipated prolonged surgical procedures associated with large fluids shifts
and/or blood loss.
Intermediate (risk generally <5%)

o Carotid Endarterectomy
o Head and neck
o Intraperitoneal and Intrathoracic
o Orthopedic
o Prostate
Low (Cardiac risk generally <1%)

o Endoscopic procedures
o Superficial procedures
o Cataract
o Breast
Cardiac functional capacity

Is a reliable predictor of future cardiac events. It is estimated from the ability to perform
daily activities expressed in metabolic equivalent (MET) levels oxygen consumption
(V02) of a 70 kg, 40 year man at rest is 3. mL/kg/min or 1 MET. MET greater than 4 is
considered the `tipping point'. Functional capacity is classified as: -
o Excellent (>7 METs)
o Moderate (4-7 METs)
o Poor (<4 METs)
o Unknown.
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Estimated energy requirements for various activities
1 MET
 Can you take care of yourself

 Eat, dress, or use the toilet
 Walk indoors around the house
 Walk a block or two on level ground at 2-3 mph or 3.2-4.8 km/h
4 METs
 Do light work around the house like dusting or washing clothes
>4 METs
 Climb a flight of stairs or walk up a hill
 Walk on level ground at 6.4 km/h
 Run a short distance
 Do heavy work around the house like scrubbing floors or lifting or moving heavy
objects
 Participate in moderate recreational activities like golf, bowling, dancing,
doubles tennis or throwing a baseball or football
10 METs
 Participate in strenuous sports like swimming, single tennis, football, baseball, or
skiing?
Euro SCORE
European system of cardiac operative risk evaluation (Euro SCORE) was constructed
from an analysis of 19,030 patients undergoing surgery at 128 centres in Europe.
During the 2000s, this score has been used and validated at across various centers
across the world making it the primary tool of risk stratification in cardiac surgery.
Factor Score
Age – per 5 yr or part thereof >60 yrs 1
Sex – male 1
COPD – on long-term bronchodilators/steroids 1
Extra-cardiac arteriopathy – any one or more of the following: claudication, > 2
50% carotid stenosis, previous or planned abdominal aortic/limb/carotid
intervention
Neurological dysfunction affecting ambulation / day-to-day functioning 2
Previous cardiac surgery involving opening of pericardium 3
Serum creatinine > 200 micromol/L 2
Active endocarditis under antibiotic therapy 3
Critical preoperative state: Any one or more of the following: VT, VF aborted 3
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sudden death, preoperative cardiac massage, preoperative ventilation,
preoperative inotropic support, preoperative IABP or preoperative renal
failure (anuria/oliguria < mL/hr)
Unstable angina requiring Iv nitrates until arrival in OT 2
Moderate LV dysfunction: LVEF 30-50% 1
Severe LV dysfunction: LVEF < 30% 3
Recent MI:< 90 days 2
Pulmonary hypertension: systolic PAP > 60 mmHg 2
Emergency surgery 2
Major cardiac procedure other than CABG ± CABG 2
Surgery on thoracic aorta 3
Post-infarct rupture 4
 Low risk : 0-2 Expected mortality 0.85
 Medium risk : 3-5 Expected mortality 3.0%
 High risk : > 6 Expected mortality 11.2%
APPROACH TO PRE-OPERATIVE CARDIAC ASSESSMENT:

Step-1: Determine the urgency of non-cardiac surgery. If patient requires immediate
surgery, there is no time for the anesthetist for further cardiac assessment or treatment.
Needs proper per-operative medical management and surveillance. Post-operative risk
stratification by cardiac assessment is done after surgery over the patient has
recovered.
Step-2: Has the patient undergone coronary revascularization in the past 5 years? or
percutaneous cardio intervention (PC[) from 6 months to 5 years previously? And if the
patient does not have S/S of ischemia in the interim the likelihood of perioperative
MI/Cardiac death is extremely low. Further cardiac testing is not necessary.
Step-3: If patient has undergone extensive coronary evaluation with either
invasive/non-invasive techniques within 2 years and findings show that he is
adequately amended with favorable findings, repeat testing is usually unnecessary. If he
has experienced a definite change or new symptoms of coronary ischemia, he should be
evaluated.
Step-4: If the patient has one of the major clinical predictors of risk, and if he is for
elective non-cardiac surgery, the surgery should be delayed or cancelled till the cardiac
problem is clarified and appropriately treated. They need medical treatment or may be
referred for coronary angiography.
Step-5: Patients with intermediate clinical predictors of risk should be evaluated of
their functional capacity as determined by HIO daily activities (Duke's activity) status
index.
Step-6: Patients with intermediate predictors with moderate or excellent functional
capacity can generally undergo intermediate risk surgery with little likelihood of
preoperative MI. Patient with poor functional capacity or those with combination of
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only moderate functional capacity and high risk surgery are considered for further non-
invasive testing.
Step-7: Non-cardiac surgery is generally safe for patients with minor or no clinical
predictors of cardiac risk and with moderate or excellent functional capacity regardless
of surgery type. Patients with poor- functional capacity facing high risk surgery are
considered for further testing.
Step-8: After the results of non invasive testing one may decide for medical
therapy/cardiac catheterization leading to coronary revascularization and may delay or
cancel the proposed non-cardiac surgery.
Laboratory testing:
Investigations –
Blood, Urine, Specialized studies.
Blood: Hb%, PCV,
Blood sugar
Serum electrolytes
Blood urea, Serum creatinine
Coagulation profile
LIFT
Chest X-ray
Specialized studies
1. ECG - Resting ECG, Exercise ECG,
Ambulatory ECG (Holter monitoring)
2. ECHO - Resting, following exercise
Dobutamine stress echo.
3. Myocardial perfusion scintigraphy
IV dipyridamole/ adenosine,
MPI Th 201, Tc 99,
4. Radionuclide ventriculography (RNVG).
7. Coronary angiography.
PREOPERATIVE TESTING FOR RISK ASSESSMENT:

Should be limited to patients in whom the result will effect the treatment and outcome.
Aims of tests:
1. To identify perioperative myocardial ischemic /arrhythmias.
2. To estimate perioperative cardiac risk and prognosis
3. To provide objective measure of functional capacity.
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Recommendations for pre-operative 92 lead resting ECG are
Class I: Recent episode of chest pain/ischemic equivalent in clinically intermediate /
high risk patients scheduled for an intermediate/high risk surgery.
Class II(a): Asymptomatic persons with diabetes mellitus.
Class II (b):
1) Patients with prior coronary revascularization
2) Asymptomatic male>45 years old or female >55 years old with two or more
atherosclerotic risk factors.,
3) Prior hospital admission for cardiac causes.
Class III: As a routine tests in asymptomatic subjects undergoing low risk surgery.
Ambulatory ECG monitoring:

24-48 hours ambulatory monitoring of ECG for ST changes may be the choice for
patients who are unable to undergo exercise stress test, but limitations are, patients
with LBBB. LVH with strain. ST-T changes with digoxin because of difficulties in
analyzing ST segment changes.
ECHOCARDIOGRAPHY:
Indications for pre-operative echocardiography examination are:
1) IHD patients with hypertension of long duration
2) IHD patients with diabetes of long duration
3) Unexplained breathlessness in a pre-operative patients
4) Patients with known, dysfunction of the ventricles with or without recent CCF.
5) Any of the above patients schedule for surgery during which there is a likelihood
of massive fluid shift.
Exercise stress testing:

Aim is to provide an objective measure of functional capacity to identify the presence of
important pre-operative Ml and the cardiac arrhythmias. In addition, it gives
information about the threshold heart rate and BP at which either ECG changes or
symptoms occur. Based on this anesthetist can have a target heart rate or BP during
peri-operative period.
TREADMILL TEST RESPONSES PREDICTIVE OF SEVERE MULTIVESSEL AND /OR LEFT

MAIN CORONARY ARTERY DISEASE:
Electrocardiographic responses:
o Horizontal or down sloping ST segment > 2mm.
o Early onset (first 3 min.) of ischemic ST segment depression or elevation with
low work load.
o Persistence of ST depression after exercise for 5 min or longer.
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o Complex ventricular arrhythmias occurring at low heart rates (120-130
beats/min.)
Non-electrocardiographic criteria
o Low achieved heart rate (<_120 breaths/min)
o Hypotension (≥ 10mm Hg fall in systolic blood pressure) during exercise.
o Rise in diastolic blood pressure ( ≥110-120 mmHg)
o Low achieved rate pressure product ( ≤ 15,000)
o Inability to exercise beyond 3 minutes.
Non-exercise stress testing:

For patients with decreased joint mobility, dementia, muscle weakness, claudication or
exertional angina.
There are two techniques:
1. Dobutamine stress echocardiography

2. IV dipyridamole/adenosine myocardial perfusion imaging.
Dobutamine stress echocardiography:

The predictive value of a positive test is 7-25% for MI /cardiac disease. The predictive
value of a negative test is 93-100% for MI/cardiac disease. Presence of a new wall-
motion abnormality is powerful determinant an increased risk for perioperative events.
Worsening of pre-existing wall motion abnormalities is also important.
IV dipyridamole/adenosine myocardial perfusion imaging:

Patients receive dipyridamole 0.5mg/kg IV over 4 minutes while their HR, BP and ECG
were monitored. After 2 minutes, when the effect of dipyridamole was maximal 2m ci of
thallium - 201 was administered IV. 5 minutes after the administration of thallium,
initial images were taken for 8 consecutive minutes. Delayed images are taken 3 hours
later. Dipyridamole causes vasodilation and increases the coronary blood flow. The
stenotic vessels cannot dilate more, so areas of myocardium supplied by them, take up
less thallium and show a filling defects on immediate image. This test is preferred to
exercise/dobutamine stress test in patients with left bundle branch block.
Recommendations for exercise/pharmacological stress testing:
Class I
1. Diagnosis of adults patients with intermediate pretest probability of CAD.
2. Prognostic assessment of patients undergoing initial evaluation for
suspected/proven CAD: evaluation of subjects with significant change in clinical
status.
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3. Demonstration of proof of MI before coronary revascularization.
4. Evaluation of adequacy of medical therapy; prognostic assessment after an acute
coronary syndrome.
Class II (a): Evaluation of exercise capacity when subjective assessment is unreliable
Class II (b):
1. Diagnosis of CAD patients with high/low pretest probability; those with resting
ST depression less than 1 mm, those undergoing digitalis therapy, and those with
EGG criteria for LVH.
2. Detection of re-stenosis in high risk asymptomatic subjects within the initial
minutes after PCI.
Class III:
1. For exercise stress testing, diagnosis of patients with resting EGG abnormalities
that preclude adequate assessment e.g pre-excitation syndrome, electronically
paved ventricular rhythm, rest ST depression greater than 1 mm or LBBB.
2. Severe co-morbidity likely to limit life expectancy or candidacy for
revascularization.
3. Routine screening of asymptomatic man1women without evidence of CAD.
4. Investigation of isolated ectopic beats in young patients.
CORONARY ANGIOGRAPHY:
Recommendations for coronary angiography in pre-operative evaluation before (or
after) non-cardiac surgery:
Class I: Patients with suspected/known CAD
1. Evidence for high risk of adverse outcome based on non-invasive test results.
2. Angina unresponsive to adequate medical therapy.
3. Unstable angina, particularly when facing intermediate risk/high risk non-
cardiac surgery.
4. Equivocal non-invasive test results in patients at high clinical risk undergoing
high risk surgery.
Class II (a):
1. Multiple markers of intermediate clinical risk and planned vascular surgery
(noninvasive testing should be considered first)
2. Moderate to large region of ischemia on non-invasive testing but without high
risk features and without lower LVEF.
3. Non-diagnostic non-invasive test results in patients of intermediate clinical risk
undergoing high risk non cardiac surgery.
4. Urgent non cardiac surgery while convalescing from acute MI.
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Class II (b):
1. Peri operative MI
2. Medically stabilized class III,'IV angina and planned low risk or minor surgery.
Class III:
1. Lower risk non cardiac surgery with known CAD and no high risk results on non-
invasive testing.
2. Asymptomatic after or re-vascularization with excellent exercise capacity
(greater than or equal to 7 METs).
3. Mild stable angina with good L V function and no high risk non-invasive test
results.
4. Non-candidate for coronary revascularization owing to concomitant medical
illness, severe LV dysfunction (LVEF <0.2) or refusal to consider
revascularization.
5. Candidate for liver/lung/renal transplant more than 40 years old on part of
evaluation for transplantation unless non-invasive testing reveals high risk for
adverse outcome.
MYOCARDIAL:
CK - MB rises within 4 to 8 hours after MI and returns to normal by 48 to 72 hours.
CK - MB: CK - 2.5 --) suggests MI,
cTnl - remain elevated for 7 to 10 days after acute MI.
cTnT - remain elevated for 10 - 14 days.
CK and CK - MB levels generally do not rise in unstable angina.
Pre-operative therapy: Surgical /medical

percutaneous coronary intervention (PCI)
There are no proper studies conducted with regard to benefit of PCI before a non
cardiac surgery.
Delaying surgery 2-4 weeks after stent placement or after stopping of antiplatelet
agents, non cardiac surgery can be performed.
Pre-operative CABG:
It is indicated in patients with following conditions
1. Suitable viable myocardium with left main stenosis
2. 3-vessel CAD
3. 2 vessel disease involving severe proximal LAD obstruction
4. Intractable coronary ischemia despite maximal medical therapy.
The timing of the procedure depends on the urgency of the non-cardiac surgical
procedure balanced against stability of underlying CAD. Patients undergoing elective
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non cardiac procedure who have high risk coronary anatomy and in whom long term
outcome would likely to be improved by CABG should undergo revascularization before
their elective non cardiac procedure of high intermediate risk.
THERAPEUTIC INTERVENTIONS IN ACTUE INFARCTION:

Following classes of drugs are used
1. Nitrates: Commonly used are -
a. Nitroglycerin (NTG)
b. Isosorbide dinitrate
Mechanism of action: It releases No, which activates guanylate cyclase. This increase
the CGMP levels which inhibits Ca entry into vascular smooth muscle and may increase
Ca uptake in SER to produce vasodilatation.
On heart:
Peri-operative NTG therapy:

Indication:
Arterial hypertension 20% above the baseline values.
2. PCWP > 18-20 mmHg
3. AC and V waves greater than 20 mmHg on PCWP wave form
4. ST segment changes > 1 mm
5. Regional wall motion abnormalities
6. Acute right / left ventricular dysfunction
7. coronary arterial spasm.
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Recommendations are:
 Class I: High risk patients previously taking NTG who have active signs of MI
without hypotension.
 Class II (b): As prophylactic agent for high risk patients to prevent MI and cardiac
morbidity, particularly in those who have required nitrate therapy to control
angina. The recommendation for prophylactic use of NTG must take into account
the anesthetic plan and patient hemodynamics and must recognize that
vasodilatation and hypovolemia can readily occur during anesthesia and surgery.
 Class III: Patients with signs of hypovolemia/ hypotension.
Peri-operative anti-hypertensive therapy

IV 1-3 pg/kg min
Same are resistant: SNP may be added
Peri-operative ischemia treatment

Prophylactic ischemic protection 0.5 – 1 µg/kg/min
Peri-operative treatment of LVF

Side effects
1. Methemoglobinemia, theoretical concern - in clinical practice - rare

2. V/Q mismatch by depressing HPV
3. Known to cause inhibition of platelet function
4. Nitrate tolerance/dependency.
 Blockers
They are subdivided based on –
a) Cardio selectivity
b) Intrinsic sympathetic activity (ISA)
c) Membrane stabilizing activity (MSA)
d) Concomitant a blocking properties.
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Drug Cardio selectivity ISA MSA

Propranolol No 0 ++
Nadalol No 0 0
Pindolol No + ±
Timolol No ± 0
Sotalol No 0 0
Metaprolol Yes 0 ±
Atenolol Yes 0 0
Acebutolol Yes + ±
Esmolol Yes 0 0
Mechanism of action:
Bind to  receptors and inhibit the ability of catecholamines and other
sympathomimetic to provoke  responses. Effect is more when there is more
sympathetic stimulation. Decreased heart rate because of predominant
parasympathetic tone.
Increased SVR because

(a) Direct effect through blockade of peripheral R2 adrenergic mediated
vasodilatation and
(b) Indirect effect by reflex a mediated vasoconstriction occurring because of
decreased BP.
Decreased heart rate → increased diastolic time → increased cardiac perfusion
Decreased heart rate, decrease BP, decrease contractility → decreased myocardial
oxygen demand.
 blockers are primarily used for the management of –

Peri-operative hypertension
Peri-operative MI
Dysrrhythmias
Esmolol: It is a water soluble cardio selective, (3 blockers with no ISA/MSA.
Mainly useful in acute care setting because of its titrabiiity and short duration of action.
Useful for acute treatment of SVT, AMI, Peri-op tachycardia, Per-op, hypertension
Loading dose of 0.5 - 1 mg/kg - slow bolus over 30-60 sec.
Maintenance 25-300 µg/kg/min.
Reversal of blockade occurs 10-20 min after the infusion is stopped.
Metaprolol: Used in AMI - 5 mg every 2-5 minutes IV, for a total of 3 doses.
Propranolol: It is the proto type  blockers against which all others are compared.
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Hemodynamic effects - Decrease heart rate
Decrease contractility
Available in oral 40-800 mg/day
IV 0.05 mg/kg given in increments of 0.5 to 1 mg and every 5 minutes. Also used to
suppress the hemodynamic stress associated with intubation.
Labetalol
Has both a and  blocking properties. a: blocking effectiveness is 1:3 when given oral
and 1:7 when given IV.
Decreases SVR without significant changes in CO & HR (so can be used in patients who
cannot tolerate bradycardia).
Used for controlled hypotension (25-50 mg IV) and hypertensive emergencies.
Side effects of  blockers:

Bradycardia
Heart block
Worsening of CHF
Bronchospasm
Sedation
Calcium channel blockers:

They block the calcium channels when they are open and also cause allosteric
modulation of calcium channels and thus reduce intracellular calcium and cause
vasodilatation.
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Comparative CV effects of the calcium channels blocking drugs:
Average Metabolic
Available
Drug elimination activity and Indications Dosage
from
half-life excretion
Diltiazem 30 & 60 mg 4-5 Hepatic SVT oral HTN Initial: 30 mg 4
tab. metabolism; treatment times daily,
metabolites maximum 240
partially active: mf/day (probably
70% GL higher) IV 0.25
excretion mg/kg over 2 min.
repeated in 15
min. if needed
infusion
10mg/hr/24 hr
Nifedipine 10 mg 3-4 (wide Hepatic Angina HTN Initial 10mg ¾
capsules individual metabolism; emergencies times daily
variation) inactive maximum 120-
metabolites; 180 mg/day
80% renal
excretion
Verapamil Injectable 3-7 Hepatic SVT IV bolus of 0.075-
solution metabolism; 0.15 mg/kg
80 and 120 active (average in adults
mg tablets metabolites; 5-10 mg);
70% renal maintenance
excretion infusion of 0.005
mg/kg/min Oral:
initial 70mg ¾
times
Daily: Maximum
480mg/day
Nicardipine Injectable 10 min Hepatic Residual HTN IV bolus of 2.5 – 5
solution metabolism; despite  - mg; maintenance
30mg inactive blocker 1-5 µg/kg/min
capsules metabolites therapy oral initial 20mg 3
times daily:
maximum 40mg 3
times daily.
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Side effects of anti anginal drugs:
Hypotension Decreased HR Interaction
GI Broncho
flushing LVD atrioventricular with
symptoms constriction
headache block anesthetics
 blockers 0 ++ +++ + +++ Halothane
Mask
hypoglycemia
Nitrates +++ 0 0 0 0 -
Diltiazem + + + 0 0 Myocardial
Nifedipine +++ 0 0 0 0 depression and
Nicardipine +++ 0 0 0 0 per
Verapamil + + ++ 0 vasodilation
produced by
volatile
anesthetics
exaggerated
Recommendation for peri-operative medical therapy:
Class I
1.  Blockers required in the recent past to control symptoms of angina or patients
with symptomatic arrhythmias/hypertension.
2.  Blockers patients at high cardiac risk owing to the finding of ischemia on pre-
operative testing who are undergoing vascular surgery.
Class II (a)
 Blockers pre-operative assessment identifies untreated hypertension, known
coronary disease or major risk factors for coronary disease.
Class II (b)
α2 agonists: peri-operative control of hypertension or known CAD or major risk factors
for CAD.
RISK FACTORS FOR REINFARCTION FOLLOWING ANESTHESIA FOR NONCARDIAC

SURGERY
1. MI with CHF
2. Angina, TJVP, TPCWP
3. Intra thoracic/ upper abdominal surgery
4. Intraoperative hypertension (9.2%), hypotension (11.5%, tachycardia.
5. Time internal of previous MI.
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0-3 months - 30%
3-6 months - 15%
> 6 months - 06%
6. Emergency operations.
7. Ejection fraction EF < 0.35 – 75-85%
EF 0.35 – 0.4 -19-20%
8. Duration of surgery > 3 hours.
Pre-anesthetic evaluation:
 Thorough history taking → eliciting relationship between symptoms and activity

levels. Including drug history, previous hospital admissions, any interventional
procedures.
 Complete physical examination
 Airway assessment.
Routine lab investigations.

PRE-OPERATIVE PREPARATION
 Continue the anti-hypertensives/anti anginal drugs till the time of surgery

 ACEI is skipped on the day of surgery
 Aspirin/clopidogrel - stopped 7 days before
 Ticlopidine-stopped 14 days before,
 Platelet GPllb/Illa inhibitors:
 Abciximab - 24 -48 hours
Eptifibatide & tirofiban -4-8 hours
 Warfarin - Should be discontinued 4 - 5 days prior to surgery.
 If emergency - CNB can be done if INR < 1.5
Vitamin K 10-25 mg im/IV - slowly 12-24 hours prior to surgery.
 Heparin: Delay the heparin administration - 1-2 hours after the procedure.
Remove the catheter after 2-4 hours of last heparin dose. Re-heparinized only
after 2 hours of removal of catheter.
 LMWH: Risk of bleeding/spinal hematoma are decreased. CNB can be performed
safely after 12-24 hours of administration. Catheter should be removed 12 hours
after the last LMWH administration.
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 High risk patients - pre-operative NTG infusions may be started.
 Prophylaxis for venous thromboembolism may be required for some surgeries
like major surgery in a patient with clinical conditions associated with venous
thromboembolism risk or patients older than 60 years without risk factors, total
hip replacement, intracranial neurosurgeries etc.
INTRAOPERATIVE MONITORING
1. Pulse oximetry - Pulse rate, rhythm, volume and oxygen saturation
2. NIBP
3. Blood sugar monitoring - diabetic patients need careful treatment va6ith
infusions of short acting insulin based on frequent blood sugar determination.
4. ECHCO,
Esophageal ECHO (TEE) - TEE provides a visual assessment of left ventricle (LV)
volume and function during the surgery. It can give a more accurate assessment of
ventricular filling than the P.A. catheter. New alterations in wall motion can help assess
the presence and significance of intraoperative ischemia a view of right ventricle
function and most of the ascending aorta are added benefits of TEE.
Doppler TEE
Commonly used for cardiac surgery. But less frequently used in non-cardiac
surgery.
It may show mild hypokinesia to severe hypokinesia or worsening of earlier wall
motion abnormalities, akinesia or dyskinesis.
5. ECG
Intracardiac ECG
Endotracheal ECG - Most useful in pediatric patient:
Intracoronary ECG: Has greater detection of acute ischemia than with surface ECG.
Selection of monitoring leads is based on pre-operative ischemic site, evidence of
ischemia on exercise ECG and stenosed vessels.
ECG leads Coronary artery responsible for ischemia
II, III, aVF RCA
I, avL CCA
V3 – V5 LAD
Sensitivity of leads to monitor ischemia

V3-61%, V5-75% V4+V5-90%, II + V5 -80%, II + V4+V5-98%
MI is defined as persistent ST-T changes lasting 60 seconds.
If only one lead can be displayed, V5 should be used because lead V5 has the greatest
sensitivity.
(75% intraoperatively and 89% during exercise treadmill testing).
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Criteria for diagnosis of ischemia (under anesthesia)
Up sloping ST segment - 2mm depression; 80 ms after J point
(The use of computerized STsegment analysis in high risk patient improves MI

detection).
5. Pulmonary artery pressure monitoring
Mainly two changes:

 Increased in PCWP (because increased LVEDP → because decreased atria
l/ventricular compliance acute LV dilatation). Papillary muscle dysfunction.
 Large AC & V waves - (because alteration in diastolic and mitral valvular
function).
6. Temperature monitoring
In a RCT, it is found that hypothermia was associated with increased risk of MI.
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7. CVP: Use right atrium (RA) as zero reference point (mid axillary line, 4th
intercostal cartilage). Normal range with spontaneous respiration is 0-6 cm Hz0.
ischemia causes abnormal V waves.
8. ETCO2: To avoid hypercapnia
9. Intra-arterial pressure monitoring
10. U.O.P: To know renal function, renal perfusion and appropriate, fluid
replacement. (Input - output chart)
HAEMODYNAMIC GOALS DURING ANESTHESIA ARE:

Objective is to maintain a favorable myocardial supply - demand relationship.
1. Autonomic mediated increases in HR and BP should be controlled by deep
anesthesia or adrenergic blockade and excessive reductions in coronary
perfusion pressure or arterial oxygen content are to be avoided.
2. Diastolic arterial pressure should be generally maintained at 50mm Hg or above.
Higher diastolic pressure may be preferable in patient with high grade coronary
occlusion.
3. Excessive increase in LVEDP (such as those caused by fluid overload) should be
avoided because they ↑ L,V. after load and can ↓ sub endocardial perfusion.
4. Adequate blood Hb > 9-10 mg/dl and arterial oxygen tension (>60mm Hg)
should generally be maintained.
Choice of anesthesia:
 There is. No best myocardium protective anesthesia techniques.
 It is based on physical status of the patient i.e., co-existing diseases and surgical
procedure.
 With ASA4 and 5 - regional anesthesia has higher mortality. So GA is used.
 For ASA 3 Patients - regional anesthesia may be used with precautions.
 For ASA 2 Patients - regional is preferred over general anesthesia.
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Regional Anesthesia General Anesthesia
Patient is awake, easy assessment of complications Unconscious, difficult to assess
Decreased stress response Increased stress response: Ischemia
Decreased catecholamines Increased catecholamine: ischemia
Decreased bleeding may increased
Less use of drug that cause Increased
myocardial depression Increased
Post-operative analgesia decrease
Decreased DVT risk
FRC is preserved with epidural anesthesia
Not suitable for uncooperative patients Hypotension, Suitable
bradycardia is unpredictable, difficult to control can Hypotension with induction and
cause ischemia stroke predictable and can be controlled
Not suitable for surgeries with volume shift only for quickly. Suitable
ASAI-3 Any patient
Regional Anesthesia/ Local Anesthesia
 Proper premedication
 Supplemental oxygen
 Monitoring - Sa02, ECG
 Good verbal communication
 Careful titration of dose / level of block
Adrenaline may increase heart rate and BP
Plasma concentration of LA may be increased (P blockers, CCB)
Hypotension and bradycardia should be treated aggressively
Monitored anesthesia: Includes the use of local anesthesia supplemented with
intravenous sedation I analgesia and is believed to be associated with the greatest
marginal safety.
Monitored anesthesia care is however associated with greatest incidence of "30 day
mortality". Although this technique can eliminate some of the undesirable effects of
general or neuraxial anesthesia.
Inadequate local anesthetic block could result in an increased incidence MI and cardiac
dysfunction. To achieve the desired effect. Excess sedation may be needed,
compromising the overall safety.
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Preparation:
Emergency drug tray: load the drug with appropriate dilution and label properly.
Laryngoscope with two Macoy blades, Macoy blade,
Flexi metallic stylet

Appropriate ET tubes
Defibrillator
Suction apparatus
OT table - in working condition.
Senior / colleague to assist in case of emergency.
Pre-medication:
 Allaying fear, anxiety, pain preoperatively are desirable goals in patients with
CAD.
 Satisfactory premedication prevents sympathetic activation which adversely
effects myocardial oxygen - supply demand balance.
 Over medication is equally detrimental. However, should be avoided because it
may result in hypoxemia, respiratory acidosis and hypotension.
 Benzodiazepines alone or in combination with a opioid is most commonly used.
(morphine 0.1 - 0.15 mg/kg).
 Concomitant administration of oxygen via nasal cannula helps to avoid
hypoxemia following premedication.
 All antianginal medications especially  blockers should be continued up to time
of surgery. As sudden withdrawal of antianginal, and  blocker can precipitate
sudden increase ischemic episodes (rebound).
 Prophylactic  blockade has been shown to reduce the incidence of intra-op and
post-op ischemic episodes and appears to be superior than calcium channel
blockers prophylaxis.
α2-agonists: Stimulate prejunctional receptors and decrease nor-epinephrine release

producing sedation, anxiolytic, and analgesia.
Clonidine: As a premedication reduces HTN, tachycardia, and nor-epinephrine levels. It
also suppresses normal post-operative increase in fibrinogen levels and antagonizes
epinephrine induced platelet aggregation, also shown to decrease intraoperative MI.
Dexometomedine and mivozerol - are more selective α2-agonists → reduce
postoperative MI events in high risk patients.
Control the heart rate 20% below the ischemia threshold or about 60 bpm with esmolol.
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Induction:
A smooth induction is essential to 'prevent hypotension, hypertension, and tachycardia,
which can precipitate MI.
In patients with
Good left ventricular function

 Anesthesia is induced with fentanyl 5-10 µg/kg and thiopentone 2-4 mg/kg,
patient is ventilated by mask with 100% oxygen. After administration of
Succinylcholine 1 mg/kg or pancuronium 0.1 mg/kg the patient is intubated.
 Alternatively anesthesia is induced with thiopentone 4mg/kg and deepened with
fentanyl 5 to 10 µg/kg and 2.0% isoflurane for 3 to 5 min. When adequately
anaesthetized, the patient is given muscle relaxant and intubated.
 If the patient has a h/o hypertension or initial BP is more than 150 mmHg
systolic, fentanyl 10µg/kg is usually required to blunt HTN and tachycardia from
intubation.
Poor left ventricular function

 Potent inhalation agents enflurane, isoflurane and halothane are avoided during
induction and maintenance of anesthesia.
 More midazolam 2-5 mg and less thiopentone 1-2 m4/kg will be given for
induction.
 Ketamine - Ketamine by itself is relatively contraindicated because its indirect
sympathomimetic effects can adversely affect myocardial oxygen demand supply
balance.
 The combination of benzodiazepines and Ketamine may be most useful in patient
with poor ventricular function (EF < 30°lo).
 Alternatively, Etomidate 0.2mg/kg may be given for induction.
ETOMIDATE: (a carboxylated imidazole derivative)

0.3 mg/kg IV acts in 10-60 seconds and its duration of action is 6-8 min. etomidate is
non-cumulative with repeated administration.
It appears to have a better hemodynamic profile than other commonly used induction
agents, especially in the setting of CHD. It also attenuates the reaction to tracheal
intubation to a greater extent than thiopentone. If the patient has poor LV, etomidate is
a good choice of induction.
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Induction agents:
HR MAP SVR Contractility Pressor effect Does
Thiopentone ↑↑ ↓↓ ± ↓ - 5-6 mg/kg
Propofol - ↓↓ ↓ ↓ ↓ 1-5-2.5 mg/kg
Ketamine ↑↑ ↑↑ ↑ ↑/↓ - 1-2 mg/kg
Midazolam - -/ ↓ + - - 0.1-0.2 mg/kg
Fentanyl -/↓ - - - ↓↓ 3-30 µg/kg
Relaxants:
Intermediate acting neuromuscular blocking agents such as vecuronium, Cisatracurium,
and Rocuronium can be used safely because they do not produce significant
cardiovascular changes.
Autonomic margin of safety: The difference between the dose of neuromuscular
blocking drug that produces neuromuscular blockade and circulatory effect is defined as
"autonomic margin of safety".
 An ED95 dose of pancuronium that produces neuromuscular blockade is also
likely to produce circulatory (heart rate changes) and the autonomic margin of
safety is narrow.
 Vagolytic effect of pancuronium can be used to balance bradycardia caused by 
blocker / opioid.
 Sch. can also be used for intubation.
Succinylcholine
 Circulatory effects of Succinylcholine are due to stimulation of autonomic ganglia
and cardiac muscarinic receptors → variable effect on HR and BP.
 Net effect influenced by pre-existing relative sympathetic and parasympathetic
tone, pre-medication with anticholinergic and  blockade.
 Bradycardia may be seen in patient taking  blocker following administration of
Succinylcholine.
Intubation
 Attenuation of pressor response is done by:
Short and smooth intubation less than 15 seconds.
 Lignocaine spray
Inj. Lignocaine 1.5 -2 mg/kg IV 90 sec. -3mm. before or
Inj. Fentanyl 2 - 3 µg/kg IV 3-5 min before or
Inj. Esmolol 2-3 mg/kg IV 60 sec-I min before used
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Inhalation agents:
When LV function is good, both isoflurane and halothane are commonly used along with
N2O.
With compromised LV function - titrated dose of isoflurane with or without N2O is used.
Controlled ventilation is preferred avoiding hyperventilation.
Maintenance
As we have to extubate the patient at the end of surgery, it is better to use nitrous oxide
and a combination of low-dose isoflurane and fentanyl for maintenance.
02 + N2O (50:50): graded doses of halothane I isoflurane + vecuronium and IPPV. or 02 +
air, titrated dose of isoflurane, fentanyl, vecuronium and IPPV.
High dose of narcotics should be avoided if postoperative ventilation is not planned.
Circle system with C02 absorber is used to prevent hypercapnia.
Reversal:
Reversal of muscle paralysis with neostiogmine doesn't have any determental effects in
patient with CAD. Use of glycopyrrolate instead of atropine may decrease likelihood of
transient tachycardia.
Extubation
At the end of surgery extubate when patient is awake, breathing adequately and
neuromuscular blockade is fully reversed, to prevent tachycardia and HTN, associated
with extubation a emergence, low dose of 1 mg/kg lidocaine or esmolol or 0.1 mg/kg
labetalol, diltiazem 2 min before extubation.
Post-operative ventilation may be required if:
a. Intra operative complications.

b. Unstable patients.
c. Compromised cardiac state
d. Peri-operative ischemia
Peri-operative fluid management

 Well hydrated before induction to avoid hypotension.
 In compromised cardiac function, it is guided by CVP.
 Patients on chronic diuretic therapy, require monitoring for hypovolemia and
hypokalemia
 Colloids are preferred to avoid volume over load.
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Peri-operative Complications
A. Myocardial ischemia
Prevention
 Continue cardiac medications until the time of operation.
 Tachycardia prophylaxis before intubation with 1 mg/kg IV esmolol.
 Maintaining hemodynamic parameters.
Treatment
A) Ischemia associated with tachycardia hypertension / both
 Ensure adequate depth of anesthesia, oxygenation (100%) and ventilation.

 Esmolol 50-100 µg IV (or propranolol 0.5-1 mg/kg IV, until heart rate is <
90/min)
 Start NTG 1-2 µg/kg/min to maintain SBP 90 to 110.
 NTG has been shown to reverse MI intraoperatively. However prophylactic use
of NTG in high risk patient may have no effects and actually lead to
cardiovascular decompression, through decrease in preload.
 NTG should be restricted to high risk patient previously an NTG, who have active
signs of MI without hypotension. NTG patch / paste may have uneven absorption
intra operatively and so NTG IV infusion is preferred.
 If hypotension (SBP < 80%) → judicious volume or phenylephrine 100, µg/min
infusion.
B) Ischemia with severe hypertension, no tachycardia
 Nicardipine 0.3 mg IV every 30 seconds.

 Start NTG infusion or
 Nifedipine 10 mg S/L
C) Ischemia with no apparent cause
S - NTG infusion
Nicardipine infusion - 3 mg/hour
Sublingual nifedipine
D) Ischemia resulting in severe hemodynamic compromise- treated according to BP
MI with normal/high BP-NTG followed by  blockers.
Hypotension (< 85mm SBP)
Dobutamine 5 µg/kg/min
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2. Myocardial infarction
 Commonly seen on 2nd or 3rd post operative day.

 Intra operative ischemic episodes → Increase the incidence of MI post-
operatively
 Other contributing factors are – Postoperative pain, tachycardia, and BP
variations.
Treatment
1. 100% oxygen
2. Tab aspirin '160-32`5 mg orally - then daily PO
3. Tab NTG S/L - 0.4 mg-every 5.minutes.
4. Inj. Morphine 2 - 4 mg every 5 minutes for the control of pain. –
5. Inj. Metoprolol 5 mg every 2-5 minutes for a total of 3 doses. Decreases the pain
of AMI by decreasing oxygen.
6. β-blockers
7. Statins.
8. ACEI
9. IABC (Intra aortic balloon counter pulsation)
Thrombolysis should not be done preferably within 7 days
PTCA l stenting may be done on emergency basis if pain is persistent.
Arrhythmias
 Cause may be due to:
Hypoxia
Pre-existing cardiac disease
Hypokalemia
Sympathetic/parasympathetic stimulation anesthetics
Treatment
Identification and correction of causes.
Tachyarrhythmia’s treated by slowing heart rate.
Sinus bradycardia - Inj. Atropine IV
PAT / PA flutters
Vagal maneuvers
DC cardio version (if patient is hemodynamically unstable).
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PVCs
Inj. Lidocaine I mg/kg IV bolus followed by an infusion of 1-4 mg/min.
VF: DC shock
Pulmonary edema: Most commonly seen in early post-operative period. Careful fluid
resuscitation guided by CVP monitoring is needed.
Treatment
 Propped up position.
 100% oxygen
 Diuretics
 Morphine - 4mg IV followed by 2mg IV increments.
 Bronchodilators
 Steroids
 If hypoxemia continues -> IPPV
Cardiac Arrest:
In an emergency surgery for a high risk patient, this problem is commonly encountered.
100% oxygen
CPR
Preventing Peri-operative Ischemia
Low risk patients
Aggressively treat tachycardia
Maintain euvolemic
Medications that are cardiac stable should be given in pre/intra/post operative patients
Aggressively prevent pain for 72 hours – Analgesics
Regional anesthesia techniques.
Aggressively prevent hypothermia
High risk patients

All the above factors
Aggressive monitoring of ST segment on ECG and PCWP
Obtain 12 lead ECG on the day of operation and day 2.
Prophylaxis with nitrates/0 blockers/calcium channel blockers.
POSTOPERATIVE COMPLICATIONS
 Highest risk for cardiac morbidity for non cardiac surgical patient. Postoperative
monitoring should be continued upto 7 days.
 Postoperative MI is usually preceded by severe ST segment depression for more
than 24 hours.
 HR increase due to pain
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 Pain control patient controlled IV/epidural analgesia.
 Fentanyl lozenges, transdermal fentanyl patches, diclofenac suppository.
 Effective pain management leads to a reduction of postoperative catecholamine
surge and hyper coagulability.
 Postoperative anemia – transfuse packed cells to raise hematocrit to 30%
 Postoperative hypothermia – unintentional hypothermia (sub-lingual
temperature) less than 350 C on arrival to postoperative ICU is significantly
higher incidence of MI forced air warming in hypothermic patient.
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Chapter 9 - ANESTHESIA FOR OPEN HEART SURGERY
INTRODUCTION
The term "open heart surgery" embraces all those procedures in which the operative
requirements preclude maintenance of an effective circulation by the heart.
During this period, some form of extracorporeal support is required, and the heart can
then be opened widely and accurate surgery carried out under direct vision in a
virtually bloodless field.
To provide satisfactory anesthetic conditions for both the patient and the surgeon and
to maintain optimal cardiovascular function, all details of the anesthetic plan must be
carefully considered. Communication with the cardiologist and cardiac surgeon is
essential; they should be made aware of the role the anesthesiologist is prepared to play
in seeing the patient successfully through the pre operative period, and the advances
that have been made in the anesthesia, monitoring, and life support of patients
undergoing cardiac surgery.
Anesthetic care of the patient undergoing cardiac surgery encompasses management of
patients with concurrent diseases and medication, airways that must be properly
managed; Central and autonomic nervous systems that must be adequately
anaesthetized. The critical difference from the normal operative procedures is that in
these operations the heart is directly affected by the surgical procedure and for most
patients extra corporeal circulation is required.
HISTORY
 Successful use of the First Heart - Lung Machine by Dr. John Gibbon 6th May 1953.
 First Successful CABG Operation was performed by Sabiston in 1962. This was an
end - to - end anastomosis of a saphenous Vein graft from the Aorta to the right
Coronary Artery in a patient with an occluded prior end arterectomy. Pt
unfortunately died 3r`' day post operatively of CVA and a report was not
published until 1974.
Indication for open heart surgery

chronic valve disease
Mitral valve disease

Aortic valve disease
Multiple valve replacement
Reoperation for valve disease
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Ischemic heart disease
Myocardial revascularization
Resection of left ventricular aneurysm
Congenital heart disease

Closure of secundum atrial septal defect
Closure of ostium primum atrial septal defect
Closure of ventricular septal defect
Relief of pulmonary stenosis
Total correction of the tetralogy of Fallot
Glenn procedure for the relief of tricuspid atresia
Emergency open heart surgery

Pulmonary embolectomy
PREOPERATIVE EVALUATION
The "Pre Operative Visit" with the prospective cardiac surgery patient should serve to
allay the apprehension of the patients and their families because of the awareness of
life-threatening risks and adverse consequences.
In particular, explanation of what to expect on emergence in ICU (tracheal tube, Arterial
Catheter, pulmonary artery or central venous catheter, provisions for pain relief) can
obviate the distress that may otherwise arise.
All patients undergoing cardiac surgery require a comprehensive evaluation of the
cardiovascular system. They may also have Co-existing diseases which have contributed
to the development of their cardiac dysfunction. Therefore it is important that these
patients should undergo multi system pre op-evaluation with the help of detailed
History, Invasive and non invasive screening tests.
Clinical Assessment of Cardiac Disease

Cardiac surgery is performed commonly for Coronary Artery Disease (CAD) and
structural heart disease, each manifest by some combination of 5 symptoms complexes -
Angina Pectoris, MI, Heart Failure, Cyanosis, Dysrrhythmias.
Angina pectoris:
Key clinical findings
 Exercise tolerance.
 Unstable angina.
 Ischemia without angina.
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Prior myocardial infarction
 Interval between infarction and surgery.
 Location and extent of infarction.
 Complication of infarction - heart failure or dysrrhythmias.
 Residual dysfunction.
Congestive heart failure:

Key clinical findings.
 Dyspnea on exertion, orthopnea, PND.
 HIO CHF
 Digitalis use
 Diuretics use
 Rales on physical examination.
Cyanosis:
Key clinical findings - central vs. peripheral.
Associated findings –
 Clubbing.
 Congenital heart lesion.
 Pulmonary Lesion.
 Polycythemia.
Dysrrhythmias:
Key clinical findings –
 Palpitations - chronic or acute.
 Dizziness.
 Syncope or near syncope.
 Associated angina or dyspnoea.
 Drug therapy.
 Pre disposing factors.
Non-invasive cardiac diagnostics studies:

Chest x-ray clinical findings
 Heart size - LV size (decreased LV function).

 Cardio thoracic ratio (decreased LV function).
 Presence of CHF.
 Pulmonary vascular flow.
 Presence l absence of respiratory infections.
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ECG
Resting ECG
 Rhythm disturbances.
 Ischemia.
 Conduction defects.
 Infarction.
 Hypertrophy.
Exercise ECG
 Relatively inexpensive and safe test.
 It has significant predictive value if characteristic S-T segment changes of large
magnitude occur.
a) At early stages of test and are sustained.
b) With sub-normal increase in Heart Rate or blood pressure. (Particularly if associated
with Hypotension).
 Are accompanied by angina or arrhythmias.
Pts with these findings are likely to have severe CAD.
 Computerized scoring of the ECG during stress testing may be more sensitive
than standard visual criteria.
 Scoring systems combining ST segment changes with exercise performance may
be more predictive of adverse myocardial events.
 The product of HR and SBP (Systolic BP) at which S-T Segment changes and Pain
occur is the "Rate-Pressure Product" (RPP) (HR X BP).
 "Myocardial Viability Ratio" - which suggested that there is a HR/BP quotient
that should be avoided to reduce ischemia. (Imperfect predictor of myocardial
ischemia).
 Positive findings on exercise ECG are
Ventricular irritability.
Hypotension - denotes poor LV function.
ST segment depression > 1 mm at very low exercise levels.
Poor exercise tolerance from any cause.
All these describe a group of patients at high risk for morbid coronary events.
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Echocardiography:
Key findings
 Segmental Wall Motion Abnormalities (SWMA) (When Caused by Ischemia occur
prior to ECG Changes).
 Ejection fraction (2D echo).
 Valvular function.
 Congenital anatomic defects.
*Stress Echocardiography (using exercise, dipyridamole or dobutamine).
*Contrast Echocardiography.
Nuclear medicine techniques

 Use newer perfusion agents and single - photon emission computed tomography
(SPECT) imaging.
 Thallium – 201
 Stress testing, using exercise or dipyridamole, with detection of perfusion
abnormalities has been used as a screening test for IHD.
 Technetium-99m.
 To detect RV and LV volumes, SWMA's, abnormal pulmonary blood flow.
 Technetium-99m methoxy isobutyl isonitrite (Te-99m MIBI).
Invasive studies
Coronary angiography:
1. It is the "gold standard" for defining the extent of CAD.

2. Vessels suitable and unsuitable for bypass are redefined.
3. High risk patients can be identified (reduced EF).
i) Extent and distribution of obstructive coronary lesions.

ii) Ventricular function as assessed by abnormal contracting segments and EF.
iii) Intra cavitary pressures.
iv) Valvular function.
v) Pulmonary vascular compliance.
Contrast ventriculography
1. Demonstrates areas of abnormal wall motion.

2 Used to determine EF.
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SYSTEMIC DISEASE:
Atherosclerotic vascular disease.
1. Carotid bruits
2. Cerebrovascular accident
3. HTN
4. Claudication
Hypertension
1. Duration
2. Drug history
3. Hypokalemia
4. Palpitation
5. Headaches
Diabetes Mellitus
1. Duration
2. Insulin - type and requirements
3. FBS
4. Autonomic instability
5. Renal insufficiency.
Hepatic
1. H/O Hepatitis
2. Ascites
3. Serum bilirubin
4. Serum albumin (<3)
5. Prothrombin time.
Renal
1. Daily urine output

2. Serum creatinine, Blood urea
3. Serum electrolytes
4. Urine analysis.
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Pulmonary
1. Cigarette smoking
2. Sputum production
3. Dyspnea
4. Wheezing
5. Recent RTI
Coagulation
1. Family H/O
2. Coagulation studies PT, PTT, platelet count, BT, ACT
Hematological
1. Hb
2. TC, DC, ESR, Hematocrit
Allen's test
To ascertain the collateral circulation in the hand for arterial cannulation.
Previous history of surgical procedures
1. Vein stripping in the legs (Vein Grafts from arms)

2. Previous surgery in neck e.g. thyroidectomy or carotid endarterectomy. (Relative
contra indication to IJV cannulation)
3. Cardiac catheterization - (Femoral artery-Hematoma / aneurysms).
4. Previous Surgery in the mediastinum and heart
Airway assessment - teeth, dentures, TMJ assessment, neck movement, M.P.
Preoperative risk assessment:

The most feared complication following CABG is mortality. A simple method of risk
assessment is to classify the patients according to the presence or absence of following
risk factors.
1) Unstable Angina / Recent MI

2) Poor LV function
3) Evidence of Heart failure
4) Obesity (BMI > 30)
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5) Emergency Surgery
6) Re Operation
7) Other Significant and uncontrolled systemic disturbances.
Normal risk: None of above factors present
Increased risk: If any one of the above factors is present
High risk: If more than one factor is present.
According to a recent risk computation scale scores are given for risk factors as follows:
Parsonett scale
Female 1
Obesity (More than 15% Ideal body weight 3
Diabetes 3
Hypertension 3
Ejection fraction % > 50 0
30-50 2
< 30 4
Age 70-74 7
75-79 12
80 20
Re-operation 1 5
2 10
Pre operative IABP 2
LV Aneurysm 5
Emergency surgery 10
Dialysis Dependency 10
Catastrophic conditions 10-50
Valve surgery
Mitral valve 5
Aortic valve 5
CABG + Valve surgery 2
Risk score Mortality

0-4 1%
5-9 5%
10-14 9%
15-19 17%
> 20 31%
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PREOPERATIVE DRUG THERAPY
Beta-Adrenergic blocking drugs:
Used primarily for stable exercise induced Angina, with good LV function with out
Coronary vasospasm, SVT, HTN
 Continuation is beneficial in limiting the intra-operative tachycardia, arrhythmia,
HTN and MI
 Discontinuation is dangerous because it may produce rebound exacerbation of
Angina pectoris, Infarction and HTN.
 Should be continued until morning of surgery and better substituted with short-
acting beta blocker (Nadolol).
Calcium channel blockers

 Diltiazem, Nifedipine, Verapamil.
 Used primarily for IHD, Supra Ventricular dysrrhythmias, HTN.
 Beneficial in Peri Operative Period of IHD patients. Due to their effects -
improved myocardial 02 supplies - Demand ratio, decreased coronary vascular
resistance, reduce Inotropy, dilate systemic vasculature.
 Continue through the morning of surgery.
Anti Hypertensive Drugs

 Continued through the night before and the morning of surgery.
 ACE inhibitors may increase the requirement for vasoconstrictors following CPB.
 Beneficial in attenuating hemodynamic stress during surgery.
Heparin
 In patients with Unstable Angina, Heparin infusion may be continued upto the
time of surgery t ½ of Heparin is 1 hrs).
 Prolonged exposure to Heparin may induce Heparin Resistance (Relative def. of
antithrombin Ili) an ill defined entity in which larger than normal doses of
heparin may be required to provide sufficient anti-coagulation for CPB.
 Patients with near Total Coronary occlusion symptoms may benefit from
continuing the heparin infusion until anticoagulation is achieved prior to CPB.
Aspirin
 It prevents platelet adhesion - so used for treatment of coronary thrombosis -
more over CPB induced platelet dysfunction is thought to be an important
mechanism in post bypass coagulopathy.
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 Aspirin is stopped one week before surgery in some centers (can be continued
till the time of surgery).
Digitalis
 If given for control of heart rate as in pts with atrial fibrillation it is continued
pre-operatively.
 However, the arrhythmogenic properties of digoxin may be accentuated by the
Peri Operative Hypothermia and electrolyte changes.
 If given for its inotropic properties - digoxin is with held on the morning of CABG
operation - substituted with other inotropes I.V. if needed.
Vasodilators
 Oral/Sublingual Nitrates (Venodilators) [Nitroglycerine; Isosorbide dinitrate]
can be replaced by I.V. Nitroglycerine intra operatively to reduce the risk of MI.
 Arteriolar vasodilators [Hydralazine/prazosin / Nitroglycerine] used in AR or
MR or severe ventricular dysfunction should be continued approximately 8 hrs
prior to operation and if additional vasodilation is needed titrated Sodium
Nitroprusside IV (1 micro gram/Kg) can be substituted.
Anti dysrrhythmias
 Quinidine, Di-isopyramide or Procainamide or oral drugs like mexilitine,
amiodarone or calcium channel blockers-continued peri operatively.
 Disopyramide is associated with difficulty in terminating CPB sometimes, so if
possible substituted.
 Amiodarone causes hypotension and bradycardia unresponsive to
catecholamines and difficulty in weaning, so should be discontinued 2 weeks
prior or at least pre operatively.
Magnesium
 Is now given frequently following acute Mi. (Reduces the incidence of mortality
and heart failure, may be arrhythmogenic).
 Hypermagnesemia can cause sedation and prolongation of neuromuscular
blockade at levels reached in treatment of an MI (0.96 to 1.54 mmol/L).
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Chapter 10 ANESTHESIA PROTOCOL FOR ADULT
CARDIAC SURGERY
Cardiac anesthesia and cardiac surgery has become a rapidly advancing and changing
field. Newer techniques, newer medicines as well as monitoring devices are being
continuously introduced. There could be several effective and safe methods of
conducing anesthesia for a patient undergoing cardiac surgery. Indeed, the practice
varies from centre to centre, although the anesthetic principles remain the same.
Duty of anesthesiologist
 Control of coagulation
 Maintenance of unconsciousness and relaxation
 Hemodynamic monitoring
 Control of ventilation
 Indication of elective cardiac arrest
 Restoration of heart beat
 Termination of perfusion
 Myocardial support
 Post –op monitoring
The room and set up:

The cardiac operating room should be large enough to comfortably contain the patient,
Anesthesia Machine and monitoring equipment, the perfusionist’s equipments including
devices other than pump-oxygenator (such as IABP and cells Saver devices) and the
requisite nursing supplies and sterile areas.
 This normally requires a space of 600 to 800 square feet.
 Designed so that rapid movements of both the patient and equipment are
possible.
 Anesthesiologist should have access to a wide variety of anesthetic and vaso
active drugs as well as the ability to infuse them via infusion pumps.
Anesthetic check list for cardiopulmonary bypass:

Boyle's machine:
 Bain's circuit-test for leaks.
 Oxygen (O2), nitrous oxide (N2O) sources plugged in correctly.
 Vaporizer off
 Ventilator: secure circuit and test for leaks.
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Intubation:
 Laryngoscope
 Endotracheal tube
 Connection
 Catheter mount
 Cut the endotracheal tube; generally 23 cm for adult male and 21 cm for adult
female.
Monitoring trolley:
 ECG, arterial and central venous pressure (CVP).
 ECG cable and pressure transducers ready for use.
 Thermodilution Swan Ganz catheter and cardiac output (CO) monitor in selected
poor risk patients.
 Transoesophageal echocardiogram (TOE), if needed in selected patients (poor
left ventricular (LV) function, valve repair surgery).
 Defibrillator available with external paddles.
 Suction apparatus available.
 Check blood availability.
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Anesthesia for open heart surgery
Monitoring established prior to open heart surgery. A catheter introduced at operation

will be used to monitor left atrial pressure postoperatively.
Syringe pumps:
2 to 3 mounted on the right hand pole
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Lay up:
 Morphine 10 mL syringe 16 mg in 8 mL
or fentanyl 10 mL syringe 500 µg in 10 mL
 Diazepam 2 mL syringe 10 mg in 2 mL
or 2 mL syringe 5 mg in 5 mL
midazolam 5 mL syringe 5 mg in 5mL
(with the availability of fentanyl and midazolam, they are preferred over
morphine and midazolam).
 Pancuronium or 5 mL syringe 8 mg in 4mL
Vecuronium 5 mL syringe 8 mg in 4 mL
 Thiopentone or 10 mL syringe 250 mg in 10 mL
Propofol 10 mL syringe 100 mg in 10 mL
 Calcium gluconate 10 mL
 Atropine 0.6 mg in 1 mL 2 mL syringe
 Scalp vein needle / 21/23 G
Y-cannula
 Cannula 21/23 G
 Cannula 14 G x 1
Internal jugular lines:

- Triple lumen or long central lines (cavafix) x 2 with 14 G Jelco/Optiva x 2 with 2
mL syringes x 2.
- 2 mL syringe + blue needle.
 Pulmonary artery catheter if indicated.
 Temperature probe.
 Heparinized saline: 500 units in 500 mL.
– 10 mL syringe of heparinized saline + t connector (for aspirating and flushing the
arterial cannula).
– 10 mL syringe of heparinized saline + 3 way tap (3 syringes for aspirating and
flushing the luminal of triple lumen catheter).
– 10 mL syringe of heparinized saline + 3 way tap + 200 cm pressure monitoring
line for connecting the arterial cannula to the transducer.
 500 mL Ringer’s lactate + blood transfusion set + 3 way + wide bore drip
extension set.
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Intubation trolley:
 Endotracheal tube: 7:5 or 8mm for females, 9mm for males.
 Scissors
 Long catheter mount
 Laryngoscope
 Stylet (malleable)
 Bougie
 Cuff inflating syringe
 Airway: size 2 and 3
 Jelly
 Thread, dynaplast and bandage for fixation of the tube
Anesthesia trolley
Top:
 Tray for anesthetic drugs
 Syringe trays ; 20, 10, 5, 2, 1 ml
 Needle trays: 16, 18, 20, 22, 24, 26 G
 Kidney tray or sharps disposal box for the used ampoules
 Three way taps
The various drugs and other material should be readily available and arranged in the
drawers of the anesthetic trolley.
Drawer 1:
Dopamine Propranolol
Isoprenaline Metoprolol
Adrenaline Atenolol
Dobutamine Calcium Gluconate
Isoprenaline Dexamethasone
Atropine Hydrocortisone
Diazepam Aminophylline
Midazolam Sodium bicarbonate
Heparin Xylocard ( 2 percent vial)
Protamine KCI
Nitroglycerin Furosemide
Nitroprusside Pancuronium
Morphine Vecuronium
Fentanyl Propofol
Thiopentone
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Drawer 2:
Adhesive plaster
Scissors
Towel clips
Dressings (transparent and others)
Labels
Drawer 3:
Glucose saline 500 mL x 2
Ringer’s lactate 500 mL x 2
Haemacel/ starch 500 mL x 2
Blood transfusion sets
Micro drip sets with chamber
PREOPERATION:
Read all the case notes and investigations and check pre-anesthetic check-up and
consent.
Premedication
 All the oral drugs such as propranolol, nifedipine etc.
 Morphine 0.2 mg/kg and phenergan 25mg, intramuscularly, 1 to 2 hours before
operation.
Transfer to operation theatre:

 Water blanket on table.
 Underneath towel to tuck over the arms later.
 ECG on.
 Preoxygenation if necessary (but usually not required).
 Y cannula or scalp vein needle in right hand and give morphine (3 to 5
mg)/fentanyl (50 µg) or diazepam/midazolam (1 mg), but not both.
 Left radial artery: percutaneous 22 G cannula, attach T-connector, then 200 cm
extension line to the transducer. Strap securely and note blood pressure (BP)
(use right radial artery for cannulation, if the left one is to be used as arterial
conduit in patients undergoing CABG).
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Induction:
 Morphine: 10 to 30 mg (0.5 mg/kg) or
 Fentanyl: 1 to 2 mg (10 to 20 Vg/kg) (decrease the dose appropriately, if early
extubation is planned).
 Diazepam / midazolam: 2.5 to 5 mg (be careful as benzodiazepines in
combination with opioids may lead to severe hypotension).
 Pancuronium: 6 to 8 mg. or vecuronium: 6 to 8mg
 Thiopentone: 50 to 100 mg slowly or propofol: 40 to 80 mg
Note: The choice of doses should also be determined by the preoperative cardiovascular
status of the patient. For instance, in a frail patient, restrict the dose of
morphine/fentanyl and avoid diazepam / midazolam as it can lead to precipitous
hypotension if used with opioids. Diazepam / midazolam can also be administered after
intubation.
 Intermittent positive pressure ventilation (IPPV) with 6 liters N20 and 3 liters O2,
but increase the oxygen in sick patients.
Intubation:
 Intubate with appropriate size endotracheal cuffed tube.
 Manual ventilation first and then switch over to mechanical ventilation FiO 2 of
0.33 to 0.5 (N2 O/O2) .
NITROUS OXIDE:
Nitrous oxide can be used to supplement both potent inhaled anesthetics and
intravenous opioids.
 Nitrous oxide tends to decrease cardiac output and increase SVR when given
alone or in combination with opioid (increased pulmonary vascular resistance).
 The degree of hypotension and myocardial depression may be sufficient to
discontinue it.
 It expands air filled spaces including air emboli.
 Nitrous oxide has a solubility 20 times that of oxygen at 37°C and can cause air
emboli to increase in size, thus increasing the degree of vascular obstruction.
 If arterial embolization is suspected nitrous oxide is discontinued and avoided
for the rest of the procedure.
 Should not be used in the presence of pneumothorax unless a functioning
thoracotomy tube is in place.
 Nitrous oxide limits the inspired oxygen concentration and does not allow for
apnea ventilation.
 The advantages of nitrous oxide as a rapid onset / offset inhaled anesthetic are
now shared by desflurane and sevoflurane.
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Peripheral venous cannula for infusion:
 14 G cannula: right hand / wrist, attach Ringer's lactate drip with extension
looped to the head end.
Right internal jugular vein cannulation:

 Triple lumen catheter. Or
 30 cm long 16 G central venous catheter (cavafix): 2 lines usually requires either
both in internal jugular vein (IJV) or one each in internal and external jugular
vein.
 Introduce about 15 to 20 cm.
 Careful with aortic aneurysm, coarctation of aorta and aortic regurgitation (i.e.
avoid carotid artery).
 7 F Swan Ganz catheter in poor risk patients. (IJV catheter will not be required if
Swan Ganz catheter is used).
 Connect the line to the transducer and note central venous pressure (CVP) or
pulmonary artery (PA) pressure.
 Note: in poor risk patients, the 14 G peripheral line and triple lumen or Swan
Ganz catheter should be inserted under local anesthesia before induction.
 Additional 7 F check flow in femoral artery for pressure monitoring or easy
access for intra-aortic balloon pump (IABP) catheter later on in poor risk
patients.
 Temperature probe.
 Naso-gastric / oro-gastric tube.
 Tuck towel over arms and under trunk.
 Anesthetic screen.
 Diathermy pad.
 Urinary catheter.
Patient is now ready for the surgical procedure.
Check the ventilation of the patient at this stage:

 Rate 12 to 16/min.
 Minute volume to give PaCO2 of about 35 to 40 mm Hg.
 Bacterial / viral filter with heat and moisture exchanger.
 Check CVP and BP.
 Arm drip functioning well.
 Additional doses of morphine / fentanyl may be considered at this stage if BP is
high.
 Fill in the anesthetic chart.
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 Towel up One wing clipped to the right drip pole and the other clipped to the left
hand pole.
 Both firmly clipped at the corners of anesthetic screen. One manometer line from
surgeon to transducer for on table pressure measurements in selected patients.
Check: Defibrillator - paddle leads passed from the table - switch on.
 Pacemaker availability.
 Bleed the patient if Hb is > 10 gm percent for auto-transfusion.
 Collect the blood in citrate phosphate dextrose (CPD) bag via central venous
catheter, approximately 7 percent of estimated blood volume if Hb is 10 to 12 gm
percent and 10 percent of the estimated blood volume if Hb is more than 12 gm
percent.
 Estimated blood volume (mL).
Male’s 75 x weight in Kg.
Females: 65 x weight in Kg.
 Simultaneously, perform TOE at this stage (standard views) and confirm the
diagnosis. Also, note the myocardial contractility and volume status in the trans-
gastric midpapillary view.
Blood pressure control:

 Hypertension commonly occurs during surgery.
 Ensure that the patient has received sufficient analgesia (morphine/fentanyl).
 Halothane / isoflurane 0.5 to 2 percent.
 Give chlorpromazine 2.5 to 5 mg increments, if halothane / isoflurane is not
enough.
 Start nitroglycerin infusion (0.5 to 1 µg/Kg/min) for patients undergoing
coronary artery bypass grafting (CABG).
 Nitroprusside/nitroglycerin infusion (0.5 to 1 µg /Kg/min) in patients
undergoing mitral valve surgery with high PA pressure and aortic valve surgery
for finer control of BP.
 Metoprolol/atenolol: 1 mg increments if heart rate is more than 100/min and BP
are not controlled with above measures.
Note: BP will often rise with the sternal split and fall 20 to 30 mm Hg when the heart is
lifted by the sternal retractor.
Vecuronium: 2 mg increments, only if patient moves before CPB or rarely after one
hour of induction, if bypass is not established by then.
Take samples for activated clotting time [(ACT), no heparin]: 5 mL syringe, and arterial
blood gases (heparin) 2 mL syringe.
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Disconnect ventilator during sternal split to avoid injury to pleura
Have ready:
 Calcium gluconate: 10 mL syringe (not in aortic stenosis).
 Adrenaline 4 mg in 500 mL glucose saline.
 Dopamine 400 mg in 500 mL glucose saline (in addition to or with anticipated
renal problem).
 Dobutamine 500 mg in 500 mL glucose saline (in poor risk patients).
 Blood is rarely required before bypass.
 Add vecuronium 4 to 6 mg, morphine (10 to 15 mg)/fentanyl (250 to 400 lug)
and diazepam (5 to 10 mg)/midazolam (5 to 10 mg) to the pump prime.
 Draw up heparin 3 mg/kg.
 Give heparin at the request of the surgeon, as he inserts aortic purse string.
Usually given via central venous line, after aspirating blood to make sure, it is
certain to reach the circulation.
 Start timer as the heparin is given and record the time and dose on anesthetic
chart.
 Check ACT 5 min. after the heparin dose. If less than 400 seconds give additional
heparin in the dose of 1 mg/Kg (note, it is not safe to institute CPB, if ACT is less
than 300 seconds).
ON BYPASS:
Partial bypass:
 When bypass commences
 Give 100 percent O2
 Chart the time
 Turn off halothane / isoflurane
 Look at venous pressure: it should fall
 Look at arterial pressure: usually small pump pulsations only.
 There should be no diaphragmatic movement.
Record: Urine volume on the chart, Temperature on the chart.
Total bypass:
When ascending aorta is clamped, ventricular fibrillation (VF) or venaecava snared.
 Ventilation to manual circuit.
 Spill valve open: nil fresh gas flow
 Chart the time
 Start the timer for myocardial ischemic time.
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Administration of cardioplegia:
Cardioplegia solution:
Although, several methods of producing cardioplegic arrest have been described, the
most common agent used to produce electrical and mechanical quiescence is potassium.
The composition of a typical cardioplegia solution is
Component Approximate concentration (mmol/L
Potassium 20 to 30
Sodium 109
Chloride 114
Calcium 1
Bicarbonate 27
Glucose 28
Mannitol 54
In general, the cardioplegia is solution should produce immediate arrest. It should be
cold, hyperosmolar and provide substrate for continued metabolism during aortic cross
clamping. In addition, it should also have membrane stabilizing property and buffering
capacity to counteract anaerobic acidosis.
Various types of cardioplegia used in clinical practice:

Antegrade (cold / warm)
 Intermittent crystalloid (only cold)
 Intermittent blood
 Continuous blood
Retrograde (cold / warm)

 Intermittent crystalloid (only cold)
 Intermittent blood
 Continuous blood
 Continuous crystalloid (only cold)
Combined antegrade and retrograde (cold / warm)
Hot shot
Following cold crystalloid or blood cardioplegia
Tepid cardioplegia (290C)

Substrate enriched cardioplegia
 Adenosine
 L-Arginine
 Magnesium
 Insulin
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Delivered by the perfusionist by using one of the pump heads. Record the amount
delivered and time on the anesthesia chart.
Chart major events only:

 Commencement of CPB.
 Volume of pump prime.
 Aortic cross clamp time.
 Release of aortic cross clamp.
Drugs on bypass:
 Heparin repeated as half dose at one hour.
 1/4th dose at 2 hours and every hour thereafter, if CPB continues.
 Vecuronium 2 mg after each hour of bypass.
 Morphine (5 to 10 mg) / fentanyl (100 µg) after each hour of bypass.
 Vecuronium 4mg, if diaphragm moves.
 Chlorpromazine 5 to 10 mg sometimes indicated, if mean arterial pressure
(MAP) is more than 100 mm of Hg.
 Nor-epinephrine (5 to 10p,g), if MAP is less than 40 mm Hg.
 Propofol at 5 to 10 min. interval, while re-warming to prevent awareness. (Note:
In patients undergoing normothermic bypass, begin propofol infusion (5 to 10
mg / hour) at the onset of CPB.
 Check arterial blood gases every 1/2 hour on bypass (sample to be drawn from
the pump).
 Monitor ACT every '/2 hour during CPB. If less than 400 seconds at any stage,
administer additional heparin in the dose of 1 mg/Kg. This dose will be in
addition to the hourly dose of heparin that has already been described.
 Chart temperature and MAP at regular intervals and urine output at the
termination of CPB and before transferring the patient to ICU.
Aortic clamp off:

When the heart has been closed or distal coronary grafts have been completed.
 Assist de-airing (in open cardiac procedures), by giving a head down tilt to the
table and gently ventilating the lungs.
 Coronary perfusion is restored after aortic clamp is released, but heart may be in
VF.
 Charge defibrillator to 20 to 30 Joules.
 Shoot when requested by the surgeon.
 Observe both heart and ECG.
 Give 50mg xylocard into the CVP line if more than one defibrillation is required.
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End of bypass
 Recommence ventilation.
 Only 100 percent oxygen (no nitrous oxide).
 For safety reasons (not forgetting to initiate ventilation), start ventilation when
final proximal vein graft is being sutured in CABGs and as soon as acceptable
cardiac rhythm is established in other surgeries.
 In addition, gently breathe the patient using oxygen when the final cavity (e.g.
aorta, left atrium (LA) or right atrium (RA)] is being tied.
 Recommence ventilation WITHOUT FAIL.
 LA pressure line will be inserted by the surgeon in some patients if necessary.
Coming off bypass:

 RA pressure, pulmonary capillary wedge pressure (PCWP) or LA pressure and
appearance of the heart will guide you regarding optimum filling for an adequate
systemic pressure.
Inotropes: Timely start inotropes if necessary e.g. patient with poor LV function,
showing poor myocardial contractility, low BP with rising RA, PCWP or LA pressure.
Take help of TOE, if available.
Off bypass:
 Make sure ventilator is ventilating (oxygen only).
 No nitrous oxide. It can depress the myocardium and increase the size of air
bubbles in circulation.
 Check
- Inflation pressure
- Tidal volume / minute volume.
- Lung movement.
Note: Time the end of bypass on chart.
Record BP, CVP, LA pressure and urine volume during bypass on chart.
Maintain optimum CVP / LA pressure by giving bagged pump blood, if Hb is more than
8gm percent.
Transfuse autologous blood first, if collected (after Protamine). Consider transfusing
fresh warm blood and cold blood thereafter.
Protamine: 1.3 x initial dose of heparin given slowly when requested by surgeon (after
venous decannulation).
Additional 50mg, if bagged (heparinized) pump blood is given.
Adverse effects of Protamine:

 Hypotension - decreased SVR treated with fluid administration, alpha adrenergic
agonists, and calcium chloride.
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 Myocardial depression and LV failure - Requiring Inotropic support.
 Pulmonary vaso constriction - relieved by inotropes and calcium chloride.
 Some adverse effects can be due to rate and site of administration so it is advised
to give Protamine slowly over 10 min and in a peripheral vein. (Patients who
receive NPH insulin are at increased risk of adverse reactions. Vasectomies men
are also at increased risk due to increased incidence of Protamine specific
antibodies).
Blood sample: 5 to 10 min after Protamine is completed, (ACT and arterial blood
gases).
If bleeding
Think ahead and order blood well in advance.
Enough Protamine give 50mg.
Consider transfusing FFP, platelets.
End of operation:
 Continue IPPV.
 If systolic BP more than 120mm Hg, give halothane / isoflurane to ensure that
patient remains settled during transfer to ICU and does not become
hypertensive. Alternatively, give morphine (5 to 10mg) / fentanyl (50 to 100 µg)
or diazepam (2.5 to 5mg) I midazolam (1 to 2 mg).
 Secure IJV line firmly.
 Inotropes: Usually not necessary to run while transferring, but it fragile patients
may be necessary. Run adrenaline infusion with syringe pump during transfer.
 Transfer after clamping chest drains, removing all drips, and urine bag,
unplugging ECG cable and finally disconnecting pressure line with three way tap
attached. Leaves arterial pressure display until last.
 Transfer the patient with portable ventilator and ECG monitor.
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Chapter 11 PROTOCOL FOR OFF-PUMP CABG
Patients undergoing off-pump CABG can be extubated early (within 4 hours of surgery).
Therefore; the dosage of opioids should be appropriately reduced. For instance,
induction dose of morphine can be decreased to 0.3 to 0.5 µg/Kg and that of fentanyl to
5 mg/Kg. In essence, the protocol is similar to the one outlined above except for the
following changes.
Heparin: 1.5 mg/Kg before the coronary artery stabilizer (octopus or Guidant) is placed
on the myocardium.
 Repeat 0.75 mg/Kg heparin each hour to maintain ACT of ≥ 300 sec.
Placement of the coronary artery stabilizer leads to considerable hemodynamic
instability, especially when it is placed on the lateral walls of the myocardium to
stabilize the circumflex coronary artery (and its branches) or the right coronary artery.
In order to maintain the hemodynamics, following maneuvers can be performed:
 Infusion of volume: 100 to 200 mL of Ringer's lactate or pentastarch.
 Trendelenberg position (10 to 200).
 Dopamine (5 to 10 l µg/Kg/min) or epinephrine (0.025 to 0.05 µg/Kg/min) can
be infused.
 MAP of 70 mm Hg or more is desirable, but lower values (up to 60mm Hg) may
be accepted in exceptional situations.
 If it is difficult to maintain MAP of 70 mm Hg, the coronary stabilizer should be
removed and the heart allowed to recover, before it is placed again.
 Monitor ECG, MAP. CVP and PCWP carefully during the anastomosis and try to
maintain MAP of ≥ 70 mm Hg at all times with the help of intravenous fluids and
inotropes.
 Sometimes, there can be substantial blood loss during the distal anastomosis.
The following methods can be utilized for blood conservation.
o Acute normovolaemic haemodilution.
o Use of cardiotomy reservoir to collect the blood lost from the operative
field.
o Use of cell saver to collect the blood lost from the operative field.
Off-pump CABG can be converted into the conventional CABG with cardiopulmonary
bypass at any point of time. The usual criteria for such a decision are
o Technical difficulty faced by the surgeon.
o MAP decreasing to very low values (≤ 50mm Hg) with PCWP rising to ≥
20mm Hg.
o Intractable arrhythmias and significant ST segment changes (? 4mm).
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Chapter 12 - CARDIAC INTENSIVE CARE
 Attach to ventilator, giving 40 percent oxygen and aim to ventilate to a PaCO2 of
35 to 40 mm Hg. Auscultation both sides of the chest for air entry.
 Attach radial artery pressure line to appropriate transducer and ensure that
pressure is satisfactory.
 Attach CVP, PA, and LA pressure line (if present) to transducer, exclude air
before flushing. Check the transducers for zero.
 Plug in ECG.
 Chest drains unclamped.
 Tell the surgical resident, arterial and venous pressures, inotropes rate to be set
on infusion pump and last potassium measurement.
 Immediate X-ray chest, ECG and routine arterial blood gases and electrolytes to
be arranged by resident in-charge.
 Sedate with morphine 3 to 5mg.
 Many patients should be sufficiently stable, wide awake with good respiratory
and cardiovascular parameters to come off the ventilator in 4 to 6 hours time.
Some patients particularly those who have undergone valve surgery (with high
PA pressure) and poor LV function should be ventilated overnight.
Regional anesthesia:
Survey suggested that most anesthesiologists do not use epidural anesthesia or
analgesia for cardiac surgery.
Since conventional methods of anesthesia allow early extubation and favorable pain
relief. It is suggested that although, thoracic epidural anesthesia should not be viewed
as irrational, routine selection of technique still seems inadvisable.
Intrapleural analgesia:
Intrapleural injection of 20ml of 0.25% bupivacaine followed by clamping of chest
drainage tubes for 20 min offered superior analgesia as compared with thoracic
epidural analgesia.
Post op monitoring:
HTN: Good sedation and pain relief after cardiac surgery is an important contributing
factor towards control of the post op hypertension.
Sodium nitroprusside (arteriolar dilator): 0.5 to 2 µg / kg / min.
NTG - (Venodilators) - 0.5 to 2 l-µg / kg / mm.
 Blockers (atenolol) in incremental dose of 0.5 to 1 mg.
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Sympathetic blockade: Thoracic epidural analgesia for cardiac surgery is used in some
centers. Sympathetic blockade is associated with increased subendocardial blood flow,
improved myocardial oxygen safely and improved ventricular wall motion during
stress.
Post operative MI:

– Tachycardia, anemia, hypothermia, shivering and less than optimal analgesia can
be contributing factors.
– Patients are most likely to manifest myocardial ischemia in the immediate post
operative period usually within 48 hours of surgery.
Antianginal drugs:
Beta adrenergic blockers due to their ability to suppress tachycardia appear most
efficacious in preventing myocardial ischemia. Diltiazem and NTG infusions have been
used.
High dose narcotics
Anemia
Hypothermia
FAST-TRACKING
In this new era of cardiac surgery, the emphasis has been on the reduction of ICU stay
(which is a major determinant of cost) after cardiac surgery. Due to the safety and cost
effectiveness, "Fast-track" protocols have become increasingly popular.
The goal is often to have patient’s extubated within 4 to 6hours of surgery, so that he is
transferred to the postoperative ward and then discharged from the hospital, usually by
the postoperative day 4.
A vapor based technique with modest doses of opioids and benzodiazepines and
propofol infusion are used.
Once the patient is awake and making respiratory efforts; extubation can be
accomplished after a brief trial of unassisted or partially assisted breathing. Once
extubated, patients who are doing well can be transferred to the `step down' unit with
minimal monitoring.
This approach has mostly been described in patients undergoing CABG.
The patients undergoing valvular surgery in India often have severe pulmonary artery
hypertension. In these patients, it seems rather unwise to practice 'fast-tracking' and
elective ventilation for a prolonged period is always beneficial.
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Conclusion:
Responsibilities of the anesthesiologist are not limited to the cardiac operating room. He
is actively involved in the postoperative management of these patients.
Anesthesiologists are well suited to provide postoperative care because the respiratory
and cardiovascular management are an extension of the operation theatre management.
Intensive respiratory management of the patients is his primary concern but is now
required to face a peculiar challenge of providing adequate sedation, analgesia and
hemodynamic stability, without prolonging recovery time.
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Chapter 13 - CLINICAL PRACTICE OF CARDIAC
ANESTHESIA
Table 3.1: Standard formulae and normal values of hemodynamic parameters
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Acute treatments for suspected intraoperative myocardial
ischemia
Associated Hemodynamic Therapy Dosage
Finding
I Hypertension, tachycardia + Deepen anesthesia Esmolol 2-100 mg, + 50-
IV  - Blockade 200
Metoprolol 0.5-2.5 mg
Labetalol 2.5 – 10mg
33-330 µg/min +
Ii Normotension, tachycardia + IV Nitroglycerin As above
Assure adequate anesthesia
change anesthetic regimen
IV - Blockade
III Hypertension, normal heart Deepen anesthesia 0-20 mg
rate sublingual/intranasal Nicardipine 1-5 mg, + 1-10
nicardipine µ
Phenylephrine 25-100 µg
IV. Hypotension, tachycardia + IV α-agonist Nor-epinephrine 2-4 µg
V Hypotension, bradycardia Lighten anesthesia 5-10 mg
IV Ephedrine 4-8 µg
IV Epinephrine 0.3-0.6 mg
IV Atropine As above
IV Nitroglycerin when
normotensive
VI. Hypotension, normal heart IV α- Agonist As above
rate IV Epinephrine
alter anesthesia (eg, lighten)
IV Nitroglycerin when
normotensive
VII. No abnormality IV Nitroglycerin As above
sublingual/intranasal nifedipine As Above
IV Nicardipine As above
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Cardiac Drugs
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Chapter 14 - PAEDIATRIC INTENSE CARE UNIT
Quick calculations: Drug concentrating for infusions
Desired Calculation Drug Dose Range
concentration
1ml/hr =
Mcg/kg/min Dose in MG in a 50 mL Mcg/kg/min
Syringe
0.01 mcg/kg/min = 1 ml/hr 0.03 x Wt (kg) Epinephrine 0.01-1.0 mcg/kg/min
nor-epinephrine 0.01-0.5 mcg/kg/min
alprostadil EI 0.01-0.1 mcg/kg/min
Isoprenaline 0.025-1.0 mcg/kg/min
0.02 mcg/kg/min=1 hl/hr 0.06 x Wt (kg) Epinephrine 0.5-2 mg/kg/day
Nor-epinephrine 0.01-1.0 mcg/kg/min
0.05 mcg/kg/min = 1 ml/hr 0.15 x Wt (kg) Epinephrine Nor- 0.01-1.0 mcg/kg/min
epinephrine 0.01-0.5 mcg/kg/min
0.1 mcg/kg/min = 1 ml/hr 0.3 x wt (kg) Epinephrine 0.01-1.0 mcg/kg/min

(concentrated) Nor-epinephrine 0.01-0.5 mcg/kg/min
isoprenaline 0.025-1.0 mcg/kg/min
0.03 mcg/kg/min = 1 ml/hr 1.0 x Wt (kg) Milrinone 0.33-0.99 mcg/kg/min
1 mcg/kg/min=1ml/hr 3 x Wt (Kg) Nitroprusside 0.5-10 mcg/kg/min
nitroglycerine max Nitroglycerine 0.5-10 mcg/kg/min
75mg in 50 ml midazolam 1-6 mcg/kg/min
2 mcg/kg/min = 1 ml/hr 6 x Wt (kg) Midazolam 1-6 mcg/kg/min
5 mcg/kg/min – 1 ml/hr 15 x Wt (kg) Dopamine 5-20 mcg/kg/min
amiodarone 5-15 mcg/kg/min
Dobutamine 2-20 mcg/kg/min
20 mcg/kg/min – 1 ml/hr 60 x Wt (kg) max Lidocaine 20-50 mcg/kg/min
1000mg/50ml
Mcg/kg/hr Dose in Mg/50 Ml Mcg/kg/hr
syringe
10 mcg/kg/hr=1 ml/hr 0.5 x Wt (kg) Morphine 10-40 mcg/kg/min
20 mcg/kg/hr – 1ml/hr 1 x Wt (Kg) Morphine 10-40 mcg/kg/min
2 mcg/g/hr=1 ml/hr 0.1 x wt (kg) fentanyl 2- mcg/kg/hr
titrate as required
as per order
Mcg/kg/hr Dose in units/50Ml syringe Units/kg/hr
10 U/kg/hr = 1 ml/hr 10x 50 x Wt (kg) Heparin – Standard
28 U/kg/hr = 1 ml/hr 28 x 50 x Wt (kg) concentration
Heparin – High dose
Mg/kg/hr Dose in Mg/ 50 Ml Syringe Mg/kg/hr
0.25 mg/kg/hr=1ml/hr 12.5 Wt (kg) Furosemide 0.25-0.5 mg/kg/hr
Mg/kg/day Dose in Mg / 50 ML syringe Mg/kg/day
1mg/kg/day = 1 ml/hr 2 x Wt (kg) Phenoxybenzamine 0.5-2 mg/kg/day
Units/kg/min Dose in Units / 50 Ml Units/kg/min
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syringe
0.0001 U/kg/min=1 ml/hr 0.3 x Wt (kg) Vasopressin
(max. 50 units/50ml) sepsis ; 0.0001-0.001 units/kg/min
Vasodilatory shock post CVS Survey: 0.0001-0.002
units/kg/min
brain Death: 0.0003 U/kg/min
Diabetes Insipidus: 0.0001-0.00025 u/kg/min
Nanogram/kg/min Dose in MCG / 50 ML Nanogram/kg/min
syringe
5 nanogram/kg/min = 1 15 x Wt (kg) Eprostenol 5-40 mg/kg/min
ml/hr (Prostacyclin/Elolan)
(0.005 mcg/kg/min =1
ml/hr)
Dose in Grams/ 40 Ml Mg/kg/hr
syringe
Standard concentration 1 g in 40ml of sterile 1120 = Thiopentone 2-4 mg/kg/hr
Tirrate as per order. 25 mg/ml concentration
ESMOLOL Refer: 0 pharmacy manual
Wockhard hospitals (incorporated from HSc Toronto Canada)
This drug protocols is specific to wockhard ICU internal activities wockhard hospital
does not accept responsibility for use of thus by any person or organization not
associated with Wockhard 05/09/2006.
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PEDIATRIC ICU INFUSIONS
Maximum Syringe
Drug Diluents and comments
concentration
Alprostadil 1000 mcg/50ml D5W, NS
Amiodarone PIV 100 mg/50ml D5W, Non PVC tubing
CVL 600 mg/50 ml
Calcium gluconate 11.6 mmol/50 ml Undiluted CVL may run undiluted
Dobutamine 625 mg/50ml CVL may run undiluted
Dopamine CVL 1000 mg/50ml CVL
PIV 3x body weight / 50 m
(Pending CVL insertion).
Epinephrine 30 mg / 50 ml CVL Dextrose / NaCL combination
Esmolol PIV 500 mg/50ml See dosing charts in ICU Hand book
CVL 2500 mg/50ml
Fentanyl 2500 micrograms / 50 ml NEAT
Furosemide 500 mg/50 ml May run undiluted
Heparin 30000 u/50ml Use 1,000 u 7 ml strength
Insulin (Regular) 50 u / 50 ml If dose . < 5U, order the “diluted insulin 10
50 u / 50ml U/ml”
Isoproterenol 4 mg / 50 ml
Labetalol 250 mg/50 ml Undiluted May run undiluted
Lidocaine 1000 mg/50 ml Undiluted May run undiluted
Magnesium sulphate 20 mmol/ 50 ml
Meperidine 250 mg/50 ml
Midazolam 250 mg / 50 ml Undiluted May run undiluted
Milrinone 50 mg/ 50 ml Undiluted D5W, NS May run undiluted
Morphine Standard Diluent: D5W, NaCL.
Nitroglycerine 75 mg / 50 ml No exception to max concentration
Nitroprusside 200 mg/ 50 ml D5W Protect from light
Nor-epinephrine 8 mg / 50 ml CVL Must be in Dextrose or DNS
combination.
Phenoxybenzamine Protect from light, non-PVC tubing
Phenylephrine 50 mg/ml CVL
Procainamide 2000 mg/50 ml NS
Propafenone 175 mg/50ml D5W may run undiluted
Potassium Chloride 25 mmol/50ml CVL Standard Diluent D5W
Potassium phosphate P-15 mmol/50 ml CVL
Sodium phosphate P-15 mmol/ 50 ml
Vasopressin 50 units/ 50 ml CVL D5W or NS
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Chapter 15 - Anesthesia for patients with Congenital
Heart Disease
Common congenital heart diseases and anesthetic management of these patients
coming for non cardiac surgeries
 Fetal circulation and its transformation into adult type
 Individual cardiac lesions
Atrial septal defect (ASD) Definition
Ventricular septal defect (VSD) Incidence
Patient ductus arteriosus (PDA) Pathophysiology and hemodynamics
Tetralogy of fallot (TOF) Clinical manifestations
Diagnosis
Treatment
Anesthetic management of patients with CHD coming for non-cardiac surgeries.
o Pre-operative diagnosis, evaluation and preparation
o Premedication and antibiotic prophylaxis
o Anesthetic management
o Post-operative management
o CHD and pregnancy
Fetal and perinatal circulation:

Knowledge of fetal and perinatal circulation is an integral part of understanding the
natural history, Pathophysiology and the approach to anesthetic management patients
with CHD.
Fetal circulation:
Is a parallel circulation and has 4 low resistant shunts
 Placenta
 Ductus venous
 Foramen ovale
 Ductus arteriosus
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Changes in circulation after birth:

 The primary change in circulation after birth is a shift of blood-flow for gas
exchange from the placenta to the lungs.
 Placental circulation disappears and the pulmonary circulation established.
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Normal cardiac catheterization findings in a child:
Etiology of CHD:
Etiology of majority of CI-ID is not known, advances in molecular biology have
provided new understanding of the genetic basis of CHI).
Hereditary plays an important role in the etiology of CHD.
Sexes are equally affected though in individual lesions there may be predominance of
one sex over the other, but in general.
Right, sided lesions → Female
Left sided lesions → Male
Genetic and chromosomal aberrations are also known to predispose to CF-1D.
- CATCH 22: (CHD, abnormal facies, thymic hypoplasia, cleft palate and
hypocalcemia) due to defect in chromosome 22.
- VATER AND VACTERL SYNDROMES
- Pierre robin syndrome, Treacher Collins syndrome, Goldenhar syndrome, Nagar
syndrome.
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Extracardiac anomalies associated with cardiac lesions:
Extracardiac anomalies Most likely congenital cardiac lesion
Abnormalities of forearm like absence Ventricular septal defect
of radius or ulna
Syndactly and polydactyl Ventricular septal defect
Down syndrome (Mongolism) Atrial septal defect of the endocardial cushion
type
Arachnodactyly Atrial septal defect
Turner syndrome Coarctation of aorta, pulmonic stenosis and
aortic stenosis
Ellis-van Creveld syndrome Atrial septal defect, single atrium
Rubella syndrome Patent ductus arteriosus and/or pulmonic
stenosis
Moon facies and hyperaldosteronism Pulmonic stenosis
Holt Oram syndrome Familial atrial septal defect
Marfan’s syndrome Aortic or pulmonary artery dilation
Hurler syndrome Mitral or aortic regurgitation
Trisomy 13-15 Ventricular septal defect
Trisomy 17-18 Ventricular septal defect, patent ductus
arteriosus
 Environmental factors: like high attitude may predispose higher incidence of
PDA and ASD.
 Alcohol and drug abuse (thalidomide) during pregnancy
 DIABETIC mother
 Infections: congenital rubella (PDA and PS)
 Metabolic: idiopathic Hypercalcemia
Classification of CHD:
CHI) have been traditionally classified into CYANOTIC and ACYANOTIC heart defect.
Defect Incidence %
Acyanotic defect
Ventricular septal defect 35%
Atrial septal defect 9%
Patient ducts arteriosus 8%
Pulmonary stenosis 8%
Aortic stenosis 6%
Coarctation of aorta 6%
Atrioventricular septal defect 3%
Cyanotic defects
Tetralogy of fallot 5%
Transposition of great vessels 4%
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Depending upon the Pathophysiology of the defects CHD are classified as:
1. Simple shunts Restrictive
Nonrestrictive
2. Obstructive lesions
3. Complex shunt lesions (shunt + obstruction)
 Simple shunts: These arc lesions with an abnormal communication between
systemic and pulmonary circulation.
 Ex. ASD, VSD, PDA
 The amount of blood flow across the shunt depends upon the size of the orifice
and the relative difference in the PVR and SVR.
Restrictive (non dependent):

Small defects, with pressure gradient across the defect and flow largely fixed by orifice
size.
Changes in down stream impedance, to flow have little influence (i.e. changes in SVR &
PV).
Ex. small ASD, VSD
Nonrestrictive (Dependent):
 Large defects with very little or no pressure gradient across the defect and shunt
flow is lamely dependent on the down stream impedance to flow (dependent
shunts).
Ex: Large ASD, VSD
Obstructive lesions:
 May be right sided (PS) or left sided (AS)
 May be valvular, subvalvular or Supravalvular Dynamic Fixed
Complex-shunt lesions
 Simple shunts + obstructive lesions
Ex: Tetralogy of fallot
Classification of CHI by their effect on blood flow:

 Volume overload of the ventricle or atrium resulting in the increased pulmonary
blood flow.
o ASD, VSD, PDA, endocardial Cushion defect
 Cyanosis resulting from obstruction to PBh
o TOF, tricuspid atresia, pulmonary stenosis
 Pressure overload of the ventricles
o AS, coarctation of aorta, PS
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 Cyanosis due to common mixing chambers
o Total anomalous venous return
o Truncus arteriosus
o Double outlet right ventricle
o Single ventricle
 Cyanosis due to separation of the systemic and pulmonary circulation
o Transposition of the great vessels
Atrial septal defect (ASD):

 Is an abnormal communication between the 2 atria.
 ASD occurs as an isolated anomaly in 5-10% of all congenital heart defects, and
30-50% of children with CHDs have ASD as part of the cardiac defect.
 More common in females with a ratio of 2:1
Pathology:
Types: 1. Septum secundum type
2. Septum Primum type
3. Sinus venosus Superior venaecaval type
IVC type
rarely a coronary sinus type
Pathophysiology and hemodynamics of ASD:

Physiologically atrial septal defect results in leaking of oxygenated blood from
the left to right atrium at a minor pressure difference between the two atria.
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In an ASD the magnitude of the L-R shunt is determined by the size of the defect and the
relative compliance of the right and left ventricle.
L → R shunt through ASD
↓
Right atrial volume overload and enlargement
↓
Tricuspid delayed diastolic murmur
↑
right ventricular overload and enlargement
↓
↑ Flow through PA and a ejection systolic murmur in pulmonary area
Clinical Picture:
 Children with ASD are generally asymptomatic or mild effort intolerance, with
dyspnea on exertion, frequent chest infections may the only symptoms with
relatively slender body build (< 10th percentile).
Auscultation:
 A widely split and fixed S2 with delayed and accentuated P2 .

 A ejection systolic murmur in pulmonary area.
 Delayed diastolic murmur in tricuspid area.
 Typical auscultatory findings may be absent in infants with large ASD.
 Severity of ASD is directly proportional to intensity of the 2 murmurs and the
cardiac enlargement.
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Natural history prognosis and complications:
 All most all ASD of < 3mm closes spontaneously by 1 ½ years of age.
 ASD of > 8mm rarely closes spontaneously.
 A large untreated ASD may lead to CHF and pulmonary hypertension in adults
who are in their 20s and 30s.
 Atrial arrhythmias can occur.
 SABE doesn’t occur in children with isolated ASD.
 Cerebrovascular accident from paradoxical embolization through an ASD is a
rare complication.
Diagnosis:
ECG: shows right axis deviation and RVH
RBB with rsR pattern in V1
Chest x-Ray:
Cardiomegaly with right sided enlargement
Prominent PA segment and ↑ pulmonary markings with plethoric lung fields.
Echocardiography and color Doppler studies:

 Shows position and size of the defect
 Reveals characteristic flow patterns and direction of the shunt.
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Cardiac catheterization:
Treatment:
Medical management
 Treatment of chest infection.

 Prophylaxis for SABE if associated with other defects.
 In infants with CHF, medical management is recommended because of its high
success rate and possibility of percutaneous closure of the defect.
Surgical treatment:
Indications:
Not responding to medical management
QP: QS →1.5:1
Contraindications
 11 PVR (> 10 units I m2 or > 7 units / m2 with vasodilators) and development of
PVOD
Timing of surgery: usually until 3-4 years of age because of high rates of
spontaneous closure.
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Procedure: Traditionally repaired through a midsternal incision under CPB by
either a single suture of Teflon graft.
Nonsurgical closure; for secundum ASD with an adequate septal rim (< 20 mm)
Ex: 1. Clamshell device
2. Angel wings ASD device
3. Cardio-selective device
Advantage being rapid recovery with < 24 hr hospital stay, no risk of thoracotomy.
Complications: CV accidents and arrhythmias in immediate post operative
period.
 MR may occur in patients who have undergone repair of an ASD primum.
Ventricular septal defect (VSD):

 Is a communication between the 2 ventricles.
 VSD is the commonest CHD and accounts for about 30-35% of all CHD.
Pathology:
Types of VSD:
o Perimembranous
o Inlet
o Outlet (infundibular)
o Muscular
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 Anatomically 90% of VSD are located in the membranous septum with variable
extension into adjoining muscular part of the septum.
 May be multiple and the defect may vary in size ranging from tiny defects
without hemodynamic significance to large defects with accompanying CHF and
pulmonary HTN.
Pathophysiology and hemodynamics

 AVSD results in shunting of oxygenated blood from the left to right ventricle
(Acyanotic)
 The magnitude of the shunt is determined by the size of the shunt and level of
PVR and not the location of the defect.
 With a small VSD, a large resistance to L-R shunt is offered at the defect and the
shunt does not depend on the level of PVR.
 With large VSD, the resistance offered by the defect is minimum and L-R shunt
depends on the level of PVR.
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CLINICAL MANIFESTATIONS:
History: with a small VSD, the child is asymptomatic with normal growth and
development.
 With moderate to large VSD, delayed growth, and development, decreased

exercise tolerance, repeated pulmonary infections and CHF are relatively
common in infancy.
 With long standing cases of large VSD pulmonary HTN, history of cyanosis and
decreased level of activity may be present.
On physical examination:
 With large VSD, signs of CHF may be present.
On auscultation:
 Murmurs: a pansystolic murmur due to shunting of blood across the defect,

which starts early in systolic and masks S1.
 Ejection systolic murmur due to increased PBF.
 Delayed diastolic murmur at the apex.
 S2 is widely split but varies with respiration and intensity of P2 is increased.
Natural history, prognosis and complications of VSD:

 Spontaneous closure occurs in 30-40% of patients with small membranous and
muscular VSDs during first 6 months of life.
 CHF develops in infants with large VSDs, but usually not until 6-8 weeks of age.
 Pulmonary vascular obstructive disease may begin to develop as early as 6-12
months of age in patients with large VSDs. But the resulting R-L shunt usually
does not develop until the teenage years.
 Infundibular stenosis may develop in some infants with large defects and result
in ↓ in the magnitude of L-R shunt (i.e. Acyanotic TOF) with occasional
production of R-1 shunt.
 Infective endocarditis rarely occurs.
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Diagnosis:
ECG
 In small VSD, ECG in normal

 In moderate VSD LVH with occasional LAH may be seen.
 In large VSD, ECG shows combined VH with or without LAH.
 With development of pulmonary vascular obstructive disease (PVOD), ECG
shows only RVH.
Chest x-ray
 Cardiomegaly of varying degrees is present and involves LA, LV and RV (some
times), pulmonary vascular markings increase. The degree of Cardiomegaly and
the I in PV markings directly related to the magnitude of L-R shunt.
 With development of PVOD, the main PA and the hilar pulmonary arteries
enlarge, but the peripheral lung fields are ischemic and the heart size is usually
normal.
Echocardiography:
 2 dimensional and Doppler echo can identify the number, size and exact location
of the defect and to estimate the PA pressure and identify other associated
defects and estimate the magnitude of the shut.
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Management:
Medical management:
 Treatment of CHF → with digoxin and diuretics for 2-4 months to see If the
growth failure can be improved, frequent feedings with high calorie formulas
either by Naso-gastric tube or oral feeding may help and correction of anemia if
present with oral iron therapy.
 Maintenance of good dental hygiene and prophylaxis against SABE.
 Nonsurgical closure of selected muscular VSDs is possible using “UMBRELLA”
device.
 PA bonding as a palliative procedure (rarely)
Surgical management:
Indications:
 CHF in infancy not responding to medical management with first 6 months of
age.
 After 1 year of age, QP: QS of at least 2:1 indicates for surgical closure regardless
of pulmonary artery pressure.
Contraindicated:
 With the development of PVOD and reversal of shunt
 Direct closure of the defect with a use of DACRON patch, ↓ CPB and or deep
hypothermia preferably carried out through and RA approach or right
ventriculotomy.
Complications:
 Right and left ventricular failure.
 Complete heart block.
 RBB
 Residual VSD
 Cerebrovascular accidents rarely
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Chapter 16 - Patient ductus arteriosus (PDA):
 PDA is an abnormal communication between PA and the descending aorta after
birth.
 It is present in fetal life in all, but closes both functionally and anatomically after
birth.
 PDA occurs in 5-10% of CHD, excluding premature infants.
 More common in females with a ratio of 3:1
 More common in children born at high altitudes.
Pathology
 There is a persistent patency of a normal fetal structure between left PA and
descending aorta, that is 5-10mm distal to the origin at left subclavian artery.
 Usually cone shaped with a small orifice to PA which is restrictive to flow.
 Duct may be short or long, straight or tortuous.
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Pathophysiology and hemodynamics:
Hemodynamics of PDA is similar to those of VSD.
The magnitude of L-R shunt is determined by the resistance offered by the ductus
(diameter, length, tortiousity) when the duct is small (nondependent) and depend upon
level of PVR when ducts is large (dependent).
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Clinical manifestations:
History:
 Patients are usually asymptomatic when the duct is small, a large shunt PDA may
cause recurrent LRT, atelectasis and CHF accompanied by poor weight gain.
On physical examination:
 Tachycardia and exertional dyspnea in children with large shunt PDA.
 With chronically elevated PA pressure results in development of PVOD and
reversal of shunt (R →L) leading to differential cyanosis (lower half of the body).
 Hyperactive pericardium with systolic thrill at upper left sternal border.
 Bounding peripheral pulse with wide pulse pressure.
Auscultation:
S1→ Accentuated
S2→ normally split
S3→ small L – R shunt
Murmurs:
 Shunt murmur →
continuous machinery murmur
 Flow murmurs
Delayed diastolic murmur in mitral area
 Aortic ejection systolic murmur
Assessment of severity:
 Heart size
 3rd heart sound (S3) (mild)
 Delayed diastolic murmur large
 Wider the pulse pressure larger is the L – R shunt
Natural history, prognosis and complications:

Unlike PDA in premature infants, spontaneous closure of a PDA does not usually occur
in full term infants. This is because PDA in full term infants results from a structural
abnormality of the ductal smooth muscle cells rather than decreased responsiveness of
premature ductus to oxygen.
 CHF and recurrent pneumonia if shunt is large.
 Subacute bacterial endocarditis.
 Aneurysm of PDA and rupture is a rare complication.
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Diagnosis:
ECG:
 A normal ECG or LVH with small to moderate PDA
 CHV with large shunt PDA
 Only RVH with the onset of PVOD
Chest-x-ray:
 Normal with a small shunt PDA
 Cardiomegaly of varying degrees occurs with enlargement of the LA, LV and
ascending aorta, with increased pulmonary vascular markings.
 With PVOD, the heart size is normal with marked prominence of PA segment,
hilar vessels and peripheral lung fields are ischemic.
Echocardiography:
 2 dimensional and Doppler echocardiography can help in assessing the size,
functional information.
 The dimensions of LA, LV provide indirect assessment of the magnitude of L-R
shunt.
Management
 If diagnosis is made within 2 weeks and in premature infants.
 → Indomethacin 0.1 mg/kg/dose orally 12th hourly for 3 doses.
→ But not useful in term infants.
 Medical management of CIIF with digoxin and diuretics.
 SAGE prophylaxis.
 Non surgical closure: with stainless coils for PDA of up to S mm in length.
 Surgical closure: anatomic existence of a PDA, regardless of its size is an
indication for surgery.
Timing: Between 6 months to 2 years age in premature infant and soon after the
diagnosis is made in older children.
Procedure:
 Ligation and division of PDA through left posterolateral thoracotomy without
cardiopulmonary bypass (CPB).
 Recently Video assisted thorocoscopic surgery (VATS) is being used.
Complications:
 Injury to recurrent laryngeal nerve, left phrenic nerve and thoracic duct.
 Re-opening of the duct is rate.
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Tetralogy of fallot (TOF):
TOF is the most common cyanotic CHD accounting for about 10% of all CHDS.
Anatomically TOF consists of

A large VSD
Right ventricular out flow obstruction Dynamics
Fixed
RHV
Overriding of aorta (25%)
Pathophysiology and hemodynamics:

A large VSD with right ventricular outflow obstruction
↓ Continuous murmur in large L – R shunt
concentric RHV and RV pressure over load
↓
Reversal of shunt and decreased pulmonary artery blood flow
↓
cyanosis
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CLINICAL MANIFESTATIONS:
History:
 A heart murmur is audible at birth.
 Most patients are symptomatic with cyanosis at birth or shortly thereafter.
 Dyspnoea on exertion, squatting or hypoxic spells develop later in life.
 Infants with Acyanotic TOF may be asymptomatic or shows signs of CHF due to
large L-R shunt.
 Severe cyanosis soon after birth is seen in infants with TOF and pulmonary
atresia.
Physical examination:
 Varying degree of cyanosis; tachypnea and clubbing.
 Squatting position for relief of Dyspnoea.
Hypercyanotic spells (TT'f gpens)

 It is seen specially ii) first 2 years of life with a peak incidence at 2-4 months in
children with TOF.
 Usually occur in the morning, after crying, feeding or defecation.
 It is characterized by a paroxysm of hyperapnoea, arterial desaturation,
associated with worsening cyanosis and even loss of consciousness, seizures, CV
accidents and even death in untreated cases.
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Mechanism:
Mechanism of hypoxic spell. A decrease in the arterial PO2 stimulates the respiratory
center, and hyperventilation results. Hyperpnoea
increases systemic venous return. In the presence
of a fixed right ventricular outflow tract (RVOT),
the increased systemic venous return results in
increased right –to-left (R-L) shunt, worsening
cyanosis. A vicious circle is established. SVR,
systemic vascular resistance.
Treatment of Hypercyanotic spells:

 Infant should be picked up and held in
knee-chest position.
 100% oxygen supplementation
 Injection morphine 0.2 mg/kg SC or IV.
 Acidosis corrected with sodium bicarbonate 1 mEq/kg IV.
 If not responding to the above measure.
o Vasoconstrictors → phenylephrine – 0.02 mg/kg/IV
o Inj ketamine 2 mg/kg IV
o Inj propranolol – 0.05 mg/kg/KV
o Inj esmolol – 300-500 µgm/kg/IV
Auscultation:
Sounds: S1 is normal
S2 is single → only A2 is heard
P2 being soft, delayed and inaudible.
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Murmurs:
Shunt murmur: usually absent
Flow Murmur: Pulmonary ejection systolic murmur (intensity inversely proportional

to the severity of right ventricular out flow tract obstruction)
Aortic ejection click.
Natural history, prognosis and complications:

 Infants with Acyanotic TOF gradually become cyanotic; patients who are already
cyanotic become more cyanotic as a result of the worsening condition of
infundibular spasm or pulmonary stenosis.
 Polycythemia secondary to chronic hypoxemia (Hct > 65%) may lead to systemic
thromboembolism (renal, CNS)
 Relative iron deficiency anemia.
 Growth retardation
 Brain abscess and anoxic infarction in CNS and hemiplegic are not uncommon.
 SABE
 Coagulopathy in long standing cases with chronic hypoxemia
DIAGNOSIS:
Chest-X-ray:
 Heart size is normal or even small with decreased pulmonary vascular markings.
 Boot shaped heart (Coeur en sabot)
 Right aortic arch is 25% of patients.
ECG:
 RVH with right axis deviation
 `P' pulmonary maybe seen
 CVH in Acyanotic TOF (large L-R shunt)
Echocardiography:
 2 dimensional and Doppler echo studies can snake the diagnosis and quantative
the severity of TOF.
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Management:
Medical management:
 Medical management of CHF and other complications.

 Maintenance of good dental hygiene with SABE-prophylaxis.
 Correction of relative iron deficiency anemia.
Surgical management:
 Palliative shunt surgery
 Conventional repair surgery
Palliative shunt procedure:

Indications:
 Neonates with TOF and pulmonary atresia
 Infants with hypoplastic pulmonary annulus which requires a transamural patch
for complete repair.
 Children with hypoplastic pulmonary artery stenosis.
 Severely cyanotic infants < 3 months of age.
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 Infants of 3-4 months with unsuccessful medical management of hypoxic spells.
Figure 14-20. Palliative procedures that can
be performed in patients with cyanotic cardiac
defect with decreased pulmonary blood flow.
The Gore-Tex interposition shunt (or modified
Blalock-taussig shunt) is the most popular
systemic-to-pulmonary artery shunt
procedure. AO, aorta; LV left ventricle; PA,
pulmonary artery; RA, right atrium; RV, right
ventricle.
Types:
 Blalock - Taussig shunt → between
subclavian artery and the ipsilateral pulmonary artery.
 Gore-Tex interposition shunt (modified B-T shunt)
 The Waterson shunt (ascending aorta and right pulmonary artery)
 Potts operation (between descending aorta and left pulmonary artery)
CONVENTIONAL REPPAIR SURGERY

Indications and timing
 Symptomatic infants who have favorable anatomy of right ventricular out flow
tract, PA, without coronary artery anomalies may have primary repair at any
time after 3-4 months of age.
Procedure:
 Total repair of the defect is carried out under CPB and circulatory arrest. •
Procedure includes patch closure of VSD and widening of the right ventricular
outflow tract by resection of the infundibular tissue and placement of a fabric
patch.
Complications:
 Bleeding problems in postoperative period, especially in polycythemia patients.
 Right and left ventricular failure.
 Complete heart block, RBB.
 Residual VSD.
 Pulmonary valve regurgitation.
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ANESTHETIC MANAGEMENT OF PATIENT WITH CHD COMING
FOR NON CARDIC SURGERIES
Approach to the patient with CHD is the same whether the procedure is cardiac or non
cardiac.
Pre-operative preparation:
 Successful anesthetic management of patients with CHD is based on complete
and accurate pre-operative assessment, adequate pre-operative preparation and
early post-operative management.
 The approach to CHD patients must emphasize cardiac concerns but the basic
tests of pediatric anesthesia cannot be overlooked because they form the
formulation on which more complex interventions are built.
 In general, patients with CHI) requiring non-cardiac surgery may present in the
following situations.
o Before the congenital lesion is diagnosed.
o After the diagnosis but before surgical intervention.
o After surgical palliation
o After surgical correction
o Inoperable cardiac lesions
 The anesthesiologist caring for the patient with CHD should understand.
o The patient specific intracardiac and extra-cardiac defects and resulting
pathophysiology of the hemodynamic changes.
o The sequels of surgery or residual defects after the surgery.
o Cardiovascular effects of the anesthetic agents to be administered.
Pre-operative diagnosis and evaluation:

Goals of pre-operative evaluation are as follows
o To develop a detailed understanding of the patient cardiac anatomy and its
physiologic consequences.
o Ascertain anesthetic problems related to the patient non-cardiac medical
conditions or concomitant congenital syndromes.
o Educate the patient and family concerning the expected course of the planned
anesthetic.
o Reduce anxiety and fear relating to the operative procedure through
psychological preparation of both patient and family.
 In addition to the routine history about the patient, anesthesiologist should be
particularly concerned about the
o Functional status of the patient
o Details about surgery to be taken & kind its complications.
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 Apart from the regular examination, airway assessment requires special
attention in patients with CHID.
 For symptoms arising from the compression of major airways.
 Anticipate difficult airway for tracheal intubation in patients with facial
dimorphic changes such as
o Large tongue, hypoplastic mandible and teeth
o Patients with Down's syndrome are more prone for cervical dislocation.
 Special attention should be paid to the cardiopulmonary status of the patient and
any abnormalities that pertain to the planned surgical procedure.
Symptoms and signs of cardiac-failure in a neonate and infant:

a. Failure to thrive - poor feeding, diaphoresis
b. Increased work of breathing: tachypnea, wheezing, grunting, flaring of ala
nasi and chest wall retraction.
c. Altered cardiac output: tachycardia, gallop rhythm – Cardiomegaly,
hepatomegaly, cyanosis.
2. Pulse and BP should be recorded in all the 4 extremities as patients with CHD are
at a increased risk for an abnormal origin of the arterial supply to the extremities
and for unsuspected stenosis of peripheral vessels.
3. Special attention should be paid for the presence of upper and lower respiratory
tract infections and should be treated promptly.
Laboratory studies:
1) Hemoglobin (Hb%)
 For relative iron deficiency anemia due to polycythemia.

 Chronic hypoxemia in CHD patients lead to the development of Hb% > 20gm%
and such high levels of hematocrit (>65%) results in hyperviscosity and
peripheral sludging of blood leading to reduced tissue perfusion, acidosis, ↑ level
of 2,3 DPG and right ward shift of oxyhaemoglobin dissociation curve.
 If the hematocrit > 65%, pre-operative isovolumic exchange transfusion or RBC
pharesis is considered.
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2) Coagulation profile
 Patients with CHD especially with polycythemia are at a risk of having

coagulation abnormalities due to
o Reduced number of functional platelets.
o Increased fibrinolysis
o Decreased concentration of clotting factors.
 Hence all the patients with CHD requires a detailed coagulation profile
evaluation which-includes
o Prothrombin time (PT)
o Activated partial thromboplastin time (APTT)
o Fibrinogen levels
o Platelet count
3) Serum electrolytes
 Pre-operative electrolytes evaluation, especially for K+ in patients on digitalis

and diuretics and prompt treatment of the imbalance.
4) Blood glucose
 Pre-operative blood glucose should be evaluated and monitored as the patients

under stress and with CHD are more likely to acquire hypoglycemia.
5) Blood gases: ABG
 For patients with respiratory compromise and severe cyanosis.

 A PaO2 of 30-40 mm of Hg and SPO2 of >70% is an indication for the development
of metabolic acidosis.
6) Renal function test
 Blood urea
 Serum creatinine
7) Chest x-ray:
 For cardiac size, signs of pulmonary congestion or pulmonary vascularity.

 X-ray may give a clue of any underlying airway problem including n1ajor airway
compression from the enlarged pulmonary vessels.
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8) Electrocardiogram (ECG):
 For information about rhythm, volume and pressure burdens on the ventricles
due to anatomic defect.
 The pre-operative ECG should be evaluated for pre-existing arrhythmias and as a
baseline for intraoperative and postoperative wave forms.
9) Echocardiography and color Doppler studies:
 For the anatomic location of the defect

 To know the direction and magnitude of the shunts and pressure gradients.
 To access the wall motion abnormalities.
 For intraoperative and postoperative assessment of the cardiac function.
10) ECG gated Magnetic resonance imaging and angiography (MRI/A):
 MRA has emerged as an important diagnostic modality in the evaluation of

cardiovascular system.
 Provides an excellent 3 dimensional images to qualitatively assess valve and
ventricular function, and to quantify flow, ventricular volume, mass and ejection
fraction.
11) Cardiac catheterization
 Cardiac catheterization remains the gold standard for assessing anatomy and
physiologic function in congenital heart disease.
 Important catheterization data for anesthesiologist include
o Patient response to sedative medications.
o Pressure and oxygen saturation in all chambers and great vessels.
o Location and magnitude of intra- and extracardiac shunt (QP:QS).
o Pulmonary vascular resistance, systemic vascular resistance,
o Chamber size and function.
o Valvular anatomy and function.
PREOPERATIVE ORDERS:
1) Fasting ORDERS:
 Standard guidelines for the fasting interval based on the age must be adjusted
according to the individual needs.
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 Preoperative dehydration should be avoided especially in children with cyanotic
CHD and elevated hematocrit.
 Current recommendations for fasting interval in children and infants are
o Solids and milk products until 6-8 hrs prior to surgery.
o Clear liquid until 2 hrs prior to surgery.
o Breast milk until 3 hrs prior to surgery.
2) Medications:
 Patients with CHD should receive all cardiac medications till the day of surgery
except anticoagulants and diuretics.
3) Antibiotics: for SABE prophylaxis
Surgical procedures that do & do not require endocarditis prophylaxis

Endocarditis prophylaxis recommended Endocarditis prophylaxis not
recommended
Dental procedures known to induce gingival Dental procedures not likely to induce
or mucosal bleeding, including professional gingival bleeding, such as simple
cleaning adjustment of orthodontic appliances or
fillings above the gum line.
Tonsillectomy or adenoidectomy Injection of local intraoral anesthesia
(except intraligementary injections)
Surgical operations that involve intestinal Shedding of primary teeth
or respiratory mucosa
Bronchoscopy with a rigid bronchoscope Thmpanostomy tube insertion
Sclerotherapy for esophageal varices. Oral endotracheal intubation
Gallbladder surgery Cardiac catheterization
Cystoscopy Endoscopy with or without gastrointestinal
biopsy.
Urethral dilatation Cesarean section
Urethral catheterization if urinary tract In the absent of infection for urethral
infection is present catheterization, dilatation and curettage,
uncomplicated vaginal delivery, therapeutic
abortion, sterilization procedures, or
insertion or removal of intrauterine devices.
Urinary tract surgery if urinary tract
infection is present
Prostatic surgery
Incision and drainage of infected tissue
Vaginal hysterectomy
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Table 23-5. RECOMMENDATION-IONS FOR PROPHYLAXIS AGAINST SUBACUTE
BACTERIAL ENDOCARDITIS
Oral Regimen for Dental, Oral, or Upper Respiratory Tract Procedures

Standard
 Amoxicillin, 50 mg/kg, orally 1 hr before procedure Penicillin-Allergic Patients
 Clindamycin, 20 mg/kg, orally 1 hr before procedure Azithromycin or
Clarithromycin, 15 mg/kg, orally 1 hr before procedure
IV/IM Regimen for Dental, Oral, or Upper Respiratory/ Tract Procedures
Standard
 Ampicillin, 50 mg/'<g, IV/IM 30 min before procedure Penicillin-Allergic Patients
 Clindamycin, 20 mg/kg, IV/IM 30 min before procedure Regimens for
Genitourinary and Gastrointestinal Procedures Standard
 Ampicillin, 50 mg/kg, IV/IM + gentamycin, 1.5 mg/kg, 30 min before procedure;
6 hrs later, ampicillin, 25 mg/kg, IM/ IV or amoxicillin, 25 mg/kg, orally
 Penicillin-Allergic Patients
 Vancomycin, 20. mg/kg, IV over I hr + gentamicin, 1.5 mg/ kg, IV/IM completed
30 min before procedure
Adapted from Dajani AS, Taubert KA, Wilson W: Prevention of bacterial endocarditis.
Circulation 96:358-366,1997.
Pre-medication:
 The potential advantages of pre-operative sedative patients with CHD
o Easy separation from points and less crying.
o Decreased sympathetic activity
o Decreased oxygen demand and consumption
o Decreased requirements of intraoperative anesthetics.
 But this should be balanced against the respiratory depressant effects of the
drugs used.
 Thus, premedication should procedure a sedate and cooperative patient plus
maintenance of airway reflexes and a smooth induction of anesthesia.
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PREMEDICATION RECOMMEDATIONS FOR CHILDREN WITH CONGENITAL HEART
DISEASE OVER 1 YEAR OF AGE*
Minutes prior to
Drug Dose
induction to be given
Oral premedicant Combinations
Meperidine 3 mg/kg (maximum 100mg)
60-90
pentobarbital 4mg/kg (maximum 100mg)
Atropine 0.02 mg/kg (maximum 0.4 mg)
Or
Meperidine 1.5 mg/kg (maximum 100mg)
Diazepam 0.15 mg/kg (maximum 10mg) 30-60
Atropine 0.02 mg/kg/ (maximum 0.4 mg)
Or
Meperidine 2-3 mg/kg (maximum 100mg)
Diazepam 0.1 mg/kg (maximum 10mg) 60
Pentobarbital 2-4 mg/kg (maximum 100mg)
Or
Fentanyl (oral/ 15-20 µg/kg
30-45
transmucosal)
Or
Midazolam 0.5-0.75 mg/kg (maximum 5 mg) 20-30
Intramuscular premedicant combinations
Scopolamine 0.01 mg/kg (maximum 0.4 mg)
Pentobarbital 2 mg/kg (maximum 100mg) 60
Morphine 0.1 mg/kg (maximum 10mg)
Or
Pentobarbital 2 mg/kg (maximum 100mg 60
Morphine 0.1 mg/kg (maximum 10mg)
Or
Midazolam 0.08 mg/kg (maximum 5 mg) 10
Nasal premedication
Midazolam 0.2-0.3 mg/kg (maximum 5mg) 10
Or
Ketamine 1-5 mg/kg 5-15
Or
Sufentanil 0.3-3 µg/kg 10
Rectal premedication
Midazolam 0.3-1.0 mg/kg 20-30
Under 6 months of age only atropine should be used; between 6 months and 1 year,
atropine in combination with a sedative can be used. For all children premedication
recommendations should be modified based upon the severity of the illness, airway
patency, and any associated problems.
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Operating room preparation:
 An operational anesthesia machine with suitable breathing circuit.
o Airway and intubation instruments
 Variety of pharmacologic agents
 Cardiac resuscitative drugs and a defibrillator.
 Equipment for thermal hemostasis
 Functional suction apparatus
Venous access:
o Consideration should be given to placement of an IV catheter in all the
patients with C11D undergoing any surgical procedure because rapid
administration of cardiac medications may be required.
 EMLA cream can be used for painless access especially in pediatric cases.
 The introduction of air bubbles is extremely dangerous in patients with Shunt
lesions, precautions must be taken to prevent the inadvertent introduction of
venous air.
o Meticulous preoperative dabbling of all invasive tubing and intravascular
monitoring catheters.
o Allowing free flow of fluid from tubing and intravascular catheters before
connection.
o Ejection of any air from syringe and needle before injecting drug into an
IV catheter.
o Avoiding injection of the last milliliter of fluid from I syringe because of
micro bubbles on the plunges.
o Using IV air traps whenever possible.
o Positioning syringes vertically before injection to allow air to rise away
from the outlet.
o Never allowing arty central venous catheter to be open to air.
o Avoiding use of nitrous oxide whenever possible and discontinuing its use
if air embolization is suspected.
Monitoring:
 Standard monitoring devices for patients with CHD undergoing noncardiac

surgeries include.
 Pulse oximetry
 Precordial stethoscope
 NIBP
 ECG
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 ETCO2
 Temperature monitoring
 CVP monitoring
 Urinary catheter
 Transoesophageal echocardiography is reserved for procedure in which patient
is placed at risk of embolization arising from the surgical field.
 Interatrial blood pressure, pulmonary artery catheterization and PCWP are
reserve for more complex surgeries and in patients with compromised cardio-
respiratory status.
 Thermal stabilization: low environmental temperature brings about
cutaneous vascular constriction and a significant increase in blood viscosity.
Therefore children already polycythemia encountering the combination of
peripheral constriction and sludging of blood secondary to viscosity increase,
will be predisposed to metabolic acidosis, increased oxygen consumption and
cardio respiratory depression. Hence all anti hypothermic actions should be
taken.
 Fluid management: fluids must be individualized For each patient based on
the patients cardiac physiology, age specific fluid needs, preoperative deficit and
expected third space fluid and blood losses associated with the planned surgical
procedure. Care should be taken not to fluid overload a child with borderline
myocardial dysfunction. The ultimate goal of fluid management is to produce a
hemodynamically stable child during the anesthesia while maintaining a urine
flow of 0.5-1.0 ml/kg/hr.
o Maintenance of an optimal preload is essential in these patients, ideally
guided by CVP monitor.
o In R-L shunt preload must be increased.
In L-R shunt fluid overload must be avoided.
A variety of pharmacologic and physiologic differences exist for each anesthetic agent
and muscle relaxant. The choice of which agent to use for a specific patient is based on
NPO status, hemodynamic status, and requirement of the patient determined by cardiac
grid, age of the patient, venous access, airway competency, level of anxiety of expertise
of the anesthesia.
General anesthesia:
General anesthesia with tracheal incubation and positive pressure ventilation should be
used in all but shortest procedure to avoid the potential complications of transient
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hypoxia and hypercarbia in patients with reduced pulmonary blood flow and
pulmonary hypertension,
Breathing system:
 Jackson Rees circuit (<20kg)
With a fresh gas flow twice the minute ventilation.
 Bain's circuit: 70ml/kg for controlled ventilation
 Closed circuit: 2-4 ltr of fresh gas flow
Induction techniques:
 No drug is absolutely contraindicated, slow and smooth induction of general
anesthesia should be done avoiding myocardial depression, excessive
vasodilatation and hypotension.
 The technique of induction depends on various factors including age, NPO status,
level of anxiety and pathophysiology of anatomic defect, cardio respiratory
status of the child, IV access and the expertise of the anesthesiologist.
Inhalation induction:
 Is preferred for children with good cardiac reserve and without an IV access.
 Halothane is used for a awake and steal mask induction in children because of its
easy acceptance and minimal effect on PVR and SVR and ability to titrate depth of
anesthesia.
 Other agent such as sevoflurane is gaining more popularity as an induction agent
in children because of its less myocardial depressant effect.
Nitrous oxide:
 Can be used for induction and maintenance along with other inhalation agents in
50% concentration.
 Nitrous oxide increases SVR and PVR so should be avoided in patients with
pulmonary hypertension.
Intravenous (IV) induction:

 Is usually used in patients with significant cardiovascular compromises
Inj. Thiopentone - 3-5 mg/kg/IV
Inj. Ketamine - 1-2 mg/kg/IV
2-10 mg/kg/IM
Inj. Midazolam - 0.05-0.1 mg/kg/IV
Inj. Etomidate - 0.3 mg/kg/IV
 High dose narcotic techniques are useful in patients with minimal cardiac
reserve and when post-operative mechanical ventilation is planned.
o Inj. Fentanyl - 25-75 µg/kg/IV
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o Inj. sufentanyl - 5-20 µg/kg/IV
 A useful combination that can be used in a sick cyanotic CHD child is IV ketamine
+ IV phenylephrine + IV fentanyl with glycopyrrolate Which maintains the best
arterial oxygenation during anesthesia.
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Speed of induction:
1) Left-Right shunt
 L-R shunts have a relative over perfusion of the pulmonary circuit. The blood
from lungs which already contains anesthetic agent is recirculated, there by
acquiring additional anesthetic, the result is a higher peak concentration of the
anesthetic agent in the blood allowing a more rapid induction with inhalation
agent.
o IV induction agents hate a slower onset of the action as a result of a delay
in reaching the brain during the period of recirculation through the
pulmonary circuit.
2) Right-Left shunts
o R-L shunts slow the rate of rise in alveolar concentration off inhalational
agents and prolong induction and emergence of anesthesia.
 IV induction should have a more rapid onset of action in patients with limited
PBF, since the agent would more rapidly reach the systemic circuit.
MUSCLE RELAXANTS
For tracheal incubation
Inj. Succinylcholine 1-2mg/kg/IV
o But can cause bradycardia so reserved only for rapid sequence induction.
o Rapid onset and intermediate acting non-depolarizing muscle relaxant such as
inj. Rocuronium – 0.06-0.8 mg/kg IV can be used as a alternative.
Other non-depolarizing NMB agents

o Inj. pancuronium -0.1-0.15 mg/kg/IV
o Inj. Vecuronium – 0.07-0.1 mg/kg/IV
o Inj. Atracurium – 0.3-0.5 mg/kg/IV
Maintenance:
 O2 + N2O + inhalational agent + muscle relaxants + analgesia + IPPV.
 N2O is avoided in patients with pulmonary HTN.
 Controlled ventilation is used in all patients. PaCO2 is maintained between 30-
40mg HG.
 In TOF, excessive positive pressure ventilation is avoided as it may lead to
increased R-L shunt across the VSD and decreased PaO2.
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Analgesia:
Narcotic analgesics such as
 Inj. Morphine – 0.10.2 mg/kg/Iv

Inj. Fentanyl – 1.2 µg/kg/IV
Inj. Remifentanyl - 1µg/kg/min IV.
 Postoperative mechanical ventilation should be considered in patients with
preoperative CCF and in case of prolonged and extensive surgeries involving
massive fluid shifts.
Reversal:
 At the end of the surgery the patient is reversed with
 Inj. Neostigmine – 0.05 mg/kg
+
Inj. Glycopyrrolate – 0.01-0.02 mg/kg
 Is used whenever possible and suitable.
 But, care should be taken when initiating the surgical blockade, which may cause
decrease in SVR and increase R-L shunts resulting in rapid desaturation.
o Coagulation abnormalities are contraindicated for regional anesthesia.
 Regional anesthetic techniques are useful adjuncts to general anesthesia in
patients with CHD. The advantage included
o Decrease requirements of other general anesthetics that might cause
delay in extubation.
o Provision for postoperative analgesia.
POSTOPERATIVE MANAGEMENT:
 Immediate post-operative care of' the patients with CHD who has undergone
surgery is an important period in the overall sequence of anesthetic and surgical
management.
 Patients with CHD are susceptible to deleterious effects of hypoventilation and
decreased oxygen saturation. Therefore it is advisable for postoperative oxygen
administration.
 As a member of the operating team, it is necessary the anesthesiologist
understand and become involved during the immediate postoperative care.
 One important area in which anesthesiologist can aid the recover; of these
patients in the form of providing adequate postoperative analgesia and sedation.
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The main aim is to reduce cardio-respiratory work by attenuation of stress
response.
 Patients with CHD and poor cardio-respiratory reserve, who have undergone
major coincident of surgeries should be ventilated for some hours and should be
under the supervision of an anesthesiologist familiar with the specific cardiac
disease.
 Postoperative pain relief is considered as part of the anesthesia plan.
 Regional analgesia such as caudal epidural analgesia in pediatric patients for
genitourinary surgery - Inj. bupivacaine 0.25% 1 ml/kg Inj morphine 0.05-0.75
mg/kg
 Epidural analgesia with injection bupivacaine 0.1 % with
 Inj. fentanyl – 2 µg/ml
 Inj. morphine – 30 µg/kg/hr
 NSAIDs - provide effective analgesia for mild to moderate postoperative pain.
The drugs most commonly used are acetaminophen - 15mg/kg po, Diclofenac - 1-
3mg/kg/day PO/PR and ketorolac - 0.5mg/kg.
 Systemic analgesia: patient controlled analgesia (PCA) is a method of giving adult
patients small doses of opioids at frequent intervals to minimize the side effects.
CHD AND PREGNANCY:

 CHD has overtaken RHD as the most common type of heart disease seen in
pregnancy women with a L-R shunt tolerate pregnancy, labour, delivery and
surgery well ; whereas women with a R-L shunt are associated with a high
maternal and fetal mortality. The risk of the fetus is in the proportion to the
degree of maternal hypoxemia with a 50% risk of fetal death if maternal oxygen
saturation is less than 85%.
L- R shunts: pregnancy creates tin additional burden by increasing blood volume,

heart rate and cardiac output. Parturient with small shunts who are asymptomatic prior
to pregnancy tolerate this additional stress; whereas those with large shunts develop
symptoms of congestive cardiac failure.
Anesthesia consideration:
 Should receive antibiotic prophylaxis for SBE.
 Avoid hypotension which may cause shunt reversal.
 Conditions that increase PVR such as hypoxemia, hypercarbia and acidosis are
avoided.
 Avoid aortocaval compression by left uterine displacement.
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 Epidural analgesia and anesthesia is appropriate as it brings about minimal
changes in vascular resistance.
R-L shunts: A few women with these lesions reach child bearing age and are associated
with high maternal and fetal mortality. Pregnancy results in up to 50% maternal
mortality and 80% fetal loss. Pregnancy in these women is not advised. The decreased
SVR in pregnancy promotes increased R-L, shunting and cyanosis.
Anesthesia consideration:
 Prime importance is to avoid myocardial depression and to maintain normal
SVR, venous return and blood volume.
 Epidural analgesia is chosen as it allows a gradual onset of block. Epidural
opioids are used which improve quality of block and allow use of lower
concentrations of local anesthesia.
 General anesthesia is preferable during cesarean section as it allows optimal
airway management and titration of drugs to maintain vascular resistance and
volume.
CONCLUSION:
 Anesthesiologists should be familiar with the anatomy and pathophysiology of
the specific CHD, before anaesthetizing these patients, a discussion with the
cardiologist prior to anesthesia provides valuable information regarding the
status of the individual cardiac pathophysiology and help to anticipate
intraoperative problem.
To goals of anesthesia for these patients with CHD coming for non cardiac
surgeries are the maintenance or even improvement of the hemodynamic status
in the face of destabilizing surgical manipulation.
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Chapter 17 - ANESTHESIA FOR VASCULAR SURGERY
(ABDOMINAL AORTIC ANEURYSMS)
Introduction:
The perioperative management of a patient undergoing vascular surgery is one of the
most challenging and controversial areas in the field of anesthesiology. The challenges
faced by the anesthesiologist in a vascular patient are unique given the high incidence of
co-existing disease, the hemodynamic and metabolic stress associated with cross-
clamping and unclamping, and the ischemic insults to the brain, heart, kidneys, and
spinal cord. Therefore the perioperative morbidity is relatively high than other surgical
procedures.
The controversy associated with routine preoperative screening for coronary artery
disease (CAD) has been fueled by issues related to cost containment and clinical
efficiency. Ongoing controversy continues over anesthetic technique and outcome
because vascular procedures often lend themselves to local, regional, general, or
combined regional and general anesthetics.
More recently the multidisciplinary field of endovascular surgery has provided less
invasive approach to conventional vascular reconstruction.
ANEURYSMS
The International Society for Cardiovascular Surgery (ISCVS) has defined an aneurysm
as a permanent localized dilatation of an artery with increase in diameter of greater
than 50% (1.5times) its normal diameter.
Other related terms:

 Ectasia: Increased diameter of artery less than 50% of its normal size. Same as
arteriomegaly.
 Arteriomegaly: Diffuse enlargement of arterial tree but not large enough to
meet criteria of aneurysm.
HISTORY OF AORTIC ANEURYSMS

 Aneurysms were first described by Galen in his Methodus Mendi
 3rd Century: Greek Antyllus described a procedure involving proximal and distal
ligation of a peripheral aneurysm followed by incision and evacuation of the sac.
 1585: Ambrose Pare implicated atherosclerosis in pathogenesis of aneurysm
 1728: Lancisi advocated ligation of aneurysms as definitive treatment, noting
that involved aneurysms develop gangrene
 1854: Baumgarten and Wurtenburg described the technique of galvano-
puncture of aneurysms.
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 1951: Schafer and Hardin excised an abdominal aortic aneurysm and replaced
with a homograft.
 1957: Teflon and Dacron became materials of choice for grafts.
 1991: Parodi first used endovascular surgery for graft placement in abdominal
aortic surgery.
CLASSIFICATION OF AORTIC ANEURYMS

Aortic aneurysms can be classified on various criteria:
Shape
 Fusiform: Affects entire circumference of a segment of vessel resulting in
diffusely dilated lesion.
 Saccular: Affects only a portion of circumference, resulting in outpouching of
vessel wall.
 Dissecting: Have an intramural separation within aortic media, most prone for
rupture.
Size
 Macro aneurysm
 Micro aneurysm
Structure
 True aneurysm: Involves all 3 layers of vessel wall, namely inner tunica intima,
middle tunica media and outer tunica adventitia.
 False aneurysm: Intimal and medial layers are disrupted and the dilatation is
lined by adventitia only and sometimes by perivascular clot.
Location:
Aneurysms are mostly segmental involving the ascending, arch, descending thoraco-
abdominal or abdominal aorta.
 Ascending aorta aneurysms occur between annulus of aortic valve and the origin
of the innominate artery.
 Transverse aortic arch aneurysms arise in conjunction with brachiocephalic
vessels.
 Descending thoracic aneurysms begin distal to the origin of the left subclavian
artery.
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ETIOLOGY
Degenerative:
 A Nonspecific (Atherosclerotic): Most common cause.
 Fibrodysplasia
 Previous Graft
Congenital
 Idiopathic
 Marfan’s Syndrome (Cystic Medial Necrosis)
 Tuberous Sclerosis
Infectious
 Bacterial
 Syphilitic
 Mycotic - Seen mostly in intravenous drug abusers and immunocompromised
individuals.
Inflammatory
- Rheumatoid arthritis and Scleroderma causes panaortitis. Other causes include giant
cell arteritis and Takayasu's disease.
Trauma
- Blunt injury chest is a common cause of aortic rupture.
Iatrogenic
- False aneurysms occur postoperatively at a site of aortic cannulation, at patch graft
sites, and at aortic anastomosis sites.
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Dissecting
ABDOMINAL AORTIC ANEURYSMS (AAA)

Anesthesia for conventional abdominal aortic reconstruction require an
understanding of the pathophysiology, an extensive knowledge of surgical procedure,
optimization of patient preoperatively, the ability to interpret sophisticated
hemodynamic data and skilful pharmacological control and manipulation of
hemodynamics.
Despite the development of effective surgical treatment, the abdominal aortic
aneurysm remains a significant cause of morbidity and mortality in world.
PREVALENCE:
Population based studies between 25yrs and 84yrs of age reported prevalence of AAA
to be 8.9% in males and 2.2% in females. Therefore it is 4times more common in males.
However, rupture of aneurysms is more commonly encountered in females.
ANATOMY
Understanding of anatomy of abdominal aorta is important for expecting the
hemodynamic changes that occur during clamping of aorta at various levels.
The branches of abdominal aorta are:

Anterior group Celiac trunk, superior mesenteric, inferior mesenteric
artery
Lateral group Suprarenal artery, renal artery, gonadal artery
Dorsal group Inferior phrenic artery, lumbar a
Terminally its divides into two common iliac arteries.
Normal average diameter of Aorta at

11th rib-2.7cm
Suprarenal – 2-4cm
Infrarenal – 2.1cm
bifurcation-1.9cm
based on age, the aorta dilates with increasing age:
< 40 yrs – 2.1 cm
≥ 70 yrs – 2.4 cm
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Risk Factors:
 Age: One of the major factors. With advancing age, the risk of occurrence of AAA
also increases. Also the symptoms of an enlarged AAA also occur with increasing
age.
 Family History: Occurrence of AAA has a familial tendency. Various investigators
have linked aneurysms from autosomal dominant inheritance to X-chromosome
linked traits.
 Atherosclerosis: It is a progressive disease process that compromises the arterial
blood supply to any or all of the vital organs or the extremities. It affects large to
medium sized arteries. Inflammation in the arterial wall plays a fundamental role
in the initiation and progression of atherosclerosis.
 The most common sites are the coronary arteries, the carotid bifurcation, the
abdominal aorta, and the iliac and femoral arteries.
 Morphologically, atherosclerosis produces a fusiform aneurysm in thoracic aorta
and a more saccular aneurysm in the abdominal aorta.
HISTOPATHOLOGY
Basically the collagen present in the tunica is gradually destroyed during expansion of
an aneurysm; whereas elastin finally gives away during rupture of aneurysm.
The basis of dilatation is degeneration and fibrotic replacement of the media
underlying atherosclerotic lesions. Local vascular nutrition is compromised by
increasing tension on the dilated aneurysmal wall, with increasing wall tension in
accordance with the Laplace principle. The resultant diminished aortic wall nutrition
causes further degeneration and enlargement of aneurysm. Mural thrombosis fails
because of the pulsatile movement of the wall. Eventually, the aneurysm consists solely
of dense acellular and avascular connective tissue, and only traces of the media can be
seen microscopically.
COMMON PRESENTATIONS
Incidental: On physical examination (as palpable, pulsatile, non-tender mass), plain
x-ray or-most commonly abdominal ultrasound. Even large AAA's are difficult to
feel, so many remain undetected until they rupture.
Pain: In central abdomen, back, loin, iliac fossa or groin.
Thromboembolic Complications: Thrombus within the aneurysm may be a source

of emboli to lower limb. Less commonly, the aorta may undergo thrombosis
occlusion.
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Compression: Surrounding structures such as duodenum (Obstruction and
vomiting), Inferior vena cava (edema and deep vein thrombosis)
Rupture: Into the retroperitoneum, the peritoneal cavity or surrounding

structures.(most commonly into NC leading to aortocaval fistula)
DIAGNOSIS
 All patients with atherosclerotic disease and/or a family history of aortic
aneurysms should be routinely screened at least once a year.
 Plain X-ray - Usually the basic investigation, calcified lesions can be made out
easily.
 Ultrasound - Can identify the extent of aneurysm and involvement of various
other visceral organs.
 CT scan - Plain CT scan is a very useful tool for pinpointing size and exact
location. Spiral CT helps in 3D reconstruction of aorta.
 MRA -Magnetic resonance arteriography helps in functional analysis of aorta
 Arteriography - Very rarely indicated, but highly sensitive.
MANAGEMENT
The natural history of AAA is one of progressive enlargement and ultimate rupture and
death.
The Joint council of American association for vascular surgery and Society for vascular
surgery published revised guidelines for treatment of AAA
 Aneurysms < 4cms → Benign aneurysm
 4 to5.5cms → Surveillance of Aneurysm, conservative
management
 > 5.5cms → Surgery indicated.
More than the size, the RATE OF EXPANSION of aneurysm is important.
A rate of expansion of >0.5cms in 1 year, surgery is absolutely indicated.
PERIOPERATIVE EVALUATION
Preoperative assessment focuses primarily on the cardiac, renal, pulmonary systems.
Patients presenting for aortic surgery have a very high incidence of significant
concurrent medical diseases.
Pre-op cardiac evaluation:

Cardiac complications are the leading cause of perioperative morbidity and mortality in
patients undergoing vascular surgery. The risk of MI or cardiac death is 2.5% in general
surgical population whereas it is 6.2% in vascular surgical patients.
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- Increased Perioperative cardiac complication is a function of:
1) Patient population - vascular surgery patients have high incidence of CAD

2) Surgical procedures - vascular repair is associated with significant hemodynamic
shifts and neuro-endocrine stress.
- GOALS of preoperative cardiac assessment
→ Identify the presence of underlying cardiac disease.
→ Evaluate its severity
→ Determine need for preoperative interventions to minimize the risk of
perioperative cardiac complications
History and Physical Examination

 Symptoms of CAD should be sought.
 CAD manifests (after 75-90% arterial lumen occlusion) as angina, arrhythmias,
heart failure or infarction.
 Myocardial ischemia may be silent, in which case the patients are asymptomatic
and carries poor prognosis.
 Patients in CCF will have ankle or sacral edema and shortness of breath.
Co-existing Disease
 Previous MI: Current guidelines recommend waiting 6weeks after an

uncomplicated MI before proceeding with an elective surgical repair.
 Hypertension: Fifty percent of all patients have HTN according to WHO. High
incidence in elderly population is a major factor in pathogenesis of
atherosclerotic disease.
Patients on anti-hypertensive medication should continue right upto the day of

surgery and afterwards if possible.
Patients with untreated HTN who require urgent surgery, a single dose of beta-
blocker given with premedication reduces incidence of intraoperative MI from 28% to
2%.
Congestive Heart Failure: present in 10-15% patients preoperatively and 30%

postoperatively. All patients in heart failure must be treated vigorously with diuretics,
inotropes and vasodilators prior to surgery.
CAD Radiologically significant atherosclerotic disease of coronary arteries is present in

almost two-thirds of all patients coming for vascular surgery.
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Some of the tests used for risk assessment:
Electrocardiogram: Advised for all patients undergoing vascular surgery. It is

necessary for comparison if myocardial ischemia or infarction is suspected
postoperatively.
Exercise ECG:A majority of vascular patients cannot attain target heart rates that allow
detection of ischemia. So this test cannot be used in many patients.
Myocardial Perfusion Imaging: Dipyridamole thallium Imaging (DTI) is the most

commonly used noninvasive test used to screen vascular surgery patients. Eagle and
colleagues in 1989 stratified vascular surgery patients first by clinical predictors and
then by thallium distribution.
Ambulatory ECG (AECG) Monitoring: It has almost same predictive value as DTI but
the advantage is it one-third the cost of DTI.
Echocardiography: Two dimensional ECHO is widely used tool that provides

measurements of left ventricular function, ejection fraction, regional wall motion and
ventricular function.
Stress Echocardiography: It can be used with pharmacologic stress testing

(dobutamine or dipyridamole) to provoke myocardial ischemia, as detected by new or
worsening wall motion abnormalities. Dobutamine stress echocardiography (DSE) has a
sensitivity and specificity of 80% to 90% for predicting perioperative cardiac morbidity.
Schema of Cardiac Evaluation on patients with Asymptomatic AAA

 Class I Asymptomatic, Cardiac status => AAA Repair
 Class II Mild, stable cardiac symptoms => Non invasive cardiac study:
Study positive → Coronary Angiography
Study negative → AAA repair.
 Class III Significant cardiac symptoms => Coronary Angiography
Significant CAD → CABG, then staged AAA
Insignificant CAD → AAA repair
 Class IV Very elderly or LVEF <30% or non-reconstructible CAD
AAA <6cm → careful surveillance of aneurysm.
AAA ≥ 6cm → AAA repair with invasive monitoring.
In summary, the three of the most commonly used preoperative ischemia tests,
i.e., DTI, AECG, DSE, have relatively high negative predictive values. If a patient tests
negative most likely perioperative cardiac morbid event is unlikely, but negative result
should never be interpreted as CAD free patient. In case the patient tests positive,
further workup with cardiologist is necessary, with the patient requiring a Coronary
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artery bypass graft(CABG) or percutaneous transluminal coronary angioplasty (PTCA).
In case PTCA is done, the surgery should be postponed for at least 6weeks.
PRE-OP PULMONARY EVALUATION

Chronic obstructive pulmonary disease (COPD) is present in approximately one-third of
patients presenting for vascular surgery. History of smoking should be sought and the
patient advised to give up smoking.
Antibiotic therapy should be aggressively continued for controlling infection in case of
Pneumonia. Pulmonary function tests (PFT) should be used to assess the ventilatory
reserve of the patient.
PREOP RENAL EVALUATION

Renal function is vulnerable in patients with hypertension or heart failure and is
manifest in 10-15% of patients as elevated blood concentrations of urea and creatinine.
Operative mortality is 19% when aortic reconstruction is performed on patients with a
serum creatinine greater than 2mg/dL. Hypertensive patients have marked increase in
total body sodium and water retention. The impaired blood autoregulation may lead to
renal ischemia. Also the atherosclerotic plaques found in renal arteries make the
kidneys relatively vulnerable to hypotension during aortic surgery.
Diabetes Mellitus
Patients with DM constitute 10% of vascular surgery patients. Silent myocardial
ischemia is associated with DM. Steady blood glucose levels should be maintained by
intravenous insulin treatment.
Lab investigations:
Other investigations that should be done before taking the patient for surgery are:
Complete Blood Count
Blood Grouping and Typing
Blood Urea and Serum Creatinine
Arterial Blood gases
Serum electrolytes
Arrange at least 4-6 units of compatible whole blood.
SURGICAL ISSUES RELEVANT TO ANESTHESIOLOGIST

Goals Of Surgery Are:
Avoidance of rupture of aorta

Relief of symptoms of aneurysm
Restoration and maintenance of blood flow to viscera and legs.
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Aneurysm is replaced with a graft made either from knitted or woven Dacron or
Polytetrafluoroethylene (PTFE) by a procedure called "Endoaneurysmorraphy". The
newer grafts are made up of ‘Expanded – PTFE’
Two surgical techniques are used:

 Open abdominal aneurysm repair (OAAR)
 Endovascular aneurysm repair (EVAR)
In open repair of aorta, there are two approaches

→ Tran peritoneal approach
→ Retroperitoneal approach
Trans-peritoneal approach
It is indicated when:
 Abdominal organs are to be accessed.
 Right renal or iliac artery is to be accessed.
 Aorto-femoral graft is to be performed.
The disadvantages of this technique are

- Severe postoperative pain which may limit chest and abdomen movement.
- Loss of heat and fluid from intestines.
- Paralytic ileus which may persist for days.
Retro-peritoneal approach:
It is performed with the patient in right lateral decubitus position.
It is indicated in
→ Inflammatory aneurysms. Retroperitoneal fibrosis
→ Previous abdominal surgery with adhesions.
Advantages are
→ Rapid return of GIT function
→ Decreased postoperative pulmonary complications
→ Decreased postoperative pain
SURGICAL PROCEDURE OF OAR

Incision: Vertical midline or Transverse supra-umbilical incision.
Exposure of Aorta: The abdominal contents are thoroughly explored, following which
the transverse colon, greater omentum, and small intestine are lifted superiorly and
placed outside the abdomen between moist packs. The posterior peritoneum is incised
and dissected to expose the aorta from the left renal vein superiorly to the common iliac
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arteries inferiorly. Dissection near the aneurysms is kept to a minimum to keep
bleeding to minimum.
Stage of Clamping: Systemic heparin (5000 – 10000 units) is given to prevent distal
thrombus formation during the cross –clamp period. Vascular clamps are then applied,
first to both common iliac arteries (to prevent embolization) and then to the aorta at the
required site (supraceliac, suprarenal or Infrarenal).
Grafting and anastomosis: The aorta is incised longitudinally. All atherosclerotic
debris and thrombus are removed from the aortic lumen and the paired Ostia of the
lumbar arteries is overseen. The chosen graft is sutured into the infrarenal aorta at its
proximal end and the anastomosis tested by brief unclamping of the aorta. If necessary
repairs are made to the suture line. The distal anastomosis is then sutured (aorta-tube
graft or iliac arteries – bifurcation graft) and, before completion, the distal vascular
clamps are released to permit back bleeding and the vessel is flushed to remove any
residual intraluminal debris.
Stage of Unclamping and closure: It should be done in a slow, controlled fashion, one
leg at a time to minimize unclamping hypotension.
The original aortic wall is then wrapped round the graft and sutured, the peritoneum
closed, the intestines are returned to the abdominal cavity, and the abdominal wall is
repaired.
PATHOPHYSIOLOGY OF AORTIC ANEURYSMAL SURGERY

An elaborate understanding of the pathophysiology of aortic cross clamping and
unclamping is necessary for successfully executing the therapeutic interventions to
reduce the morbidity associated with these procedures.
AORTIC CROSS-CLAMPING
It is defined as the obstruction to blood flow in aorta by application of clamps (proximal
and distal) for the purpose of facilitating repair of aorta. The pathophysiology of aortic
cross clamping is multifactorial.
It depends on:
 Level of cross-clamp
 The extent of CAD and myocardial function
 The degree of periaortico lateralization
 The intravascular volume and distribution
 Anesthetic agents and techniques.
The main factor determining the consequences of aortic cross clamping is the level of
aortic occlusion.
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Clamping may be done:
 Infrarenal → Majority of AAA are infrarenal aneurysms.
 Suprarenal → Indicated for juxtarenal or inflammatory aneurysms and
aorto-iliac occlusive disease with proximal extension.
 Supraceliac → Reconstruction of celiac trunk or mesenteric artery.
HEMODYNAMIC CHANGES
Cardiovascular changes are similar in all three levels of clamping but their severity
differs. It is profound in supraceliac clamping, mild to moderate in suprarenal and
minimal in infrarenal cross-clamping. The most consistent change is Arterial
Hypertension, occurring in all the levels of cross clamping of aorta.
 In infrarenal cross clamping: blood pressure increases by 7 to 13%
 Cardiac output decreases by 9 to 33%
 Percentage change after occlusion
Supraceliac
Cardiovascular variable Supraceliac Infrarenal
infrarenal
MABP 54 5 2
PCWP 38 10 0
End-Diastolic area 28 2 9
End-Systolic area 69 10 11
Ejection Fraction - 38 - 10 -3
Pts. With wall motion 92 33 0
abnormalities
PERCENT CHANGE IN CV VARIABLES ON INITIATION OF AORTIC

OCCLUSION
Cardiac function during aortic cross clamping, particularly in infrarenal cross clamping,
is generally maintained in the presence of sufficient coronary blood flow and
myocardial contractility. In patients with good ventricular function, contractility could
actually increase in the setting of increased after-load and preload. In contrast, in
patients with significant heart dysfunction, the left ventricle could decompensate and
contractility worsens, especially if concomitant CAD does not allow an increase in
myocardial oxygen supply. In the patients, even the minor insult of an infrarenal clamp
could precipitate ischemia and heart failure.
THERAPEUTIC INTERVENTIONS
Patients with impaired ventricular function requiring supraceliac aortic cross clamping
are most challenging. Goals of therapeutic strategies are
 Reduce after load
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 Normalized preload
 Optimize coronary blood flow and contractility
These are achieved through:
Controlled Cross clamping:

 The surgeon is advised to clamp the aorta slowly (especially supraceliac portion)
to avoid abrupt and extreme stresses on heart. This helps in preventing
myocardial ischemia.
After load Reduction

 Most commonly accomplished by Sodium nitroprusside (SNP), a predominant
arteriolar dilator. It is necessary to "unload" the heart and reduce ventricular
wall tension. SNP also allows adequate volume loading before unclamping which
resulted in stable unclamping hemodynamics.
Normalizing Preload
 Careful fluid titration and if required a Venodilators like Nitroglycerin
administration is necessary.
 Blood flow below the clamp is pressure dependent. So care must be taken not to
reduce perfusion pressure (in collaterals) drastically with vasodilators.
RENAL PATHOPHYSIOLOGY DURING CROSS-CLAMPING

- Preservation of renal function is of paramount significance during aortic
reconstruction.
- Incidence of renal failure in patients undergoing AAA repair is 5.4% (3% in
infrarenal aortic repair) Mortality resulting from postoperative renal failure is
40%.
- Much of the morbidity associated with significant postoperative renal dysfunction
is "nonrenal" in nature,
Risk factor for developing post-operative renal failure is:

1) Preoperative renal insufficiency
2) Preexisting cardiac disease
3) Renal ischemia for > 30mins duration.
- Adequacy of renal perfusion cannot be assumed by urine output because
intraoperative urine output doesn't predict postoperative renal function.
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Infrarenal aortic cross-clamping causes:
o 75% increase in renal vascular resistance.
o 38% decrease in renal blood flow.
o Redistribution of intra-renal blood flow towards renal cortex
o Etiology of renal failure in aortic surgery is due to "Acute Tubular
o Necrosis"
- Other contributing causes include
→ Intravascular volume depletion and low cardiac output.

→ Embolization of atherosclerotic debris to kidneys.
→ Surgical trauma to renal arteries.
Mechanism:
Sustained deterioration in renal perfusion during and after infrarenal aortic clamping is
attributed to renal vasoconstriction mediated by renin-angiotensin system and
sympathetic nervous system. However epidural anesthesia or ACE inhibitors do not
alter the renal outcome when administered in these patients.
Therapeutic Interventions for Renal Protection

The most important and effective means of renal protection is to maintain adequate
intravascular volume.
Various drugs can be used to maintain urine output, increase renal blood flow and
minimize ischemic injury. Best options available are:
 Mannitol (most commonly used)
 Loop diuretics (Furosemide)
 Dopamine (renal dose 1-3 µg/kg/min)
 Fenoldopam (DAI receptor agonist)
 MANNITOL: Dose used is 12.5- to 25g.
- Administered before aortic clamping to induce osmotic diuresis.
- Other advantages of administering Mannitol are:
 Increases renal cortical blood flow.
 Decreases ischemia induced renal vascular endothelial cell edema and vascular
congestion.
 Acts as scavenger of free radicals.
 Decreases rennin secretion.
 Increases renal prostaglandin synthesis.
- Use of Furosemide and dopamine is controversial and is currently limited to patients
with preoperative renal insufficiency.
- Intraoperative use of these agents requires heightened monitoring of serum
electrolytes (K & Mg) and fluid requirements.
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SPINAL CORD: Spinal cord ischemia is a very rare but potentially devastating
complication of aortic cross-clamping. The incidence of paraplegia is less-than 1% for
infra-renal aortic repairs but high-in thoraco-abdominal aneurysm repair.
It is caused due to interruption of flow in artery of Adamkiewicz (arteria radicularis

magna) supplying the anterior spinal artery. Various methods utilized to reduce
incidence of spinal cord ischemia are spinal cord cooling, hypothermia, aortic and left
heart bypass with retrograde perfusion and lumbar Intrathecal drainage.
BOWEL: The incidence of GI complications after aortic surgery is 1 to 7%. Infrarenal
cross clamping produces little effect on splanchnic blood flow whereas supraceliac
clamp causes marked reduction in blood flow. Ischemic colitis occurs in 0.6% cases after
AAA repair.
AOTRIC UNCLAMPING
It results in restoration of blood flow to the ischemic tissues and vasodilator blood
vessels of the lower torso.
The immediate hemodynamic changes occurring after unclamping can be termed as
"Unclamping Shock". It includes:
 Hypotension (most important)
 Decreased S VR
 Decreased CO
Unclamping shock is of short duration (<10mins) and its magnitude can be reduced by:
 Slow, controlled release of clamp over 2-3mins.
 Release of blood flow to one leg at a time (in case of bifurcation graft used)
 Stop any vasodilator infusion.
 Reduce the concentration of volatile anesthetic 5-10 mins before unclamping.
 Start heavy volume loading.
In case of refractory hypotension after Unclamping:

→ Administer Vasopressors (phenylephrine or NE)
→ Reclamping of aorta is the last option.
The goals of anesthesia for abdominal aortic surgery should meet the following goals
1) Ensure adequate preoperative assessment of risk and optimize management of
coexisting diseases.
2) Maintain adequate intravascular volume, cardiac output, and tissue oxygenation
in the presence of surgical events that affect blood pressure, volume and
myocardial performance.
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3) Recognize the major risks of aortic surgery, including MI, visceral organ
ischemia, coagulopathy and hypothermia.
The goal at the conclusion of surgery is to provide a hemodynamically stable,
comfortable, normothermic and non coagulopathy patient.
PREMEDICATION
Premeditation should be individualized according to patient's preoperative
condition. Anxiolytic premeditation is desirable to minimize the release of endogenous
catecholamines and decrease sympathetic nervous system stimulation that occurs from
surgical stress in preoperative period.
Low dose benzodiazepines (diazepam 5-10mg oral) can be given night before
surgery and on morning of surgery. The reminder of preoperative medications can be
given intravenously after arrival in the operating room.
MONITORING:
Standard monitors should include:
 Pulse Oximetry
 Standard 5 lead ECG monitoring
 End tidal C02 monitoring.
 Continuous arterial BP measurement via Radial artery cannula.
 CVP monitoring
 Core temperature monitoring via a thermistor on PAC or esophageal probe.
 Transoesophageal echocardiography (TEE)
 Pulmonary artery catheter (PAC) - Regular use remains controversial. Highly
indicated in patients with significant cardiac disease or renal insufficiency.
ANESTHETIC TECHNIQUE
1) General anesthesia as a sole technique.
2) Epidural anesthesia alone: can be used in small uncomplicated infrarenal
aneurysm repairs.
3) GA + Epidural anesthesia is ideal.
INTRAOPERATIVE MANAGEMENT
General Anesthesia + Epidural Anesthesia
First an epidural catheter is put in place and test dose given to check correct placement.
Next 100% oxygen is administered for 3-5mins.
The choice of agents and methods for premedication; induction and maintenance of
general anesthesia is not unique to aortic surgery. It is important to recognize that these
patients are often frail and elderly with significant coexisting diseases that affect
multiple organ systems. Careful titration of medications in small doses is the most
prudent approach.
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FLUID MANAGEMENT
- Fluid and blood losses are large compared with abdominal surgery.
- Adequacy of circulating volume is judged form CVP and PAOP values.
- CVP should be maintained between 5-10mm Hg and PAOP around 15minllg.
- Balanced salt solutions like Ringer's lactate or DNS should be used. Rate of
infusion is 6 to 16 mL/kg/hr. Some 3-6 L crystalloid may be required
perioperatively.
- Hb should be monitored carefully. A l gm/dL should be maintained in cardiac
patients.
- Blood loss averages 2L (± 1 L). So around 4 units of blood should be ready for
transfusion.
- Preoperative autologous donation, intraoperative cell salvage, and acute
normovolaemic haemodilution should be used during aortic surgery to reduce or
eliminate exposure to allogenic and related complications.
BODY TEMPERATURE
- Core temperature decreases by up to 3-4 C in a large abdominal incision with
evisceration of intestines.
- Various methods to reduce heat loss:
 Operating room temperature to be maintained at 20 C minimum.
 Use of heated mattress
 Forced air warming devices.
 Pts head should be covered with heat reflective cap.
 Use of warm IV fluids.
COMPLIATIONS OF AAA REPAIR

Intraoperative:
 Myocardial infarction
 Hypertension (during cross-clamp)
 Hypotension (after clamping)
 Metabolic acidosis (mild, transient after unclamping)
 Bleed from graft site.
Mesenteric traction syndrome: It causes hypotension associated with sudden
tachycardia and facial flushing. It is of short duration of less than 30mins, and is
primarily due to increased plasma Prostacyclin.
Renal failure:
 Renal failure – ARF carries a mortality > 30% postoperatively.
 Paralytic ileus
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 Colonic ischemia
 Spinal cord ischemia and paraplegia
 Lower extremity ischemia
 Coagulopathy
 Venous thromboembolism
POSTOPERATIVE MANAGEMENT
 Patient is shifted to ICU for mechanical ventilation if he was not extubated and
also stabilization of vital parameters.
 First 48 hrs after surgery is most important as significant cardiac morbidity and
MI can occur during this period.
Analgesia
Good pain relief is most important for speedy recovery. It is given by epidural catheter
in place. (0.125% to 0.25% bupivacaine with fentanyl 1 µg/kg or tramadol 1mg/kg)
- Fluid management: Adequate maintenance of circulating volume is monitored
via CVP or PAOP for 24hrs.
- Post op ileus is common and feeds should be withheld for minimum 48hrs.
- Renal sufficiency should be monitored by hourly urine output chart.
ENDOVASCULAR ANEURYSM REPAIR

This is the latest, minimally invasive treatment of aortic aneurysm, introduced in mid
1990's.
Advantages
 Useful in very elderly or those deemed unfit for open repair (ASA class ill or 1V)
 Reduces risk of open surgery.
 Duration of surgery short (< hrs of EVAR vs.>4 hrs of OAAR)
 Shorter patient recovery periods.
 Cost saving
 Significant reduction in fluid and blood requirements.
Disadvantages:
 Uncertainty over long term effectiveness of the graft.
 “Endoleaks” common.
Preoperative assessment:
The Endovascular Graft Committee recommended the following as appropriate workup
of a potential endovascular patient: cardiac evaluation involving either an
echocardiogram or stress thallium to assess function or ischemic potential, renal
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function tests, pulmonary function tests, hematology profile, including hemoglobin and
coagulation studies and liver function tests.
Surgical Technique:
The current approach uses a bilateral femoral arterial exposure. Patient is
anticoagulated with 5000U heparin and femoral arteries clamped. A small incision is
made in femoral artery to pass delivery sheath. Diagnostic angiography is done to
delineate proximal and distal fixation points. The endograft limbs are delivered into iliac
arteries where the graft is uncovered and fixed proximally at aneurismal neck and
distally into the iliac arteries. A completion angiogram is performed to check for
endoleaks and then the femoral artery sites repaired.
Anesthesia Plan:
Regional anesthesia: It is the most preferred technique. Epidural or Combined Spinal-

Epidural anesthesia can be used with intravenous sedation. Local anesthesia: at femoral
sites with mild sedation has also been used.
RUPUTURED AORTIC ANEURYSM

 It is a surgical emergency and nearly always fatal.
 Rupture is retroperitoneal in 75% cases where tamponade effect is protective
against massive blood loss. In 25% cases aorta ruptures intraperitoneally and
carries grave prognosis.
 Management: Rapid diagnosis is very important with immediate resuscitative
measures starting with administration of massive IV fluids and administering
100% oxygen and shifting the patient for emergency laparotomy.
 Intraoperatively, rapid sequence intubation should be done with minimal
sedation and relaxation with Succinylcholine. Maintenance is done with 100%
oxygen, atracurium and minimal does of fentanyl. At least 6-10 units of blood
may be required.
 Postoperatively, the patient should be ventilated until physiologically stable.
 Mortality occurring early is due to cardiac failure whereas ate death is attributed
to multiorgan failure.
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Chapter 18 - DELIBERATE HYPOTENSION
Synonyms:
- Induced hypotension
- Controlled hypotension
- Hypotensive anesthesia
Definition:
Reduction in SBP to 80-90 mmHg or mean arterial pressure (MAP) to 50-65 mmHg in
normotensive patients.
Indications:
- Neurosurgery
- Orthopedic procedures e.g.: Total hip arthroplasty complicated back surgery
corrective spinal surgery.
- Surgery of head and neck
- Surgery where blood loss is anticipated to be high
- Cancer surgery
o Surgery on large tumors, aneurysms.
o A-V fistula, large vessels etc.
- Plastic surgeries especially those of hand /foot
- Extensive evisceration procedure.
- Inability to replace blood loss
- Control of dangerous hypertension intra and post operative.
- Religious beliefs preclude blood transfusion. JEEVOH s witness
- To treat pulmonary edema secondary to pulmonary HTN.
Contra indications:
Disease states:
1. Severe cardiac disease
2. Cerebro vascular disease
3. Liver and renal dysfunction
4. Peripheral vascular disease (less likely to have good) organ perfusion.
5. Arteriosclerosis
6. Degenerative C.N.S disorders
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Clinical conditions:
a. Un corrected anemia Reserves for adequate
b. Patients with hypovolemia organ perfusion 
c. Shock / preoperative Haemorrhage.
d. Uncontrolled HTN- autoregulation of C.B.F is  or lost.
 Intracranial pressure -hypotension should be induced after opening the
dura.
e. Patients with myocardial disease/IHD deliberate hypotension not done unless
proper monitoring is available.
Technical factors:
I. Inadequate skill
II. Inadequate fluid and blood reserves
III. Poor team work.
Techniques: 5 P’s
I. Positioning, (pressure + local infiltration).
II. Positive pressure ventilation.
III. Phlebotomy.
IV. Pharmacological sympathectomy
V. Pharmacological hypotensive agents.
Physiologic:
These techniques reduce the needed dose of hypotensive drugs. They include
Body positioning:
Operating parts put at the higher level to minimize blood loss. Studies have
proved that for each 2.5 cm of vertical height / 30 tilt there will be  in S.B.P by 2 mmHg.
The part above the heart level will be hypotensive and below heart level have BP raised.
Mechanical ventilation: Because of mechanical ventilation there is inhibits of thoracic
respiratory pump which controls venous return. Hence there is decrease in venous
return and decrease in the capacity and the pulmonary vascular bed also.
By hypoventilation there will be increased fall in SBP due to raised PaCO2.
Further  in PaCO2 will maintain SBP at low levels, so venous tone is inversely related to
PaCO2. i.e.  PaCO2 decrease in venous tone  V.R.
Changes in circulatory volume (phlebotomy) - The method is very unsatisfactory. It is
done by doing arteiotomy and narrowing around 1000 ml of blood.
Changes in heart rate.
Inducing hypothermia -this method is unsatisfactory.
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Pharmacologic:
1. Spinal and epidural anesthesia.
2. Volatile anesthetics, halothane, isoflurane, sevoflurane.
3. Direct acting vasodilators – Na – nitroprusside nitroglycerin, hydralazine.
4. Autonomic ganglion blockers e.g. Trimethaphan.
5. -blockers e.g. phentolamine
 blockers e.g. propranolol, esmolol
6. Combined & blockers
7. Ca-blockers – nicardipine
8. PGE1
Effect of hypotension on organ function:

CNS.
o Lowest MAP at which autoregulation of C.B.F. is maintained in
normotensive patients is 50-55 mmHg (73  9 mm Hg). In hypertensive
patients it is 113  17 mmHg.
o Once MAP falls below this limit CBF decreases in parallel with pressure.
o Deliberate hypotension doesn’t produce permanent change in cerebral
hemodynamics.
o It also causes decrease in electrical activity of the brain.
o There is increase in I.C.P because of cerebral vasodilation.
CVS:
Normal arterial hypotension

Tachycardia
 metabolism  diastolic period

 
 O2 demand  O2 supply
Myocardial ischemia
General anesthesia depresses the baroreceptor control of heart rate there by no

change in the heart rate by deliberate hypotension.
I.V. anesthesia also depresses baroreceptor control of HR except ketamine and
Etomidate.
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The inhibitory effect on baroreceptor mechanism is minimum with Halothane
and enflurane and least with isoflurane.
In C.V.S. disorders isoflurane is the volatile anesthetic of choice.
 To avoid tachycardia
 Along with vasodilators we can use
o Esmolol
o Ganglion blockers.
 Labetalol and because of their concomitant 1 antagonistic action cause less
tachycardia.
 Adenosine causes less tachycardia by inhibiting S.A. node directly.
CAUTIONS:
 Nitroglycerine improves perfusion to jeopardized area
 ADENOSINE AND SODIUM NITROPRUSSIDE should not be used without a
monitor because they cause coronary steal.
 Haemodilutation reduces coronary vasodilatory reserve and causes tolerance to
M.I. during hypotension.
Lungs:
1. CO2 tension in the blood.
2. Combined effect of hypotension, increase means airway pressure; head up
position and surgery increases the dead space. If cardiac output is maintained
there will not be any increase in dead space.
3. Decrease arterial oxygenation.
4. Because of changes in oxygenation and CO2 elimination, controlled ventilation is
preferred.
Renal:
Normal renal blood flow = 20 – 25% of total cardiac output.
Renal arterioles have got low resting vascular tone and hence limited ability to
dilate further in response to hypotensive drugs. Therefore renal blood flow is near to
normal.
 GFR = maintained until MAP falls below 75 mm Hg.
 Renal function not altered.
 Renal function are best preserved with a combination of labetalol and isoflurane
than with isoflurane alone.
Splanchnic circulation:
Pressure flow autoregulation is limited in hepatic arterial blood and absent in
portal venous system. Therefore profound changes are seen in deliberate hypotensive.
Baroreflex activation, surgical stress or exogenous vasopressors will decrease
hepatic and splanchnic blood flow by vasoconstriction.
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Isoflurane preserves hepatic blood flow better than Halothane and enflurane.
Isoflurane + I.V. adjutants will preserve hepatic blood flow better than isoflurane alone.
Combination of haemodilution and isoflurane has got adverse effect on hepatic blood
flow.
EYE:
 IOP
Symptoms = Blurring of vision, rarely blindness.
Skin and muscle:
There will be decreased blood flow to the skin but it is non injurious to the tissue.
The blood flow to the skeletal muscles is increased; O2 pressure in the skeletal
muscle is decreased. Lactate, pyruvate and HCO3 levels will be normal.
Routine monitors:
I. B.P. Invasive non invasive.
II. Pulse oximetry
III. ETCO2
IV. ABG analysis
V. Temperature
VI. Urine output
VII. ECG
VIII. Electrolytes
IX. Hematocrit
Monitoring: During deliberate hypotension.
1. Beat to beat measurement of arterial B.P.
This is done by arterial catheter placed in radial artery, the transducer being
placed at the level of circle of Willis. B.P. measurement by sphygmomanometer
can also be used. Oscillometric method is preferred than auscultatory method.
2. Intermittent blood sampling for arterial blood gas analysis.
3. This is to know the adequacy of oxygenation and ventilation.
4. E.C.G. (V5/ CB5.)
5. To detect signs of inadequate myocardial perfusion, because of excessive
hypotension. V5 lead / CB5 configuration is used. Signs of ectopic beats / ST
changes.
Capnography:
 Sudden  in end expiratory PCO2 indicates sudden  in cardiac output or
disconnection of breathing system.
 This also helps to avoid hyperventilation, which by decrease PaCO2 decreases the
CBF.
 Pulse oximetry
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 Temperature monitoring
 This can be done by tympanic or nasopharyngeal probes for the brain temp
measurement and by using rectal / mid esophageal probes for measuring core body
temp.
 This is done because body heat loss will be more by dilated blood vessels.
1. Urinary output:
2. This indicates adequacy of circulatory status and tissue perfusion as well as renal
function.
3. Serum electrolytes
4. Hematocrit
Non routine monitors:
1. Evoked potentials
2. Pulmonary artery pressure
3. E.E.G.
4. Esophageal stethoscope for breath sounds and heart sounds.
5. Tissue pH.
Complications:
Non fatal:
1. Reactionary haemorrhage (most common)
2. Delayed haemorrhage.
3. Blurred vision
4. Renal disturbances = Anuria, oliguria
5. Thrombosis = cerebral, coronary
6. Rebound hypertension
7. I.C.P.
Fetal:
1. Cerebral thrombosis.
2. Anoxia
3. Renal failure
4. Cardiac arrest
5. Coronary thrombosis.
6. C.V.S. collapse.
Precaution
 Careful pre evaluation of the patient regarding function of each and every organ.
o – 1.5 hrs is the upper limit of the length of time that hypotension should
be permitted, more complications occurs if duration is more.
 Maintain normal blood volume by replacing blood loss.
 Maintain airway and complete oxygenation.
 Proper post operative care should be given.
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COMMONLY USED HYPOTENSIVE AGENTS
Mechanism
Drugs Dosage Advantage Disadvantage
of action
1. Sodium 0.5 to Nitric oxide Rapid onset Cyanide toxicity,  ILP
nitroprusside 10g/kg/iv mediated and offset rebound HTN, 
direct pulmonary shunt
vasodilator coagulates abnormal
2. NTG 1 to 10 Same of Rapid onset Cyanide toxicity,  ILP
nitroglycerine /kg/iv nitric oxide and offset rebound HTN, 
pulmonary shunt
coagulates abnormal
3. 1 to 5mg/iv Ganglion Rapid onset Histamine release,
Trimethaphan blockade and offset pseudocholinesterase
cerebral compression
below MAP 55mmHg
4. Esmolol 0.2 to -adrenergic Rapid onset Cardiac depress and
5mg/kg/iv blockade and offset bronchospasm
loading, 50-
200g/kg/iv
5. Labetalol 20mg tab 0.5  and  -  probability Bronchospasm
to 2mg iv, adrenergic of adverse
total 300mg blocked effects
6. PGE1 0.1 to 0.65 Direct Rapid onset, Slow offset, bradycardia
g/kg/iv vasodilation decreases hypotension
reflex
tachycardia
and stable
CBF
7. Nicardipine Begin 5mg/hr Coronary and rapid onset, Slow off, resists
max 15mg/hr peripheral decreases antihypotensive therapy.
vasodilator reflex  pulmonary. shunt
tachycardia
and stable
CBF
8. Inhalation Titrate by Vasodilation Provides  ICP,  cerebral edema,
anesthetics inspired conc. and surgical  vital organ blood flow
myocardial therapy
depression
FUROSEMIDE:
Loops: I.V. Furosemide 0.1 to 1mg/kg IV
Orally 0.1 to 3mg/kg
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Etharynaic acid:
Orally 0.1 to 3mg /kg
I.V. 0.5 to 1mg kg
SODIUM NITROPRUSSIDE:
NO
C CN–
N
Fe+2
CN– CN–
CN–
- Relaxes both arteriolar and venous smooth muscle.

- Form nitric oxide – activates Guanylcyclase – synthesis of CGM. Intracellular
Ca+2 – vascular smooth relaxation.
Nitric oxide (N = O) – naturally occurring vasodilator released by endothelial cells
(endothelium derived relaxing factor) .
– Plays important in regulating vascular tone
– Ultra short half life < 5 sec.
– Inhaled NO – selective pulmonary vasodilator in treatment of reversible
pulmonary HTN.
– In ARDS patients – NO improves perfusion in ventilated areas of lung.
– One lung ventilation.
– Anti inflammatory effects – promote lung healing.
– PPM
– Color of cylinders
Dose
IV diluted to 100 g/ml.

- Continuous infusion 0.5 – 10 g/kg/min
- Laryngoscopy 1-2 g/kg
- Bolus – 50 to 100 g
- Rapid onset 1-2 min
- Short duration (5 min)
- Mechanical infusion pump
- Intra arterial monitoring
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- Protected from light (due to photo degeneration)
Metabolism: IV  enters RBC’s
SNP + oxyhemoglobin  SNP– + methemoglobin.
SNP– 5 CN– + No.
CN– + methemoglobin  cyanomethemoglobin.
B , Rhodonas e
CN– + Thiosulfate 12 Thiocyanate
Liver and kidney
CN+ + Cytochrome oxidase  cyanide toxicity
(interference normal O2 utilization)

Metabolic acidosis, cardiac dysrthymias,  venous O2 content. Early sign –
tachyphylaxisis.
Avoided if cumulative dose of SNP is less than 0.5 mg/kg/hr.
Treatment:
– Mechanical ventilation with 100% O2.
– Sodium thiosulfate 150 mg/kg over 15 min  Thiocyanate excreted by renals.
– 3% sod nitrate 5 mg/kg over 5 min.
– Hydroxo cobolamine – cyanocobalamine
Methemoglobinemia:
From excessive doses SNP or sodium nitrate – treatment 1% methylene blue 1-2 mg/kg
of over 5 min) reduced hemoglobin.
Effects on organ systems:
CVS  after load – C.O. normal in normal patients.
C.O  in CHF, MR, AR
 preload -  myocardial work so  ischemia
 BP  reflex mediated responses
Tachycardia
 myocardial contraction
Coronary dilation
(+) intracoronary steel
Cerebral:
o Dilates cerebral vessels.
o Abolishes cerebral autoregulation.
o CBF maintained or 
o ICP
Renal– decreased B.P -release of Renin and catecholamines causes rebound HTN after /
stopping SNP, blocked by propranolol or high epidural (T1).
Respiratory: Pulmonary vasculature dilates.
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– Reduction in pulmonary artery pressure -  perfusion of some normally
ventilated alveoli -  physiological dead space.
– Abolishes hypoxic pulmonary vasoconstriction.
– Mismatch ventilation to perfusion -  arterial oxygenation
Drug interactions:
– Phosphodiesterase inhibitors – Aminophylline  cGMP potentiates hypotensive
effects.
 BP -  muscle flow – NMDR – delayed onset and prolonged duration of
action.
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Chapter 19 - SHOCK
Shock: A rude unhinging of the machinery of life - Samuel gross, 1872.
The term shock (Fr, choke) was first used by French physician Le Pran in 1773 to
describe the clinical characteristics of patients after severe gunshot trauma.
Definition:
 Shock is a state in which failure of the circulatory system to maintain adequate
cellular perfusion results in wide spread reduction in delivery of oxygen and
other nutrients to tissues. OR
 Shock is a syndrome of failure of heart to pump blood in sufficient quantity or
under sufficient pressure to maintain pressure flow relationship necessary for
adequate tissue perfusion. OR
 Shock denotes circulatory failure leading to inadequate vital organ perfusion ,
oxygen delivery and other tissues
 Hypoperfusion of organs may occur due to,
 Myocardial failure  Decrease in cardiac output.
 Perivascular failure  Maldistribution of adequate cardiac
Output O2 delivery (DO2)
O2 conoumpth (VO2)
 Maintains organ function 

I. BP  IV fluids, Vasopressors or vasodilators
II. Demand of O2 maintain MAP  60 mm Hg; Hb  10 gm%.
III. PaO2 60 mm Hg ; SaO2 90%
a. VO2 prevent seizures, maintain normothermic,
Mechanical ventilation with high FIO2
Physiology (of tissue perfusion):

The determinants of tissue perfusion are cardiac factors.
Cardiac output = stroke volume x heart rate
 Cardiac output – the amount of blood ejected by ventricle per unit time.
 Heart rate – the number of times heart beats per minute.
 Stroke volume – the amount of blood ejected by either ventricle per contraction.
This is determined by,
 Per load: venous return represented by ventricular end diastolic volume.
 Myocardial contractility: ability of the ventricular myocardial fibres to shorten
during systole. This is assessed by calculating ejection fraction.
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Stro kevo lume
 EF = Endd iastolicvo lume(N  0.70)
 After load: the load that the ventricle has to overcome after it starts contracting.
 S.V.R. constitutes the after load of the L.V.
MAP - CVP
 SVR = X 80 (n = 900 – 1500 dynes/s/cm5)
CO
 Starling’s curves: relates preload and contractility to stroke volume.
High compliance
Contractility
SV
Low compliance
Preload
Stages of shock:
1. Compensated shock (initial non progressive stage).
2. Decompensated shock (progressive stage)
3. Irreversible shock.
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Pathophysiology of shock:
Hemodynamic mechanism of shock occur at eight different levels.
Vascular factors:
 Resistance to flow of blood is directly proportional to vessel length and viscosity
and inversely proportional to the fourth power of the vessel radius.
 Arteriolar smooth muscle tone is the most important determinant of SVR., which
in turn is regulated by,
Extrinsic factors:
Neural regulation: sympathetic vasoconstrictor innervation.
Hormonal regulation – Endogenous adrenaline and nor adrenaline.
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Intrinsic (Local) factors:
a. Myogenic response
b. Metabolic autoregulation
c. Endothelial mediated regulation
Microcirculatory factors:
Microcirculation is that part of the cardiovascular and lymphatic systems in
intimate contact with active tissues to facilitate metabolic exchange and promote the
fully integrated activity of the whole organism.
Microvascular flow is influenced by the balance between COP and capillary
hydrostatic pressure, which in turn determines the balance between intravascular and
extra vascular fluid.
MICROCIRCULATORY RESPONSE IN SHOCK:
 The relationship between Pre and Post CAP sphincters is important

 Reversible stage: (compensatory mechanism)
BP – Sympathoadrenal stimulation

PRE CAPILLARY SPINCTER CONSTRUCTION

CAPPILARY HYDROSTATIC PRESSURE.

FLUID MOVES INTO INTRAVASCULAR SPACE
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 HR because of stimulation of baroreceptors.
 Renal conservation of fluid through renin-angiotensin mechanism
 Maintains adequate perfusion pres. To vital organs.
IRREVERSIBLE STAGE:
If hypoperfusion continues

Hypoxia – Anaerobic metabolism

 LACTIC ACID +  [H+]

 CAP. HYDR. PRES  Post cap. Sphincter tone
 +
Weakening of pre cap sphincter tone
Fluid loss into extra vascular space.
 Adhesion of activated leukocytes to endothelial cells - cap. Permeability +
obstruction to micro vessels
 Accumulation of micro thrombi because of activation of coagulation system
with fibrin deposition.
CLASSIFICATION OF SHOCK:
Hypovolemic shock:
Haemorrhage
 External – trauma, GIT bleeding
 Internal – hematoma, hemothorax / hemoperitoneum
Fluid depletion
 External – vomit & diahorrea, sweating, hyperosmolar states.
 Internal – third space loss
 Loss of plasma – burns and exflovative dermatitis.
Cardiogenic shock:
Myopathic:
– Acute myocardial infarction
– Dilated cardiomyopathy
– Myocardial depression
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Mechanical
– Mitral regurgitation
– Ventricular septal defect
– Ventricular aneurysm
– Left ventricular outflow track obstruction (A.S.)
Arrhythmic
– Tachyarrhythmia
– Brady arrhythmia
Extracardiac obstructive shock:

a. Pericardial tamponade
b. Massive pulmonary embolism.
c. Severe pulmonary hypertension
d. Aortic dissection
e. Tension pneumothorax
Distributive shock:
a. Septic shock
b. Toxic products (drug overdose)
c. Anaphylaxis
d. Neurogenic shock
e. Vasodilator drugs
Endocrine:
a. Myxedema coma.
b. Adrenal crisis
c. Thyroid crisis
Organ Dysfunction in shock:

Depends on
1. Severity of tissue perfusion deficit.
2. Underlying cause of shock.
3. Prior organ dysfunction.
 If circulatory failure persists and sufficient cellular dysfunction occurs. It leads to
multiple organ dysfunction syndrome (MODS) which may be fatal.
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Organ dysfunction and outcome:
Organ dysfunction Mortality rate
One organ 40%
Two organs 60-80%
Three organs (> 72 hrs) 100%
 Tachycardia – because of reflex neuro humoral response to decrease myocardial
performance.
 Low pulse volume: because of decrease S.V. exception early septic shock.
 Decrease CO - because of
1. In hypovolemia shock  decrease preload.
2. Cardiogenic shock  decrease myocardial control and / or dysryhtmias.
3. Septic shock  Multi organ failure and decrease myocardial responsiveness to
circulating catecholamines.
 Decrease coronary perfusion pressure  because of increased LVEDP and
decrease arterial pressure.
 LVF  decrease pulmonary cap hydrostatic pressure  pulmonary edema 
respiratory fail.
 Abnormal mentation, confusion / restlessness or frank coma.
 Because of,
1. Hypoperfusion: autoregulation of C.P.P. fails when M.A.P < 60 mm Hg.
2. Hypoxemia
3. Acid base abnormalities
4. Electrolyte disturbances
 Renal perfusion is compromised because blood flow is directed preferentially
towards vital organs.
 Decrease afferent arterial tone initially compensates for decrease RBF and
maintains glomerular filtration.
 Severe / late stages failure of compensatory mechanism  decrease renal
cortical blood flow  A.T.N. and renal failure.
 Work of breathing increase  increase resp. muscle O2 requirement  resp.
muscle fatigue  ventilatory failure.
 Endogenous mediators damage interalveolar cap. Endothelium endothelial
dehiscence’s, leakage, increase extra vascular lung fluid, abnormal platelet
deposits, W.B.C plugging and micro vascular thrombosis.
 Increase alveolar dead space, impaired dead space,
 V/Q inequality, micro shunting  hypoxia results in acute lung injury and later
A.R.D.S.
 Hepatic injury results from (1) Hypoperfusion (2) Cytokines released from
activated kuppfer cells.
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 Shock liver – parenchymal injury – increase SGOT, SGPT, increase LDH –
decrease synthetic capacity –decrease albumin and decrease clotting factor and
increase bilirubin.
 In septic shock  dysfunction of bile canaliculi  intrahepatic cholestasis.
 Decrease splanchnic B.F  intestinal ischemia which may be exacerbated by
release of free O2 radicals during reperfusion following resuscitation.
 Decrease Hb, decrease Hct, thrombocytopenia because of haemodilution
association with volume repletion.
 Activation of coagulation cascade and consumption of clotting factors in
microvasculature  D.I.C. + thrombocytopenia, microangiopathic hemolytic
anemia, decrease fibrinogen and increase F.D.P’s.
General management of shock:

Prime importance in any critically ill patient
In shock, work of breathing increase and excess of CO2 and O2 supply is diverted to work of
breathing.

 O2 supply to vital organs
Therefore intubate and ventilate such patients with high FiO2.

Enhances O2 delivery and optimizes (decrease) O2 consumption.
Arterial blood pressure:

 To prevent major organ dysfunction, treat severe hypotension aggressively.
 Fluid loading is the mainstay of treatment in hypovolemic shock, but
Vasopressors may be necessary to maintain vital organ perfusion.
History:
 A quick but accurate history which gives valuable clues to the etiology.
 Heart rate and rhythm: tachycardia is almost always present. Dysrrhythmias
may be present in cardiogenic shock.
 Quality of pulse: usually “Thready”, bounding in early septic shock.
 Arterial blood pressure: hypotension - ++.
 Pallor: because of (i) hemorrhage and / or
(ii) Marked vasoconstriction.
 Body temperature:
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– Increase in early septic shock.
– Core to skin temp gradient widened
– Good index of severity of shock
 Cyanosis: indicates hypoxemia and / or poor peripheral perfusion.
 Signs of ventricular failure: III heart sound S3 and jugular venous distension – in
cardiogenic.
 Signs of dehydration:
– Loss of skin turgor – sunken eye balls
– Dry mucous membranes – oliguria / anuria
 Pulmonary rales – because of
I. Interstitial / alveolar edema or
II. Pulmonary secretions.
Monitoring:
 Cardiac rate and rhythm – ECG.
 Arterial BP – invasive and non invasive
 Arterial O2 saturation – pulse oximetry.
 Left and right ventricular filling pressures and cardiac output.
 Urine output.
 Temperature
 ET CO2 concentration – Capnography
Investigations:
 ECG – MT and / or dysrrhythmias.
 Hb and Hct
 Blood grouping and cross matching.
 ABG for evaluation of ventilation, pulmonary O2 transfer and acid base status.
 Plasma levels of cardiac injury enzymes.
 CXR – serum lactate levels (N  1.5 m.mols/L)
 Blood glucose – blood urea and plasma creatinine
 Plasma and urinary osmolality.
 Serum Ca++, P, Mg+ levels and other electrolytes
 LFT
 Culture / sensitivity of blood/urine/other body fluids.
 Gastric tonometry
 SJVO2
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Hypovolemic shock:
There is absolute / relative deficiency of I.V. volume which results in decrease in
venous return  preload.
Etiology:
Hemorrhagic shock:
Traumatic
– Blunt / penetrating injury, hematoma
– Fracture of lung bones and pelvis hemothorax hemoperitoneum.
Non – traumatic
– G.I. bleed
– Aortic dissection
– Rupture of aneurysm
Non hemorrhagic shock

Traumatic
– Burns
– Crush injuries
Non-traumatic
– Vomiting
– Diarrhea
– D.K.A
– Hyperosmolar states
Third space loss
– Intestinal obstruction.
– Pancreatitis.
– Ascites.
Features:
1. Cold clammy, pale skin / extremities
2. Rapid thready pulse – reduced peripheral pulses.
3. Tachycardia and tachypnea
4. Hypotension
- Reduced filling pressure
-  CVF,  SO  BF
- Diminished heart sounds
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1. Oliguria
2. Confusion / Coma
3. CVP - 
4. PCWP - 
5. CO - 
6. Core – peripheral temp gradient - 
Hemorrhagic shock:
Classification with features:
Parameters Class – I Class – II Class – III Class – IV
Blood loss (%) < 15 20 – 25 30 – 35 > 40
Blood loss (ml) < 750 - 1250 - 1800 - 2500
Pulse rate (bpm) 72-84 > 100 > 120 > 140
Blood pres (mm Hg) 116/80 110/76  30% 70-90/50-60  40% < 60
Pulse pres. (mm Hg) 36 30 20-30 10-20
Resp. rate (bpm) 14-20 20-30 30-40 > 40
Urine output 30-35 25-30 5-15 <5
(ml/hr)
Mental status Anxious Anxious Confused Lethargic
Vicious cycle in hemorrhagic shock:
Heart failure
Haemorrhage

 blood volume  CO HR
Fluid loss  BP
Compensatory Major organ

Cap. Endothelial
mechanism failure
damage
Vasoconstriction
Cellular
Anoxia
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Pathogenesis of hemorrhagic shock:
 With loss of 10-20% B.V.  compensatory mech.
 Increase sympathomimetic adrenergic activity  vasoconstriction, increase
venous return and tachycardia.
 Decrease cap hydro press because of pre cap arteriolar vasoconstriction 
transudation of fluids in to in space.
 Decrease I.V. volume  activation of rennin angiotensin system + release of ADH
and increase ACTH and aldosterone  renal sodium and water retention.
 Maintain perfusion to vital organs and orthostatic hypotension may be the only
sign of early hypovolemia.
 With loss of > 20%  clinical shock syndrome.
 CO and hypotension in spite of generalized vasoconstriction
 Tissue perfusion  anaerobic metabolism  lactic acidosis.
 Reflex adrenergic response  redistribution of flow to perfuse brain and heart.
 Excessive vasoconstriction  cellular damage / hypoxia
 Cap endothelial damage  loss of fluids and proteins  hypovolemia.
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Non hemorrhagic shock pathogenesis:
Volume loss
Survival
  autonomic tone Fluid shifts from extra
 Catecholamine release cellular to I.V. space
Intervention /
Partial restoration of
stabilization   venous capacitance
intravascular volume
  HR
Maintenance of perfusion
Blood flow shunted to
Continued volume loss Vital organs (heart and brain)
Survival / delayed
Cellular hypoxia /
morbidity
anaerobic metabolism
Intervention /
 A.T.P. production /
stabilization
lactic acidosis
Cellular function impaired
Continued volume loss
 membrane porosity
Movement of fluid Lysozomal

from intravascular to leakage
interstitial space
Irreversible shock Cellular auto
digestion
Intervention Nonintervention
Death
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Management of hypovolemic shock:
AIM: To restore cardiac filling pressure promptly and adequately without
inducing pulmonary edema  oxygenation.
Measures:
1. Arresting ongoing blood loss.
2. Restoration of organization blood volume.
3. Correction of metabolic acidosis
Arresting ongoing blood loss:
 External haemorrage by pressure elevation and tourniquet.
 Internal haemorrhage by immediate surgical exploration.
Restoration of circulating blood volume:
 Start two large bore I.V. cannula,
 Debate still exists over the type, amount and rate of infusion of fluids.
 Fluid challenge test is the guideline for rate of infusion.
Initial CVP mm Hg PCWP Fluid to be infused

<5 < 12 200 ml in 10 mins
5-8 12-15 100 ml in 10 mins
>8 > 15 50 ml in 10 mins
Response from baseline Therapy

CVP mm Hg & PCWP
 by > 5  by > 7 Stop fluid administration
 by 2-5  by 3-7 Wait for 10 mins
Still > 2 Still > 3 Stop fluid administration
 by < 2  by < 3 Continue fluids
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Types of fluid available:
Crystalloids: They are balanced salt solutions.
 They lack macromolecules.
 Equilibrate rapidly between interstitial and I.V. fluid.
 Ratio – 1:3-4.
RL NS DNS-0.45 DNS-0.9
pH 6.5 5.0 4.5 4.2
Osmolality 280 308 430
Na++ 131 154 77 154
K+ 5 0 0
Cl – 112 154 77 154
HCO3 – 29 0 0
Glucose 5 gms/L 5 gms/L
Colloids:
 They are plasma volume expanders.
 They contain macromolecules – therefore increase COP
 Ratio – 1:1
 Ideal colloid should
– Normalize blood volume losses.
– Normalize micro circulatory flow.
– Restore hemodynamic balance
– Improve Delivery of O2 and organ functions.
– Have sufficient long intravascular residence time
– Be readily metabolized and excreted
– Be well tolerated and
– Not interfere with blood grouping and cross matching
Types:
Natural colloids:
– 5% human serum albumin
– 25% human serum albumin
Synthetic colloids:
– 3.5% polygelatin – haemacel
– Dextran – 40, 70 and 110
– Hydroxyl ethyl starch – 40 and 200
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Colloids Vs crystalloids:
Advantages Disadvantages
Colloid Smaller volume required Expensive
Sustained  in plasma volume Coagulopathy
Less peripheral edema Pulmonary edema in leak states
Lower intra cranial pressure  G.F.R.
Osmotic diuresis
Impaired cross match
Crystalloid Inexpensive Transient hemodynamic effects
Promotes urinary flow Peripheral edema ++
Restores third space losses Pulmonary edema CCF
No impaired cross match
No coagulopathy
No anaphylaxis
Blood and blood products:

 Ideal solution because it increases O2 carrying capacity.
 Ratio – 1:1
 Disadvantages – expensive and delays in grouping and cross match
 High incidence of allergic phenomena
 Risk of transfusion reactions.
End point of resuscitation should be based on factors reflecting adequacy of perfusion.
 Establishing urine output > 0.5 ml/kg/Hr.
 Reappearance of peripheral pulses.
 Correction of hypothermia, with reduction of core to peripheral temp gradient to
< 10C.
 Improvement of mental status.
 Return of B.P. to normal
 Capillary refill < 3 sec
 Correction of metabolic acidosis (blood lactate level  1.5 mmol/l) with
normalization of pH.
Cardiogenic shock:
Characterized by primary decrease in myocardial contractility which results in
decrease ventricular output accompanied by increase in preload and vascular
resistance.
Cardiogenic shock syndrome is defined as systolic BP < 80 mm Hg, CI < 2lt / min
/ m , LVEDP or PCWP > 18 mm Hg and MAP is 30 mm Hg below previous basal values.
2
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Etiology:
Acute myocardial infarction:
1. Severely reduced left ventricular function (> 40%).
2. Ventricular septal rupture
3. Acute mitral regurgitation
4. Right ventricular infarction
Other cardiac entities:

1. Dilated cardiomyopathy / severe myocarditis
2. End stage valvular heart disease, AS / AR, MS / MR.
3. Tachycardia or bradyarrhythmias
4. Following C.P.B.
Pharmacological causes:
1. Blocking drugs
2. Ca++ channel blockers
3. Chemotherapeutic agents (adriamycin)
4. Anti arrhythmic drugs (quinidine)
5. Inhalation anesthetics (halothane)
Clinical features:
Manifest as 2 sets,
Circulatory insufficiency (forward failure)
 Restlessness, mental obtundation
 Skin is moist, cool, cyanotic
 Weak and rapid peripheral pulses
 Hypotension
 Reduced urine output (< 20 ml / Hr).
Circulatory congestion (backward failure)
 Pulmonary edema
 Raised J.V.P
 Tender Hepato splenomegaly
 Pedal edema
Pathophysiology:
 Decrease myocardial contractility and function.
 Sympathetic stimulation  HR and contractility + renal fluid retention 
increase preload.
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 Increase HR and contraction  increase myocardial O2 demand and exacerbate
ischemia
 Tachycardia  decrease diastolic filling time  decrease myocardial perfusion.
 Fluid retention  increase I.V. volume  pulmonary congestion and hypoxemia.
 Ischemia  decrease ventilatory Compliance  increase left atrial pressure 
pulmonary congestion.
 Vasoconstriction to maintain BP and perfusion pressure to vital organs 
decrease renal, splanchnic and skin perfusion.
 Increase SVR  increase after load  impairs cardiac performance and increase
myocardial O2 demand + inadequate perfusion leads to worsening of ischemia
and vicious cycle.
Management of cardiogenic shock:

Three steps:
1. Initial stabilization
2. Evaluation of the patient
3. Definitive therapy
Initial stabilization:
1. Establishment of ventilation and oxygenation to maintain PaO2> 70 mm Hg.
2. Restore MAP > 70 mm Hg with volume correction and vasopressors.
3. Treatment of pain, arrhythmias and acid base abnormality.
Evaluation of the patient:
Brief history, physical examination and investigations.
 ECG-look for ischemic changes, cardiac enzymes Good compliance
 Cardiac filling pressure – CVP, PCWP, LVEDP
 Chest x-ray, ABG
SV
 2D echo  for ventricular function

 Arterial O2 saturation
Poor
 Starling function curve. compliance
Definitive therapy: Preload (LVEDV)

The goals of therapy are,
1. CI  4.5 l/min/ m2 (N – 3.0 – 3.4 l/min /m2).
2. DO2 600 ml/min/ m2 (N – 480 – 600 ml/min /m2)
3. VO2 – 140 – 180 ml/min /m2 (N – 130 – 160 ml/min/ m2)
Achieved by,
1. Pharmacological support and / or
2. Surgical intervention
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1) Pharmacological support:
Aimed at – increase C.O., improving coronary blood flow and decrease
transudation of fluid into the lung.
Done by – modifying preload, after load and by increase inotropic function of the
myocardium.
a) Reduction in preload (diuretics):
 Decrease volume where excusive preload exists.
 Overzealous use my result in organ hypoperfusion and renal failure.
 Loop diuretics– chlorthiazine, hydrochlorothiazide, chlorthalidone.
b) Improving myocardial contractility (inotropes):
 Inotropes are indicated where preload is optimal but low cardiac output and
hypotension exists.
 Sympathomimetic amines are potent inotropes which act via  and  adrenergic
receptors.
Epinephrine:
 Powerful cardiac stimulant
 Increase HR, shortens systole.
 Increase cardiac work and O2 consumption.
 1-2 g / min -  stimulation
 2-10 g/min – mixed  and  stimulation
 10 g / min -  stimulation.
Dopamine: (3-4 di-hydroxy phenyl ethylamine)
 1-5 g/kg/min – dopaminergic receptors – renal and mesenteric vasodilation.
 5-10 g/kg/min -  action, receptor positive inotropic and positive chronotropic
effects on heart.
 10 g/kg/min -  receptor– vasoconstriction.
Side effects:
Renal and mesenteric ischemia Tachyarrhythmias
 Gangrene – extremities 
Lactic acidosis Myocardial ischemia

Dobutamine: synthetic sympathomimetic amine
 Acts mainly on 1 receptor with little effects on 2 / 
 Useful in cardiogenic shock due to MI with tachycardia.
 Increase CO without increasing infarct size or causing malignant arrhythmias.
 Dose – 5-20 g/kg/min.
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Dopexamine:
 Positive inotropes with both direct and indirect effects
 Agonist for 2 and dopaminergic receptors with little 1 and no  adrenergic
effects.
 Decrease SVR, decrease PVR, decrease Lt and Right ventricular filling pressure, 
HR,  CO and  SV.
Reduction in after load (vasodilators):
 Vasodilators decrease after load by decrease SVR and decrease PVR which
improves cardiac output.
 Useful in patient with
– Normal / increase preload-PCWP > 15 mm Hg.
– Adequate perfusion pressure SBP > 110 mm Hg.
– High vascular resistance
– Low cardiac output
Types:
– - adrenergic blockers – phentolamine, prazocin.
– Ganglion blocking agents – Trimethaphan
– Direct vasodilators – Hydralazine, SNP, NTG, Isosorbide dinitrate.
– 2 adrenergic agonists – salbutamol.
– SNP and NTG are commonly used – because rapid onset of action and short ½ life
therefore dose can be titrated against response.
SNP:
– Both arteriolar and Venodilators
– Onset of action within 2 mins
– Rapidly metabolized to Thiocyanate and cyanide
– Dose 1-10 g/kg/min (20-500 g/min)
NTG:
 Venodilators, + coronary vasodilator  treatment myocardial ischemia
 Onset within sec
 ½ life – 4 mins
 Dose 1-10 g/kg/min (10-400 g/min)
INOLATORS:
 Inotropic + vasodilator
 Act by inhibition of Phosphodiesterase – type III
 Bipyridine derivative – amrinone, Milrinone
 Imidazoline derivative– enoximone, pyroximone
 Causes dose dependant increase in C.O.
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– But decrease SVR and PVR, decrease PCWP and Lt Ventricular filling
pressure.
– Increase C.I. by 30-100%
– HR and BP remain unchanged.
S/E of vasodilators
– Hypotension due to decrease in SVR therefore monitor B.P. closely.
– Coronary ischemia – due to decrease in DBP
– Intracranial hypertension – in patients with decrease intracranial compliance.
– Hypoxemia – by reversing H.P.V  pulmonary shunting.
II. Surgical intervention:
1) IABP 2) Angioplasty 3) CABG. 4) Cardiac transplant.
Intra aortic balloon counter pulsation:

Indication:
 Extensive myocardial ischemia / infarction
 Mechanical defects – papillary muscle or ventricular septal rupture.
 Balloon is inserted per cutaneosly and placed in thoracic aorta.
 Inflates during diastole and deflates prior to systole
– Diastolic inflation – creates a pressure gradient, where in aortic diastolic
pressure increase and LVEDP decrease  increase cardiac perfusion
pressure.
– Presystolic deflation  decrease resistance to ventricular ejection which
mimics ventricular after load reduction.
IABP
– Increase C.O. by – 15-20%.
– Increase myocardial O2 supply
– Myocardial O2 demand – improves Myocardial Ischemia.
Obstructive shock:
Here increase in extracardiac pressure impairs ventricular diastolic filling  decrease
preload  decrease SV  decrease C.O.  decrease perfusion pressure.
Etiology:
– Pericardial tamponade or constriction.
– Massive pleural effusion / hemothorax
– Massive pulmonary embolism
– Tension pneumothorax
– Coarctation of aorta
– Severe hypertrophic cardiomyopathy
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Pathogenesis:
 Pericardial tamponade: Results from accumulation of fluid in the pericardium
with increase in intra pericardial pressure  decrease gradient between
peripheral venous and atrial pressure  compromised diastole Filling  SV
 CO.
 Pulmonary embolism: When more than 50-60% of pulmonary vascular bed is
obstructed by thrombus, acute (R) ventilator failure can occur and (L) ventilator
filling impaired.
Clinical features and treatment:

Pericardial tamponade: Hypotension, jugular venous distension and pulsus
paradoxus.
Echocardiography.
Treatment: Pericardial drainage via needle pericardiocentesis or surgery.
 Pulmonary embolism: Restlessness, chest pain, hypotension.
Inv: Ventilation perfusion lung scanning and pulmonary angiography.
Treatment: systemic anticoagulation (thrombolytic therapy) or emergency
surgical pulmonary embolectomy.
Distributive shock:
Here decrease tissue perfusion will be present because of  S.V.R, even in the presence
of normal or  C.O., association with normovolaemic /hypovolemia.
Etiology:
Septic shock Anaphylaxis
Neurogenic shock Endocrinology shock
Toxic products (drug over dose)
SEPTIC SHOCK
Sepsis is the response of the host to bacteremia or endotoxemia and is
characterized by fever, tachycardia and tachypnea and respiratory alkalosis.
Systemic inflammatory response syndrome (S.I.R.S) defined as a systemic response
to an ongoing inflammatory process and is said to be present when at least 2 of the
following are present.
1. Temperature > 380 C or < 360 C
2. Heart rate > 100 beats / min.
3. PaCO2< 32 mm Hg or respiratory rate > 20/min
4. W.B.C count > 12,000 or < 4,000 cells / mm3
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Septic shock is defined as S.I.R.S induced hypotension with perfusion abnormalities.
Septic shock is a state in which initially there will be hyperdynamic state with
increase C.O., normal / decrease cardiac filling pres and decrease S.V.R. In the later
stages there will be hypovolemia, myocardial depression and abnormal distribution of
blood flow in the microcirculation leading to hypoperfusion and its consequences.
 S.S. is the common cause of death in I.C.U (50%).
 S.S. develops in approximate 40% of cases of sepsis.
 Mortality ranges from 50-90%.
Septic shock: Sepsis associated with hypotension (SBP < 90 mm Hg) signs of
hypoperfusion despite adequate fluid resuscitation.
 Characterized by inadequate tissue perfusion and wide spread cellular
dysfunction.
 Cellular dysfunction may be a metabolic block at cellular level that contributes
septic shock.
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Pathogenesis:
Nidus of infection
(Abscess, pneumonia, peritonitis, cellulites)
Organism
Exotoxin Structural component

- TSST-1 - Teichoic acid
- Toxin-A antigen - Endotoxins
Act on - Plasma, platelets

Monocytes/macrophage,
lymphocytes
Endothelial cell
Release Neutrophil
Endogenous mediators
Cytokines  Arachidonic acid metabolites
 INF  Cyclooxygenase
 IL1,2,6,8  Lipoxygenase
 PAF  Prostaglandins
 Endorphins  Leukotrienes
 EDRF  Coagulation
 MDF  Complement – C5a
 KININS
Act on -
Myocardium
Vasculature Organs
 Vasodilation  Dysfunction
 Vasoconstriction  metabolic effect
 Leukocyte aggregation
 Endothelial cell dysfunction
SHOCK
Refractory
Multiple organ Recovery
hypotension
system failure
Death
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Hemodynamic subsets: depend on:
a. Pre existing cardiac function
b. Intravascular volume
c. Where patient is on spectrum of response
Hyperdynamic septic shock Hypodynamic septic shock
- N /  C.O -  C.O
-  SVR -  /N SVR
- Myocardial depression - Marked myocardial depression
- MVSO2 - MVSO2 severely hypovolemic
Features of septic shock:

Site of infection:
 Pneumonitis, empyema, UTI, cellulites, peritonitis, abscess, sinusitis, meningitis.
Systemic inflammatory response:
 Fever / hypothermia, chills
 Tachycardia
 Tachypnoea
 Leukocytosis / leukopenia (ominous sign) (with left ward shift)
Shock induced organ dysfunction:

 CVS – hypotension, myocardial depression
 RS – ARDS (Hypoxemia).
 Renal – ARF, oliguria
 Hepatic – hyper blirubinemia
 Coagulation – thrombocytopenia, DIC
 CNS – confusion, stupor
 Others -  lactate production.
Management of septic shock:

Identification and elimination of septic NIDUS:
 Antimicrobials depending on C/S report of blood, urine, tracheal aspirate or
other body fluids.
 Till C/S report comes, broad spectrum antibiotics, aminoglycoside (gentamycin,
tobramycin, amikacin) + semisynthetic penicillin (piperacillin) + semisynthetic
penicillin (piperacillin) or second generation cephalosporin (cephazolin)  anti
anaerobic drug (metronidazole).
 Surgical drainage of abscess / exploration of peritonitis.
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Optimization of organ system perfusion:
By optimizing BP, DO2 and VO2.

 B.P: perfusion pres is maintained by appropriate use of fluid volume,
Vasopressors or vasodilators packed RBC’s (Hb > 109 %).
 DO2:
I. Maintaining MAP  60 mm Hg
Because DO2 is the product of
II. PaO2 of at least 60 mm Hg
Hb concentration SaO2 and CO
III. SaO2 of at least 90%
 VO2
 Prevention of seizures
 Maintaining normothermia
 Mechanism ventilation with high FiO2
Interruption of pathogenic sequence leading to SEPTIC SHOCK:

 Large dose glucocorticoid – no more used.
 Inhibition of toxic mediators like endotoxins, TNF, IL by anti-endotoxins
antibody, anti-TNF-Ab, IL-1 receptor antagonists, naloxone, PG inhibitors and
lipid -X.
Supportive treatment of complications:

Such as ARDS, ARF, GI bleeding, DIC , acidosis.
Agent BP CO O2 delivery
Dopamine   
Dobutamine  or O  
Epinephrine (2-8 g/min)   
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Chapter 20 - CARDIOMYOPATHIES
 Comprise a diverse group of disorder characterized by myocardial dysfunction
unrelated to the usual causes of heart such as CAD, cardiac valve dysfunction and
essential HTN.
 Are clarified on morphologic and homodynamic bases as
1) Dilated 3) Hypertrophic
2) Restrictive 4) Obliterative.
Etiology:-
Idiopathic
Ischemic
Infectious - viral (HIV), Bacterial
 Toxic – Alcohol, Danuorubicin, Doxorubicin, Cocaine
 Systemic – Muscular dystrophy, phaeochromocytoma
 Myotonic dystrophy, Acromegaly
 Collagen vascular disorder thyrotoxicosis
 Sarcoidosis, Myxedema
Infiltrative – Amyloidosis
Haemochromotosis
Primary or metastatic tumors.
Nutritional
Familial (genetic)
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Classification of cardiomyopathies on morphologic and hemodynamic basis
Parameter Dilated Restrictive Hypertrophic Obliterative
Morphology Biventricular Decreased Hypertrophy of Thickened
dilation ventricular left ventricle endocardium
compliance and usually or mural
interventricualr thrombi
septum
Ventricular Marked Normal to Normal to Moderate
volume increase moderate moderate decease
increase decrease
Ejection Marked Normal to Marked Normal to
fraction decrease Moderate increase moderate
decrease decrease
Ventricular Normal to Marked Marked Marked
compliance moderate decrease decrease decrease
decrease
Ventricular Marked Marked Normal to Moderate
filling increase increase moderate increase
pressure increase
Stroke volume Marked Normal to Normal to Normal to
decrease moderate moderate moderate
decrease increase decrease
Idiopathic Dilated cardiomyopathy:-

Primary myocardial disease of unknown cause
– Characterized by left ventricular or biventricular dilation, impaired myocardial
contractility, decreased cardiac output and increased ventricular filling
pressures.
– May be associated with essential HTN, use of β- adrenergic agonists, and
moderate alcohol consumption.
– Familial and genetic factors are imp, as 20% of patients with cardiomyopathies
have 1st degree relative with a decreased EF and Cardiomegaly.
– African – Americans increased risk of developing idiopathic dilated
cardiomyopathy.
– May occur in peripartum patients, most often manifesting 1-6 weeks after
delivery
– Clinical course is unpredictable, most deaths occur within 3 year of diagnosis
owing to progressive congestive heart failure.
– Ventricular dysrrhythmias and sudden deaths are common
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Clinical presentation:-
– Patients seen b/w 20-50 years of age, may also involve children & elders. Initial
manifestation is congestive heart failure (CHF).Chest pain on exertion
indistinguishable from angina pectoris.
– Hemodynamic abnormalities that predict poor prognosis are EF <0.25%, left
ventricular end-diastolic dilatation and a hypokinetic left ventricle on Echo.
– PCWP >20mmHg, cardiac index <2.5 lt/min/m2 systemic hypotension and
increased CVP.
– Ventricular dilatation  leads to functional MR/TR.
– ECG  LVH, ST and T waves abnormality and BBB.
– Cardiac dysrrhythmias  ventricular premature beats and AF
– Chest X-nay  cardiac enlargement of all 4 chambers
– Systemic embolization is common seen in dilated and hypokinetic cardiac
chamber.
Treatment:-
– General supportive measures  adequate rest, weight control, abstinence from
tobacco use, moderate alcohol consumption and decreased physical activity
during periods of cardiac decompensation.
– Vasodilator therapy –initial treatment in symptomatic patients.ACE inhibitors
and smooth muscle relaxing drug such as Hydralazine and Isosorbide dinitrate.
– More prone for systemic or pulmonary embolization because of blood stasis in
hypo-contractility ventricle leads to coagulation process for this reason
anticoagulation with warfarin. Long term anticoagulant is often adjusted to
prolong the PT to an INR of 2-3
– More prone for asymptomatic cardiac dysrrhythmias (VT). Drug therapy does
not improve, so automatic cardioversion – defibrillator can be decrease risk of
sudden deaths in patients with CHF.
– Digitalis  controls symptoms of CHF and normal sinus rhythm
– Idiopathic dilated cardiomyopathy - is a principle indication for heart
transplantation in adults and children
Management of Anesthesia:
Goals:
 Avoidance of drug induced myocardial depression
 Maintenance of normovolaemic.
 Prevention of increased ventricular after load
 Regional anesthesia is an alternative to GA in selected patients.
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 Excessive cardiovascular depression in response to induction of anesthesia in
patients with a H/o alcohol abuse may reflect unimpeded idiopathic dilated
cardiomyopathy
 Surgical stimulation that produces undesirable increase in heart rate or SVR may
be treated with - antagonists, such as esmolol, keeping in mind the potential for
these drugs to cause cardiac depression
 Intraoperative hypotension is logically treated with Vasopressors such as
ephedrine, which provides some degree of  stimulation.
 Intravenous infusion of crystalloid solution or blood should be guided by cardiac
filling pressure to decrease the likelihood of volume overload. A pulmonary
artery catheter facilities early recognition of the need for inotropic support or
administration of peripheral vasodilator drugs.
Restrictive cardiomyopathy:
 Is the least common of cardiomyopathies
 Cardiac amyloidosis, Sarcoidosis and idiopathic variety are most common
etiologies.
 Increased stiffness of myocardium causes pressure within ventricle or ventricles
to increase suddenly and with only small increase the volume.
Clinical presentation:
 May resemble that of constrictive pericarditis decreased ventricular compliance.
 Normal to modest increase in EF and ventricular volume.
 Marked decrease of ventricular compliance
 Marked increase of ventricular filling pressure
 Stroke volume – normal to moderate decrease
 In advanced cases all signs of CHF are present except Cardiomegaly.
 Thromboembolic complications and cardiac conduction disturbances are
common.
– Treatment: - Diuretics – decrease venous congestion in pulmonary and systemic
circulation.
– Excessive effects  co  hypoperfusion and hypotension.
– Amiodarone Rx in AF, cardioversion
– External cardiac pacemaker
– Implantable defibrillator in malignant ventricular dysrrhythmias
– Anticoagulation-warfarin - view of risk of embolus seen in AF and low CO.
– Cardiac transplantation – not usually considered because of recurrence of
disease (Sarcoidosis) in transplanted heart
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Management of Anesthesia: (same as cardiac tamponade)
 Maintain intravascular fluid volume
 Avoid abrupt bradycardia
 Maintain normal sinus rhythm
Hypertrophic Cardiomyopathy:-
Hypertrophic cardiomyopathy is a common (1 in 500 individual) genetic malformation
of the heart.
Clinical features:-
 Clinical course varies widely, with most individuals remaining asymptomatic
throughout life, some have symptoms of CHF and others die suddenly
presumably from ventricular tachyarrhythmia, often in the absence of previous
symptoms.
 Angina pectoris – relieved by assumption of the recumbent position that
decreases LV outflow obstruction.
 Syncope may represent aborted sudden death
 Tachydysrhythmia
 CHF
 Massive cardiac hypertrophy – echocardiography may reveal a slit like left
ventricular chamber.
 EF >0.8
 Cardiac murmur reflecting left ventricular outflow obstruction – confused with
aortic or mitral valve disease.
 Sudden death
Marked LVH make these patients particularly vulnerable to myocardial
ischemia, especially when endocardial blood flow is decreased owing to excessive
pressure in the left ventricle.
– Sudden death is a recognized complication of hypertrophic cardiomyopathy (the
risk parallels the magnitude of the hypertrophy)
Treatment:-
Rx of these patients with hypertrophic cardiomyopathy is undertaken
recognizing that these individuals are at risk for sudden death and these must be
treated aggressively.
Medical therapy 
– - Adrenergic blocking drugs and Verapamil have been used extensively in the
treatment of hypertrophic cardiomyopathy.
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– In patients also are at high risk for sudden death from ventricular dysrrhythmias
– therapeutic options are Amiodarone and implantable cardioversion –
defibrillator.
– Management of AF patients who develop AF is at increased risk of
thromboembolism, CHF and sudden deaths.
– Amiodarone is considered most effective antiarrhythmics drug to prevent
recurrence of AF.
Surgical therapy
Surgical reduction of the outflow gradient is usually achieved by removing a
small amount of cardiac muscle from ventricular septum.
Intraoperative echocardiography is useful for determining the extent of surgical
resection and defining mitral valve structure. A marked decrease in the intraventricular
systolic and end-diastolic pressures is the most tangible consequence of surgery.
1. Non-surgical techniques to relieve LV outflow obstruction  dual chamber
pacing  outflow gradient and symptomatic improvement that are
unresponsive to medical therapy.
Management of anesthesia:-
Aim toward minimizing LV outflow obstruction
Events that increase outflow obstruction

Increased, myocardial contractility
 -adrenergic stimulation
 Digitalis
 Tachycardia
Decreased preload
 Hypovolemia
 Tachycardia
 Vasodilators (nitroprusside, nitroglycerine)
 Positive – pressure ventilation
Decreased after load
 Hypotension
 Vasodilation
 hypovolemia
Events that decrease outflow obstruction
Decreased myocardial contractility

 -Adrenergic blockade (esmolol)
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 Volatile anesthetics (halothane)
 Calcium channel blockers
Increased preload
 Hypervolemia
 Bradycardia
Increased after load
 - Adrenergic stimulation (phenylephrine )
 Hypervolemia.
Anesthesia and surgery in patients with previously unrecognized
hypertrophic cardiomyopathy may manifest intraoperatively as hypotension and
sudden increased in intensity of a systolic murmur, typically association with acute
hemorrhage or drug induced vasodilation.
Pre operative medication 
 Ideally decrease anxiety and the activation of sympathetic nervous system.
 Atropine is questionable – as tachycardia could increase left ventricular outflow
obstruction.
 Expansion of the intravascular fluid volume during the preoperative period is
useful for maintaining the intraoperative stroke volume and minimizing the
adverse effects of PPV of patient’s lung.
Induction of Anesthesia:
 With IV agents (except ketamine) is acceptable, precaution – important of
sudden drug induced decrease in SVR.
 Duration of laryngoscopy - should be brief to minimize activation of the
sympathetic system (consider administration of volatile anesthetic or  -
adrenergic blocker before direct laryngoscopy)
Maintenance of anesthesia:-
 Is deepened to produce mild depression of myocardial contractility
(volatile anesthesia plus N2O) and at the same time preserve intravascular fluid
volume.
 IABP and cardinal filling pressure –monitoring
 TEE and Doppler color flow imaging provides useful information
intraoperative left ventricular and mitral valve function as well as
intravascular fluid volume.
Hypotension due to decreased preload or after load Rx with
phenylephrine and replacement of blood loss.
Hypertension Rx increased concentrative of volatile anesthetics.
Parturient with hypertrophic cardiomyopathy seem to tolerate pregnancy
and delivery despite pregnancy induced decease in SVR and the risk of impaired venous
return caused by uterine compression of IVC.
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Parturient with hypertrophic cardiomyopathy may present major
challenges as events such as catecholamine release and bearing down (Valsalva
maneuvers) may increase lt ventricular outflow obstruction.
 Epidural anesthesia – is useful in these parturient with emphasis on CVP
monitoring and maintaining euvolemic or slight hypervolemia. In case
hypotension because of regional technique phenylephrine may be preferred to
increase the after load.
 Pulmonary edema had been observed in parturient with hypertrophic
cardiomyopathy following delivery.
 Rx bolus fluid to increase venous return.
 Esmolol to slow the heart rate, decreased myocardial contractility
and allow prolonged diastolic filling time to decrease the LV
outflow obstruction.
Obliterative Cardiomyopathy:-
 Considered as variant of restrictive cardiomyopathy
 Thickened endocardium or mural thrombi.
 Normal of modest decrease in EF and ventricular volume.
 Marked decrease in ventricular compliance
 Modest increase in ventricular filling pleasure
 Normal to modest decreased in stroke volume.
Peripartum Cardiomyopathy:-
 Onset of LV dysfunction during the last month of pregnancy or with in 5 months
following delivery
 Absence of an identifiable cause
 Absence of known heart disease prior to the last month of pregnancy
 Left ventricular dysfunction demonstrated by echocardiography diagnosis 
onset of unexplained LV dysfunction during limited period surrounding
parturition.
It may be difficult to differentiate b/w symptoms of CHF and dyspnea, fatigue
and peripheral edema also with pregnancy.
Rx  is designed to alleviate symptoms of CHF (diuretics, vasodilators, digoxin)
 ACE inhibitors are teratogenic during pregnancy but useful for Rx following
delivery.
 Prognosis depend on normalization of LV size and function within 6 months after
delivery.
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Management of anesthesia 
 Assessment of cardiac status and careful planning for providing analgesia and
anesthesia for delivery.
 Continuous IV infusions of Remifentanyl and or propofol may be considered.
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Chapter 21 - CARDIO PULMONARY BY PASS (CPB)
As the term implies, CPB involves the temporary substitution of the functions of the
heart and lungs with mechanical devices, placed outside the human body.
History:
Dr. John gibbon: Performed first successful intracardiac operation with the aid of heart
lung machine in 1953 (Philadelphia).
C. Walton Lillihei: Introduced a cross circulation technique for oxygenation of venous
blood during intracardiac operations in March 1954 (Minneapolis)
Dr. John Kirklin: Began the first successful series of intracardiac repairs using the heart
lung machine.
Goals of CPB
A. To provide a stilled bloodless heart with blood flow temporarily diverted to an
extra corporeal circuit that functionally replaces the heart and lungs.
B. Respiration
 Ventilation
 Oxygenation
C. Circulation.
D. Temperature regulation
Types
Total CPB:
Tapes are snugly drawn around both the superior and inferior venaecava to
prevent any flow of systematic venous blood around the cannula into the right atrium.
It is used when the cardiac chambers are to be opened or when the systemic venous
blood return to the heart proves troublesome.
Partial CPB:
 It allows blood to enter the heart and this is satisfactory for most aortocoronary
bypass grafting operations or other procedures in which the heart is not opened.
It is advantageous for the following purposes.
 To check the CPB system before establishing total CPB
 To fill the heart to its usual size and facilitate more precise estimation of
coronary graft length
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 Near the end of CPB to allow some pulsatile flow to improve tissue perfusion,
facilitate rewarming of peripheral tissues and for washout of cardioplegia
components from the heart.
 To assess the heart’s function at the end of CPB by increasing its filling and work
gradually to prevent excessive ventricular distention and failure
 To allow coronary sinus blood to drain into the venacavae and reduce flow into
the pulmonary vasculature and left heart.
ROLE OF ANESTHESIOLOGIST
Even though perfusionist is responsible for the safe conduct of CPB, the anesthesiologist
is particularly responsible for,
 Acid base management
 Anticoagulation maintenance
 Delivery of cardioplegia
 Maintenance of arterial pressure (use of vasodilators, vasoconstrictors)
 Use of inhalational agents
 Cerebral protection, especially when deep hypothermia and circulatory arrest
are employed.
INDICATIONS:
Surgical correction of congenital, ischemic and/or valvular heart diseases.
E.g. Coronary artery bypass
Valve replacement
Correction of septal defects
Advances of CPB technology have been utilized in the development of other complex
medical devices like
 Artificial hearts
 ECM0
 Ventricular assist devices
Basic circuit for CPB:
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The path of blood flow is as follows:
Desaturated venous blood drains by gravity into a venous reservoir, which is
either a separate component or an integral part of an oxygenator,
The oxygenated blood then passes through a heat exchanger, several filtering
devices and finally is actively pumped back into the systemic circulation.
The order of the above components may vary. Additional components may include,
 Alarm systems: to warn of low blood levels-in the oxygenator/ reservoir
 In-line pressure monitors
 Blood gas analyzers
 Vaporizers: to allow the introduction of volatile anesthetic agents during bypass.
Positioned in inflow circuit
 Separate circuit for infusion of crystalloid/ blood cardioplegic
BRIEF NOTE ON EACH COMPONENT:
1) Venous cannula
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These drain blood from the patient into the CPB circuit. One or two cannula are used,
depending on the type of cardiac surgical procedure or surgeons preference. These
drain the blood by gravity.
2. Arterial cannula
- These cannula return the blood from the CPB circuit to the patient.
- Commonly ascending aorta, just proximal to the innominate artery is the site for
arterial cannulation.
- Axillary femoral artery can be used in cases of
 Dissecting aortic aneurisms
 Patients who require reoperation
 In emergencies
3. Blood reservoir:
This stores the blood
It can be of two types
Venous reservoir: collects the blood drained from the patient
Arterial reservoir: collects the oxygenated blood coming from the oxygenator
The reservoir provides a 5-10second reserve of blood in case
venous return is temporarily interrupted.
4. OXYGENATORS:
It is an apparatus where O2 and Co2 exchange
Takes place
There are two types
Bubble oxygenator
Membrane oxygenator
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a) Bubble oxygenator:
This type of oxygenator is used when CPB is needed for less than 2 hours.
 In this, O2 is directly infused into a column

of systemic venous blood through a diffusion
plate. The diffusion plate produces
thousands of small O2 bubbles within
the blood. Gas exchange occurs across
a thin film at the blood gas interface around
each bubble.
 Co2 diffuses into the bubble and O2 diffuses
into the plasma.
 Diffusion of Co2 is 25 times more rapid than O2
 Smaller the bubble, more efficient is the
exchange because of the larger surface area.
 Co2 transfer is proportional to total gas flow
 O2 transfer is dependent on bubble size
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The bubble oxygenator consists of,
Oxygenating chamber: Where oxygenation takes place
Deforming chamber: Here the oxygenated blood is passed through a polypropylene
mesh treated with a surface tension reducing agent or charged silicon polymer
(antiform A) so that debubbling takes place.
Advantages:
- Easy to assemble and operate
- Lower cost
- Need relatively small amount of priming solution
Disadvantages:
- Blood cell trauma due to the gas interface and excessive Co2 removal. This can
lead to capillary plugging and organ damage from RBC debris
- Micro embolization of air and particular material
- Blood has to be deformed
- Platelet destruction/ impaired platelet activity
- Decrease in WBC count
- Activation of complement system
- Denaturation of blood proteins.
b) Membrane oxygenator:
This type of oxygenator is used when CPB is needed for more
than 2-3 hours.
In this type of oxygenator, gas doesn’t come in direct contact
with the blood.
A membrane, made up of silicon rubber or polypropylene or Teflon, separates blood and
gas compartments. Blood is made to flow in small streams (hollow fibers) or thin sheets
over the membrane.
CO2 diffuses outwards and O2 diffuses into the blood. O2 diffusion depends upon
concentration gradient and Co2 diffusion depends upon PvCo2.
Therefore O2 tension is controlled by the FIO2 of the inspired gas and Co2 is regulated by
total gas flow.
Types of membranes:
 Solid: made up of the silicon rubber sheets.
 Microporus: made up of Teflon / polyacrylamide contains multiple small pores
(0.1-5m).
Advantages:
 Less blood trauma
 Better platelet preservation
 Allows independent control of PaCO2 and PaO2
 Decreased protein denaturation
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Disadvantages:
 More expensive
 Can’t tolerate perfusion pressures > 125mmHg and gas exchange capacity
deteriorates after 5 hours of continuous use. (Especially seen with microporus
membrane).
5) HEAT EXCHANGER
These are necessary to cool and rewarm blood during CPB.

It adjusts the temperature of the perfusate to provide moderate systemic hypothermia
during the period of cardiac repair and gradually rewarms the blood during the
discontinuation of CPB.
Water circulates within the heat exchanger in a counter current fashion to the flow of
blood at temperatures between 1-2°C and 42°C. The temperature gradient between the
water and blood is kept at 10°C or less and the water temperature is not allowed to
exceed 42°C during the rewarming phase to avoid injury to blood proteins.
As the gas solubility gets reduced during rewarming, there is a tendency to form bubble
in the heat exchanger. Hence an arterial line filter should ideally be placed distal to the
heat exchanger.
There are the devices, which are used to generate the pressure required to return the
perfusate to the patient. These are driven by electrical motors. In the event of
mechanical/electrical failure, these motors can be hand cranked. There are two types,
a) Roller pump
b) Centrifugal pump
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a) Roller pumps:
 Consists of two rollers 180 apart, which rotate through a metal raceway that has
an arc of approximately 200°.
 A polyvinyl silicon rubber or polyurethane tubing is placed between the rollers
and raceway so that the rollers barely occlude the tubing at 180mm Hg back
pressure.
 As one roller begins to compress the tubing, the opposite roller releases, so that
the blood within the tubing is continuously propelled in one direction.
 Generated flow = Revolutions of pump head per minute (rpm) x boot capacity (rt)x2
 Pump output is directly proportional to

- The speed of rotation of the rollers
- The diameter of compressible tubing
Advantages:
 Reliable and safe
 Comparatively inexpensive
 Easy to operate
Mainly used for,
 Cardiotomy and vent suction
 Delivering cardioplegia
 To produce pulsatile flows along with special attachments
b) Centrifugal pump:
 These are conical, hardened plastic housings containing rapidly rotating cones,
which generate a centrifugal force to propel the blood.
 The flow rate is determined by both inflow and outflow pressures and pump
head speed
 Forward flow is measured by an inline electromagnetic flow meter. (Direct
calculation is not possible)
Advantages:
 Safe and reliable
 Disposable
 Simple to operate
 Doesn't produce
- High back pressure where tubing is temporarily obstructed/ kinked
- Separation of emboli from compression of the tubing
 Can't pump large amount of air emboli
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7) Filters:
 These are designed to trap particulate matter and gaseous emboli. The effective
pore size: 40m they should not significantly add to the flow resistance.
Sites:
- In the suction line: Prevents the debris from the operating site from reaching the
oxygenator
- Arterial filter: This removes the emboli from the blood in the arterial tubing prior
to entering the body.
- Venous filler: Remove the particulate matter from the cardiotomy suction
devices.
8) Circuits:
The CPB circuit drains venous blood by gravity into the oxygenator and returns
the oxygenated blood under pressure to the systemic circulation.
The tubings used in the circuit should have the following characteristics.
a. Non-thrombogenic and chemically inert
b. Smooth internal finish with non-wettable luminal surface and low surface
tension
c. Durable enough to withstand the use of roller pump and high pressures on the
arterial side.
9) The Connectors:
These should be designed to ensure smooth laminar flow while providing secure
connection.
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10) Accessory devices:
a) Cardiotomy suction:
Aspirates the blood from the surgical field and returns it to the main pump reservoir
and hence avoids blood losses. Excessive suction pressure contributes to red cell
trauma.
A cell saver Auction device which returns to a separate reservoir can also be used
instead of cardiotomy suction. But this depletes the CPB circuit volume.
b) Left ventricular vent:

Blood keeps on accumulating in the L.V, because of direct opening of thebasian veins
and bronchial arteries into the L.V. This may compromise myocardial preservation by
removing cardioplegia solution and warming the myocardium.
This blood is removed by a catheter inserted into the L.V via the right superior
pulmonary vein and left atrium.
c) Cardioplegia pump:
It provides optimal control over the cardioplegia infusion pressure and temperature.
d) Ultra-filter:
Used to increase patient's hematocrit without blood transfusion.
Review of a typical CPB setup:
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Pulsatile flow:
The flow produced by the pumps is non pulsatile. By using a different type of pump or
insertion of additional components into a circuit, allows the production of a pulsatile
waveform.
Advantages:
 Improved perfusion at the capillary level
 Lower SVR during bypass.
 Improved O2 extraction
 Lower production of pyruvate and lactate
 Decrease in the need for pharmacologic or mechanical support after bypass.
It is proved that pulsatile flow is beneficial over the non-pulsatile flow, in patients
with impaired ventricular function.
Dextran not used because of the interference with the clotting mechanisms. Blood if
at all used, preferably CPD blood < 7days old has to be used.
Ideal priming solution = RL / D5 + K+ and Ca+ < 30-40ml/ng
Electrolyte abnormalities:
Changes from 30mm after 20hrs after
During bypass
control bypass bypass
Total Ca+ Lower No change No change
Ionized Ca + Highest Higher Higher
Mg + Lower Lower Lower
Phosphate No change N/C N/C
Total proteins Lower Lower Lower
 Ca+, Na+, RBS and catecholamines

 Mg+, K+, proteins and clotting factors
Priming:
The composition of the fluid used for priming, varies according to the preference of
institutions. But its composition should be close to that of ECF. The volume depends
upon the capacity of the CPB circuit. The prime for most adult perfusions contains a
balanced salt solution.
Individual recipes add
 Albumin or hetastarch (to increase oncotic pressure)
 Mannitol (to promote diuresis)
 Heparin
 Bicarbonate
 Calcium
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In neonates, children and adults with significant preoperative anemia, in whom
profound haemodilution might decrease O2 carrying capacity; blood is used as priming
solution.
1500-2000ml of prime is added to the patient’s blood volume because of priming.
This will lead to acute normovolaemic haemodilution. Hct of 20-30% is the acceptable
limit. Dilution more than this, can be lethal. Blood is added if the Hct is < 25% after
dilution.
PATHOPHYSIOLOGY OF CPB
CPB attempts to simulate the functions of the patients heart and lungs. But it is a
complete departure from the normal circulation. The physiological effects of this are
summarized as follows,
A. The circulation:
(a) Cardiac output:

As systemic blood flow is controlled by the revolution of the pump, output
remains constant at the predetermined level and will not alter with the metabolic
demand of the body.
Optimal flow rates 2.2-2.5 lt/min/m2 in anesthetized, normothermic patients.
The flow may be reduced by 7% for each degree Celsius decrease in body temperature
as the BMR falls by 8% per degree Celsius decrease in body temperature (BMR will
be 50% of normal at 28°c).
b) Arterial pressure wave:
The normal pulsatile flow replaced by non pulsatile flow. ABP controlled by flow rate
and by infusion of peripheral vasodilators/ vasoconstrictors.
c) Systemic vascular resistance:

 Falls abruptly on instituting CPB. The reasons include,
 Reduced viscosity of the blood
 Dilution of circulating catecholamines
 Baroreceptor triggered reflex vasodilation
After the initial fall, SVR gradually rises to above normal levels. Changes in BP are
mainly determined by SVR changes.
Increase in SVR is due to,

Actual decrease in vascular cross sectional area due to closure of portions of
microvasculature
Constriction of vascular tree due to hypothermia and increasing levels of
catecholamines.
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Acceptable perfusion pressure during CPB=50-100mmHg. Variations beyond this
range may be corrected with vasoactive drugs.
d) Venous tone:
Gradually increases during CPB and remains elevated for a few hours afterwards.
CVP and pulmonary venous pressures should be at zero during CPB. Pulmonary venous
pressures more than 10mmHg may lead to increase in extra-vascular lung water.
B. Respiration:
Oxygenators mite over the function of the lungs. Rates/of gas transfer depend on the
type of oxygenator. Acceptable ABG values include PaO2 should be >85mmHg. pH = 7.4
PCO2 = 35-45mmHg. To maintain these levels high inspired oxygen concentration and
longer transit time are used.
C. Haemodilution:
"Why whole blood is not used for priming?
 Because of the problems like,
 Post perfusion bleeding diathesis
 Allergic and incompatibility reactions
 Demand on blood banks
 Hence exsanguinous fluids are used which will cause haemodilution
Physiological effects of haemodilution include,

 Fall in the blood viscosity (Decrease Hct)
 Decrease SVR
 It should be remembered that hypothermia increases the viscosity, balancing the
effect of haemodilution.
 O2 carrying capacity of the blood is reduced. But tissue hypoxia is usually not a
problem unless the Hct Tails below 20%.
 Fall in the osmolality of the blood, leading to fluid shifts outside the vascular
compartment.
 Dilution of other blood constituents e.g., coagulation factors
Hypothermia to :< 300 = 10 min
Mild = 35-280C <200 = 1hour
Moderate = 21-270C
Deep = < 200C
 Arrhythmias at 300C
 Ventricular fibrillation at 280C
 Apnea at 230C
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RS: MV
Bronchial dilatation leads to  dead space
Respiratory acidosis
With controlled ventilation, alkalosis may occur ( CO2 production  solubility)
Hence MV has to be decreased according to ABG values
Metabolism: Acidosis ( O2 availability)
 Viscosity  tissue perfusion is greater than  in BMR
Lactic acidosis on rewarming
 insulin activity and decreased enzymes of glucose metabolism  RBS
CVS: myocardial O2 uptake,  BP, ventricular dysrrhythmias (extra-systole /AV
dissociation)
ECG = prolonged PR, QRS and QT.
< 250C  ST, T wave changes
Causes: temp / pH gradients in the myocardium and disproportion in conduction
velocities.
Liver: metabolism,  blood flow,  coagulation time.
Kidney: blood flow, O2 consumption and GFR  UOP, UOP ceases at  200C.
CNS: metabolism
Premedication with chlorpromazine IV cause vasodilatation and facilitates heat
loss. Anticholinergics prevent cold induced bradycardia.
Cooling techniques:
Surface cooling  immersion (40C water) (for correction of cardiac abnormalities
within 8min) Evaporation
Cooling blanket
Core cooling  extracorporeal circuit
D) Metabolic rate:
Falls because of hypothermia. For every 10° decrease in body temperature. MR of O2
consumption is roughly halved.
E. Body composition:
Increase in,
 ECF volume,
 Plasma volume
 Total exchangeable sodium and potassium
 Intracellular potassium
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F. Effects of hypothermia:
 Decreased metabolic rate
 Decreased O2 requirement
 Increased blood viscosity
 Increased solubility of O2 and Co2
 For each degree decrease in temperature pH increase by 0.0147units
 Reductions in blood volume due to generalized vasoconstriction, plasma
sequestration and/ or leakage into interstitial compartment. This causes
increased volume requirements during rewarming.
 Shift of ODC to the left.
 Thermal deficit: patient kept at low temperatures, will have basal energy deficit
after rewarming. This is called as thermal deficit as the consequent increased
metabolic demand stresses the cardiopulmonary system in the postoperative
period.
Monitoring: Heart temp: mid esophageal probe
Brain temp: nasopharyngeal or tympanic membrane.
Temperature gradient: rectal
Systemic effects of CPB:
Hematology:
RBC:
- Become stiffer and less distensible
- They are also exposed to non-physiologic surfaces and shear stresses.
- All these will lead to hemolysis and increase free Hb levels
- The degree of hemolysis depends on flow rate.
WBC: Marked decrease will occur shortly after the onset of CPB.
Platelets: Platelet interaction with synthetic surfaces of the CPB circuit is the major
cause for platelet dysfunction and reduced platelet counts seen during and after CPB.
'Plasma proteins: Protein denaturation because of gas liquid interface.
This leads to,
- Altered enzymatic function.
- Aggregation of platelets
- Altered solubility characteristics
- Release of lipids
- Absorption of denatured proteins into cell membranes.
Activation of humoral cascade systems i.e.,
- Coagulation and fibrinolytic systems
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- Complement systems
Fluid: Alteration in the determinants of fluid flow during CPB, favors fluid accumulation
in the interstitial spaces.
CNS changes:
Embolic phenomenon - Air, preexisting thrombi, platelets and leukocyte aggregates, fat
globules or foreign substances in the CPB apparatus can get embolized.
- Haemodilution causes mild cerebral edema.
- When MAP drops below 40mmHg during CPB, CBF decreases proportionately
thereafter with decrease in MAP
Renal: Many variables that influence renal function during CPB,
Decreased U.O.P.:
- Micro emboli
- Production of vasoconstrictors
- Precipitation of plasma hemoglobin in renal tubules leading to ATN.
Increased U.O.P:
- Haemodilution
- Diuretics
Pulmonary:
(A-a) O2 increases after bypass, (max 18-48hrs afterwards). This is due to V/Q
imbalance and increased pulmonary interstitial fluid.
Activated neutrophils containing elastase and lysosomal enzymes accumulate within
the lungs during CPB.
An increase in the pulmonary venous pressure, secondary to elevated left atrial filling
pressure increases the risk of pulmonary interstitial edema.
Following CPB, pulmonary compliance falls and airway resistance increases leading to
increased WOB. Atelectasis is quite common.
Neuroendocrine response to CPB:
Serum catecholamine levels:

- Circulating levels of both adrenaline and nor-adrenaline increase during CPB and
aortic cross clamping.
- This is due to reflexes initiated by Baro chemoreceptors in the heart and lungs
when the organs are excluded from the circulation
- Other stress hormones whose levels are increased are ADH, cortisol, glucagon
and GH.
- Glycogenolysis and gluconeogenesis are enhanced
- Effect of insulin on glucose metabolism are inhibited
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ANESTHESIA FOR THE SURGERIES WHERE CPB IS USED
- The task confronting the anesthesiologist is to render the patient undergoing
cardiac surgery, analgesic, amnesic and unconscious while simultaneously
suppressing the endocrine and autonomic responses to intraoperative stress.
Equally important is preservation of compensatory cardiovascular mechanism
and prevention of perioperative episodes of myocardial ischemia.
- There is no one best technique of anesthesia. Familiarity with all anesthetics and
their physiologic and pharmacologic effects in the patient with severe cardiac
disease allows great flexibility in anesthetic selection.
- During anesthesia, amnesia is obtained by benzodiazepines; - Dilution by the
priming solution and sequestration of narcotics on oxygenator membrane may
necessitate administration of additional doses just before/ initiation of CPB.
Narcotics:
- Fentanyl and sufentanyl are preferred because of their less hemodynamic
impact.
Volatile agents:
- An anesthetic vaporizer attached to the CPB circuit adds inhalation agent directly
to the patient’s blood.
- It's use reduces the need of benzodiazepines and hence hastens the recovery.
Neuromuscular blocking agents:

The agents, which have less impact on hemodynamics, are used. The blockade should be
maintained to prevent shivering during induction of hypothermia or inadvertent
inspiration, which might result in air entry into open cardiac chambers.
Hypertension during bypass should be treated only with direct vasodilators or
inhalational agents and not with negative inotropic agents because heart is replaced by
the bypass pump.
CONDUCT OF CPB:
The various steps associated with the conduct of CPB may be described in the following
order,
a. Pre bypass preparations
b. Initiating CPB
c. Maintenance of extracorporeal circulation
d. Weaning from CPB
A. Pre by pass preparations:

- The heart lung machine should be partially assembled 45-60min before bypass is
scheduled to begin.
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- The system is primed with priming solution and recirculated for several minutes
through a sterile 0.5u filter to remove all air bubbles and particulate emboli from
the system.
- The calculated flows are written down for easy reference.
- The patient positioned in trendlenberg position and anesthesia induced.
- The surgeon prepares the sites for arterial and venous cannulation
Anticoagulation:
 As bypass circuits are thrombogenic, appropriate systemic anticoagulation is a
must before initiating bypass.
 Heparin 300-400Ukg-1 or 2-3 mg/kg given into the central vein / directly into the
right atrium.
 Activated clotting time is measured 2-5minutes later and additional heparin
given as required. ACT for CPB = > 400-480 sec.
 Supplemental dose of heparin given every hourly at the dose of 1/3 of initial
dose.
Heparin resistance is seen in,

 Ongoing active coagulation
 Antithrombin III deficiency
 Prior heparin therapy
 Drug interactions (OCP’s)
 Drug error
 Advanced age
 IV nitroglycerin
Treatment:
 Increase the dose of heparin up to 800U kg-1
 FFP to increase AT III levels
Patient with heparin induced thrombocytopenia coming for open-heart surgery:

 Delaying the case until heparin-induced antibodies are no longer present.
Usually up to 12 months.
 Plasmapharesis
 lloprost administration (Prostacyclin analogue which prevents platelet
aggregation).
Alternative methods of anticoagulation:

 Aneroid: an extract of Malayan pit viper venom cleaves fibrinogen.
 Hirudin and dermatan sulfate
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o Leech derived anticoagulant factors
o Direct inhibitors of thrombin
 Development of bypass components that have reduced or completely lack
thrombogenic activity.
 Heparin bonded circuits
CANNULATION:
 After full heparinization, cannulas are placed.
 Arterial cannula is usually placed first because, it is technically more difficult to
do and after placement, the perfusionist can give additional volume via the
arterial cannula to support the patients BP.
 The ascending aorta is most often used.
 Reduction of systemic BP to 90-100mm Hg systolic facilitates placement of aortic
cannula.
 Once the arterial cannula is placed, it is then connected to the arterial tubing
from the bypass machine and a careful search is done for any air bubbles left in
the tubing. Even a small amount of air may lead to cerebral air embolus with dire
neurological consequences.
 A small fluid bolus through the arterial line (back flow of blood) is given to check
for proper flow dynamics and to confirm placement of the cannula in the aortic
lumen.
 The anesthesiologist should palpate both carotids to confirm the cannula is not
obstructing right-sided carotid blood flow.
 High arterial inline pressures may indicate,
o Improper positioning of the arterial cannula or
o Can be an initial warning sign of an aortic dissection
Checklist Prior to Initiating Cardiopulmonary Bypass
Laboratory values
ACT or measure of adequate heparinization
Hematocrit
Anesthesia/machine
Adequate anesthesia and muscle relaxants given Nitrous oxide off (if used)
Monitor
Arterial pressure—initial hypotension and then return CVP—indication of inadequate venous drainage PCWP—
LV distention—inadequate drainage, Al—pull back pulmonary artery catheter 1-2 cm
Patient/field
Cannulas in place: no air locks, clamps, or kinks: no bubbles in arterial cannula Facial appearance
Suffusion (inadequate SVC drainage)
Unilateral blanching (innominate artery cannulation)
Heart
Signs of distention (especially in Al, ischemia)
Support
Usually not required
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 Once the surgeon, perfusionist and anesthesiologist are satisfied with the
functioning and placement of the arterial line, the venous cannula is then placed.
 Two cannula one in SVC and another in IVC or a single cannula in the right
atrium are used. Single cannula often has 2 ports 1 in the RA and other in the IVC
 Placement of the venous cannula may be associated^ with episodes of

hypotension that usually occur secondary to impaired venous return or an atrial
arrhythmia. (PAC, Atrial fibrillation, SVT)
 Usually these situations resolve quickly without intervention, but occasionally IV
medications, cardio version or the rapid placement of the patient on bypass may
be necessary.
Final preparation:
 Calibrate all monitoring transducers
 Empty the bladder to accurately track urine output while on bypass
 Inspect the patient’s eyes for Conjunctival edema and pupil size discrepancies.
 Anesthetic agents and adjuvants are supplemented to overcome the dilution
effect of CPB and the consequent lightening of the anesthetic state.
INITIATING CARDIOPULMONARY BYPASS

 Bypass begins when the surgeon unclamps the venous lines, and blood begins to
enter the extracorporeal circuit. As the blood starts to fill up the venous
reservoir of the oxygenator, the arterial pump is turned on.
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 The perfusionist gradually increases the bypass flow rates until all systemic
perfusion is machine generated.
 Left ventricular vent introduced through right superior pulmonary vein and
tapes around the SVC and IVC are tightened.
 The anesthesiologist adjusts the doses of vasoactive drugs, narcotics or inhaled
agents and corrects metabolic derangements. An additional dose of muscle
relaxant is given to prevent subclinical shivering.
 The TEE is turned off, all IV fluids are adjusted to maintain venous patency and
the pulmonary-artery catheter is withdrawn to prevent accidental perforation of
the pulmonary artery as the catheter cools.
 Once the machine is at fall flow all the venous blood is bypassing the
cardiopulmonary circulation. Ventilation at this point is discontinued.
Three methods have been suggested for the lungs during CPB.
 Disconnection of the airway from the anesthesia circuit allowing passive lung
deflation (preferred technique)
 Maintaining low flow rates (0-21/min) and /low levels of CPAP (PEEP = 5cm
of H2O)
 Continuing ventilation with reduced tidal volumes.
Potential problems that can occur during initiation,

a. Hypotension - decrease >30mmHg
b. Treatment = vasoconstrictors, increase pump flow.
c. Inadequate venous drainage (because of catheter malposition /kink/airlock)
d. Asymmetric swelling or discoloration of the face or eye indicating arterial
cannula obstruction.
e. Elevated inflow line pressures and dampened distal arterial pressures - indicate
aortic dissection.
f. Inadequate oxygenation
g. Hypertension due to inadequate anesthesia/excessive vasoconstriction from
elevated catecholamine levels. (Treatment: Decrease pump flow or add
isoflurane/ vasodilator therapy)
h. Elevated pulmonary artery pressures due to,
 Over wedged or kinked catheter (most common cause)
 Left ventricular distention
 Aortic valve insufficiency prior to the placement of the aortic cross clamp,
Elevated CVP due to
 Inadequate venous drainage
 The catheter becoming ensnared in a suture securing the venous cannula.
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Air embolism
 Inattention to venous reservoir levels
 Failure by the perfusionist to act quickly enough to prevent air from being
pumped into the arterial cannula.
Once the circulation begins, the aorta is cross-clamped and cardioplegic
myocardial protection given before surgical correction is undertaken.
Initiation of Bypass: On-Bypass Checklist*

1. Assess arterial inflow
 Is arterial perfusate oxygenated?
 Is direction of arterial inflow appropriate?
 Evidence of arterial dissection?
 Patient's arterial pressure persistently low
 Inflow line pressure high
 Pump/oxygenator reservoir level falling
 Evidence of arterial cannula malposition?
 Patient's arterial pressure persistently high or low
 Inflow line pressure high
 Unilateral facial swelling, discoloration
2. Assess venous outflow
 Is blood draining to the pump/oxygenator's venous reservoir?
 Evidence of SVC obstruction?
 Facial venous engorgement or congestion
 CVP elevated
3. Is bypass complete?
 High CVP/low PA pressure Impaired venous drainage
 Low CVP/high PA pressure Large bronchial venous blood flow Aortic
insufficiency
 Arterial and PA pressure nonpulsatile
 Desired pump flow established?
Discontinue drug and fluid administration
Discontinue ventilation
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MAINTENANCE OF BYPASS
The primary goal of this period is to obtain desired levels of hypothermia,
maintain adequate systemic perfusion, ensure//appropriate tissue oxygenation, and
manage arterial blood gases.
Aortic cross clamping during CPB completely abolishes coronary blood flow.
Hence CPB > 120 min is undesirable.
Ischemic depletion of high energy phosphate compounds and accumulation of
intracellular calcium depletes the energy stores of the myocardium. To maintain normal
myocardial cellular integrity and function during CPB, the available high energy
phosphate compounds have to be spared. This is accomplished by,
a. Hypothermia (to decrease 02 consumption)
b. Cardioplegia (to decrease energy expenditure)
c. Intermittent periods of myocardial perfusion
a) Hypothermia:
 Hypothermia of 20-30°C is routinely used for CPB.
 O2 consumption is reduced 5-7% per degree centigrade decrease in the
temperature.
 10°C drop in temperature will halve the BMR.
Advantages:
 Lower pump/flow rates, better organ/protection, less blood trauma and
improved myocardial protection. (lower flow rates decrease the volume of
collateral blood flow and therefore decrease warming of the myocardium)
 Monitoring of temperature gradient between core body temperature and
peripheral temperature is more beneficial during rewarming. Larger gradient
indicates incomplete rewarming.
b) Cardioplegia:
Cardioplegic solution:
o A number of different solutions are described. Most common compounds
are,
 Potassium = 15-40 mEq/l
 Sodium = 100-120 mEq/l
 Chloride = 110-120 mEq/l
 Calcium = 0.7 mEq/l
 Magnesium = 15 mEq/l
 Glucose = 28mmol/l
 Bicarbonate = 27mmol/l
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 St. Thomas hospital solution (supplied in 20ml ampoules)
 MgCl2 6H2O = 16mmol
 KCl = 16mmol
 Procaine 272.8mg
 Water to 20ml
 This ampoule is added to 1 liter of non-lactated Ringer’s solution at 40C and used.
Functions of each component:

 K+ = level kept < 50meq/L because higher levels can be associated with a
paradoxic increase in myocardial energy requirements and excessive potassium
loads.
 Na+ = ischemia tends to increase intracellular Na+ content, hence its level should
be kept less than that of plasma.
 Citrate = to decrease Ca+ concentration
 Ca+ = added to maintain cellular integrity
 NTG = to improve distribution of the cardioplegia solution
 Mg+2 = controls an excessive influx of calcium intracellular.
 Bicarbonate = acts as a buffer to prevent excessive build up of acid metabolites.
 Other buffers which can be used are = histamine and promethanine.
Additional components include,

 Hypertonic agents = e.g., Mannitol (to control cellular edema)
 Glucocorticoid = for membrane stabilization
 Prostacyclin = antiplatelets activity
 Ca+ channel blockers and B blockers: to reduce metabolic demand
 Free radial scavengers e.g., Mannitol
 Procaine (0-1mmol/l) = for membrane stabilization and antiarrhythmics effect
 Glucose / glutamate / aspartate = energy suppliers
o The question of whether to use crystalloid or blood as a vehicle for
achieving cardioplegia remains controversial.
Method of cardioplegia arrest:

 After the initiation of CPB and induction of hypothermia, the left heart is vented
and the aorta cross-clamped proximal to the cannula.
 The myocardium is now ischemic.
First phase: (induction of cardiac arrest and hypothermia)

 14G needle is inserted into the aortic root below the cross clamp.
 1 liter of cold (0-40C) cardioplegic solution is rapidly infused through the needle.
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 In presence of aortic incompetence, the infusion is done directly through cannula
inserted into each coronary ostium, each of which receives 500ml of solution.
 Cardioplegia may not reach areas distal to high-grade coronary obstructions.
Then cardioplegia is administered retrograde through coronary sinus catheter.
Method of injection: via a separate circuit on the bypass machine / manually using
pneumatic infusion device.
 Cardioplegia must be repeated several times (about every 20min) because of
gradual washout and rewarming of the myocardium. This also prevents
excessive build up of metabolites, which inhibit anaerobic metabolism.
Mechanism of action:
Increased extracellular potassium

Decrease in transmembrane potential

Impairment of Na+ transport

Abolition of action potential generation

Cardiac arrest in diastole
Other sites of injection,

Coronary sinus
Indicated in
 Severe coronary steal stenosis
 Multiple severe lesions
Directly down newly constructed bypass grafts
Excessive cardioplegia can result in,
 Absence of electrical activity
 A.V conduction block
 Poorly contractile heart at the end of bypass
 Persistent systemic hyperkalemia
Second phase: (Maintenance of a low myocardial temperature by topical cooling)

 Done by flooding the pericardial cavity with ice-cold Hartmann’s solution
(61/hr). A sucker removes and discards the surplus volume.
 The postero inferior aspect of heart is separated from warmer structures i.e.,
descending aorta and diaphragm, by swabs or corrugated rubber.
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 ECG monitoring is essential. Returning electrical activity implies inadequate
protection and heart should be re-cooled and by repeating a smaller volume of
cardioplegia solution.
 The atria are often first to show return of contractile activity.
c) Intermittent periods of myocardial perfusion:
Done by,
 Intermittent aortic cross clamping
 Intermittent coronary perfusion with arterialized blood from heart – lung
machine via 2 small cannula inserted into the coronary ostia.
 Alternating ventricular fibrillation with defibrillation to allow the heart to beat
intermittently.
Blood gas management:

Acid base management during CPB is done by two methods
 Alpha stat method
 pH stat method
Alpha stat method:

It considers the alkaline pH seen during CPB is physiological (increased solubility
of carbon dioxide seen during hypothermia raises the pH. Hence no additional measures
to correct the pH/Pco2 levels are undertaken. This is the more commonly used method
and it appears to preserve cerebral autoregulation & improve myocardial preservation.
pH stat method:
In this, pH & Pco2 are maintained at normal values regardless of the body temperature.
In order to maintain Pco2, Co2 is added to the ventilating gas mixture. This method is
not preferred because patients tend to have higher CBF because of increase in Co2
content and there will be loss of cerebral auto regulation. More flow, more chances of
micro-embolization.
Blood pressure and flow rate management:

 A 50 —60 ml/kg of flow rate maintains mean arterial pressure at 40-60 mmHg.
 From the myocardial protection point of view, both higher and lower perfusion
pressures are acceptable.
 To preserve CNS function MAP should be maintained >50mmHg.
 Patient who is free from cerebrovascular disease can tolerate MAP up to
30mmHg with hypothermia. As the patient is rewarmed, the MAP should also be
increased accordingly, to ensure adequate CBF.
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 In patients with peripheral vascular diseases MAP should be maintained at
60mmHg with hypothermia.
 Renal function is maintained with pump flows of  = 1.6L/min
Monitoring during CPB:
Systematic arterial pressure:

Higher pressures:
 Increase risk of cerebrovascular complications
 Increase in the non-coronary blood flow to the heart and consequent warming of
the ischemic myocardium.
Lower pressure:
 Increase the incidence of neurological complications.
CVP and pulmonary capillary wedge pressure should be close to zero.
 Increased CVP = compromises cerebral circulation.
 Increased PCWP= indicate LV distention and possible myocardial damage.
 Rectal and nasopharyngeal (near to brain temperature) temperatures
 ECG: Should show a flat line that is complete absence of activity. Once myocardial
blood supply is restored and heart defibrillated, ECG is monitored for
dysrrhythmias and ST-T changes.
 Urine output: Should be maintained at or more than 1ml/kg/hr. It is an indirect
evidence of organ perfusion.
 Blood gases and mixed venous Po2 are also monitored.
 Hematocrit monitoring: Should be maintained at 20-30%
 Level of anticoagulation: To be monitored and maintained at optimal levels. The
methods include,
 ACT (Activated Clotting Time) >480sec.
 High dose thrombin time (HITT)
 Thromboelastography: Gives information about the quality of the clot and
dynamics of its formation.
 Heparin concentration: correlates with anti factor X a activity.
Clinically observe:
 For the brisk capillary refill
 Size of the pupil (should be small and equal)
 Diaphragmatic motion Monitors in connection to CPB circuit
 Venous return to the venous reservoir.
 Arterial line pressure
 Suction pressure in the vent and cardiotomy suction lines Temperature of the
perfusate.
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Checklist during Cardiopulmonary Bypass*
Laboratory values
 ACT or measure of adequate heparinization
 ABGs (uncorrected)—acidosis
 Hematocrit, potassium, calcium levels
Anesthesia/machine
 Discontinue ventilation
Monitor
 Arterial pressure
 Hypotension
o Venous cannula—kink, malposition, clamp, air lock
o Inadequate venous return (bleeding, hypovolemia, IVC obstruction, table, too
low)
o Pump—poor occlusion, low flows Arterial cannula—misdirected, kinked,
partially clamped,-dissection
o Vasodilation—anesthetics, haemodilution, idiopathic
o Transducer or monitor malfunction, stopcocks the wrong way
 Hypertension
o Pump -  flow
o Arterial cannula—misdirected
o Vasoconstriction—light anesthesia, response to temperature changes
o Transducer or monitor malfunction
 Venous pressure—above level of atrium—obstruction to return LV filling
pressure—LA, PCW (if available)—any elevation?
 ECG—electrical quiescence (if cardioplegia used)
 EEG
 Adequacy of perfusion??
o Flow and pressure??
o Acidosis
o Mixed venous oxygen saturation
 Urine output
 Temperature
Patient/field
 Conduct of the operation
 Heart—distention, fibrillation
 Cyanosis, venous engorgement, skin temperature
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 Movement
 Breathing, diaphragmatic movement (hypercarbia, light anesthesia)
Support
 Vasodilators, anesthetics, or constrictors to control blood pressure when flow is
appropriate
REWARMING:
 When the surgeon begins the last phase of the procedure, the perfusionist begins
to rewarm the patient.
 The rewarming should be gradual and is done over a 30 minute period.
 A gradient of I0°c is maintained between the patient and the perfusate to prevent
formation of gas bubbles due to their increased solubility as the blood gets
warmed.
 Anesthesiologist should ensure amnesia of the patient by administering
additional doses of benzodiazepines, as the amnesic effect of hypothermia is lost.
 Avoid inhalational agents as they have negative inotropic property.
 Upon completion of the surgical repair, any residual air in the ventricles to be
removed.
 The anesthesiologist vigorously inflates the lungs to remove air from the
pulmonary veins and aids in filling of the cardiac chambers.
 TEE assesses the effectiveness of desiring process,
 The aortic clamp removed to resume myocardial perfusion
 The heart is defibrillated and allowed to beat empty and replace some of its
oxygen debt.
 The field is tidied up and preparations are made to separate from
cardiopulmonary bypass.
WEANING FROM CPB-

 Ensure that the patients are rewarmed adequately and myocardial contractility
rhythms are acceptable. If necessary, heart rate and rhythm can be regulated
either pharmacologically/ electrically with appropriate pacing.
 Rule out hyperkalemia and treat accordingly
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Preparation for Separation-from-Bypass Checklist*
Air clearance maneuvers completed
Rewarming completed
Nasopharyngeal temperature 37°-39°C
Rectal/bladder temperature >35°C
Address issue of adequacy of anesthesia and muscle relaxation
Obtain stable cardiac rate and rhythm a. Pacing if necessary
Pump flow and systemic arterial pressure
Pump flow to maintain mixed venous saturation ^70%
Systemic pressure restored to normothermic levels
Metabolic parameters
Arterial pH, PO2, PCO2within normal limits
Hct: 20-25%
K7: 4.0-5.0 mEq/L
Possibly ionized calcium
Are all monitoring/access lines functional?
Transducers re-zeroed
TEE (if used) out of freeze mode
Respiratory management
Atelectasis cleared/lungs re-expanded
Evidence of pneumothorax?
Residual fluid in thoracic cavities drained
Ventilation reinstituted without nitrous oxide
Intravenous fluids restarted
Inotropes/ vasopressors /vasodilators prepared
 Ventilation begun with 100%-O2
 Venous drainage lines are gradually occluded, allowing, arterial return to
progressively raise the circulating volume.
 During this time, cardiac function is continuously evaluated from the monitors/
direct inspection of the heart.
 When sufficient volume has been transformed to optimize preload, blood
pressure and cardiac output, arterial pump is stopped.
 Venous cannulas are removed following a satisfactory interval of stable
hemodynamic functions.
 Reversal of anticoagulation done with protamine, (at this point arterial cannula
will be still present)
 Protamine: A protein molecule derived from salmon sperm and is highly cationic
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 Dose = 1 to 1.3ml (10mg/ml) for every 1000U of heparin administered 2-4
mg/kg or dose is calculated based on the heparin dose response curve
/automated heparin - protamine titration assay.
 Protamine is administered in an infusion, into a peripheral vein and the rate
should not exceed 50mg/min.
 Rapid infusion increases white blood cell sequestration in the pulmonary
circulation.
 ACT As measured after 5min of protamine administration. An adequate reversal
will return the ACT to within 10% of the baseline value.
 Anesthetics are administered where clinically indicated
 Removal of atrial cannulas may trigger cardiac, dysrrhythmias but they are
usually transient. Atrial or junctional dysrrhythmias often disappear once the
cannulas are out.
 Arterial cannulas remain in place for continued transfusion of pump contents.
When this is completed and bleeding is controlled, the arterial cannula is
removed and the chest is closed.
 During decannulation, the possibility exists for unexpected bleeding from the
atrial or aortic suture lines.
 Continued vigilance for new ischemia, is important because it may indicate a
correctable problem with the grafts.
 Valve patients should have the adequacy of the repair/ replacement assessed by
TEE.
POST BYPASS PERIOD
 Patient should be shifted to the ICU, kept on mechanical ventilatory support (2-
12hr)
 He should be continuously monitored for his hemodynamic stability and cardiac
electrical activity. SBP should be maintained at 90-110mmHg. HR=70-80bpm.
Hct kept at 25-30%.
 Frequent ventricular ectopy may reflect electrolyte disturbance or residual
ischemia and should be treated.
 Hypokalemia/ hypomagnesia should be corrected
 Oozing following heparin reversal may be due to
o Incomplete reversal
o Reduced platelet count or function
o Inadequate surgical hemostasis
o Dilution of coagulation factors
o Heparin rebound phenomenon
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 If hypotension doesn't respond to volume/inotropic therapy, the chest should be
reopened to rule out cardiac tamponade, a kinked graft or other serious
problems.
 Medicated infusion must be regulated with portable infusion pumps
 Sedation and analgesia provided by Inj morphine 2-3mg or propofol infusion 20-
30g/kg/min.
 Hypertension may be due to pain and should be treated with analgesics and
sedatives. If not responding, then NTG/nitroprusside/ B blockers should be
given.
 Fluid replacement should be guided by filling pressures.
 Extubation considered when muscle paralysis has been worn off and patient is
hemodynamically stable. Most patients can be extubated by the following
morning
Complications of CPB and its signs
1. High aortic tubing pressure Aortic tubing occlusion/kinking Too small aortic cannula.
Improperly placed aorta cannula
2. Low venous return Aortic dissection Bleeding from an open blood vessel
Obstruction of venacaval cannula/ tubings Leak in
venous return tubing, connectors or CPB reservoir
3. Hypotension Anything limiting CPB pump flow Aortic dissection Low

peripheral resistance
4. Abnormal blood gases Oxygenator failure (decrease PaO2 increase PaCo2)

Inadequate perfusion (decrease pH, base deficit Pvo2<
40mmHg) Increased 02 demand
5. Oliguria/ anuria Aortic dissection

6. Suffusion, Plethora, If unilateral aortic cannula flow into carotid artery
Cyanosis/edema of head, Obstruction of SVC cannula
face, eyelids and conjunctivaObstruction of jugular venous drainage by neck
compression, head position.
7. Isoelectric encephalogram Inadequate cerebral perfusion
High anesthetic concentration
Extreme hypothermia
8. Abdominal distention Obstruction of IVC cannula
Intra-abdominal hemorrhage, Ascites
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GIT distention by gas or fluid
9. Elevated CVP Obstruction of venacaval cannula
10. Elevated pulmonary Obstruction of venacaval cannula on partial CPB
artery pressure and distention Incompetent aortic valve
of the heart Excessive coronary sinus and bronchial artery flow.
Malposition of the heart
11. Diaphragmatic movement Hypercarbia
Inadequate muscle relaxation or anesthesia
12. Hypertension Excessive CPB flow
Inadequate anesthesia
Drug induced
13. Fibrin deposition or clot in Inadequate heparin concentration
CPB reservoirs Insufficient heparin cofactor
 Most serious complications that indicate immediate cessation of CPB and

reestablishment of the patient's own cardiac output are —
 Aortic dissection Super fusion of a carotid artery
 Air in the aorta inflow tubing.
COMPLICATIONS WHICH OCCUR DURING TERMINATION OF
CPB
 Injury to the ventricles by over distention
 Low cardiac output
 Abnormal heart rate and rhythm
o Asystole / heart block
o Supraventricular tachyarrhythmias
o Recurrent ventricular tachycardia or fibrillation.
 Air embolism to the brain, or heart or into the coronary arteries
 Complication of heparin neutralization(Protamine)
o Myocardial depression leading to hypotension
o Histamine release
o Systemic vasodilation
o Pulmonary vasoconstriction
o Anaphylactic/ anaphylactic reactions
o Bronchospasm
o Pulmonary edema
 Deficient platelets and clotting factors
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EXTRACORPOREAL SUPPORT DURING VASCULAR SURGERIES

Thoracic and thoraco abdominal aortic surgeries can be performed without
extracorporeal support. Clamp and run techniques and passive conduit or shunt are
useful when clamp time requirement is less than 20-30 min.
 For aneurysms involving the ASCENDING AORTA
o Femoro-femoral bypass
o RA to femoral bypass
o RA to ascending aorta bypass
 For aneurysms involving ARCH OF AORTA
o Femoro femoral bypass
o Retrograde cerebral perfusion
o Antegrade cerebral perfusion or
o Deep hypothermic circulatory arrest.
 For aneurisms involving DESCENDING AORTA
o Distal perfusion is obtained by
o LA to Femoral artery bypass
o RA to Femoral artery bypass
o Femoro-femoral bypass
MINIMALLY INVASIVE CARDIAC SURGERIES

Economics, combined with patient comfort, is the driving force behind latest
innovations in cardiac surgery. These include:
MIDCAB: Minimally Invasive Direct Coronary Artery Bypass
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OPCAB: Off Pump Coronary Artery Bypass
PORT ACCESS SURGERY

MIDCAB: In this, coronary anastomoses are performed on a beating heart, without the
support of CPB. This is useful for the repair of single coronary artery. It involves
parasternal / inframammary incision or mini-thoracotomy or partial sternotomy.
OPCAB: In this, full myocardial revascularization is accomplished through a Median
sternotomy without CPB.
PORT ACCESS SURGERY
 Both coronary artery lesions and valve lesions are repaired without the need of
median sternotomy. But full CPB support is used for this type of surgery.
 In this anesthesiologist has to place a coronary sinus catheter (for cardioplegia
administration) and a pulmonary artery catheter (to effect LV drainage) via right
UV.
 It involves parasternal / inframammary approaches.
Anesthetic implications:
 Mild hypothermia and anticoagulation are provided even though surgeries are
performed on a beating heart.
 The choice of anesthetic agent should be oriented towards early awakening and
extubation if possible.
 Preparations for external cardioversion or epicardial pacing are made Bilateral
radial arterial line B.P. is measured
 Loss of right radial artery pressure tracings indicate migration of aortic cannula
into the aortic arch
 Continuous TEE monitoring is recommended for the early detection of aortic
dissection / catheter migration etc
 Complications that may arise during
 Right coronary repair - Atrial arrhythmias and bradycardia
 Left coronary repair - Left ventricular dysfunction
 During repair, more critically stenosed vessel has to be repaired last (To
establish blood flow to the remainder of the heart prior to the greatest ischemic
insult)
 During repair, before graft placement, test occlusions should be performed (This
is to precondition the myocardium and also to know the conditions which may
occur during repair after clamping)
Benefits of minimally invasive surgeries
 Decreased blood loss, infection, sepsis and length of hospital stay
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Complications
 Poor cardiac protection
 Arrhythmias
 Perforation of IVC and RV
 Stroke
 Difficult to deair after mitral and aortic valve replacement
 Difficult to resuscitate the patient
 Full CPB administration may become necessary sometimes because of LV
dysfunction, aortic dissection etc.
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Chapter 22 - CARDIOVASCULAR MONITORING
– Non-invasive and invasive monitoring
INTRODUCTION:
The fundamental basis for the circulatory monitoring remains in the eyes, hands and
ears of the anesthesiologist. Just as inspection, palpation and auscultation are the corner
stones for standard physical examination of the cardiovascular system. These
procedures remain the critical elements of perioperative cardiovascular monitoring.
The cardiovascular system perfuses organs to maintain function and viability.
The goal of cardiovascular hemodynamic monitoring is to maintain adequate organ
perfusion and systemic stability.
Cardiovascular monitoring is divided into non-invasive and Invasive monitoring.
NON-INVASIVE MONITORING:
a. Stethoscope heart sounds and breath sounds
b. Heart rate monitoring
c. Pulse rate monitoring
d. Electrocardiogram (ECG)
e. Blood pressure measurement - Non-invasive
INVASIVE MONITORING:
a. Invasive blood pressure measurement
b. Central venous pressure (CVP)
c. Pulmonary artery catheterization (PAC)
d. Cardiac output
e. Transesophageal echocardiography (TEE)
STETHOSCOPY:
 Stethoscope is used as a routine continuous cardiopulmonary monitoring device
during surgery. Today intraoperative monitoring with either a precordial or
esophageal stethoscope has become a fundamental extension of the physical
examination for all anesthetized patients.
 Transoesophageal stethoscope with ECG may be useful to diagnose atrial
arrhythmias, right ventricular ischemia or posterior left ventricular ischemia.
Thus stethoscope remains a valuable additional safety monitor for pediatric
surgery and diagnosing important respiratory problems.
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HEART RATE MONITORING:
The simplest and least invasive form of cardiac monitoring remains the measurement of
heart rate. Heart rate is estimated by counting the pulse or with electronic monitoring
such as ECG. Electrocardiographic measurement of heart rate begins with accurate
detection of R wave and measurement of R-R interval. Some times electrical artifacts
prevents accurate ECG measurement of heart rate. Other artifacts result from muscle
twitching, and fasciculation, as well as various medical devices including lithotripsy
machines, cardiopulmonary bypass equipment and fluid warmers, electrical diathermy
etc.
Pulse oximetry:
Detection of saturation of hemoglobin by spectrophotometry is based on Beer-Lambert
law which relates the con. of solute to the intensity of light transmitted through a
solution. Two LEDs  two wavelength of light (red and near infrared).
PULSE RATE MONITORING:

Monitoring pulse rate is more important than monitoring heart rate in terms of
perioperative hemodynamic assessment. Electrical depolarization and systolic
contraction of heart is heart rate which generates a palpable peripheral arterial
pulsation is called pulse rate.
Pulse deficit means, the pulse rate is less than the heart rate. The most common
cause is electro-mechanical dissociation or pulse less electrical activity seen in patients
with cardiac tamponade, extreme hypovolemia, and other conditions in which cardiac
contraction does not generate a palpable peripheral pulse.
Pulse oximeter will provide a suitable pulse measurement source for most
patients except those with severe arterial occlusive disease or those with marked
peripheral vasoconstriction.
ELECTROCARDIOGRAPHY (ECG):
"It is summation of electrical activities of the myocardium represented in wave form".
The apparatus consists of string Galvanometer or Radio-amplifier. The waves are traced
on standardized graph paper or fluorescent screen.
STANDARD ECG RECORDINGS:

 Speed - 25 mm/sec
Horizontal line - Represents time - 1mm  0.04 sec.
- Large square (5mm) - 0.2 sec.
- Small square (1mm) - 0.04 sec.
Vertical line - Represents voltage - 10mm lm volt.
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PARTS OF WAVE PATTERN:
 P-wave: P-wave is produced by atrial depolarization. Normal P-wave <0.11 sec.
and Height 2-5 mm.
 QRS complex: Produced by ventricular depolarization.
QRS (capital) wave >5mm (Ht)
QRS - <5mm
 'Q' wave: Initial negative deflection, It is due to depolarization of the ventricular
septum from left to right.
 'R' wave: First positive deflection of QRS complex, It is due to depolarization of
ventricles.
 S-wave: First negative deflection after 'R' wave
 T wave: Produced by ventricular repolarisation.
 U wave: Represents slow repolarisation of purkinje fibres and septum.
INTERVALS:
 R-R interval: Between two successive 'R' wave from same point.
o HR/Min. = 300/ R-R interval
 PP interval: Between two successive 'P' from same point. If regular rythm PP=RR.
 PR interval: AV conduction time, onset of P to beginning of QRS.
o Normal = 0.12 - 0.2 sec.
 VAT (Ventricular activation time): Beginning of Q to peak of R. Time of
endocardial to epicardial traveling of impulse.
o <0.3 sec. in VI - V2
o >0.05 in V5 - V6
 QT interval: Onset of Q to end of ‘T’ wave
o Normal = <0.42 sec.
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SEGMENTS:
 PR segment: End of 'P' to onset of QRS. It is Isoelectric in character. N = 0.04 sec.
 RS-T segment: ‘J' point to onset of T".
(J = Junction of end of QRS and Beginning of ST segment) Normal  0.04 sec.
I, II, III, aVR, aVL and aVF  detect front plane activity.
VI to V6  detects horizontal plane activity.
 Mean axis: It is net amplitude and direction of cardiac electric force.
o Normal: -30° to 110°
o Rt. axis: 110° to 180°
o Lt. axis: -30° to-90° (210°-330°)
o 0 to -30°: Horizontal heart
o 75° to 110°: Vertical heart
Right axis deviation:

I. Right ventricular hypertrophy
II. Thin lean bite
III. Lateral hall infarction
IV. Dextrocardia
Left axis deviation:

I. Obese, built
II. Old age
III. Pulmonary - COPD
Intermediate:
 Severe right ventricular hypertrophy
 Aneurysm of left ventricular
DETERMINATION OF AXIS:
There are two methods
I. Perpendicular method
II. Quadrant method
 The perpendicular method is the most accurate method for determining QRS
axis. It requires examining all six limb leads. The QRS axis is oriented towards
the positive end of the lead axis that has the tallest positive deflection or toward
the negative end of the lead axis, which has the deepest negative deflection.
Additionally the axis points perpendicular to the lead axis with the smallest or
most biphasic deflection.
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Normal direction:
V1 V2 septal
aVL -300 V3 V4 anterior
aVR 2100
V5 V6 lateral
V1 V4 anteroseptum
V3 V6 anterolateral
Lead I 00 L1 aVL  high lateral
L II, L III aVF  inferior
Coronary artery spasm
Lead II 600 Left ant disease artery – V1V2V3V4
Lead III 600
Left coronary are – L1 aVL, V5V6
aVF 900 Right coronary art – L II L III aVL
ECG MONITORING SYSTEM:

NON INVASIVE:
a. Three electrode system (standard)
b. Modified 3 electrode system
i) Central sub clavicular (CS5)
ii) Central back lead (CB5)
iii) Mid clavicular (MCL1)
iv) Central manubrium (CM5)
v) Central chest (CC5)
Five electrode system
INVASIVE:
i) Esophageal ECG
ii) Intra cardiac ECG
iii) Endotracheal ECG
iv) Intra coronary ECG
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Three electrode system:
One electrode acts as ground. Bipolar lead explores activity between other two
electrodes.
Modified three electrode system:

CS5 type (central subclavicular)
 RA - Under Rt. clavicle
 LA - at V5 site
 LL - Lower It. chest (ground)
 Leads  I, II
For anterior wall ischemia.
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CB5 type (central back lead)
 RA - Centre of Rt. scapula
 LA - V5 position
 Lead - I
 Good detection of supraventricular arrhythmia.
MCL1 (Mid clavicular)

 LA - below left distal clavicle
 LL - Rt. MCL at 4th 1CS
 Lead - III.
CM5 (central manubrium)

 RA - Sternal angle
 LA - Lt. anterior axillary line
 Lead - I
CC5 (central chest)

 RA: Rt. ant. Axillary line.
 LA - Lt. Ant. axillary line (5th ICS)
 Lead - I.
These leads show greater 'R' amplitude and amplification of ST segment response.
Five electrode system:

 Used to record I, II, III, aVR, aVL, aVF.
Site of electrode:
RA - Rt. shoulder RL - Rt. lower chest
LA - Lt. shoulder LL - Lt. Lower chest
V5 - V5 position
 It is well suited for detection of intra operative ischemia.
Combination and sensitivity of detection of ischemia:

V5 alone  75%
V4  61%
V4 + V5  90%
II + V5  80%
II, V5 and V4  98%
 ST segment up-sloping  2mm depression 80m sec after JP
 Horizontal ST  1mm depression 60-80 msec
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 Down sloping ST -->> 1mm from top of curvature to PQ junction
 ST elevation
 T inversion
Ischemia is represented by T-wave changes in the ECG. The normally upright,
asymmetrical T-wave becomes deeply inverted and symmetrical.
ST segment is displaced upward from the baseline and its shape is convex in
subepicardial injury, ST segment is depressed in subendocardial injury.
INVASIVE METHODS:
Esophageal ECG:
 Electrodes placed through esophageal catheter or stethoscope.
 100% detection of arrhythmia
 Detection of complex arrhythmias
 Posterior wall ischemia is detected well.
Intra cardiac
 Electrodes placed through CVP or PAC
 Atrial, ventricular and AV nodal arrhythmias and conduction blocks can be
detected.
 Recording intracavitary ECG.
Endotracheal
 ETT attached with electrodes
 When surface electrodes are impracticable or impossible.
 Useful for atrial arrhythmias in pediatric age.
Intra coronary
 Electrodes placed with coronary guide wire
 During angioplasty
 Great accuracy for acute ischemia.
FACTORS AFFECTING ECG (Artifacts):

 Hair on the body surface
 Dirt on the skin / electrode
 Shivering
 Loose electrodes
 Broken electrodes
 Dry electrodes (without jelly)
 Lead insulation
 Other electric field - e.g.: Electrocautery etc.,
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BLOOD PRESSURE MEASUREMENT  Non-invasive
Non invasive blood pressure measurement is currently performed either manually or
with a variety of automated electromechanical devices employing techniques such as -
 Auscultatory method
 Oscillometric method
 Blood flow detection: Palpation, ultrasonic and photoelectric.
 Infra sounds
 Finapres
 Arterial tonometry
 Photo plethysmography is a recent sophisticated technique relying on
Oscillometric changes in the pressure in finger cuff.
Non invasive blood pressure (NIBP) measurement involves occluding an artery by a
pressurized cuff and then measuring the oscillation in cuff pressure, or the pressure at
which flow resumes through the artery as the cuff is deflated. Multiple techniques exist
for determining blood pressure by this method.
AUSCULTATION OF KOROTKOFF'S SOUNDS:

An occlusive cuff is inflated above the systolic blood pressure. As the cuff is slowly (3-5
mm Hg/s) deflated, a pressure will be reached at which blood begins to flow turbulently
through the artery. The pressure at which the sound of this turbulent flow is heard
through a stethoscope is the systolic blood pressure. As the pressure in the cuff
decreases below the diastolic blood pressure, the sounds muffle or disappear.
Various Korotkoff’s sounds -

I phase : Sounds appear clear, sharp and snapping sound.
II phase : Sounds softened
III phase: Sounds clear, and banging
IV phase: Muffled
V phase : No sounds.
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Commonly available blood pressure cuff sizes:
Width (cms) Length (cms)
Newborn (< 1 month) 2.5 5

Infant (1 year) 4 12
Child (1-4 yrs) 6 15
Child (4-10 yrs) 9.5 23
Adult arm 15 33
Adult obese 18-20 35
Adult thigh 18 36
OSCILLOMETRIC METHOD:
This method of arterial blood pressure measurement involves double-cuff system with a
proximal cuff for occlusion of arterial inflow and a distal cuff to measure arterial
pulsations. The distal cuff begins to pulsate when the proximal cuff deflates below SBP.
These pulsations are transmitted to a detecting device.
PALPATION OR DOPPLER DETECTION OF FLOW:
As the cuff is deflated, the distal pulse is palpated or detected by Doppler ultrasound.
The pressure in the cuff at which the pulse is first detected correlates with the systolic
blood pressure. This technique only measures systolic blood pressure.
TONOMETRY:
Tonometry is a variant of the oscillometric method, in which the artery is only partially
occluded and oscillations in arterial pulsation are measured. Most commonly, the radial
artery is chosen. This method offers the advantage of continuous pressure
measurement. The measurements are affected by motion and uncertain at extremes of
pressure.
INVASIVE MONITORING
INVASIVE BLOOD PRESSURE MEASUREMENT:
Direct intra-arterial monitoring remains the gold standard against which all non-
invasive technique has been compared for several decades.
Cannulation of a peripheral artery provides access for the measurement of intra-
arterial pressure. It allows ready access for blood analysis in addition to beat to beat
pressure measurements.
Indications for intra-arterial monitoring:

 Major surgical procedures involving large fluid shifts or blood loss.
 Surgeries requiring cardiopulmonary bypass.
 Surgery of aorta
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New devices allow continuous monitoring of ABG using fiberoptic sensors placed
directly into artery through the vascular catheters.
 Patient with pulmonary diseases requiring frequent arterial blood gas.
 Patient with recent MI, unstable angina or severe coronary artery disease.
 Patient with CHF.
 Patient in hypovolemic, cardiogenic or septic shock with multiple organ failure.
 Massive trauma cases
 Patient with right heart failure, COPD, pulmonary hypertension.
 Patient requiring inotropes or intra aortic balloon counter pulsation.
 Patient with massive ascites
 Patient with electrolyte and metabolic disorders requiring frequent blood
samples.
 Inability to measure arterial pressure non invasively (e.g.-morbid obesity
and extensive burns).
INTRA ARTERIAL CANULATION:

Radial artery pressure monitoring is most common in anesthesia and critical care. It is
technically easy to perform and rarely associated with complications due to good
collateral circulation of hand. Before attempting radial artery cannulation, adequacy of
collateral flow to the hand should be assessed by alien's test.
Allen test: Examiner compresses the radial and ulnar arteries and asks the patient to
make a tight fist to exsanguinating the palm. As the ulnar occlusion is released, the color
of the open palm is observed. Normally the palm will have a striking flush in several
seconds; severely reduced ulnar collateral flow is present when the palm remains pale
for more than 10 seconds.
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Procedure:
 Wrist and hand are immobilized in mild dorsiflexion and course of the radial
artery is identified by gentle palpation.
 After sterile preparation of the skin, LA solution is injected
intradermally and subcutaneously along side of artery.
 A small nick is placed on the skin at the intended puncture site. Next arterial
catheter is checked and 3ml syringe without plunger is attached to catheter.
 20G Teflon catheter: is most commonly used. The catheter is advanced
towards the palpated artery at a comfortable angle for the operator, usually 30°-
45°. A successful puncture is confirmed by identifying a 'flush' of arterial blood
into the needle hub. Then angle should be slightly lowered and catheter is
advanced. Then needle is removed with occlusive pressure held transiently to
reduce blood loss.
 Pressure tubing is then attached to the catheter and sterile dressing applied.
Alternative sites:
 Ulnar artery
 Brachial artery
 Dorsalis pedis, posterior tibial, superficial temporal artery
 Axillary artery - long term pressure monitoring
 Femoral artery - largest artery with less risk of distal ischemia.
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COMPLICATIONS:
 Distal ischemia
 Arterial thrombosis
 Arterial spasm
 Infection
 Haemorrhage - compartment syndrome
 Retrograde arterial embolism
Arterial pressure monitoring system has number of components:

 Intra vascular catheter
 Coupling system (tubing, stopcocks, flush device)
 Transducer
 Analysis and display screen.
ARTERIAL PRESSURE WAVE FORM:

 The systolic arterial pressure wave form results from ejection of blood from the
left ventricle into aorta during systole, followed by peripheral arterial run off of
this stroke volume during diastole.
 The systolic components follow the ECG R wave and consists of a steep pressure
upstroke, peak and decline and correspond to the period of left ventricular
systolic ejection.
 The down slope of the arterial pressure wave form is interrupted by the dicrotic
notch. Then continues its decline during diastole following the ECG-T
wave reaching at end diastole.
 The dicrotic notch recorded directly from central aorta is termed incisura. It
is sharply defined and is related to aortic valve closure.
 As the arterial pressure wave travels from central aorta to the
periphery several characteristic changes occur. The arterial upstroke becomes
steeper, the systolic peak becomes higher, the dicrotic notch appears later, the
diastolic wave becomes more prominent and end -diastolic pressure becomes
lower.
CONTRAINDICATIONS:
 Local infection
 Coagulopathy
 Proximal obstruction - Such as thoracic outlet syndrome and congenital
anomalies of the aortic arch vessels.
 Reynaud’s syndrome.
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CENTRAL VENOUS PRESSURE
CVP is the pressure measured at the junction of the venacavae and right atrium. It
reflects the driving force for filling of right atrium and ventricles. CVP is an index of the
right ventricular filling pressure as it is the determinant of stroke volume.
It is highly dependent on intravascular blood volume and intrinsic vascular tone of
these capacitance vessels.
INDICATIONS FOR CVP MONITORING:

 Major operative procedures involving large fluid shift and blood loss.
 Intravascular volume assessment when urine output is not reliable or
unavailable (renal failure, urologic surgeries).
 Major trauma
 Surgical procedures with high risk of air embolism, such as sitting position
craniotomies.
 Venous access for vasoactive or irritable drugs.
 Chronic drug administration.
Seldinger technique right IJV:

I. O2 mask is applied; patient head is turned toward the left and slightly extended.
 Under aseptic precaution
 Midpoint between mastoid process and sternal attachment of the SCM is located
(depending on approach)
 IJV can be entered medial to SCM at this approach.
 Placed – Trendelenberg position (50-150) except cardiac patients
 LA is infiltrated with 1% lidocaine and needle is advanced laterally to the artery
at 300 angle to skin towards ipsilateral axilla (anterior approach) or nipple
(central approach).
 Needle is removed and catheter is inserted at same angle and depth. Blood
should be easily aspirated.
 Guide wire is advanced through catheter.
 The frequent blood sampling in patient who will not require an arterial catheter.
 Inadequate peripheral intravenous access
 Rapid infusion of intravenous fluids
 Insertion of pulmonary artery catheter
 Insertion of transvenous pacemaker.
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The sites of cannulation are:
 Internal jugular vein
 Sub clavian vein
 External jugular vein
 Femoral vein
 Basilic vein
TECHNIQUES OF VEIN PUNCTURE:
The techniques used for introducing the definitive catheter into central circulation can
be categorized into 3 basic types -
 Catheter over needle
 Catheter through needle
 Catheter over a guide wire (Seldinger) technique.
Technique through internal jugular vein (IJV):
Advantage:
1. High success rate
2. Short straight course to right atrium or sup. vena cava.
3. Easy access from head of table
4. Fewer complication than subclavian
Right IJV is preferred because -
 It leads straight into SVC
 Thoracic duct is on the left side
 The IJV is localized under the medial border of lateral head of
sternocledomastoid carotid artery is consistently deep and medial to UV.
There are three approaches:
 Middle approach: Between the two heads of sternocleidomastoid
 Anterior (high) approach; At the level of laryngeal cartilage, needle enters at
medial border of sternocleidomastoid and directed lateral to carotid A.
 Posterior approach: At intersection of EJV and lateral border of SCM. Needle
directed along posterior surface of SCM towards sternal notch. Needle is aimed
at direction of carotid A. Therefore incidence of carotid A puncture is higher.
Subclavian vein cannulation:

The subclavian vein is an important site for central venous cannulation for emergency
volume resuscitation and long term intravenous therapy.
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There are two approaches.
Infraclavicular approach: Most common technique used for subclavian vein cannulation.
Supraclavicular approach
Complications: - Pneumothorax
Subclavian artery punctures. Normal CVP = 3-10 cm of H2O
Wave forms of CVP:

The normal CVP wave form consists of 3 up word deflection. A, C, and V waves, and 2
down ward deflection X, Y descents. The waves are produced as follows.
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 ‘a’ wave is produced by right atrial contraction and occurs after 'P' wave on ECG.
 ‘C’ wave is produced due to isovolumic ventricular contraction forcing the
tricuspid valve to bulge upwards into the right atrium.
 The pressure within the right atrium decreases during ventricular systole. This is
the 'X' descent. The V wave results from rapid late systolic filling of the atrium
prior to opening of the tricuspid valve. At the end of systole.
 The y descent occurs as the tricuspid value opens and the blood from the RA
empties rapidly into RV during early diastole. Normal CVP = 3-10 cm of H2O.
CONTRAINDICATIONS:
Absolute: Superior vena caval syndrome
Relative:
 Infection at site of insertion
 Newly inserted pace maker wires
 Coagulopathies which predispose to hemorrhagic complication
 Presence of carotid disease.
COMPLICATIONS:
 Arterial puncture with hematoma
 Hemothorax
 Pneumothorax/Hydrothorax
 Chylothorax
 Nerve injury -> brachial plexus, stellate ganglion phrenic nerve which lie in close
proximity to IJV.
DIAGNOSTIC IMPORTANCE OF CVP:

 Heart rate changes, conduction abnormalities, valvular pathologies all alter the
CVP wave forms.
 A short ECG PR interval causes fusion of a and c waves.
 Tachycardia - Reduces length of diastole and duration of Y descent.
 Bradycardia - Each wave becomes more distinct.
 Atrial fibrillation - ‘a’ wave disappears and 'c' wave becomes
prominent because atrial volume is greater at end-diastole and onset of systole,
owing to the absence of effective atrial contraction.
 Junctional rhythm or isorhythmic atrio-ventricular dissociation: Alters the
normal sequence of atrial contraction prior to ventricular contraction. Instead
atrial contraction now occurs during ventricular systole; when the tricuspid
valve is closed there by inscribing a tall cannon 'a' wave in the CVP wave form.
 Tricuspid regurgitation: A broad tall systolic C-V wave is inscribed which begins
in early systole and obliterates the systolic x-descent in atrial pressure.
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 Tricuspid stenosis: The mean CVP is elevated. The ‘a’ wave is unusually
prominent and the y descent is slurred.
 Respiration: During spontaneous breathing, CVP is reduced. During positive
pressure ventilation - CVP is increased.
PULMONARY ARTERY PRESSURE MONITORING

In 1970 - Swan, Ganz and colleagues introduced the flow directed pulmonary artery
catheter.
Pulmonary artery catheter allows direct measurement of several major determinants
and consequences of cardiac performance like the preload, after load, and cardiac
output.
Specific information that can be gathered using PAC include.
 Pulmonary artery systolic pressure (PASP)
 Pulmonary artery diastolic pressure (PADP)
 Pulmonary artery wedge pressure (PAWP)
 Mixed venous oxygen saturation
 Thermodilution cardiac output
 Special PAC with continuous CO
 Continuous mixed venous oxygen saturation
 Ventricular pacing or A-V sequential pacing
 Right ventricular ejection fraction.
PAWP and PADP are measured as they provide an indirect measurement of left atrial
pressure which reflects left ventricular end diastolic pressure used as an index of left
ventricular end diastolic volume i.e., left ventricular preload.
Pulmonary artery catheterization:

 PAC can be introduced from any of the CVP cannulation sites.
 Right internal jugular vein is preferred because it provides the most direct
route to right heart chambers leading to successful catheterization.
Indications for PAC monitoring:

 Major surgical procedures involving large fluid shifts or blood loss in patients
with coronary artery disease.
 Surgery of aorta requiring cross-clamping.
 Procedures requiring cardio-pulmonary bypass
 Recent myocardial infarction or unstable angina
 Hemodynamically unstable patients requiring ionotropes or IABP.
 Patients with poor left ventricular function (congestive heart failure)
Patients in hypovolemic, cardiogenic or septic shock or with multiple organ failure.
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Relative:
 Patients with right heart failure, COPD, pulmonary hypertension or pulmonary
embolism.
 Patients requiring high levels of PEEP
 Hepatic transplantation
 Patients with massive ascites requiring major surgery.
CONTRAINDICATIONS:
Absolute:
1. Tricuspid and pulmonary valvular stenosis.
2. Right atrial or right ventricular masses (tumor or thrombus) - The catheter may
dislodge a portion of mass causing pulmonary or paradoxical
embolization.
3. Tetralogy of fallot.
 Severe arrhythmias
 Coagulopathy
 Newly inserted pacemaker wires.
Catheters:
 The standard PAC has 7.0, 7.5 or 8.0 French circumference and in 110 cm in
length with the distances marked at 10cm intervals.
 Heparin bonding reduces the thrombogenecity.
 Latex balloon is fastened 1-2 mm from the catheter tip.
 PA catheters are available in wide varieties.
 Double lumen  For balloon inflation and PA pressure
 Triple lumen  II + RA pressure
 Quadruple lumen  III + thermistor for thermodilution
 CO measurement.
 Five lumen -> additional lumen for drug infusion.
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Right atrium:
 CVP wave form has a, c, v waves and x-y descent.
 Right ventricle: increase systolic pressure, wide pulse pressure, and low
diastolic pressure (RVSP  17-30 mm Hg) = PASP (except pulmonary stenosis
with RV outflow). Right ventricular diastolic pressure in equal to right atrial
pressure when tricuspid valve is open except in tricuspid valve disease.
 Pulmonary artery: step-up diastolic pressure, systolic pulmonary Art pressure
 right ventricular systolic in the absence of pulmonary .valve disease.
 PAWP: Indirect management of pulmonary venous pressure and left atrial
pressure it is identified as a venous pressure trace with a and v waves and x – y
descent .PAWP  2-12 mm Hg.}
Technique:
 The balloon should always be inflated with air using the volume limited 1.5ml
syringe provided. The air filled balloon at the tip of catheter serves following
function.
1. It prevents the tip of the catheter from contacting the right ventricular wall
during passage and hence reduces the incidence of arrhythmias during insertion.
2. It acts to flout the catheter into the PA.
3. Inflation of the balloon allows the measurement of PCWP.
The PAC is inserted through the cannulation site till the PAC lip is in the venacava or
right atrium. The balloon is now inflated, the catheter is attached to a pressure
transducer and the catheter advanced into the right atrium, through the tricuspid valve
into the right ventricle, through the pulmonary valve into the pulmonary artery and
finally into the wedge position.
 Characteristic waveforms from each of these positions confirm proper catheter
passage and placement.
 After PAWP is measured, balloon is deflated, and PAP wave form should
reappear.
The approximate distance (cm) of chamber location from venous insertion sites:
Insertion site Rt. atrium Rt.-ventricle Pulm. artery
Right IJV 20 30 45
Left IJV 25 35 50
Rt. ante cubital vein 50 65 80
Femoral vein 40 50 65
Subclavian vein 10 25 40
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PHYSIOLOGIC CONSIDERATION:
The PAC allows estimation of It. sided ventricular pressure from catheterization of the
right side of heart. At the end of diastole, the aortic and pulmonary valves are closed and
the mitral valve is open. Thus a continuous fluid chamber is created from the pulmonary
artery to aortic valve.
Therefore at equilibrium during end ventricular diastole. The pressure relationship are
–
PAEDP  PAOP  PVP ~ LAP  LVEDP
PAEDP : Pulmonary artery end diastolic pressure
PAOP : Pulmonary artery occlusion pressure
PVP : Pulmonary venous pressure
LAP : Left atrial pressure
LVP : Left ventricular pressure
LVEDP : Left ventricular end diastolic pressure
COMPLICATIONS:
PAC monitoring complication can be divided into -
1. Those associated with attempts to gain venous access
2. Those occurring during PA catheterization
 Arrhythmias - supraventricular arrhythmia, atrial fibrillation VT, VF, RBBB,
complete heart block.
 Misplaced catheter lip
 Air embolism.
Late complications associated with catheter residence
 Mechanical problems - catheter entrapment, coiling knotting, balloon rupture.
 Thrombosis, pulmonary embolism
 Thrombocytopenia
 Pulmonary infarction
 Infection – endocarditis
 Structural damage
 Endocardium, rricuspid valve, pulmonary valve.
 Pulmonary artery rupture, pseudoaneurysm.
Those associated with misuse of equipment and misinterpretation of data.
Condition resulting discrepancies between PCWP and LVEDP:
1) PCWP > LVEDP:

1. Positive- pressure ventilation,
2. PEEP
3. Increase intrathoracic pressure
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4. Non wet lung zone III PAC placement
5. COPD
6. Increase pulmonary vascular resistance
7. Left atrial myxoma.
8. Mitral valve disease (MS/MR)
2) PCWP < LVEDP:

1. Non compliant LV (Ischemia,hypertrophy LV)
2. AR (premature closure of MV)
3. LVEDP > 25 mm Hg.
Left atrial pressure:

Indications: Cardiac surgery, diagnostic cardiac catheterization.
Technique: Direct placement through right superior pulmonary vein & brought out
through the skin below the xiphoid process.
Others:
1. Retrograde arterial approach.
2. Trans-septal venous catheterization.
3. Percutaneous direct left atrial puncture.
Wave form: Normal LAP  CVP or RAP although these one changes ‘a’ wave appears
slightly later than right.
 Left side v wave is taller than the ‘a’ wave.
 a & c waves merge into composite a-c wave.
Directly measured data:
Normal intracardiac pressure (mm Hg)

Type Mean Range
Right atrial pressure 5 1-10
Right ventricular end systolic end diastolic pressure 25 15-30

5 0-8
Pulm. arterial systolic / diastolic pressure 23 15-30

9 5-15
Mean pulmonary arterial pressure 15 10-20
Pulmonary capillary wedge pressure 10 5-15
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Left atrial pressure 8 4-12
Left ventricular - end diastolic pressure 8 4-12
Left ventricular systolic pressure 130 90-140
DERIVED HAEMODYNAMIC PARAMETERS:

Formula Normal value
CI = CO/BSA 2.8-4.2 1/min/m2
SV - CO. 1000/ HR 50-110 ml/beat
SI - SV/BSA 30-65 ml/beat/m2
 PCWP)xSI
1 .3 (MAP
6 45 - 60 g/mm2
LVSWI =
100
1 .3 6(P AP CVP ) xS I 5-10 g/mm2
RVSWI =
100
(MAP  CVP) x 8 0 900-1400
SVR =
CO dyne/sec/cm5
(PAP  PCWP) x 80 150-250 dyne/sec/cm5
PVR = (PAP - PCWP) X 80
CO
CI = cardiac index,
SV = stroke volume
SI = stroke index
LVSWI = left ventricular stroke work index
RVSWI = right ventricular stroke work index
CO = cardiac output
BSA = Body surface area
MAP = mean arterial pressure
SVR = systemic vascular resistance.
PVR = pulmonary vascular resistance.
Other methods of cardiac output:

1. Direct Fick method.
2. Indicator dilution method.
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 Direct Fick method:
States that the amount of a substance taken up by an organ per unit of time is
equal to the arterial level of substance minus the venous level (A – v difference)
times the blood flow.
O consumption
Output of left ventricle = 2
[AO 2 ]  [VO 2 ]
= = 25ml/min
Indicator dilution method:

Amount of substance such as dye, or more commonly, a radioactive isotope is
injected into an arm vein and the concentration of the indicator in serial samples of
arterial blood in determined.
The output of heart is equal to the amount of indicator injected divided by its
average concentration in arterial blood after a single circulation through the heart.
CARDIAC OUTPUT
Apart from pressure monitoring, an important feature of PAC is its ability to measure
cardiac output using thermodilution method.
Cardiac output is the total blood flow generated by the heart and in a normal adult
ranges from 4.0 to 6.5 1/min.
Measurement of CO provides a global assessment of circulation.
The modified Stewart - Hamilton equation is used to calculate cardiac output.
Q = (TM B T 1).K Where,

 ΔT (t)dt
B Q = Cardiac output (L/min)
O
TB = Blood temperature
m T1 = Injectable temperature
 ΔT (t)dt
o
B K = Computation constant
= integral of temperature change over time.
CONTINUOUS THERMODILUTION CARDIAC OUTPUT MONITORING:

 New technologies allow near continuous cardiac output monitoring using either
hot or cold thermal indicators. The hot thermal technique is more widely
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accepted and involves the release of small quantities of heat from a 10cm
thermal filament incorporated into the right ventricular portion of a PAC.
 The displayed value is updated every 30 sec and represents the average cardiac
output over the previous 3-6 minutes.
CONTINOUS MIXED VENOUS OXIMETRY:

Rearrangement of FICK EQUATION reveals four determinants of mixed venous oxygen
saturation.
VO2
SV O2 = Sa O2 - Q.1.36.Hb
Where,
 SVO2 = Mixed venous O2 saturation (%)
 SaO2 = Arterial oxygen saturation (%)
 VO2 = Oxygen consumption (ml O2/min)
 Hb = Hemoglobin concentration (g/dl)
 Q = Cardiac output (dl/min)
Monitoring this variable provides more comprehensive information about the balance
of oxygen delivers' and consumption by the body. Not just cardiac output, but also the
adequacy of cardiac output.
TRANSOESOPHAGEAL ECHOCARDIOGRAPHY:
Physical principle:
 Ultrasound is sound which cannot be heard by the human ear [2.5 to 7.5 million
cycles per sec (MHz)].
 Echocardiography involves intermittent pulses of ultrasound waves with a
frequency of 2.5 10 7.5 million cycles per second (MHz) generated by a
transducer consisting of piezoelectric crystal’s.
 When these waves travel through the soft tissues of differing densities, they are
partly absorbed, partly reflected and partly scattered. The reflected ultrasound
echo waves are received by the crystal, converted into electric impulse and
displayed on a Television screen.
 No ionizing radiation is used in echocardiography and no adverse effects of
ultrasound have been demonstrated in humans.
 Transthoracic echocardiography examination is often limited by the presence of
limited acoustic windows due to the Presence of obstacle to ultrasound the form
of bones and lung. Esophageal window to TEE results in its close proximity to the
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heart separated only by soft tissues of the mediastinum and thus has advantage
of close field, high resolution imaging.
M-Mode (motion mode):

 It is the most basic form of ultrasound imaging.
 A one - dimensional view of cardiac structures produced by a single beam of
ultrasound requiring skill full interpretation.
 Used to view rapidly moving structures like valve leaflets.
2D / brightness mode:
 It creates a 2 dimensional image of fan shaped section of the heart providing an
enormous advantages in identifying anatomic and pathologic land marks.
 Images are displayed in real time.
Doppler:
 By measuring Doppler shift, modern ultrasonograph quantify blood flow
velocities.
 The Doppler shift is the shift in frequency of a wave, when the source of the wave
is moving (Moving Red blood cells).
Pulsed - wave Doppler:

 A single transducer sends out repetitive short bursts of ultrasound at a specific
pulse repetition frequency.
 P-W Doppler defines blood flow velocities and their location within the heart and
great vessels.
Continuous wave Doppler:

 Uses two separate transducers, one to emit ultrasound continuously and one to
receive it continuously.
 It cannot precisely determine the location of moving target, very useful to obtain
hemodynamic information.
Colour Doppler:
 Displays blood flow in colors, in real time. While also showing the 2D image in
black and white.
 In addition to location, direction and velocity of blood flow, it also estimates flow
acceleration and differentiates between turbulent and laminal flow.
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Equipment:
 The commonly used TEE probe has a 5 MHz transducer mounted on the tip of a
gastroscope.
 Two knobs are present at the handle, the big knob allows flexion / Extension of
the probes tip and other is for side to side motion.
INDICATIONS/PRACTICE GUIDELINES:
ASA task force 1996 divided indications for intraoperative TEE into 3 categories.
Category I Indications:
These indications are supported by strong evidence and expert opinion that TEE is
indicated, very useful and will improve the clinical outcome.
 Hemodynamically life threatening intraoperative and ICU disturbances.
 Valve repair surgery
 Congenital heart surgery
 Infective endocarditis
 Hypertrophic obstructive cardiomyopathy repair surgery.
 Thoracic aortic aneurysm/dissection in unstable patients.
 Aortic dissection with aortic valve involvement repair surgery.
 Pericardial window procedures.
Category II Indications:
Weaker evidence and less expert opinion that TEE will improve outcome.
Category III Indications:

There is little scientific support or expert opinion that TEE will improve outcome.
In General the Indications are:

 Evidence of depressed myocardial function
 Risk of myocardial ischemia.
 Patients with CAD/Angina/documented ischemia/past or recent MI/Cardiac
morbidity in previous surgery.
 Monitoring for intracardiac air.
o Open heart surgery
o Venous air emboli - Sitting position during surgery
o IVC surgery.
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CONTRA INDICATIONS:
 Esophageal stricture
 Esophageal mass/malignancy
 Massive varices
 Previous esophageal surgery
 Undiagnosed active 01 bleeding.
Complications:
Serious complications are rare:
 Oesophageal injury
 Vocal cord paralysis
 Dysryhtmias
 Hypotension
 In infants TEE probe may obstruct airway distal to ETT, and compressing
descending aorta.
Minor complications are more common:
 Oral and pharyngeal injuries.
PROBE INTRODUCTION:
 Once patient is anesthetized and the trachea is securely intubated, the contents
of stomach are suctioned. Then the patient’s neck is extended and the well
lubricated TEE probe is introduced into the midline of hypopharynx.
 Usually, with minimal force, the probe will pass blindly into the esophagus. If the
probe does not pass blindly, a laryngoscope is used to lift the larynx anteriorly,
and the probe is placed into the patient’s esophagus under direct vision.
BASIC EXAMINATION:
 The basic examination should include all the classic views both horizontal (O
degrees) and vertical (90 degrees) and off-axis view (0-180") if a multi plane
probe is used. The standard cross-sections used most often during intra
operative TEE includes the following as the probe is advanced in the esophagus.
 Basal short axis view of pulmonary artery: Bifurcation and aorta - This image
is good for pulmonary artery investigation and cardiac output measurement.
 Basal short axis view through the LA: Visualization of LA appendage and
pulmonary veins is possible.
 Coronary artery view: Coronary arteries and RA appendages can be visualized,
pulmonary vein can also sometimes be visualized.
 When the probe is advanced further the aortic valve is visible and the different
cusp can be examined.
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 Further advancement of the probe will show a 5 chamber long axis view of the
heart. The 5th chamber is the LV outflow tract.
 The aortic valve, mitral valve leaflets, papillary muscles and parts of RV and RA
can be examined.
 A little further down with mild retroflection of the probe shows the classical 4-
chamber view of the atria and ventricles, extreme retroflection will show the
coronary sinus.
 Advancement of probe into the stomach will show the transgastric short axis
view. Which is good for evaluation of mitral valve (‘fish mouth view’)and a little
further down LV function and wall motion abnormalities can be noted (mid
papillary short axis view).
 Further advancement of the probe with extreme flexion will display the deep
transgastric view.
 From the 4 chamber view, the probe can be rotated anti-clockwise to visualize
the descending thoracic aorta.
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Chapter 23 - WAVES IN ECG
P-Waves:
 Atria fibrillation: P replaced by small irregular waves.
 Atrial flutter: flutter waves (saw tooth).
 Junctional rhythm: just precedes or buried in QRS complex.
 Ventricular tachycardia: Buried in QRS complex .
 Hyperkalemia :> 5.1 mEq/Lt:
o P wave reduced in amplitude or absent. Associated with tall t-wave and
widened QRS complex.
 Inverted p-wave: WPW syndrome (retrograde activation) (accessory pathway
by -passing AV node).
 Tall p-wave ‘P’ pulmonale > 2.5 mm height  right atrial enlargement.
 Broad p wave ‘P’ mitrale  2.5 mm (width)  left atrial enlargement
Pathological Q wave MI, [> 0.04 sec > 25% (R wave)].
And also in severe angina, hypoxia, hypothermia, small infarct (Rt vent infarct &
post. Wall infarct)  absent Q wave.
Q – Wave + ST segment elevation recent MI.
Q wave without ST segment (or T wave changes) old infarction.
4-6 hrs after infarction  Q wave appears.
R – wave:
QS (V1, V2) QR (V5, V6)
Non progressive  mycardial disease,LVH, LBBB,
Tall R – wave > 4 mm in V1 RVH, RBBB, WPW syndrome.
> 25 mm in V6 LVH, LBBB.
Right ventricular hypertrophy:

1. Tall R-wave,
2. Right axis deviation
3. ST segment depression
4. T-wave inversion in V1, V2 associated with right atrial enlargement  ‘P’
pulmonale
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RBBB: Dominant deflection in V1 is upright,
QRS complex wide deflection,
RSR1 configuration. R1 means delayed right ventricular activation. {Seen in V1}
Left ventricular hypertrophy:

 Tall R wave in V5 V6
 Left axis deviation
 ST– segment depression and T wave inversion in V5 V6
 With left atrial enlargement  ‘P’ mitrale Wide QRS complex: (>0.08 sec): RBBB,
LBBB, hyperkalemia, cardiomyopathy, WPW syndrome.
LBBB: M shaped on QRS complex wide – V6
RSR! Complex is followed by S-T segment depression and T wave inversion.
T-wave:
Inversion heavy meals, smoking, anxiety, hyperventilation, tachycardia, bundle
branch block, ventricular hypertrophy, hypokalemia, cardiomyopathy, myocarditis,
pericarditis, pericardial effusion.
Tall T-wave: Hyperkalemia, Myocardial ischemia (hyperacute infarction)
U wave:
 upright, smaller than T-wave, (appreciated in V2 – V4).
 Prominent U wave  hypokalemia, drugs  digitalis, quinidine, amiodarone.
 Inverted U wave: MI, LV systolic overload, left ventricular dysfunction.
P-R segment:
Depression: Atrial enlargement & infarct. Acute pericarditis.
S-T segment-
Depression:> 0.5 mm Heavy meal, smoking, anxiety, hyper ventilation, ventricular
hypertrophy, bundle branch block, WPW, hypokalemia, digitalis.
ST–segment:
Elevation: MI, Prinzmetal angina, Post infarction syndrome, Acute pericarditis.
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Prolonged P-R interval:
1) Athletes
2) Rheumatic fever
3) Diphtheria
Shortened P-R interval:

1) Junctional rhythm.
2) WPW syndrome
Shortened QT interval:
1) Hyperkalemia.
2) Hyperclacemia
Prolonged QT interval:
1) Hypocalcemia.
2) MI, head injury, cerebral haemorrhage.
3) Mitral valve prolapses.
MI: ST segment elevation  injury
Q wave  infarction ST↑ subepicardial
T wave inversion ischaemia ST↓ sub endocardial
Hypocalcemia < 4.5 mEq/L.

1. ST – segment lengthening
2. QT prolongation.
Hypercalcemia > 5.3 mEq/L

1. Shortening of ST segment
2. Shorten QT interval
Hypomagnesaemia ≈ Hypokalemia<1.5mEq/L
Hypermagnesemia ≈ Hyperkalemia > 2.5 mEq/L
Hypokalemia: (<3.5 mEq/L ):
1) low T wave. 2) Prominent U wave. 3) Prolonged P-R interval.
Torsade – de pointer is a unique variant of VT in which the QRS complexes appear to
twist around the baseline.
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Chapter 24 - NON INVASIVE METHODS TO ASSESS
VENTRICULAR FUNCTION
Over the past decade, the number of new techniques available to assess and
monitor the patient with circulatory failure has increased dramatically. Some of these
techniques are widely available, inexpensive, portable, and simple to use, others are
available in a few centers, require expensive stationary equipments and trained
technicians or present special hazards like radiation.
With recent developments in echocardiography and computing power, non
invasive methods offer hope of continuous monitoring of ventricular function with
minimum danger or complications.
Cardiac Rhythm:
Electrocardiogram: ECG is the echocardiography and computing power, non invasive
methods offer hope of continuous monitoring of ventricular function with minimum
danger or complications.
Precordial or esophageal stethoscope also can be used for this purpose.
Mechanical Function of the Ventricles and Peripheral Vascular System

 Heart sounds: Monitored continuously using a precordial or esophageal
stethoscope, we can get some crude estimation of cardiac output from such
monitoring. Loudness of 1st heart sound is correlated with the force of
contraction of the ventricles. So it gives information regarding the stroke volume.
11nd heard sound gives some information about the after load.
 Arterial pressure: Many methods are there for measurement of arterial blood
pressure noninvasively.
a. Auscultation of 1st and 4th Korotkoff’s sounds.
b. Palpatory method.
c. Doppler ultrasound techniques.
Oscillometry technique:
Provided there is no mechanical obstruction to ventricular outflow, arterial
systolic pressure is same as the peak systolic pressure in the ventricle and is an index of
the force of contraction and hence stroke volume.
Arterial diastolic B.P. gives an estimate of the after load or impedence to
ventricular ejection. Since myocardial blood flow occurs mainly during diastole,
diastolic pressure, gives idea about myocardial perfusion pressure.
The product of systolic pressure (in mm of Hg) and heart rate (beats / min)
known as rate pressure product correlates with myocardial O2 consumption.
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CVP:
CVP is a reflection of the ability of the right heart to cope with venous return at the
moment of examination. For non invasive measurement of CVP an ultrasound probe is
placed over the external or internal jugular vein. The venous flow is usually heard as a
“hum”, where as the arterial flow signal has a pulsatile nature to it. The airway pressure
is then raised either by asking the patient to blow into a manometer or in case of the
anesthetized patient, by squeezing the reservoir bag of circuit. The CVP roughly
corresponds to the airway pressure at which Jugular venous flow ceases.
A sudden elevation of CVP associated with a decreasing cardiac output or a
decreasing arterial pressure is a sign of acute ventricular failure or tamponade.
Cardiac output:
Non invasive technique to measure cardiac output includes:-
Doppler Cardiac Output Measurement: Out of the non invasive techniques, this is the
most practical and reproducible method. A probe which emits as well as receives sound
waves of frequencies between 2 M Hz and 10 MHz is directed towards the descending
aorta either across the esophagus or through the suprasternal notch. The emitted sound
waves are reflected by red cells, which are moving away from the receiver. Frequency of
the reflected sound is less then the frequency of emitted sound. This frequency shift is a
function of the velocity of the red cells and the blood flow velocity is easily measured.
---------------------------------------------------------------------
Flow (ml/s) = Flow velocity (cm/s) X Cross Sectional area of aorta (cm2)
--------------------------------------------------------------------
Cross sectional area of aorta is usually derived from the patient’s height, weight and
body surface area using a monogram or formula. Currently, devices are available for
continuous monitoring of cardiac output which works on the Doppler principle.
Instead of descending aorta, flow velocities can be measured at the mitral annuals or left
ventricular outflow tracts by a transoesophageal ultrasound probe.
a. Cardiac output by gas exchange analysis.
b. Roentgen densitometry cardiac output.
c. Echocardiographic (M mode echo) estimation of cardiac output.
Echocardiographic Estimation of Left Ventricular Size, Function and Regional Wall

Motion.
a. Measurement of left ventricular volume and function.
b. Analysis of left ventricular regional wall motion abnormalities.
c. Determination of stroke volume and cardiac output.
d. Estimation of left ventricular filling pressures.
e. Determination of intra cardiac shunts.
f. Detection of pericardial effusion.
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g. Estimation of pulmonary artery pressure.
M MODE ECHOCARDIOGRAPHY: M mode (“Motion”) echocardiography (MME) is the

study of cardiac structures moving in one plane, forward and away from the transducer
with time. a piezo electric crystal is used for the production of a beam of sound waves to
come back after reflection is a measure of the depth of the structure.
The most important limitation of MME is its singular ‘ice-pick’ view of the heart,
which permits visualization of only a small part of my chamber at a time.
TWO DIMENSIONAL (2D) ECHOCARDIOGRAPHY: It overcomes most of the limitations
of MME, instead of emitting an ice-pick of sound waves the 2DE transducer emits a
wedge shaped 30 to 90 degree plane of sound waves. The motion of structures is
recorded at 30 frames per second as movement way and toward the transducer as well
as one dimension perpendicular to it.
Left ventricular cavity usually assumes the approximate shape of a polate ellipse,
with 3 planes one long axis and two short axes. A transoesophageal probe various
stages of cardiac cycle (left ventricular systolic diameter (LVIDs) and left ventricular
diastolic diameter (LVIDd).
The fractional shortening of left ventricle measure the extent of left ventricular
contraction along the micro axes.
100 X (LVIDd – LVIDs)
%SF =
LVIDd
The mean velocity or circumferential fiber shortening (VCF) is the ratio of LV

fractional shortening to ejection time (ET).
VCF = % SF / ET
Left ventricular volume can be calculated using 2D echocardiography. Using a 4
chamber image the LV endocardial surface may be traced and the area obtained by
planometry. The length of the LV major axis is measured and a regression equation
applied to calculate LV volume.
Ejection fraction (EF) is the fraction of the EDV that is ejected during each
systole.
EF = EDV-ESV
EDV
This is a very good index of left ventricular function. Regional wall motion
abnormalities are usually, seen after myocardial infarction. Abnormal wall movements
indicates poor ventricular function.
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Flow Pattern Using Colour Doppler:
Direction of flow of blood can be detected using Doppler principle. By noting the
frequency shift, the device detects whether the flow is towards the receiver (displayed
in red color) or away from the receiver (blue). Such colour flow imaging is very useful
for quantitative assessment of abnormal flow patterns that occur across incompetent
valves or septal defects.
Radio Nucleide Imaging

Radio isotope evaluation of ventricular function includes:-
a. Analysis of ventricular function-by labeling the blood pool within a chamber.
Technicium 99m pertechnetate (99m Tc) is the commonly used radio isotope,
which is given intravenously and radioactivity within the cardiac chambers
detected using a scintillation camera. The intensity of radioactivity is
proportional to the volume of blood in the chamber.
b. NUCLEAR CARDIAC PROBE (NUCLEAR STETHOSCOPE): This is a new tool in
radio-nucleide cardiac imaging, provides a continuous beat by beat analysis of LV
function.
Myocardial imaging – using Thallium 201, helps diagnosis and sizing of acute
myocardial infarction and diagnosis of coronary artery disease on the basis of
perfusion defects which appear during resting studies or following exercise.
99m Tc concentrate is zones of ischemic or infracted myocardium and display
“hot spots”.
Myocardial Metabolic State

Metabolic derangements such as ischemia and electrolyte abnormalities
affect the mechanical function of the heart. ECG has been used to detect these
derangements. A two lead system consisting of lead 11 and V chest lead has been
advocated for detecting ischemia. Elevation or depression of ST segment greater than
1mm and lasting longer than one minute is indicative of ischemia.
Computer aided ST segment analyzer facilitates detection of ischemia easier.
Problems in patient with complete heart block coming for

surgery:
1. Complete heart block is a condition in which conduction of impulses from atria
to ventricles is completely blocked and the ventricular rate is controlled by an
abnormal pacemaker situated in the AV node, the bundle of his or directly in the
purkinje fibres.
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2. These patients are on temporary or permanent pacemakers. Patients with
complete heart block are on permanent pacemaker and are due to fibrosis of
conduction system.
3. Permanent pacemaker are of three types
– A synchronous pacemaker
– Synchronous pacemaker
– Sequential pacemaker
Asynchronous pacemakers produce an impulse which is independent of the intrinsic
cardiac electrical activity. There is a potential risk if the pacemaker fires during
repolarization after a normal complex.
Synchronous pacemakers may be triggered by a normal ventricular complex
(discharging during the absolute refractory period to avoid the risk of dysrrhythmias)
or inhibited by a normal ventricular complex or may be triggered by the P wave.
Sequential pacemaker stimulates the atria to contract, followed after a suitable period
by ventricular stimulation. If a normal ‘P’ wave occurs, but is not conducted normally,
ventricular contraction is stimulated.
Generic code for identification of pacemaker:

First letter Second letter Third letter Fourth letter
Cardiac chamber Cardiac chamber Response functions
paced where electrical programmable
activity sensed
V – ventricle V T – triggering
A – atrial A I – inhibited
D – dual O – none O – none
(asynchronous) (asynchronous)
Pacemaker may be unipolar (one electrode on the myocardium & the second distant
from the heart) or bipolar (both on the myocardium).
Preoperative evaluation:
Before anesthetizing a patient with permanent pacemaker anesthetist should know.
1. Whether a synchronized or asynchronous pacemaker has been inserted.
2. Whether – the pacing threshold has changed.
3. What power source is in use.
a) 20% of patients have a large threshold increase each year and present a risk of
developing heart block of the threshold is increase further in anesthetic drugs.
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b) Power Failure may be indicated by a reduction of 10% or more the original rate at
which the pacemaker fired on a very rapid rate.
c) A history of palpitation or dizziness and syncope vertigo suggests that the pacemaker
is failing to make the ventricles contract
d) Ventricular triggered or ventricular inhibited synchronous pacemaker must be
checked to ensure that the ventricles capture an impulse either by slowing the intrinsic
rate by some measures such as Valsalva maneuver or carotid sinus massage or by using
a magnet to convert these to asynchronous pacing.
e) Increase in threshold produced by thiopentone results in few practical problems and
can most of anesthetist can be used successfully.
ECG – evaluated to confirm 1:1 capture.
CXR – confirming for absence of pacemaker electrodes breakage.
f) Suxamethonium: Can alter the intracellular / extracellular K+ ratio, increases the risk
of ventricular dysrrhythmias, muscle fasciculation has caused malfunction of unipolar
pacemaker, hence inhibition of fasciculation by predisposing with small dose of non-
depolarizing blocker are recommended.
g) Regional anesthesia has been recommended but the risk of complication is not
reduced.
h) Monitors: - Pulse oximetry
- ECG
- Fluid, electrolyte
- Acid base balance
i) Myocardial excitability increases if ischemia is present, and factors which increases
the risk of ischemia should be avoided.
j) Surgical diathermy interferes with synchronous unipolar pacemakers.
Continuous diathermy converts them to asynchronous mode and inhibit their function,
thus diathermy plate should be placed as far away as possible from the pacemaker. The
use should be restricted to a 1second to not more than 10 sec.
As asynchronous pacemakers are not affected, synchronous is connected to
asynchronous by activation of magnetic switch before diathermy.
k) In infusion of isoprenaline should be available in case of pacemaker failure.
(Preoperative chest x-ray taken to know the correct position of pacemaker, and to
known any break in it etc.)
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Anesthetic management of patients with artificial cardiac
Pacemakers:
1. Continuous monitoring of ECG.
2. Continuous monitoring of peripheral pulse.
3. Electrical defibrillator.
4. Electrical converter magnet.
5. Drugs (atropine, isoprenaline).
Anesthesia for pacemaker insertion:

– A functioning transvenous artificial cardiac pacemaker should be in place / or
non-invasive transcutaneous cardiac pace maker.
– Drugs (Atropine, isoprenaline) available before induction.
– Insisted intravenously (endocardial lead)
– Subcostal approach (epicardial or myocardial lead).
Indications:
a. SA node dysfunction “sick sinus syndrome”
b. AV heart block (follows CPB)
c. Neurogenic syncope
d. Cardiomyopathy.
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Chapter 25 - PAROXYSMAL NOCTURNAL DYSPNOEA
(PND)
I. Definition:
This is an acute attack of breathlessness and cough occurring at night which may arouse
the patient from sleep.
Relief is obtained by sitting up and often by finding an open window.
II. Mechanism underlying (PND):

1. Pulmonary vascular congestion due to increased venous return to the heart
during sleep i.e. in supine position.
2. Blunting of respiratory centre response to sensory input from the lung during
sleep.
3. Reduced adrenergic stimulation of myocardium at night resulting in further
impairment of myocardial function.
III. Diagnosis:
a. X-ray  shows distension of pulmonary veins in the upper lobes of the lungs.
– Perihilar and hilar haze.
– Edematous interlobar septa.
a. Pulmonary capillary pressure  increased
b. LVED pressure  increased.
c. Left atrial pressure  increased.
Radiographic pattern of pulmonary congestion may persist for 1-4 days after
normalization of cardiac filling pressures.
PND is one of the signs of CCF.
Differential diagnosis:
– Anxiety provoked hyperventilation.
– Wheezing due to accumulation of sections in patients with chronic bronchitis
Treatment:
 Head up position.
 Humidified O2 by face mask.
 Injection morphine 5-10 mg to decrease venous return to heart.
 Injection Furosemide 10-40 mg IV.
 Further
o Inotropes
o Mechanical ventilation
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Chapter 26 Endocardial viability ratio
Ratio between diastolic – pressure time index (DPTI) and tension time index
(TTI) is called endocardial viability ratio.
Normally it is 1 or more.
Ratio less than 0.7 indicate subendocardial ischemia.
 DPTI  Measure of blood flow to the left ventricle
= Coronary perfusion pressure x diastolic time.
 TTI  Measure of O2 demand.
o = Systolic BP and systolic time.
 Endocardial viability ratio can be useful in evaluating O2 supply and demand
balance.
 Myocardial O2 demand is the most important determinant of myocardial blood
flow.
 Relative contribution to O2 requirements includes.
– Basal requirement - 20%
– Electrical activity - 1%
– Pressure work - 64%
– Volume work - 15%
Myocardium normally extracts 65% of O2 in arterial but while other tissues extract only
25%. Therefore myocardium cannot compensates for decrease in blood flow by
extracting more O2 from Hb. Any increase in myocardial metabolic demand must be met
by an increase in coronary blood flow.
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Factors affecting myocardial O2 supply and demand balance.
I) DECREASE O2 SUPPLY INCREASE O2 DEMAND
Decrease coronary blood flow Tachycardia
Tachycardia Increase wall tension (↑preload & after
load )
Hypotension (diastolic) Increase myocardial contractility
Increase preload Hypertrophy
Hypocapnia (coronary vasoconstriction) Shivering
Coronary artery spasm HTN
II) DECREASE O2 CONTENT  Increase metabolic status
AVAILABILITY
Anemia Increase stress (surgery)
Hypoxemia Exercise
Decrease O2 release from Hb
Increase pH
Decrease, DPG
Decrease temp
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Chapter 27 CARDIAC PULSE GENERATORS,
DEFIBRILLATORS AND CIRCULATORY ASSIST DEVICES
Introduction:
Congestive Heart Failure (CHF) is a clinical syndrome defined as chronic,
inadequate myocardial contraction and relaxation that results in decreased cardiac
output (CO). Severe cardiac failure may be seen in the setting of,
 Post cardiopulmonary bypass.
 Advanced valvular heart diseases.
 Advanced cardiomyopathies
 Secondary to congenital heart diseases (CHD)
 Ischemic heart disease (massive MI)
 Conduction abnormalities (Idiopathic or acquired)
 Following trauma.
Primary medical therapy for CHF has always been pharmacologic and the
armamentarium available to us has grown during the past 40 years from digitalis and
mercurial diuretics to the current more potent  blockers, ACE inhibitors, aldosterone
receptor blockers, ionotropes and including cardiac resynchronization therapy by the
way of pacemakers and implantable cardioverter defibrillators (ICDS).
CARDIAC PULSE GENERATORS:

 Any rhythm other than normal sinus at an appropriate rate may be associated
with cardiac dysfunction or failure and such rhythm is termed as arrhythmia.
 Arrhythmias produce mechanical cardiac dysfunction due to bradycardia,
tachycardia or improperly synchronized atrio-ventricular contraction.
Treatment of arrhythmias with drugs / devices is indicated in case of
hemodynamic imbalance resulting from it.
 Initial treatment of arrhythmias is often with drugs, but this may not be ideal
given the disadvantages of drug therapy.
Disadvantages of drugs as treatment for cardiac arrhythmias:

Pro-arrhythmias Delayed onset of action
Untoward side effects Too long duration of effect
Myocardial depression Effects not easily reversed
Preload / after load reduction Associated toxicity
Ineffective or partially so Adverse drug interactions
Difficult to titrate the effect Bradycardia / excess tachycardia
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 Electroversion and temporary pacing are attractive options for the perioperative
arrhythmias management, because these arrhythmias are often the result of
transient imbalance and anti-arrhythmic or adjuvant drugs have recognized
potential to compound the imbalance further.
Advantages of electrical treatment compared with drugs as initial treatment for
perioperative arrhythmias
o Institute or terminate treatment at will
o Immediate and easily titrable effect
o Precise control of heart rate is possible
o No vasodilatation or myocardial depression
o Pro-arrhythmias are less likely than with drugs.
o Avoid adverse drug effects and interactions
 Cardiac pacemakers (1958) and ICDs (1980s) have revolutionized the treatment
of cardiac arrhythmias. Since implantation of the 1st pacemaker in 1958, cardiac
device therapy has been a steady expansion, this is mainly attributed to
phenomenal progress in device technology and software sophistication.
 With advancement of pacemaker technology and sophistication in their
therapeutic spectrum, there has come a need to change the nomenclature of such
implantable electric therapy devices. These permanently implantable cardiac
pacemakers or any ICD devices have been referred to by the recent American
society of anesthesiologist (ASA) advisory as “cardiac rhythm management
devices (CRMDs).
PACE MAKERS:
Design: Electronic cardiac pacemakers may be temporary or permanent (implanted)
devices that electrically stimulate the heart and they consist of an impulse generator,
circuitry with leads for sensing / regulation of the stimulus.
Generic pace-maker codes (NASPE /BPEG code):
To understand the language of pacing, it is necessary to comprehend the coding
system that was developed originally by the international conference on heart diseases
and subsequently modified by the NASPE / BPEG (North American society of pacing and
electrophysiology, British pacing and electrophysiology group).
 The five positions of the generic code refer to the order of the programmed
settings on the pacemaker.
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NASPE-BPEG FIVE-POSITION PACEMAKER CODE
I II III IV V
Pacing Sensing Response Programmability Tachycardia
0 – None 0 – None 0 – None 0 – None 0 – None
A – Atrium A – Atrium I – Inhibited C – Communicating P – Pacing
V – Ventricle V – Ventricle T – P† – Simple S – Shocks
Triggered Programmable
D – Dual D – Dual D – Dual M – Multi programmable D – Dual
(A+V) (A+V) (I+T) (P + S)
S – Simple S – Simple
(A or V) (A or V)
Indications for perioperative temporary pacing:

Class I
Any class I indication for a permanent pacemaker
For hemodynamic stabilization prior to permanent pacemaker implantation
Class II
Disadvantageous bradyarrhythmias when drugs fail to produce expected results.
Routine use of epicardial pacing wires following cardiac surgery.
Class III
Prophylactic pacing for symptoms suspected due to sinus node dysfunction.
Pacing for bifascicular heart block without symptoms attributable to
bradyarrhythmias.
Technique of temporary pacing:

Available methods for temporary pacing include
a. Invasive direct cardiac pacing via transvenous (endocardial) or epicardial routes.
b. Noninvasive indirect cardiac pacing via transcutaneous or trans-esophageal
routes.
Technique of permanent pacing:
 In permanent pacing leads are usually inserted transvenous through the
subclavian or cephalic vein with the leads positioned in the right atrial
appendage for atrial pacing and right ventricular apex for ventricular pacing. The
leads are then attached to the pulse generator, which is inserted into the
subcutaneous pocket below the clavicle.
 Epicardial lead placement is used when either transvenous access cannot be
obtained or if the chest is open during cardiac operation.
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INDICATION FOR IMPLANTATION FOR PERMANENT PACEMAKERS FOR
BRADYCARDIA IN ADULTS
Acquired AV Heart block:
Class I:
 Permanent or intermittent 30blockwith symptomatic bradycardia or congestive
heart failure.
 Ectopic rhythms or medical conditions requiring bradycardia drugs.
 Asystole  3.0 sec or escape rate < 40 beats / min without symptoms.
 Post AV junctional ablation, or myotonic dystrophy
 Type I or II, 20AVblock with symptomatic bradycardia.
 Atrial flutter-fibrillation or SVT with advanced 20or 30 AV block and symptomatic
bradycardia not due to drugs.
Class II:
 Asymptomatic 30 AV block with rates > 40 beats / min.
 Asymptomatic type II, 20AV block.
 Asymptomatic type I, 20 AV block at or below the common (His) bundle.
Class III:
 Asymptomatic 10 AV block
 Type 1, 20 AV block at the AV node.
 AV block after myocardial infarction
Class I
 Persistent advanced 20 or 30 AV block with block in the His-Purkinje system.
 Patients with transient advanced 20 AV block and bundle branch block.
Class II
 Patients with persistent advanced 20 AV block at the AV node.
Class III
Transient AV conduction disturbances without intraventricular conduction defects.
Transient AV block with isolated left anterior hemiblock, or the latter without AV block.
Persistent 10AV block in the presence of bundle-branch block not demonstrated
previously.
Chronic Bifascicular and Transfascicular block:

Class III
Fascicular block ( 10 AV block) without type II 20 AV block or symptoms.
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Sinus node dysfunction (SND)
Class I
SND with documented symptomatic bradycardia, including that consequent to chronic,
essential drug therapy for which there are no acceptable alternatives.
Class II
Spontaneous or drug-induced SND with heart rates  40 beats / min when there
is no clear association between symptoms of bradycardia and the occurrence of
bradycardia.
Class III
 SND without symptoms, including with heart rates  40 beats / min or drug-
induced.
 SND in patients with symptoms suggestive of bradycardia, but shown not due to
bradycardia.
Hypersensitive Carotid sinus and Neurovascular syndromes:

Class I: Recurrent syncope associated with clear, spontaneous events provoked by
carotid sinus stimulation.
Minimal carotid sinus pressure induces asystole > 3 sec in the absence of drugs that
depress sinus or AV node function.
Class II: Recurrent syncope without clear, provocative events, and with a
hypersensitive cardio-inhibitory response.
Syncope with associated bradycardia reproduced by provocative maneuvers (e.g., head-
up tilt  Isoproterenol), and in which temporary pacing and second provocative test
establish the likely benefits of permanent pacing.
Class III: Hyperactive cardio-inhibitory response with or without vague symptoms such
as dizziness or lightheadedness, or both.
Recurrent syncope, dizziness, lightheadedness in the absence of a cardio-inhibitory
response.
ADDITIONAL FACTORS THAT CAN INFLUENCE THE DECISION TO IMPLANT A

PACEMAKER
1. Overall physical and mental status of the patient, including associated diseases
that may result in a limited quality or prognosis for life. Desires of the patient
and family.
2. Presence of underlying structural heart disease that may be affected adversely
by bradycardia (e.g., dilated cardiomyopathy).
3. Desire of the patient to operate a motor vehicle or the need to use hazardous
tools and operate machinery.
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4. Remoteness of medical care, including patients who travel widely or live alone
who therefore may be unable to seek medical help if serious symptoms arise.
5. Necessity for administering medication that may depress escape heart rates or
aggravate atrioventricular heart block. Slowing of basic escape rates due to
whatever cause.
6. Significant cerebrovascular disease that might result in a stroke if cerebral
perfusion were to suddenly decrease.
INDICATIONS FOR PACING IN CHILDREN WITH BRADYCARDIA OR AV HEART BLOCK

Class I indications:
1. 20 or 30 AV heart block, or SND, with symptomatic bradycardia.
2. Advanced 20 or 30 AV block with moderate exercise intolerance
3. Congenital AV block and wide QRS escape rhythm or intraventricular block.
4. Advanced 20 or 30 AV block 10 to 14 days following cardiac surgery.
Class II indications:
1. Brady-tachy syndrome if digitalis or phenytoin does not control arrhythmias.
2. 20 or 30 AV block within common bundle in asymptomatic patient.
3. Transient surgical 20 of 30 AV blocks that reverts to bifascicular block.
4. Asymptomatic 20 or 30 AV block and ventricular rate < 45 beats /min (awake)
5. Complete AV block with average ventricular rate < 50 beats / min (awake).
6. Asymptomatic neonate, congenital 30 AV block and bradycardia.
7. Complex ventricular arrhythmias with 20 or 30 AV block or sinus bradycardia.
8. Congenital long QT syndrome for prophylaxis of torsades de pointes VT.
Class III indications:
 Asymptomatic, postoperative bifascicular block with or without 10AV block.
 Transient surgical AV blocks that returns to normal condition in < 1 week.
 Asymptomatic congenital heart block without profound bradycardia.
Important definitions:
Pulse generator:
It includes the energy source (battery) and electric circuits for pacing and
sensory function. Mercury-Zinc batteries that were used in the early days had a short
useful life (2-3 yrs). Currently Lithium-iodine batteries are being used which have
longer shelf life (5-10 yrs) and high energy density.
Leads:
These are insulated wires connecting the pulse generator.
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Electrode:
It is an exposed metal end of the lead in contact with the endocardium or
epicardium.
Unipolar Pacing:
There is one electrode, the cathode (negative pole) or active lead. Current flows
from the cathode, stimulates the heart and returns to anode (positive pole) on the
casing of pulse generator via the myocardium and adjacent tissue to complete the
circuit. Unipolar sensing is more likely to pick up extracardiac signals as myo-potentials.
Bipolar Leads:
They consist of two separate electrodes, anode (positive pole) and cathode
(negative pole), both located within the chamber that is being paced. As the electrodes
are very close, the possibility of external noise disturbance is less and the signals are
sharp.
Endocardial Pacing:
It is also called as transvenous pacing which implies that the leads/electrodes
systems has been passed through a vein to the right atrium or right ventricle. It can be
unipolar or bipolar.
Epicardial Pacing:
This type of pacing is accomplished by inserting the electrode through the
epicardium into the myocardium. This can also be unipolar or bipolar.
Pacing Threshold:
This is the minimum amount of energy required to consistently cause
depolarization and therefore contraction of the heart. Pacing threshold is measured in
terms of both amplitude and duration for which it is applied to the myocardium. The
amplitude is programmed in volts (V) or in milli amperes in some devices, and the
duration is measured in milliseconds.
Factors affecting pacing thresholds:
Increase Decrease
1-4 weeks after implantation Increased catecholamines
Myocardial ischemia/infarction Stress, anxiety
Hypothermia, hypothyroidism Sympathomimetic drugs
Hyperkalemia, acidosis/alkalosis Anticholinergics
Antiarrhythmics (class Ic, 3) Glucocorticoid
Antiarrhythmics (class IA/B, 2)* Hyperthyroidism
Severe hypoxia/hypoglycemia Hypermetabolic status
Inhalation-local anesthetics**
‘R’ Wave Sensitivity:
It is the measure of minimal voltage of intrinsic R wave, necessary to activate the
sensing circuit of the pulse generator and thus inhibit or trigger the pacing circuit. The
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‘R’ Wave sensitivity of about 3 mV on an external pulse generator will maintain ventricle
inhibited pacing.
Resistance:
It can be defined as impedance to the flow of current. In the pacemaker system it
amounts to a combination of resistance in lead, resistance through the patient’s tissue
and polarization that takes place when voltage and current are delivered into the
tissues. Abrupt changes in the impedance may indicate problems with the lead system.
Very high resistance can indicate a conductor fracture or poor connection to the
pacemaker. A very low resistance indicates an insulation failure.
Hysteresis:
It is the difference between intrinsic heart rate at which pacing begins (about 60
beats/min) and pacing rate (e.g. 72 beats/min). It is particularly useful in patients with
sick sinus syndrome.
Runaway Pacemaker:
It is the acceleration in paced rates due to aging of the pacemaker or damage
produced by leakage of the tissue fluids into the pulse generator. Treatment with
antiarrhythmic drugs or cardioversion may be ineffective in such cases. It is necessary
to change the pacemaker to an asynchronous mode, or reprogram it to lower outputs. If
the patient is hemodynamically unstable temporary pacing should be done followed by
changing of pulse generator.
Types of Pacing Modes:

Asynchronous: (AOO, VOO, and DOO):
It is the simple form of fixed rate pacemaker which discharges at a preset rate
irrespective of the inherent heart rate. It can be used safely in cases with no ventricular
activity. However, the problems associated with asynchronous pacemaker are that it
competes with the patient’s intrinsic rhythm and results in induction of
tachyarrhythmias. Continuous pacing wastes energy and also decreases the half-life of
the battery.
Single Chamber Atrial Pacing (AAI, AAT):
In this system atrium is paced and the impulse passes down the conducting
pathways, thus maintaining atrio-ventricular synchrony. A single pacing lead with
electrode is positioned in the right atrial appendage, which senses the intrinsic P wave
and causes inhibition or triggering of the pacemaker. This is useful in patients with
sinus arrest and sinus bradycardia provided atrioventricular conduction is adequate. It
is inappropriate for chronic atrial fibrillation and long ventricular pauses.
Single Chamber Ventricular Pacing (VVI, VVT):

VVI is the most widely used form of pacing in which ventricle is sensed and
paced. It senses the intrinsic R wave and thus inhibits the pacemaker function. This type
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of pacemaker is indicated in a patient with complete heart block with chronic atrial
flutter, atrial fibrillation and long ventricular pauses. Single chamber ventricular pacing
is not recommended for patients with sinus node disease, as these patients are more
likely to develop the pacemaker syndrome.
Dual Chamber AV Sequential Pacing (DDD, DVI, DDI and VDD):
Two leads that can be unipolar or bipolar are used, one for the right atrial
appendage and the other for right ventricular apex. The atrium is stimulated first to
contract, then after an adjustable PR interval ventricle is stimulated to contract. These
pacemakers preserve the normal atrioventricular contraction sequence, and are
indicated in patients with AV block, carotid sinus syncope, and sinus node disease. In
DDD system, both the atrium and ventricle can be sensed and paced. The advantages of
dual chamber pacemaker are that they are similar to sinus rhythm and are beneficial in
patients, where atrial contraction is important for ventricular filling (e.g. aortic
stenosis). The disadvantage of dual chamber pacing is the development of a pacemaker-
mediated tachycardia (PMT) due to ventriculoatrial (VA) conduction in which
ventricular conduction is conducted back to the atrium and sensed by the atrial circuit,
which triggers a ventricular depolarization leading to PMT. This problem can be
overcome by careful programming of the pacemaker.
British pacing and electrophysiology group recommended pacemaker modes:
Sinus node disease
Optimal AAIR
Alternative AAI
Inappropriate VVI, VDD
Atrioventricular block
Optimal DDD
Alternative VDD
Inappropriate AAI, DDI
Sinus node disease with atrioventricular
block
Optimal DDDR, DDIR
Alternative DDD, DDI
Inappropriate AAI, VVI
Chronic atrial fibrillation with
atrioventricular block
Optimal VVIR
Alternative VVI
Inappropriate AAI, VVI, VDD
Carotid sinus syncope
Optimal DDI
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Alternative DDD
Inappropriate AAI, VVI, VDD
Programmable Pacemaker:
This is being used since 1980. It provides flexibility to correct abnormal device
behavior and adapt the device to patient’s specific and changing needs. The various
factors, which can be programmed are pacing- rate, pulse duration, voltage output, R
wave sensitivity, refractory periods, PR interval, mode of pacing, hysteresis, and atrial
tracking rate.
In patients with normal cardiac contractility, the stroke volume increases to its
maximal point when only 40% of maximal activity is performed. Thus an increase in
heart rate is important during exercise to achieve the peak cardiac output. Patients with
fixed stroke volume such as those with dilated cardiomyopathy are not able to
effectively increase cardiac output by increase in contractility. They depend entirely on
their heart rate. Similarly, patients on pacemaker need to change the paced rate in
proportion to the metabolic demand so as to normalize the hemodynamic status.
Patients with “chronotropic incompetence” (atrial fibrillation, complete heart block) are
unable to change the heart rate according to their metabolic demands in these patients.
In such cases, rate responsive pacemakers (i.e. pacemakers, which not only sense the
atrial or ventricular activity but also sense various other stimuli and thus, increase the
pacemaker rate) are helpful. Various types of sensors have been designed which
respond to the parameters such as vibration, acceleration, minute ventilation,
respiratory rate, central venous pressure, central venous pH, QT interval, preejection
period, right ventricular stroke volume, mixed venous oxygen saturation, and right
atrial pressure. Out of these, sensors capable of detecting body movements (vibrations),
changes in ventricular repolarisation, central venous temperature, central venous
oxygen saturation, respiratory rate and depth, and right ventricular contractility are
commonly used in clinical practice.
Pacemaker Syndrome:
Most individuals can compensate for the reduction in cardiac output due to loss of atrial
systole by activation of baroreceptor reflexes that increase peripheral resistance and
maintain systemic blood pressure. Some individuals, particularly those with intact
retrograde VA conduction, may not tolerate ventricular pacing and may develop a
variety of clinical signs and symptoms resulting from deleterious hemodynamics
induced by ventricular pacing termed as pacemaker syndrome.
These include hypotension, syncope, vertigo, light-headedness, fatigue, exercise
intolerance, malaise, weakness, lethargy, dysponoea, and induction of congestive heart
failure. Cough, awareness of beat-to-beat variation of cardiac response from
spontaneous to paced beats, neck pulsation or pressure sensation in the chest, neck, or
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head, headache, and chest pain are the other symptoms. Symptoms may vary from mild
to severe, and onset may be acute to chronic.
The pathophysiology of pacemaker syndrome results from a complex interaction of
hemodynamic, neurohumoral and vascular changes induced by the loss of AV
synchrony. Patients with retrograde VA conduction are in a state of constant AV dys-
synchrony. Retrograde VA conduction is present in about 15% of patients with
complete antegrade AV block and in about 67% of patients with intact antegrade AV
conduction paced for sinus node disease.
SYMPTOMS AND OTHER FINDINGS WITH THE PACEMAKER SYNDROME:
Symptoms Other findings
Mild Physical examination
Abdominal or neck pulsations Cannon A waves (jugular pulse)
Palpitations, cough Palpable liver pulsations bilateral
Fatigue, malaise, weakness wheezes, rales
Apprehension, headache Peripheral edema.
Chest fullness / pain, jaw pain
Moderate Noninvasive testing
Exertional dyspnea  20 mm Hg  arterial BP (A V)
Dizziness, tinnitus, vertigo Ocular plethysmography
Paroxysmal nocturnal dyspnea Doppler echocardiography
Orthopnea, choking sensation Venous occlusion
Confusion, altered mental status. plethysmography
Intact VA conduction (ECG)
Severe Invasive testing:
Near syncope, syncope Cannot A wave on PAW + tracing
Dyspnea at rest Measurement of cardiac output.
Frank pulmonary edema Intact VA conduction (EPS)
Pacemaker Failure:
It may be due to generator failure, lead failure, or failure to capture. Failure to
capture owing to a defect at the level of myocardium (i.e. the generator continues to fire
but no myocardial depolarization takes place) remains the most difficult problem to
treat.
Hemodynamic Changes During Pacing:

In single chamber pacemaker, atrial pacing increases the cardiac output by about
26% in comparison to ventricular pacing, as atrial contraction contributes 15 to 25% of
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preload to ventricles. Also atrial systole increases the coronary blood flow and
decreases the coronary resistance.
The new AV sequential packing results in 35% increase in cardiac output in
comparison to the single chamber pacing. This is achieved by the atrial systolic boost
(atrial kick) to ventricular filling. While matching pacemaker to a patient, several factors
need to be taken into consideration such as patient’s age, symptoms, cardiac rhythm,
presence of underlying heart disease, ventricular function, and response of sinus node
to activity (chronotropic response).
BPEG have issued guidelines on the recommended pacing modes for all types of
bradyarrhythmias requiring pacing. In patients with atrio-ventricular block, the
ventricle must be paced. Ventricular pacing should follow atrial pacing or sensing to
maintain atrioventricular synchrony and cardiac output. If the patient is physically
active and node is chronotropically incompetent, a rate responsive system is advisable.
Factors important from anesthesia point of view:
Physiological:
During the first two weeks, there is an initial sharp increase in the pacing
threshold i.e. up to ten times the acute level because of the tissue reaction around the
electrode tip. Then it decreases to two to three times the acute level because of the scar
formation. In chronic state, it reaches the initial level in 80% of patients. But this has
become far less of a problem with the introduction of steroid-eluting leads and other
refinements in the lead technology.
Potassium:
Its equilibrium across the cell membrane determines the resting membrane
potential (RMP). In certain clinical situations, the RMP becomes less negative and
approaches the membrane’s threshold potential so that less current density at the
electrode tissue interface is required to initiate an action potential, making capture by
the pacemaker easier. If the RMP becomes more negative, an increased current density
wound be required to raise the RMP to the membrane threshold potential, making it
more difficult for the pacemaker to initiate myocardial contraction.
An acute increase in extracellular potassium concentrations as in patients with
myocardial ischemia, rapid potassium replacement in chronic hypokalemic patients or
use of depolarizing muscle relaxants in patients with burns, trauma or neuromuscular
disease may increase the RMP to less negative value, thus making the capture easier.
Similarly, decrease in extracellular potassium (in patients on diuretic therapy or those
undergoing hyperventilation such as neurosurgical patients) leads to more negative
RMP making the pacemaker capture difficult.
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Myocardial Infarction:
Its scar tissue is unresponsive to electrical stimulation and may cause loss of
pacemaker capture.
Antiarrhythmic Drug Therapy:
Class-Ia (quinidine, Procainamide), Ib (lidocaine, diphenylhydantoin), and Ic
(flecainide, encainide, Propafenone) drugs have been found to increase the pacing
threshold.
Acid Base Status:

Alkalosis and acidosis both cause increase in pacing threshold.
Hypoxia:
It causes increase in pacing threshold.
Anesthetic Drugs:
These drugs are not likely to change the pacing threshold. It is notable that addition of
equipotent halothane, enflurane, or isoflurane to opiate based anesthesia after
cardiopulmonary bypass did not increase pacing threshold.
Preoperative Evaluation:
Preoperative evaluation is an important aspect of the anesthetic management of
a patient with permanent pacemaker undergoing non-cardiac surgery. It includes
evaluation of the patient and the pacemaker.
Patient evaluation:
It should include not only detailed evaluation of the underlying cardiovascular disease
responsible for the insertion of pacemaker, but also other associated medical problems.
Since substantial number of these patients suffers from coronary artery disease (50%),
hypertension (20%) and diabetes (10%).
One should know the severity of the cardiac disease, the current functional status, and
medication of the patient. The patient should also be questioned about the initial
indication for the pacemaker and preimplantation symptoms such as lightheadedness,
dizziness or fainting. If these symptoms occur even after the pacemaker insertion,
cardiology consultation should be obtained.
The general physical examination should be done to rule out the presence of any bruits,
and signs of congestive heart failure. The location of the pulse generator should be
noted. Generally, generator for the epicardial electrodes is kept in the abdomen and
over one of the pectoris muscles for the endocardial electrodes.
Routine biochemical and hematological investigations should be performed as indicated
on an individual basis. A 12 lead electrocardiogram, X-ray chest (for visualization of
continuity of leads) and measurement of serum electrolytes (especially K) should be
performed.
Peri-operative management of CRMD patients should begin with a focused
preoperative evaluation for establishing.
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 Whether a patient has a CRMD
 Defining the type of device
 Determining whether a patient’s is CRMD dependent for anti-bradycardia pacing
function.
 Determining CRMD device function
Pacemaker Evaluation:
It is equally important to evaluate the function of pacemaker in the preoperative
period. Assistance from the cardiologist and the manufacturer’s representative may be
obtained for the purpose.
Most of the information about the pacemaker, such as type of pacemaker (fixed rate or
demand rate), time since implanted, pacemaker rate at the time of implantation, and
half-life of the pacemaker battery can be taken from the manufacture’s book kept with
the patient.
Ten percent decrease in the rate from the time of implantation indicates power
source depletion.
In patients with VVI generator, if intrinsic heart rate is greater than pacemaker set rate,
evaluation of pacemaker function can be done by slowing down the heart rate by
carotid sinus massage, while the patient’s ECG is continuously monitored. Carotid sinus
massage should be done cautiously in patients with a history suggestive of
cerebrovascular disease or carotid artery disease, because the atherosclerotic plaque
may embolized to the cerebral circulation. Other methods to slow the heart rate are
Valsalva maneuvers and use of Edrophonium (tensilone 5-10 mg).
Reprogramming of the pacemaker:

Reprogramming the pacemaker is generally indicated to disable rate
responsiveness. The ICD also needs to be disabled before anesthesia. ACC/AHA
guidelines advise that all antitachycardia therapy should be disabled before anesthesia.
If the risk of electromagnetic interference (EMI) is high, such as, when the electricity is
in close proximity to the generator, alterative temporary cardiac pacing device should
be available. The use of magnet may also be necessary.
Effect of Magnet Application on Pacemaker Function:
Magnet application is an extremely important function. The magnet is placed
over the pulse generator to trigger the reed switch present in the pulse generator
resulting in a non-sensing asynchronous mode with a fixed pacing rate (magnet rate).
Magnet operated reed switches were originally incorporated to produce pacemaker
behavior that would demonstrate remaining battery life and sometimes pacing
thresholds. Activation of the reed switch shuts down the demand function so that the
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pacemaker stimulates asynchronous pacing. Thus, magnets can be used to protect the
pacemakers dependent patient during EMI, such as diathermy or elector cautery.
However, not all pacemakers switch to asynchronous mode on the application of
magnet. The response varies with the model and the manufacturer and may be in the
form of no apparent change in rate or rhythm, brief asynchronous pacing, continuous or
transient loss of pacing, or asynchronous pacing without rate response.
It is advisable to consult the manufacturer to know the magnet response before use. The
patients must be connected to an electrocardiograph recorder before the magnet is
applied and, remain connected, until after the magnet is removed. The first few paced
complexes after magnet application provide information regarding the integrity of the
pulse generator and its lead system. A 10% decrease in magnet rate from the time of
implantation indicates power source depletion and is an indicator of end of life
requiring elective replacement of battery.
If no information is available from the patient about the pacemaker, magnet may
identify the particular model with the help of magnet rate, which varies among different
manufactures and thus provide clue for its identification.
Despite the previous recommendations to have a magnet available in the
operating room, routine use of magnet during surgery is not without risk and at times
may be unjustified. Switching to asynchronous pacing may trigger ventricular
asynchrony in patients with myocardial ischemia, hypoxia, and electrolyte imbalance.
The new generation pacemakers are relatively immune to magnet application and may
not convert pacemaker to asynchronous mode. Constant magnet application over the
pacemaker may alter the programming leading to either inhibited or triggered pacing,
or may cause continuous or transient loss of pacing.
It has also been seen that if a magnet is placed over a programmable pacemaker, in the
presence of EMI, the pulse generator may become inadvertently and unpredictably
reprogrammed. This new ‘surprise’ programme may not be evident until after the
magnet is removed.
A further problem with magnetic application is the variability of response between
devices, as there is no universal standard. Thus, the use of magnet may be safe in non-
programmable pacemaker, however, the most current devices should be considered
programmable unless known otherwise.
Intraoperative Management:
Monitoring:
Intraoperative monitoring should be based on the patient’s underlying disease
and the type of surgery.
Continuous ECG monitoring is however, essential to monitor pacemaker functioning. In
addition, both electrical and mechanical evidence of the heart function should be
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monitored by manual palpation of the pulse, pulse oximetry, precordial stethoscope and
arterial line, if indicated.
Presence of pacemaker is not an indication for insertion of pulmonary artery (PA) or
central venous catheter. If these are indicated, care should be taken during insertion of
the guide wire or central venous catheter as they are potentially arrhythmogenic. In a
patient in whom the pacemaker or an ICD has been recently implanted, while passing
the PA catheter, care should be taken as it can easily dislodge the freshly placed
transvenous endocardial electrode. It is best to avoid the insertion of PA catheter or use
alternative site of insertion in such patients. Multi-purpose PA catheter with pacing
facilities can also be used.
Anesthetic technique:
The anesthetic technique should be used according to the need of the patient. Both
narcotic and inhalational techniques can be used successfully. These anesthetic agents
do not alter current and voltage thresholds of the pacemaker.
Skeletal myo-potentials, Succinylcholine fasciculation, myoclonic movement, or direct
muscle stimulation can inappropriately inhibit or trigger stimulation, depending on the
programmed pacing modes. The muscle fasciculation induced by succinylcholine can be
avoided by using non-depolarizing muscle relaxant or defasiculating with non-
depolarizing muscle relaxant before giving succinylcholine. Etomidate and ketamine
should be avoided as these cause myoclonic movements.
Pacemaker function should be verified, before and after initiating mechanical
ventilation, as there may be dislodgement of pacemaker leads by positive pressure
ventilation, or nitrous oxide entrapment in the pacemaker pocket.
In patients with rate responsive pacemakers, rate responsive mode should be
deactivated before surgery. If this is not possible for some reason, the mode of rate
response must be known so that conditions causing changes in paced heart rate can be
avoided. For example, shivering and fasciculations should be avoided if the pacemaker
is ‘activity’ rate responsive, ventilation (respiratory rate and tidal volume) should be
kept controlled and constant in case of ‘minute ventilation’ rate responsive, and
temperature must be kept constant in ‘temperature’ rate responsive pacemakers.
Electromagnetic Interference:
Most pacemakers are sensitive to direct or indirect EMI. Strong ionizing beams of
radiation, nuclear magnetic resonance imaging, surgical electrocautery or dental pulp
vitality tester are the most common direct sources of EMI that could interfere with
pacemaker. The indirect sources of EMI included radar, orthopedic saw, telemetric
devices, mechanical ventilators, lithotripters, cellular telephones, and whole body
vibrations are the potential sources of mechanical interferences that could affect
pacemaker. Diagnostic radiology and computed tomographic (CT) scans do not affect
the function of the pacemaker.
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Amongst these, electrocautery is the most important source of EMI. It involves
radiofrequency current of 300-500 KHz. Fatal arrhythmias and deaths have been
reported with the use of electrocautery leading to failure of pacemaker.
One should apply the following measures to decrease the possibility of adverse effects
due to electrocautery.
1. Bipolar cautery should be used as much as possible as it has less EMI.
2. If unipolar cautery is to be used during operation, the groundling plate should be
placed close to the operative site and as far away as possible form the site of
pacemaker, usually on the thigh and should have good skin contact.
3. Electrocautery should not used within 15 cm of pacemaker. Frequency of
electrocautery should be limited to 1-second bursts in every 10 seconds to
prevent repeated asystolic periods. Short bursts with long pauses of cautery are
preferred.
4. Pacemaker may be programmed to asynchronous mode by a magnet or by a
programmer. Before using cautery, the programmer must be available in the
operation theatre (OT). During the use of cautery, magnet should not be placed
on pulse generator as it may cause pacemaker malfunction.
5. Provision of alternative temporary pacing (transvenous, noninvasive
transcutaneous) should be ready in the OT.
6. Drugs such as isoproterenol and atropine should be available.
7. If defibrillation is required in a patient with pacemaker, paddles should be
positioned as far away as possible from the pacemaker generator. If possible,
anterior to posterior positioning of paddles should be used. Although permanent
pacemakers have protective circuits to guard against externally applied high
voltage, pulse generator malfunction has been reported. In elective
cardioversion, the lowest voltage necessary should be utilized. However, even
with these precautions, defibrillation may result in acute increase in the
stimulation threshold, with resultant loss of capture. If this occurs, immediate
reprogramming or temporary pacing should be done with increased generator
output.
8. Careful monitoring of pulse, pulse oximetry and arterial pressure is necessary
during electrocautery, as ECG monitoring can also be affected by interference.
9. The device should always be rechecked after operation.
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Specific Perioperative Considerations:
Some procedures pose a greater risk of pacemaker malfunction.
Transurethral Resection Of Prostate (TURP) And Uterine Hysteroscopy:
Coagulation current used during TURP procedure has no effect, but the cutting
current at high frequencies (up to 2500 kc/sec) can suppress the output of a bipolar
demand ventricular pacemaker. Dresener et al reported a case in which electrosurgical
unit (ESU) used during operation caused pacemaker malfunction. During application of
cutting current there was a loss of pulsatile arterial flow, which returned with
interruption of ESU. Thus when ESU use is anticipated reprogramming of pacemaker
preoperatively to the asynchronous (fixed rate) mode should be performed.
Electroconvulsive Therapy:
ECT appears safe for patients with pacemakers, since little current flows within
the heart because of the high impedance of body tissue, but the seizure may generate
myo-potentials which may inhibit the pacemaker. Thus ECG monitoring is essential and
pacemakers should be changed to non-sensing asynchronous mode (fixed mode).
Radiation:
Cases where radiation therapy is planned for deep seated tumours, therapeutic
radiation can damage the complementary metal oxide semiconductors (CMOS) that are
the parts of most modern pacemakers. Generally, doses in excess of 5000 rads are
required to cause pacemaker malfunction but as little as 1000 rads may induce
pacemaker failure or cause runaway pacemaker. If pacemaker cannot be shielded from
the field of radiation, consideration should from the field of radiation, consideration
should be given to reimplanting the pacemaker at a distant site. Temporary damage to
pacemaker may recover after reprogramming but there may be permanent damage to
the pacemaker as well. This effect could be attributed to charge accumulation inside
CMOS after radiation therapy leading to failure of various components in the circuitry
and therefore, cause pacemaker failure.
Nerve stimulator testing or transcutaneous electronic nerve stimulator unit (TENS):

TENS is now a widely used method for pain relief. TENS unit consists of several
electrodes placed on the skin and connected to a pulse generator that applies 20 sec
rectangular pulse of 1 to 200 V and 0 to 60 mA at a frequency of 20 to 110 Hz. This
repeated frequency is similar to the normal range of heart rates, so it can create a far
field potential that may inhibit a cardiac pacemaker. Adverse interaction between these
devices has been frequently reported, so these patients should be monitored during
initial application of TENS. Pacemaker mediated tachycardia has been induced by
intraoperative somatosensory evoked potential stimulation.
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Lithotripsy:
Anesthesia may be required in patients undergoing extracorporeal shock wave
lithotripsy (ESWL) for immobilization and to avoid pain in flank at entry site of waves.
There may be electrical interference from hydraulic shock waves and can cause
mechanical damage. High-energy vibrations produced lithotripsy machine can cause
closure produced by lithotripsy machine can cause closure of red switch causing
asynchronous pacing. ‘Activity’ rate responsive pacemaker can be affected due to the
damage caused by piezoelectric crystals by ESWL. The shock waves can produce
ventricular extrasystoles, if not synchronized with R wave. Thus, pacemaker
malfunction can occur in patients undergoing ESWL, requiring adequate preparation
prior to procedure. One should have cardiologist’s opinion, perioperative ECG
monitoring, device programmer and a standby cardiologist to deal with any device
malfunction. Rate responsive pacemaker should have their activity mode deactivated.
Focal point of the lithotriptor should be kept at least six inches (15 cm) away from the
pacemaker. Patient with abdominally placed pacemaker generators should not be
treated with ESWL. Low shock waves (< 16 kilovolts) should be used initially followed
by a gradual increase in the level of energy. Dual chamber demand pacemaker is
especially sensitive to shock waves and should be reprogrammed to a simpler mode
(VOO, VVI) preoperatively.
Magnetic Resonance Imaging (MRI):

MRI is an important diagnostic tool. But is use in patients with pacemaker is
contraindicated due to lethal consequences and mortality. Three types of powerful
forces exist in the MRI suite.
Static Magnetic Field: An intense static field is always present even if the scanner is not
imaging. Most of the pacemakers contain ferromagnetic material, which gets attracted to the
static magnetic field in the MRI and may exert a torque effect leading to discomfort at the
pacemaker are known to close at very low magnetic field of 0.5-2 mT, thus reed switch
activation by high static filed of 0.5-1.5 T can result in switching of pacemaker to a non-
sensing asynchronous pacing.
Radiofrequency Field (RF):This field is switched on and off during magnetic resonance
imaging and has a frequency of 21-64 MHz depending on the strength of magnetic field. The
radiofrequency signals can cause interference with pacemaker output circuits resulting in
rapid pacing at multiple of frequency between 60-300 bpm causing rapid pacing rate. It may
cause pacemaker reprogramming and destruction of electronic components. Is may also cause
heating at the electrode-tissue boundary, which may cause thermal injury to endocardium and
myocardium.
Gradient Magnetic Field: Used for spatial localization changes its strength along
different orientations and operates at frequencies in order of 1 kHz. Gradient magnetic
field may also interact with reed switch in pacemaker. Inappropriate sensing and
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triggering because of the induced voltages can occur. It may induce negligible heating
effect.
The results of various studies done to evaluate the safety and feasibility suggest
that in the absence of other alternative for getting diagnostic information. MRI can be
done in the presence of a cardiologist. However, appropriate patient selection should be
done and equipment for resuscitation and temporary pacing should be available. Also
patients should be closely monitored with ECG and oxygen saturation. Further studies
are necessary to refine the appropriate strategies for performing MRI safely in a
patients with implanted pacemaker. Patients, who required head MRI scanning without
alternative diagnostic possibilities, may be best served in a carefully monitored setting.
Thus patients with pacemakers should not routinely undergo MRI scanning.
Post Anesthesia Pacemaker Evaluation:
Any pacemaker that was reprogrammed should be re-set appropriately. For non-
reprogrammed devices, most manufacturers recommend interrogation to ensure
proper functioning and remaining battery life if any electrosurgery was used. ACC
Guidelines now recommend a post-procedure interrogation.
Implantable Cardioverter-Defibrillator (ICD):
The development of an implantable, battery powered device able to deliver
sufficient energy to terminate VT or VF has represented a major medical breakthrough
for patients with a h/o ventricular tachydysrhythmia or cardiomyopathy. These devices
reduce death in the setting of ventricular tachydysrhythmia, and they remain superior
to antiarrhythmics drug.
Further, studies suggesting prophylactic placement in patients without evidence of
tachydysrhythmia.
Trial-II (MADIT-II): Multicenter automatic defibrillator implantation trail-II - ischemic
cardiomyopathy, ejection fraction (EF)<0.30
(SCD-HeFT): Sudden Cardiac Death-Heart Failure Trail: any cardiomyopathy, EF<0.35
has significantly increased the number of patients for whom ICD therapy is indicated.
Defibrillator mode codes:
In 1993 a NASPE/BPEG defibrillator code was approved. The four-position code
describes defibrillator, arrhythmia diagnostic and date storage capabilities.
1st position: Of the code indicates the shock chamber.
2nd position: Indicates the chamber in which anti-tachycardia pacing is delivered.
3rd position: Indicates the means by which tachydysrhythmia is detected, either with
the intracardiac electrogram (E) or by hemodynamic means (H).
4th position: is the three or five letter code for the pacemaker capability of the device.
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NASPE/BPG Generic Defibrillator Code (NBD)
Position IV (or use
Position I Position II Position III
Pacemaker code)
Shock chambers Antitachycardia Tachycardia Anti bradycardia
pacing chambers detection pacing chambers
O = None O = None E = Electrogram O = None
A = Atrium A = Atrium H = Hemodynamic A = Atrium
V = Ventricle V = Ventricle V = Ventricle
D = Dual (A + V) D = Dual (A + V) D = Dual (A + V)
Mechanism of ICD function:

ICDs measure each cardiac R-R interval and categorize the rate as normal, too
fast (short R-R interval), or too slow (long R-R interval). Typically ICDs deliver 6-18
shock/event. Once a shock is delivered, no further ATP can take place. Despite
improvement in detection of ventricular dysrrhythmias more than 10% of shocks are
for rhythm other than VT or VF.
INDICATIONS FOR PERMANENT ANTITACHYARRHYTHMIA PACING DEVICES:
Devices that automatically detect and pace to terminate tachycardias
Class I
 Symptomatic recurrent SVT when drugs fail to control the arrhythmia or
produce intolerable side effects, and catheter or surgical ablation failed or
refused.
 Symptomatic recurrent VT with internal cardioverter-defibrillator backup if
recurrent VT is not prevented by drugs and no other therapy is available.
Class II
 Pacing for recurrent SVT in place of drugs or other treatment.
Class III
 Tachycardias that accelerate / convert to fibrillation with pacing.
External, manually activated devices to terminate tachycardia

Class I
 Recurrent symptomatic VT uncontrolled by drugs when surgery, catheter
ablation, or ICD / automatic device implantation is not indicated.
Class III
 Recurrent SVT or VT that produces syncope.
Overdrive or Atrial synchronous pacemakers to prevent tachycardia.
Class I
 AV or AV node reentrant SVT not responsive to medical therapy.
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Class II
 Sustained VT if other therapies are ineffective or inapplicable and efficacy of
pacing is thoroughly documented.
 Long QT syndrome.
Class III
 Frequent or complex ventricular ectopy without sustained VT associated with
coronary artery disease, cardiomyopathy, mitral valve prolapse, or a normal
heart in the absence of the long QT syndrome.
 Long QT syndrome due to remediable causes.
POSSIBLE INTERACTIONS BETWEEN INTERNAL CARDIOVERTER-DEFIBRILLATOR (ICDS)
AND PACEMAKERS.
1. Transient failure of the pacemaker to sense or pace following ICD discharge.
2. Sensing of pacemaker stimuli by the ICD with inappropriate ICD discharge.
3. Over sensing of pacemaker stimuli during VF prevents appropriate ICD
discharge.
4. Reprogramming or non-intended pacemaker function caused by ICD discharge.
5. Antitachycardia pacing modes trigger inappropriate ICD discharge.
VF = ventricular fibrillation.
EARLY AND LATE COMPLICATIONS FOLLOWING PACEMAKER OR PCD

IMPLANTATION:
Early Late Early or late
Pneumo (hemo) thorax Thromboembolism Lead dislodgement
Subcutaneous emphysema Pulse generator erosion Pacemaker arrhythmias
Myocardial perforation Lead defects Pacemaker infection
Arterial lead placement Increase pacing Pacemaker syndrome
thresholds
Brachial plexus injury Battery depletion Generator malfunction
Extracardiac stimulation
PACE MAKERS
Introduction, CRMD: Advantages CRMD’s (S).
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Pace maker code by NASPEI – PSR-PT.
 P – O, A, V, , AS
 S - O, A, V, D, S P-Pacing, S-Shock, serum, T – Triggered
 R - O, I, T, D programmability, tachycardia
 P - O, C, P, M
 T - O, P, S, D
Permanent – Impulse Generator, pads, electrode, unipolar, bipolar.
Type of pacing:
1. Asynchronous (AOO, VOO, DOO).
2. Synchronized chamber atrial pacing (AAI, AAT)
3. Synchronized ventricular – (VVI, VVT)
4. Oral chamber AV sequential pacing (DD, DVI) programmable pacemaker).
Techniques
a. Temporary pacing
b. Permanent pacing.
Factor affecting pacing
Anesthetic management
Complications
a. Preoperative evaluation
b. Anesthetic technique
c. Monitoring
d. EMI
e. Special situation
f. Magnet application
g. Pacemaker syndrome
Pre-anesthetic Evaluation; ICD Reprogramming:
In addition to evaluating and optimizing co-morbid disease (s) every ICD patient
should undergo preoperative evaluation. ICD interrogation. All ICD patients should have
their antitachycardia therapy disabled during their procedure.
Intraoperative (or procedure) ICD Management:
At this time, no special monitoring or anesthetic technique (owing to the ICD) is
required for the ICD patient. ECG monitoring and the ability to deliver external
cardioversion or defibrillation must be present during the time of ICD disablement.
Should cardioversion or defibrillation be needed, the defibrillator pads should be placed
as far away as possible to avoid damage to the pulse generator to the extent possible.
Nevertheless, one should remember that the patient, not the ICD, is being treated, the
recommendations for Intraoperative (or procedure) management of pacemakers apply
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here as well. ICDs should be disabled prior to insertion of central line to prevent
inappropriate shock and possible ICD failure.
Post Anesthesia ICD Evaluation:
The ICD must be reinterrogated and re-enabled. All events should be reviewed
and counters should be cleared. The pacing parameters must be checked and
reprogrammed as necessary.
ICD magnets:
Like pacemakers, magnet behaviour in some ICDs can be altered by
programming. Most devices will suspend tachydysrhythmia detection (and therefore
therapy) when a magnet is appropriately placed. Some devices can be programmed to
ignore magnet placement.
Summary:
Electronic miniaturization has permitted the design and use of sophisticated
electronics in patients who have need for artificial pacing and / or automated
cardioversion / defibrillation of their heart. These devices are no longer confined to
merely keeping the heart beating between minimum rate (pacing function) and a
maximum rate (ICD functions), as they are now being used as therapy to improve the
failing heart. Both the aging of the population and out ability to care for a patient with
increasingly complex disease suggest that we will be caring for many more patients
with these devices, and we must be prepared for this situation. Safe and efficient clinical
management of these patients depends upon our understanding of implantable systems,
indications for their use, and the perioperative needs that they create.
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Chapter 28 New recommendations: Defibrillation
Early defibrillation is critical to survival from sudden cardiac arrest for reasons.
1. Treatment of VT/VF is defibrillation.
2. Most frequent rhythm in Sudden Cardiac Arrest is ventricular-fibrillation
3. Success of outcome depends on the earliest possible defibrillation.
4. VF becomes asystole in minutes.
 Arrest is hospital always in mediate CPR cycles, 1 cycle comprise of 30
compressions with 2 breaths, 5 cycles take 2 min and then defibrillation.
 New guidelines – 1 high energy shock and continue CPR.
 Defibrillation is electrophysiological and beat that occur in 300-500 milliseconds
after shock delivery,
 Shock success / defibrillation: defined as termination of VF for at least 5 sec
following shock.
Classification of defibrillator.
Monophasic wave form defibrillators:
2 types depending upon rate at which current decreases to zero.

a. Monophasic damped sinusoidal wave form return to O gradually. (MDS).
b. Monophasic truncated exponential waveform returns to O abruptly. (MTE).
Current
MDS tone
Shock 360 J
Biphasic waveform defibrillator:

 Have energy following Bidirectional.
 2 waveforms are used.
– Biphasic truncated waveform – 150 J- 2005
– Monophasic sectilinear waveform – 120 J
 Involve reversal of current at a specific time in the energy shock.
Automated external defibrillator:

They are sophisticated, reliable computerized diseases that use voice and visual
prompts to guide lay reassured MCP’s to safely defibrillate VF-SLA.
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Bi-truncated waveform
Public accent differentiate
Advantage of biphasic defibrillator:

1. Require less energy.
2. Smaller batteries – lithium
3. Lower costs
4. Easier maintenance
5. Longer batting storage life.
Synchronized cardioversion:
 Definition: Is shock delivery that is timed (synchronized) with QRS complex.
 This delivery of shock in the relative refractory portion of cardiac cycle,
application a shock could produce VF.
 The energy used is lower for synchronized shock , these low energy shocks
should always be synchronized because of they are delivered as unsynchronized,
they are likely to induce VF.
Indications: Unstable patients with
 Vent tachycardia with regular rhythm
 SVT due to reentry
 AF
The delivery of shock can step these rhythm because it interrupts the circulating
pattern.
Ineffective in:
 Intractable tachycardia, MAT – as these rhythm has ectopic foci.
 VF, pulseless VT, polymorphic VT.
Recommended doses:
AF: 100 J to 200 J
AF and SVT – 50 J to 100 J.
External cardiac Electroversion:

 It is the process of restoring unorganized cardiac rhythm by applying an
electrical charge to the heart through electrodes (paddles) placed externally on
the chest wall.
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History:
 Clinical application of defibrillation was achieved for the first time in 1947 by
Beck et al, who successfully defibrillated an exposed heart.
 Closed chest defibrillation was first achieved by Zoll who used an external 60
cycle A.C. device to terminate VF in his patients.
 The first D.C. defibrillator was used by Lown in 1962.
Cardiac electroversion includes:

a. Cardioversion
b. Defibrillation
Cardioversion:
 Incorporates a time delay circuit for synchronizing shocks to the ECG –‘R’ or ‘S’
waves.
Defibrillation:
 Does not synchronize shocks to the ECG waves and is used only when QRS
complex cannot be distinguished from ‘T’ wave.
Mechanism:
Defibrillation is accomplished by the electric current (D.C.) passing through a
critical mass of myocardium causing simultaneous depolarization of the myofibrils.
Through the Depolarization and

Current Heart contraction of
application chest wall
myofibrils Allows
Critical mass of SAN or other

Current Leads to
myocardium in Defibrillation intrinsic
removal recovery phase of a pacemakers to
cardiac cycle recapture the
heart
 Cardiac electroversion acts by depolarizing all excitable myocardium and

possibly prolonging refractoriness, shocks interrupt re-entrant circuits and
discharging ectopic foci, establishing the electrical homogenicity needed to
terminate reentry.
 After defibrillation, contractile function of the heart is re-established within a
few min, but initially cardiac output may be extremely low, especially after a long
period of VF. Cardiac output should continue to increase, in a minute to hours
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after successful defibrillation. This effect is called “post counter shock pulseless
rhythm” or “post counter shock myocardial depression.
Indications for cardiac electroversion:

Asynchronous shock or defibrillation
 Ventricular fibrillation
 Pulseless ventricular tachycardia
Synchronized cardioversion:
 Ventricular tachycardia
 Atrial fibrillation
 Paroxysmal atrial tachycardia
 Junctional tachycardia
 Electrical defibrillation is the only effective treatment for established ventricular
fibrillation. The success rate declines after about 4 minutes of ventricular
fibrillation because of effects of metabolic acidosis and hypoxemia on the
myocardium. It is therefore essential to defibrillate as soon as possible.
 Cardioversion is not likely to be effective or indicated for terminating automatic
or triggered tachyarrhythmias. As it merely resets the cycle of automaticity or
triggered automaticity.
Contraindications for cardiac electroversion:

 Idiojunctional or idioventricular rhythms
 II and III degree heart blocks
 DC cardioversion of digitalis induced tachyarrhythmias is contraindicated due to
the danger of inducing ventricular fibrillation.
 Cardioversion is also not necessarily indicated with acute onset atrial flutter or
fibrillation, provided the rhythm is hemodynamically tolerated and rate well
controlled without any drugs.
External defibrillator:
 The defibrillator is a variable transformer that stores a D.C. in a capacitor until
discharged through the electrodes.
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Types: there are 3 types of external defibrillator
a. Manually operated
b. Semiautomatic
c. Automatic external defibrillators (AEDs)
a. Manually operated:
The electric impulse is delivered through well protected hand held paddles or
electrodes which have a discharge button.
The time to attain maximum charge should be < 10 sec with mains operated or fully
battery powered and it should be possible to defibrillate 3 times within a minute.
b. Semiautomatic and automatic defibrillators:

 Were designed for use by nonmedical personal.
 Here the patient ECG is monitored by large 8-10 cms electrodes and interpreted
by an internal computer. The machine indicates the presence of ventricular
fibrillation and the need to defibrillate. The semiautomatic machine requires an
operator to discharge the shock; automatic machine does this by itself.
 Output of most defibrillators is indicated in energy units (joules or watt-second).
For consistency the energy level indicated on most commercially available
defibrillators is the output when discharged into 50 ohms load.
 The relations among energy, current, and impedance (resistance) are given by
the following equation.
 Energy (Joules)  power (Watts) x duration (Seconds)
 Power (Watts)  potential (Volts) x current (Amperes)
 Current (Amperes)  potential (Volts) / resistance (Ohms)
Energy (Joules)
 Current (Amperes)  Resistance (Ohms) x Duration (Seconds)
From these equations it can be determined that as impedance between the paddles
(electrodes) increases, the delivered energy will be reduced, thus optimum success of
defibrillation is obtained by keeping impedance as low as possible.
 Transthoracic impedance during human defibrillation has been measured at
between 15 and 143 ohms (Average 70-80 ohms).
 Resistance decreases with electrode size, so large paddles (8 cms in diameter)
should be used.
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Paddle size (cm)

External Internal
Infant 4.5 2
Child 8 4
Adult 13 6
 The greatest impedance is between the metal electrode and skin; this can be
decreased slightly by the use of saline soaked gauze pads or E.C.G. electrode
cream; however the lowest resistance is obtained with the specially designed
defibrillation gels or pastes.
 Firm paddle pressure of at least 11 kgs reduces resistance by improving
electrode skin contact and by expelling air from the lungs.
 The transthoracic impedance is reduced by successive shocks.
 Recently, defibrillators have been developed which measure transthoracic
impedance before the shock is delivered by passing a low level current through
the chest during the charge cycle and this technology may allow current based
defibrillation by adjusting the delivered energy for the measured resistance.
Energy requirements:
 There is a general relation between the body size and the energy requirements
for defibrillation.
Dose I attempt Dose II attempt Dose III and subsequent
Infant 2 J/Kg 4 J/Kg 4 J/Kg
Child 2 J/Kg 4 J/Kg 4 J/Kg
Adult 200 J 300 J 3360 J
Initial energy levels (joules) for cardioversion:

Atrial fibrillation 100
Atrial flutter 50
Paroxysmal supraventricular tachycardia 100
Monomorphic ventricular tachycardia 50
 However, over the size range of adults, body size does not seem to be a clinically
important variable. Therefore, currently recommended that the initial shock to
be given at 200J followed by a second shock at 200-300J if both fail to defibrillate
the patient additional shocks should be given at 360J.
 Defibrillation with excessively high energy levels is proarrhythmic and well
causes functional and morphologic damage to the myocardium.
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 Defibrillation with inadequate shock energies will be proarrhythmic refractory
VF by stimulating parts of the heart during vulnerable parts of the cardiac cycle.
Precautions:
 Do not defibrillate in the presence of flammable agents or anesthetics.
 Do not discharge the defibrillator
o With the paddles held together
o Into open air
o If the paddle handles are wet or covered with gel
o If any person is touching the patient or any equipment that is in contact
with the patient.
 Oxygen because of fire risk, defibrillation performed in the presence of oxygen
does not typically result in fire but if the localized oxygen concentration is
significantly above ambient in the vicinity of the paddles flash of fire may result.
 Disconnect the patient from equipment which may be damaged by defibrillation,
such as external pacing devices.
 Do not defibrillate in the presence of high energy electrical fields, such as those
generated by diathermy. The diathermy must be turned off first.
 Remove glyceryl trinitrate and other skin patches before defibrillation.
Technique:
Defibrillation forms part of the advanced life support protocol.
 Apply gel pads. The standard position is with the right pad to the right of the
sternum just below the clavicle and the left pad over the fifth left intercostals
space in the midclavicular line.
Select the correct paddles (during charging the paddles should either be secure in the
defibrillator or held on the gel pads applied to the patient’s chest).
 Select the required energy and clearly tell personnel ‘defibrillator charging’.
 Press the charge button (on the paddle or the defibrillator control panel).
 Wait until the defibrillator is charged
 Ensure that the paddle electrodes are placed correctly on the gel pads.
 Shout ‘stand back’.
 Check that all personnel and yourself are clear.
 Deliver the shock by pressing the discharge buttons on the paddles
simultaneously.
 Check the pulse for five seconds to see if cardiac output has been restored.
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Practical points:
 It is essential to maintain oxygenation using routine cardiac life support.
Hypoxemia and metabolic acidosis reduce the success of defibrillation. Cardiac
compression performed during the establishment of a coordinated rhythm,
following defibrillation, is unlikely to precipitate a recurrence of fibrillation.
 The operator must know how to use the defibrillator before using it for the first
time.
 The defibrillator is potentially dangerous to personnel around the patient.
Ensure that all persons, including the operator, are not in electrical contact with
the patient during defibrillation.
 Synchronized mode should not be used for ventricular fibrillation, since there
are no ‘R’ waves, and these are required for the synchronized mode.
Defibrillation would thus be delayed indefinitely.
 Current flow is determined by the shock ‘strength’ and the thoracic impedance.
The latter may be increased by inadequate electrode – chest wall interface,
inadequate electrode position and excessive disturbance between electrodes,
inadequate electrode pressure, or a pneumothorax.
 Defibrillator contact pads are preferable to electrode jelly, since the latter tends
to spread around the chest, which may cause arcing between the electrodes,
surface burning of the patient’s chest, and failure to defibrillate. This may also
occur if the patient’s chest is wet, as in cases of near drowning.
 Ensure that the defibrillator pads never overlap, since this will produce arcing.
 Always use a conductive medium between electrodes and the skin to prevent
skin burns. Ensure that all the surface of the electrode is in contact with the gel
or jelly. Saline pads may be used if conductive gel pads or jelly are not available.
 Gel pads dry out with use and lose their conductivity. They should be changed
after 10 discharges.
 Keep defibrillator paddles clean. Wet or dry gel on the electrode handles
produces the risk of electrocution of the operator.
 Glyceryl trinitrate skin patches should be removed before defibrillating to avoid
the risk of arcing between the electrode and the patch.
 A brief period of asystole may occur after defibrillation. Continue ventilation and
cardiac compression during this time.
Failed defibrillation:
 It is essential to maintain oxygenation and prevent acidosis by efficient
ventilation and cardiac compression. It might be useful to try using
another defibrillator or place the paddles anteriorly and posteriorly. The
anterior paddle is placed at the fifth intercostals space in the mid-
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clavicular line and the posterior paddle is placed just below the inferior
angle of the left scapula. Causes of failed defibrillation are listed below
Due to the patient having
 Hypoxemia  Drugs, such as digoxin or bupivacaine
 Metabolic acidosis toxicity
 Myocardial ischemia  Hypothermia
 Electrolyte imbalance  Pneumothorax
Due to technique
 Inadequate basic life support  Forgetting to recharge the defibrillator
 Inadequate energy level  Attempting to discharge the paddles before
 Incorrect paddle position the selected energy level is obtained
 Inadequate paddle pressure  Failure to press the discharge buttons
 Shorting of paddles simultaneously
Due to the defibrillator

 The battery level is low and needs  The charge has been dumped as a
recharging result of changes made to the ‘energy
 The ‘synchronize’ button has been select’ dial after the charge was
pressed, and in the absence of ‘R’ initiated.
waves the defibrillator cannot  In synchronized mode the patient is
discharge not being monitored through the
patient cable.
Complications of cardioversion:
Complications potentially associated with poor techniques
 Skin burns
 Arcing
 Electrocution
 Failed cardioversion
 Post-shock arrhythmias
Those associated with underlying disease include:
 Post-shock arrhythmias
 Congestive heart failure
 Transient hypotension
 Pulmonary or systemic embolism
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Myocardial injury:
Cardioversion performed in the usual manner does not appear to cause any significant
damage in humans.
Children:
Choose the appropriate size of electrode paddle. In some designs these clip on to
the adult paddle. A charge of 2 J/kg should be used for the first two shocks. If
unsuccessful the charge may be increased to 4J/kg. The defibrillator may have special
controls to obtain low energy levels. Defibrillator conductive pads may be cut to size to
cover the smaller electrode surface. Ensure that the pads never overlap.
Pregnancy:
A pregnant patient may require defibrillation like any other patient, since
without correction both mother and fetus may die. The standard protocol for
defibrillation may be used. Aortocaval compression must be avoided.
Pacemakers:
Alteration in pacemaker programming or a change in cardiac stimulation threshold may
occur following defibrillation. Pacemaker failure has also been described. The following
recommendations for defibrillation of a patient with a pacemaker have been made:
 Use low energy, infrequent DC shock.
 Place the paddles in a line perpendicular to the pacer axis (ideally anterior-
posterior).
 Place the paddles at least 15 cm from the electrodes and the pulse generator.
 Check the pacemaker function after defibrillation (some units will reset to a
predetermined set of values).
 Have emergency pacing equipment available.
CIRCULATORY ASSIST DEVICES:

Despite of these many medical therapies available, cardiac transplantation is the
common goal in the setting of severe cardiac failure, but because of disparity between
the availability and demand, and some of these processes are potentially reversible, a
variety of cardiac assist (circulatory assist) devices have become viable option.
Physiology of heart failure:

Heart failure can be defined as the inability of the heart to pump blood commensurate
with the metabolic needs of the body and is primarily attributed to the failure of the
ventricles to propel blood forward.
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
 systolic pump function.

 ejection fraction (EF)

 EDV Once preload exceeds equivalent of
 interstitial pressure
Enlargement and remodeling of respective ventricles

Fluid retention and congestion ensues
 The neuro-hormonal axis constitutes one of the heart’s more potent
compensatory mechanisms influencing the many manifestations of the heart
failure.
LV pump failure:
Is accompanied by decreased cardiac output and recruitment of number of
compensatory mechanisms such as stimulated rennin- angiotensin-aldosterone system,
increase in circulating catecholamines and vasopressin secretion. The activated neuro-
hormonal response leads to systemic vaso-constriction, fluid retention and increased
after load.
RV pump failure:
 The patho-physiologic manifestations of right ventricular failure are renal
insufficiency, insensitivity to circulating catecholamines, hepatic and pulmonary
congestion and as forms of coagulopathy.
 Clinically, manifestations of heart failure amenable to mechanical circulatory
support are often classified as:
“Left heart failure –forward”

Decreased EF and low cardiac output
“Left heart failure-backward”
Increased pulmonary venous pressure
“Right heart failure  forward”
Decreased ejection into pulmonary arteries and low cardiac output.
“Right heart failure – backward:

Increased systemic venous pressure.
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 Thus it’s clear that “failure begets failure” exemplifying the spiraling patterns of
circulatory shock.
 Clinically, heart failure is defined by a number of hemodynamic derangements.
 Cardiac Index (CI) < 2L/min/mt2
 Mixed venous O2 saturation MVO2< 50%.
 Systemic Bp<80 mm of Hg (or) MAP <60 mm of Hg.
 CVP >20 mm of Hg
 Pulmonary capillary wedge pressure (PCWP) >20 mm of Hg.
 Systemic vascular resistance >2000 dynes/sec/cms5
Physiology of recovery:
Once in place circulatory assist devices can quickly stabilize a patients
hemodynamics such as
 Normalization of CI
o in MAP
 Progressive  CVP towards normal
 Regression of released neuro-hormones associated with failure.
 Coronary circulation can also be improved.
 Functionally and structural restoration also known as “reverse modeling” is a
ideal outcome of mechanical circulatory support.
However, mechanical circulatory assist devices are currently being used for:
 Perioperative circulatory assistance in the patient posted for cardiac surgical
procedures.
 Acute cardiac support < month.
 Prolonged support > 1 month but <1 year.
 Permanent support as alternative transplant.
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Chapter 29 Circulatory assist devices (CAD)
Classification of circulatory assist devices (CAD):
In general circulatory assist devices (CAD) can be classified as:
1. Bridge to myocardial recovery
2. Bridge to bridge
3. Bridge to transplantation
4. Life time use (destination therapy)
Depending upon the length of the support needed circulatory assist devices have
been classified as:
I. Short term devices:

 CPB & ECMO
 ABIOMED BVS 5000 VAD
 Centrifugal (Biomedicus) pumps
 Hemopump
II. Long-term devices:

 Thoratec LVAD
 Novacor LVAD
 Heart mate LVAD
 IABP
 Total artificial heart (TAH)
INTRA AORTIC BALLOON PUMP (IABP):

 To meet the need for a nonsurgical, rapidly initiated form of short term
circulatory support. The concept of IABP was first proposed by W. Kolff et al and
first clinical use was reported by Kantrowitz et al in 1968.
 IABP is a unique volume displacement device used to invasively support and
improve the hemodynamic derangements associated with cardiac diseases.
Goals of aortic counter pulsation:

 To increase the mean Aortic blood pressure, coronary perfusion, LV stroke
volume and LV ejection fraction (EF).
 To decrease after load, myocardial O2 demand, cardiac work index and LVEDP.
Principles of IABP:
 The device in designed to augment myocardial perfusion by increasing coronary
blood flow during diastole and unloading the LV during systole.
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 This is accomplished by mass displacement of a volume of blood by alternately
inflating and deflating a balloon positioned in the proximal segment of the
descending aorta and is synchronized to the cardiac cycle.
Hemodynamic effects of IABP:
1) Physical:
IABP introduces periodic perturbations into the central Aorta that shift the phase
relations between pressure and flow in the circulatory system.
2) Physiological:
 Balloon deflation at the onset of ventricular systole diminishes the after load on
LV by suddenly decreasing central aortic pressure and thus decreases LV wall
stress, myocardial O2 demand and increases CO.
 Diastolic inflation results in the increase DBP and increase in coronary, systemic
perfusion and myocardial O2 supply.
Indications and contraindications for IABP:

Indications Contraindications
1. Cardiogenic shock 1. Aortic valvular insufficiency
Myocardial infarction
Myocarditis
Cardiomyopathy
Pharmacologic
2. Failure to separate from CPB 2. Aortic disease
Aortic dissection
Aortic aneurysm
3. Stabilization of preoperative patient 3. Severe peripheral vascular
Ventricular septal defect disease
Mitral regurgitation
4. Stabilization of non-cardiac surgical preoperative 4. Severe non-cardiac systemic
patient disease
5. Procedural support during coronary angiography 5. Massive trauma
6. Bridge to transplantation 6. DNR patients
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Design of an IABP:
 IABP consists of a catheter and a drive console. The catheter has a long balloon
mounted on the end and is triggered to inflate with helium immediately after
aortic value colure and to deflate with the opening of the aortic value.
 Fluid volume, electrolyte abnormalities, inadequate ventilation and the disorders
of the cardiac system should be corrected (or) optimized.
Insertion technique:
 A balloon catheter of appropriate size is chosen according to the height of the
patient.
o 147-162 cms  30 CC
o 162-182 CMS  40 CC
o >182 CMS  50 CC
o The diameter of the fully inflated balloon should be less than that of the aortic
diameter (=90% of Aortic diameter) and complete occlusion of the aorta should
be avoided as it dimension the physiological effectiveness of IABP.
Percutaneous  most commonly used

Insertion technique:
Surgical cut down
 In either case, the length of the balloon to be inserted is estimated by laying the
balloon tip on patient chest at angle of Louis and appropriately marking the
distal point corresponding to the femoral artery in the groin.
 The femoral artery with a greater pulse is entered with a needle and a J- tipped
guide wire is inserted to the level of the Aortic arch and the needle is removed 
puncture site is enlarged with a series of dilatators and the guide wire control is
maintained all times. The balloon is advanced over guide wire and through the
sheath to be positioned in the proximal part of the descending thoracic aorta
above the renal artery and its tip lying just 2 cms distal to the origin of left
subclavian artery.
 Remove the guide wire from the central lumen and withdraw 2-3 ml of blood and
the then flushed with 3 ml of heparinized saline  attached to the heparinized
system. Manual pressure is applied at the insertion site for 2-3 min to control
bleeding.
 Correct placement is verified by fluoroscopy if available (or) by chest x-ray (or)
Echo. Also a reasonable estimate of the position may be made by watching
balloon mediated alterations of the arterial pulse wave form.
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Trigger:
 Optimal performance of the IABP depends on the proper timing and triggering.
 The microprocessor most commonly makes use of the ECG to trigger the balloon
inflation and deflation, it uses ‘R’ wave as the central timing event and will direct
balloon inflation to occur during the T wave (diastole) and deflation immediately
before subsequent QRS complex (i.e. onset of next systole).
 Radiofrequency current from electro-cautery can interfere with the ECG
triggering.
 Alternative trigger sources are atrial pacer spikes, ventricular or atrio-
ventricular spikes and the arterial wave form.
Timing of counterpulsation:
Dicrotic notch (DN) is the land mark on the pressure wave form used to set balloon
inflation and is inflated just prior to DN.
 Early inflation: results in premature closure of aortic valve  SV and CO,  LV
EDV
 Late inflation: perfusion pressure and volume.
 Late deflation: increased work load of LV, and  myocardial O2 deemed and 
CO.
 Early deflation: no after load reduction.
 Timing will be complicated by the presence of arrhythmias and large variations
in heart rate. Changes in the HR > 10bpm requires retiming of IABP.
Monitoring:
 Physiological and clinical status of the patient is measured and monitored at
regular intervals.
 Parameters to be measured:
o Electrolytes
o Acid-base balance (ABG)
o Osmolarity
o Plasma volume, red cell mass
o CO, PAP, PCWP or CVP
o Urine output
o Coagulation parameters for the detection of activation of the haemostatic
mechanisms.
o Frequent observation of skin temperature, and peripheral pulses of the
extremity through which balloon has been introduced.
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Weaning from IABP support:
 The indications for discontinuing IABP depend on the indications for initiating it.
 Discontinuation comes under consideration some hours after hemodynamic
parameters have become normal and all the physiological derangements due to
circulatory decompensation have been corrected.
 If vasopressors are being administered, they are either withdrawn or reduced to
minimal possible dose.
 A trail of weaning is attempted by reducing the balloon augmentation in steps
from 1:1  1:2  1:4 and with the assessment of hemodynamic stability the
counterpulsation are stopped and if the patient is stable the device is removed.
 Restrictions on the duration of IABP support have not been defined; several
authors have recorded extended periods of IABP support in patients with
circulatory decompensation.
IABP in pediatric patients:

 IABP has not been widely used in children because the analogous clinical settings
in the children are relatively few and because of technical limitations.
 Children have rapid HR, more complaint aorta, small femoral vessels and all of
which tend to make counter pulsations less effective and more problematic.
 However in children with CAD from Kawasaki’s disease, anomalous coronary
artery from the pulmonary artery and patients with postoperative low cardiac
output states who are refractory to medical treatment may benefit from IABP
support.
Removal of balloon catheter:

After removal of the catheter, manual pressure is given distal to the site of
insertion and artery is allowed to bleed for 1-2 min and then pressure is given over the
proximal part and the process is repeated to ensure removal of clots in the region of
insertion.
 Manual compression is maintained for 30min
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Complications of IABP:
Vascular Miscellaneous Balloon
Arterial injury (perforation, Hemolysis Perforation (pre-insertion)
dissection) Thrombocytopenia Tear (during insertion)
Aortic perforation Infection Incorrect positioning
Aortic dissection Claudication (post-removal) Gas embolization
Femoral artery thrombosis Hemorrhage Inadvertent removal
Peripheral embolization Paraplegia
Femoral vein cannulation Entrapment
Pseudoaneurysm of femoral Spinal cord necrosis
vessels Left internal mammary
Lower extremity ischemia artery occlusion
Compartment syndrome
Visceral ischemia
Both the frequency and severity of complications depend on the nature of

indication and mechanical assistance.
IABP complications can be grouped into 4 categories
 Category I: Spontaneous restoration without treatment and with IABP in site.
 Category II: Resolve after treatment or removal of IABP.
 Category III: Residual deficit. (Ex: amputation due to ischemic injury,
neuropathy, embolization).
 Category IV: Contributory cause of the death. (cardiac arrest).
Ventricular assist device (VADs):

 A ventricular assist device (VAD) is used to take over the pumping function of the
heart, either partially or completely, allowing the damaged heart to “REST” and
possibly recover.
 When muscle recovery is not possible, a prosthetic ventricle can help to prevent
progressive end-organ detoriation and help to normalize circulatory
homeostasis.
 Mechanical circulatory support can be provided by a variety of devices and
modalities of blood flow generation and the common aim is either to assume the
blood circulatory function or to assist the native heart by unloading the
respective ventricle while maintaining the adequate flow to the systemic and
pulmonary circulation.
 For patients placed on the heart transplantation list, these assist devices may be
required to take over the hemodynamic support for many months and in some
cases lifelong.
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Physiologic and hemodynamic basis of the ventricular assist devices (VADs)
 The circulatory system may be viewed hydrodynamically as 2 pumps that
operate in series, each overcoming the load impedance defining its side of
circulation (i.e. LV  systemic and RV –pulmonary circulation).
 The device interaction with the systemic and pulmonary circulation dictates and
constrain the performance requirements of the prosthetic ventricles.
 The end systolic pressure – volume relationship (ESPVR) and the end diastolic
pressure volume relationship (EDPVR) are used to describe the systolic and
diastolic properties of the native ventricle and they constrain the operating
range of the pumping chamber.
 For the biological heart the ESPVR is determined principally by the inotropic
state of the contracting myocardium and the EDPVR is determined by the
lusitropic properties of the myocardium.
The important attributes of the pressure volume loop:

 Venous return + ESV determines the preload.
 The preload along with the lusitropic properties of the ventricle determines the
EDV.
 The ESV is determined by the relationship between EDV and the ventricles
stroke volume (SV = EDV-ESV)
 Stroke volume is affected by after load and the inotropic state of the ventricle.
 Ejection pressure is determined by the amount of blood ejected and the
impendence to that ejection. (Pulmonary, aortic)
Physiologic interaction of VADs with the native heart:
Most clinically used VADs are not timed or phased with the cardiac cycle, the
systolic and diastolic phases of LVAD may or may not be in synchrony with the systolic
and diastolic phases of the native heart.
 Maybaum et al described this interaction as having 2 phases of operation.
a. In phase
b. Out of phase
 When the VAD heart coupling is “in phase”, ventricular systole occurs during
VAD diastole resulting in stepwise maximal filling of the device and a
commensurate decrease in the left ventricular pressures.
 The “out of phase” interaction describes state whereby ventricular systole occurs
during VAD systole, and in this case the device heart coupling is such that the 2
pumps are in direct competition for blood, resulting in a decreased filling of the
prosthetic ventricle and a commensurate increase in ventricular pressure.
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Classification of VADS:
 Ventricular assist (or) replacement devices can be divided into 2 major classes of
design depending on the type of the flow generated by the pumps.
 When used for a prolonged time, the mechanical pumps are required to sustain
an adequate blood flow without damaging the blood constituents (or) activating
the coagulation pathways.
Type of flow they generate:

I. Nonpulsatile pumps (continuous flow)
II. Displacement type (pulsatile flow)
Nonpulsatile (continuous) flow: Pulsatile (displacement type)
a) Fluid dynamic rotatory pumps a) Extracorporeal
b) Axial flow pumps b) Implantable
c) Centrifugal pumps.
Continuous (or) non pulsatile flow pumps:
These include fluid dynamic rotatory pumps which consists of an spinning
impeller at a speed of 2000 –12,000 rpm in an axial (or) radial configuration and
generate continuous non pulsatile flow.
Advantages Disadvantages
Universally smaller and Un-physiological pumping principles of continuous flow
can be implanted in the on end organs such as kidneys, pituitary adrenals and
individuals of varying liver remains of concern.
size.
Hydrodynamic properties i.e. impeller rotating at 2000-
12,000 rpm and inlet cannula negative effect (suction)
might affect blood rheology and have to be resolved prior
to the long term and permanent implantation potential of
this technology.
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Types:
Axial flow pumps
Ex. Hemopump
Micro-med technology
Jarvik-Heart 2000
Centrifugal pumps Ex. Biomedicus
Pulsatile flow (displacement) pumps:
 These pumps in general represent second generation of VAD’s and most were
developed in 1980’s which provide pulsatile flow as high as 10 lts / min and are
capable of capturing the entire cardiac output.
 Pulsatile flow pumps attempt to replicate the heart anatomically and
functionally, making them more amenable to physiologically guided device
control and regulation.
 The ultimate goal of their use is to restore normal perfusion, especially to end
organs compromised by the heart failure.
 These positive displacement devices generally operate with a fixed volume,
variable beat rate but are often not time phased to the native cardiac cycle.
 Pulsatile pumps can be divided into 2 categories.
 Extracorporeal
 Implantable
Extracorporeal Implantable
Provide short to medium term right, left They are intended for left ventricular
(or) Biventricular support support only and are used as bridge to
Used for patients with post cardiotomy transplant (or) recovery.
heart failure and for the patient with These are placed in the abdomen either
implantable LVAD and compromised preperitonially (or) occasionally within
right ventricular function after LVAD the peritoneum.
placement or they may be used as bridge
to transplant or recovery. Require minimal anticoagulation.
Require long term anticoagulation
Are sensitive to electromagnetic Are susceptible to electromagnetic
interference. interference.
Example: Example:
ABIOMED – BVS 5000 Novacor LVAD
Toratec AVD Heart rate
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A note on total artificial heart (TAH):
 The first use of a TAH in humans was by Cooley et al in 1969.
 The 1st successful implant of TAH was achieved in 1982 for a patient with dilated
cardiomyopathy and underwent a implantation of a “Jarvik-7-100 TAH”.
Pre-operative considerations for the VAD insertion:
 CHF patients have low stroke volumes that make them heart rate dependent to
maintain cardiac output.
 Although they depend on adequate preload, increasing preload does not
significantly increases cardiac output, because their myocardium cannot respond
by the standard Starling’s mechanism. Conversely, decreasing heart rate and
increasing diastolic filling doesn’t increase stroke volume either, because of lack
of preload response. Increasing HR and decreasing diastolic time causes a
decrease in output.
 Autonomic tone is increased with resulting vasoconstriction and eventual down
regulation of the catecholamine receptors and myocardial nor-adrenaline.
 A reduction in cardiac output produces effects on the function of other major
organ system especially hepatic, and renal metabolism which results in
alteration in the pharmacokinetics of various therapeutic and anesthetic drugs
used because of decreased volume of distribution, altered protein binding,
slowed metabolism and decreased clearance and systemic elimination.
 Clearance and elimination of various endogenous vasoactive substances such as
cytokines, also may affect adversely the patient’s condition and render
pharmacologic intervention ineffective.
 Affected synthetic functions with resultant alteration in coagulation systemic
often produce significant pre-operative coagulopathy.
 Previous cardiovascular surgeries may result in problems at the time of VAD
insertion because of the significant pericardial adhesions that can complicate
opening the sternum and cardiac dissection with possibility of catastrophic
hemorrhage which should be always anticipated.
 Most of these VAD insertions require CPB support.
Pre-operative evaluation:
 In addition to the standard lab studies and radiographic examination,
coagulation evaluation cardiac catheterization and echocardiographic
examinations may be useful.
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Preoperative tests and examinations:
Laboratory Hb, Hct, electrolytes, BUN creatinine, liver function
Coagulation PT, PTT, fibrinogen, platelet count, platelet function
Echocardiography and LV and RV filling pressure, PAP, PVR, transpulmonary
cardiac catheterization gradient, response to pulmonary vasodilators
Temperature
monitoring
Monitoring:
 The approach for monitoring patient during VAD insertion include:
 TEE: is necessary in all patients to ascertain if a patent foramen ovale is present
and to asses LVAD inflow, valve function before and after device insertion, left
ventricular filling. Right ventricular function and completeness of air evaluation.
 EEG: monitoring is used for assessing adequate cerebral blood flow during CPB
support.
Post operative period:

 VADs support usually improves cardiac and multiorgan function and may
reverse abnormal process of myocardial cell structural damage.
 Neuroendocrine and inflammatory mediators are also normalized.
 Most patients who are stable after the immediate post-operative period show
significant clinical improvement.
 Long term, it is possible for patients with VE heart mate (or) axial flow pumps
system to leave the hospital and continue therapy on an outpatient basis and
some patients have even been able to return to work.
Summary:
VADs represent advanced therapy for cardiac failure, the anesthesiologist contribution
to the pre, intra and postoperative management of these challenging patients continues
to grow as VADs technology is refined and as more patients become eligible to receive
these life saving devices.
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Chapter 30 MYOCARDIAL ISCHEMIC PRE-CONDITIONING
Introduction
Ischemic heart disease (IHD) is one of the major causes of morbidity and mortality all
over the world. Various medical and surgical strategies have been evolved to reduce the
mortality from acute myocardial infarction (AMI), which include the use of thrombolytic
agents, -blockers, Angiotensin converting enzyme inhibitors (ACEs), antioxidants,
Percutaneous transluminal coronary angioplasty (PTCA) and Coronary artery bypass
grafting (CABG). Many reports have been shown that up to 90% of patients undergoing
CABG experience a fall in ejection fraction (EF) and cardiac index (CI) during immediate
post-op period. This has been attributed to various factors of which ischemia associated
with aortic cross clamping and inadequate myocardial preservation are important. The
myocardial protection used during surgery is varied and the viewpoints regarding the
methods to attain optimum protection differ a lot. The issue involves differences in
temperature (cold VS warm), composition (blood VS crystalloid), route (anterograde vs
retrograde) and method (continuous VS intermittent) of cardioplegia. One intervention
of myocardial preservation which has received universal acceptance and generated a lot
of excitement is the phenomenon of "myocardial ischemic preconditioning'.
What is ischemic Pre-conditioning?

It has always been firmly believed that ischemia, no matter how brief is always bad for
the tissues. Now, however it has been well established that it is not always so. Murry et
al in 1986 showed that single or multiple brief periods of myocardial ischemia that
produce reversible myocyte injury can limit the size of the infarct and the degree of
reperfusion injury after a subsequent and more prolonged period of myocardial
ischemia. This phenomenon has been termed as "myocardial ischemic preconditioning
(MIPC)" and can be defined, as “an adaptive mechanism by which brief period of
reversible ischemia increases the heart’s tolerance to a subsequent longer period of
ischemia”. MIPC has also been documented in various other animal species including
dogs, rats and rabbits. In humans the phenomenon of IPC has also been recently
demonstrated in skeletal muscle, liver, kidney, brain and spinal cord.
Two different time frames have been defined for pre-conditioning - early or the
“classical pre-conditioning” which involves the activation of various membrane
receptors and late - which is termed as the "second
window" of protection (SWOP), which is related to changes in gene expression leading
to an increased synthesis of
cardio protective stress proteins. The classical preconditioning wanes 1-2 hours after
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the ischemic insult and the second window of protection begins 12-24 hours later and
lasts for up to 72 hours. Tolerance to pre-conditioning may occur where prolonged
hours of ischemia can result in a loss of preconditioning effect. IPC can also be induced
by other forms of stress like hypoxia, stretch, heat shock and 1 receptor stimulation.
Mechanism of ischemic Pre-conditioning:

In order to understand the mechanisms of ischemic pre-conditioning it is important
to understand the pathophysiology of ischemic reperfusion injury. Investigations of
cellular pathophysiology of ischemic injury have consistently shown that a significant
part of the damage occurs not during the period of tissue ischemia but during the period
of reperfusion. This injury is termed as ischemic reperfusion injury (IRI) and is
responsible for paradoxical organ death and dysfunction after termination of the
reperfusion period. IRI can be shown in almost all organ systems. The mechanisms
involved in IRI include
a. Reduction in high energy phosphate (ATP) levels for many hours after tissue
ischemia
b. Proinflammatory cell (neutrophils and mast cell) mediated cellular and
microvascular injuries, through direct cellular toxicity of superoxide free radicals
that are generated by these cells during ischemia and subsequent reperfusion
c. Microvascular dysfunction with platelet plugging and endothelial damage
resulting in a no-reflow phenomenon with inadequate tissue perfusion during
the reperfusion period
d. Calcium overload mediated reperfusion injury.
Role of adenosine (ADO)

There are several attractive hypotheses, which try to explain the cellular protective
mechanisms of IPC; however they are not all agreed on. Most studies have shown that
adenosine (ADO) which is a naturally occurring compound in every cell of the
mammalian body, is one of tile endogenously released molecules responsible for tissue
protection. The rationale for this idea is based on the fact that large quantities of ADO
are released within seconds after the onset of ischemia in virtually all tissues types.
Tissue hypoxia is a potent stimulus for endogenous ADO production and ADO is a well-
established endogenous mediator of reactive hyperemia in many vascular beds
including cardiac and skeletal muscle. The buildup of ADO during the first brief ischemic
period (IPC period) may trigger protection through stimulating (A1 and A3) and
microvascular (A2) receptors.
ADO does not protect against IRI when administered at the time of reperfusion,
which indicates that ADO receptor activation must precede prolonged ischemia. The
protective mechanisms of ADO in IPC have been thought to be by (a) better
preservation of tissue ATP (b) inhibition of neutrophils and mast cell activity (c) anti-
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oxidant:-I and anti-free radical activity" (d) anti platelet activity (e) inhibition of no
reflow phenomenon(f) activation of K+ ATP channels and reduction of calcium
intracellularly (g) activation of proteinkinase C (PKC) and (h) premature degranulation
of mast cells.ADO mimics IPC by its ability to improve collateral muscle flow with its
vasodilation actions, its role in improved glycolytic influx and its ability to increase heat
shock protein synthesis. On an acute basis, ADO may be the most efficient way of
restoring ATP levels in viable but energy deficient myocytes by accelerating the
conversion of ADO to ATP through the action of ADO kinase and other nucleoside
salvage pathways. The half life of ADO is 2 to 10 seconds in blood but how ADO
pretreatment achieves enhanced ATP levels on a long term basis (for hours) is not clear.
IRI activates neutrophils, increases free radical production and stimulates platelet
function various studies have shown that ADO is an important modulatory inhibitor of
neutrophils and platelet function. ADO is known to inhibit neutrophils mediated free
radical production through ADO, receptor activation and may be responsible for
limiting the degree of microvascular injury during ischemia and reperfusion by
inhibiting the free radical mediated damage to endothelial cells and through its
antiplatelets activities. ADO is a potent vasodilator of the vasculature ranging from
major coronary arteries to microvasculature. ADO in addition opposes the effects of a
number of locally released vasoconstrictor substances like leukotrienes, thromboxane -
A2 (TXA2), endothelia and platelet activating factor (PAF). It also inhibits release of nor-
adrenaline release from the sympathetic mechanisms which in turn facilitates regional
blood flow in a previously ischemic bed.
The resting membrane potential remains persistently depolarized during
ischemia and subsequent reperfusion. Persistent depolarization of resting membrane
potential increases cellular energy requirements. ADO may reduce basal myocyte
metabolic demand by producing intracellular hyperpolarization with opening of
potassium sensitive ADO and / or K+ ATP channels coupled to ADO receptors. The
receptors are thought to be A1 and A3 Intracellular hyperpolarization with IPC or ADO
pre-treatment would lead to decreased phosphorylation of slow Ca++ channel by
reduced activation of protein kinase A and subsequently reduced energy requirements.
A3 receptors have been found to be present in mast cell membranes and they
function to degranulation mast cells. Increased interstitial ADO may be responsible for
prematurely degranulating these mast cells during the preconditioning period. A brief
IPC before a more prolonged ischemic period may wash out these mast cell products
and prevent subsequent mast cell mediated tissue damage. It has been documented by
Sandhu et al in rabbit myocardium that IPC prevented increased in cyclic AMP (cAMP)
levels, which invariably occurred during sustained ischemia. There is usually an
increase in intracellular cAMP during myocardial ischemia due to increased interstitial
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nor epinephrine release and stimulation of -1receptors. The blunting of cAMP by the
IPC may be caused by neither attenuation of nor epinephrine release during ischemia.
Other pharmacological agents

 In addition to adenosine, there are a few other pharmacological agents, which
influence the IPC. They include acadesine and acetylcholine.
Acadesine:
Acadesine is one of the first synthesized ADO regulating agents, which increased the
availability of adenosine and adenosine triphosphate (ATP) in tissues under ischemic
stress. The proposed biochemical mechanism of action is its formation of inosine
monophosphate (IMP), which is an intermediate substrate in the synthesis of adenosine
triphosphate (ATP) and guanosine monophosphate (GMP). The other possible
mechanisms include inhibition of ADO deaminase, ADO kinase which therefore
increases the interstitial levels of ADO. Acadesine improves the myocardial function in
hearts subjected to IRI and maintain the ventricular contractile function and lessens the
ischemic ECG changes. It also attenuates arrhythmias associated with reperfusion. It
improves post ischemic recovery in hearts undergoing CPB and global myocardial
ischemia. It has been shown to prolong the window of protection afforded by
myocardial IPC by delaying its decay. It also has an important role as an adjuvant
pharmacological agent to improve outcomes in patients with acute MI, unstable angina
and patients for CABG surgery. In addition to its beneficial effect on CABG patients, it
also decreases the need for perioperative application of ventricular assist devices.
Acetylcholine and carbachol:

It has been shown by Przyklenk and Kloner that drugs like acetylcholine (Ach) and
carbachol also mimicked IPC. They studied small I.V. boluses of Ach and nitroglycerine
(NTG), which were given prior to coronary artery occlusion to assess endothelium
dependent and endothelium independent coronary vasodilator reserve. It was found
that muscarinic agonists like Ach and carbachol could limit the infarct size in dog model.
The above workers used small (0.01 mg) and non-invasive I.V, bolus injections of Ach.
Yao and Gross had a similar report where they had used sustained infusions of high
doses of Ach (0.003 to 0.01 mgmin-1 for 10 min) directly into the soon to be occluded
coronary artery to limit the size of infarct in dog.
Volatile agents
IPC can also be mimicked by certain volatile agents in the myocardium and liver. Studies
on the canine model of myocardial stunning by Warltier et al have shown that isoflurane
or halothane administered during an ischemic period but not during reperfusion period
correlated with faster recovery of cardiac contractility. The volatile agents, which are
known to mimic IPC, include isoflurane, halothane and enflurane. The preconditioning
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effects of these agents appear to involve adenosine receptor mediated mechanisms as
pretreatment with ADO antagonists (8-p-sulpho phenyltheophylline) blocked the
protective effects of these agents. The second messengers involved appear to be PKC
and / or K+ ATP channels" Kon et al have reported that isoflurane administration before
ischemia protected rat liver from reperfusion injury as shown by reduced LDH release
and less generation of superoxide free radicals.
Ischemic pre-conditioning in cardiac surgery

The incidence of patients having a fall in ejection fraction (1ZF) cardiac index (CI) after
CABG postoperatively is approximately 90%. The cause of this can be explained on the
basis of the cellular pathophysiologic process during and after CPB. Studies on cellular
pathophysiologic process have shown that most of the cellular damage occurs during
the warm reperfusion period. Depolarizing arrest enhances calcium influx during and
after ischemia, resulting in significant calcium mediated injuries and increased energy
demands during warm reperfusion period. This is subsequently clinically manifested as
depressed myocardial performance, increased incidence of arrhythmias and prolonged
ICU stay. Experimentally the only situation where IPC has been shown to confer
additional protection to that of hypothermia and cardioplegia are long ischemic times
and non homogenous delivery of cardioplegia due to proximal coronary artery
blockade.
In clinical practice, high risk situations which would benefit from preconditioning may
include (a) extreme coronary artery disease (CAD) with poor collaterals and with
increased risk of maldistribution of cardioplegia (b) severe left ventricular (LV)
hypertrophy where subendocardial perfusion is problematic (c) anticipated long
ischemic lime including those incurred by cardiac allografts during cold storage (d) the
senescent myocardium which is more prone to develop tissue damage owing to Ca+2
overload.
Ischemic pre-conditioning in off pump CABG

The procedure of off-pump myocardial revascularization (OPCAB) requires a period of
temporary coronary occlusion of the target vessel, this possibly causing myocardial
ischemia accompanied by hemodynamic instability and arrhythmias. Animal studies
have shown that ischemic preconditioning is effective in reducing ischemic reperfusion
induced arrthymias. There is also evidence of anti-arrhythmic effects of ischemic
preconditioning in the human heart. Z K Wu et al demonstrated in their controlled,
randomized, prospective study that Ischemic preconditioning significantly suppressed
heart rate elevation, the episodes of supraventricular tachycardia (SVT) and the
incidence of ventricular tachycardia (VT) in patients who undergone off pump CABG.
Laurikka J el al investigated in a controlled, randomized, prospective study, that
ischemic preconditioning enhances myocardial performance in patients who undergone
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off-pump CABG. They found that ischemic preconditioning proved to be applicable and
safe in patients undergoing off-pump myocardial revascularization, it tended to
decrease tile immediate myocardial enzyme release, it prohibited the post operative
increase in heart rate and it enhanced the recovery of stroke volume index (SVI),
Currently, however, in view of widespread use of coronary shunts during the
performance of off-pump CABG, which maintains the distal blood flow while grafting,
ischemic preconditioning is not been widely utilized in many centers routinely.
IPC in thoracic anesthesia

Clinical situations like prolonged CPB, lung transplantation and pulmonary embolism
produce an IRI like picture in the lung which may subsequently manifest an acute
respiratory failure or ARDS. This lung injury can be attenuated by infusing ADO before
ischemic period. Marts el al who studied the effects of 2-chloradenosine (2-CA) which is
a synthetic analog of ADO, in rabbit model found that when administered I.V. before 60
mins of global lung ischemia; 2-CA was able 10 attenuate IRI. It also resulted in better
cardiac output (CO), decreased pulmonary vascular resistance, decreased white blood
cell count (WBC) and protein transudation in lung parenchyma and improved post-
perfusion PaO2.
Ischemic pre-conditioning in heart and lung transplantation
IRI is also known to be one of the major causes of post transplantation organ failure.
Presently used methods of organ storage include using hypothermic storage in
electrolyte rich solution (University of Wisconsin Solution). The storage time differs for
different organs and prolonged storage time has been shown to cause tissue edema,
vascular endothelial injury and acute organ failure soon after transplantation. The
potential of IPC has been applied lo organ preservation also. Studies by Petsikas et al
and Karen et al have shown that IPC provided additional protection than that provided
by hypothermia. This helped to improve the contractile function and cellular energy
level after global hypothermic ischemia with storage in standard medium.
Duzy el al has also shown that IPC is beneficial in lung transplantation. They studied 5
minutes of preconditioning followed by 6-12 hours of cold storage of the rat lung and
found an improved gas exchange after single transplantation. IPC also significantly
reduced the formation and release of toxic reactive metabolites in the transplanted lung.
Application of pre-conditioning in dynamic cardiomyoplasty

Cardiomyoplasty was first applied successfully in 1985. The beneficial effects of
substituting cardiac muscle with skeletal muscle include (1) ventricular mechanical
assist (2) improved collateral blood flow and/or (3) release of growth factors from the
assist muscle to the recipient myocardium. The limitation of this procedure however
has been ischemic damage to the assisting muscle. Lannuzo et al have attempted to
decrease ischemic skeletal muscle damage by combining ischemic and hyperthermic
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preconditioning prior to cardiomyoplasty. It has been previously shown that even
skeletal muscle can be preconditioned. Lamzo CD et al tested two protocols of cyclic
ischemia (IPC) consisting of 15 mins of heat shock at 42°C 24 hours prior to surgery. IPC
has also been successfully accomplished in skeletal muscle using transient noose
occlusion of the nutrient vessel to assure a no flow state in the muscle Skeletal muscle
preconditioning prior to cardiomyoplasty may augment systolic force and/or limit
diastolic function. Neovascularized skeletal muscle provides a rich source of collateral
coronary vessels to ischemic recipient myocardium. It may also initiate transcriptional
regulation of an array of protective gene expressions.
Clinical evidences of preconditioning
There are various evidences to show that preconditioning may occur in the clinical
setting. They include i) angioplasty ii) acute tolerance to ischemia iii) angina prior to MI
(iv) preconditioning and ventricular arrhythmias.
During angioplasty it has been well established that die severity of chest pain,
magnitude of ischemic changes on ECG and production of lactate is decreased on
subsequent inflation when compared to initial percutaneous transluminal coronary
balloon inflation. This protective phenomenon may be due to the opening of K+-ATP
channel. In some patients the beneficial effect of balloon occlusion has been attributed
to acute recruitment of collateral vessels whereas other studies have disposed this
concept claiming that the benefit was mainly due to preconditioning.
Another clinical evidence of IPC is the development of acute tolerance 10 ischemia in
the form of exercise or pacing. Patients with CAD were induced with ischemia by
exercise or rapid pacing and this was followed by several minutes of rest and then a
second bout of exercise. h was observed that the patients could exercise longer, had less
pain and less ST segment changes during the second challenge. This phenomenon is not
associated with acute recruitment of coronary collateral flow but is accompanied by
reduced lactate production and reduced oxygen demand during the second compared to
the first period of ischemia. A reduced oxygen demand during this second period of
stress is consistent with shorter action potential (AP) duration and supports to some
extent, the concept of the K+-ATP activation with preconditioning. Another clinical
situation in which IPC may occur is in the setting of angina prior to MI. It is shown that
this limits the amount of myocardial necrosis.
Kloner et al analyzed in hospital outcomes of patients who had history of angina prior to
MI and angina within 48 hours of MI, compared to patients without history of previous
angina. Patients who had a history of either recent angina or any angina prior to their
MI had less in hospital death and less severe congestive heart failure (CHF) and shock
than patients without a previous history angina. They also had smaller infarct size
determined from creatinine kinase curves. Anzai et al reported that the beneficial
effects of antecedent angina included a lower incidence of sustained ventricular
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tachycardia and ventricular fibrillation; less pump failure and cardiac rupture and lower
in hospital mortality rate.
Most of the deaths in AMI are due to ventricular fibrillation or ventricular tachycardia
(VT) caused by acute ischemia or induced by reperfusion, the mechanisms of with
which include reentry, enhanced automaticity and triggered activity. It has been shown
that in pre-conditioned ischemic rat heart the incidence of VT is reduced.
Future directions:
Pre-ischemic conditioning is an extremely effective reaction to limit ischemic induced
cell necrosis and preserving myocardial function. The clinical application of IPC would
be beneficial in any situation in which ischemia can be controlled by increase in the
critical ischemia time i.e. (CIT/50). CIT30 is defined as the duration of circulatory
disruption compatible with 50% tissue survival. An increase in the ischemic tissue
tolerance could decrease morbidity associated with IRI in many procedures. However
the disadvantage of IPC is that ii requires a period of pre-ischemic manipulation for
organ protection, a drawback not well tolerated in most operation rooms. It is hard to
predict, the future of cardioprotection as the present is changing so rapidly. The two
components of cardioprotection in most operations deal with the consequences of
ischemia and inflammation and the manner in which they interact. The perfect method
to utilize the protective effects of IPC would be to develop a pharmacological agent that
can duplicate the cardio-protective effects and act as a “magic bullet” against IRI.
The discovery and recognition of an ideal pharmacological agent such as ADO and other
agents would help us better to understand and therapeutically exploit this adaptive
defense system, which has proven to be one of the most effective infarct limiting
strategies reported so far.
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Chapter 31 PREOPERATIVE ASSESSMENT AND PREPARATION OF A
CARDIAC PATIENT FOR SURGERY
The number of cardiac patients presented for non-cardiac surgery is on the rise thanks
to the availability and affordability of state-of-the-art investigations and medical
treatment. The distressing fact is that the average age of the patients is on the rise (US
Dept of health and Human services-1998, the number of co-morbid conditions are also
on the rise. Therefore, the job of the anesthetist manning these patients becomes far
more demanding. The present review covers the different aspects of preoperative
cardiac risk assessment in patients suffering from heart disease (IHD) undergoing non-
cardiac surgery.
Perioperative myocardial infarction (MI) is the postoperative mortality and morbidity,
especially in the elderly. Other factors of major contribution are previous MI, congestive
heart failure, angina, hypertension and diabetes mellitus. In view of the above
mentioned factors, it becomes imperative to assess these patients preoperatively. The
patients are likely to undergo one "of the following surgeries:
1. Cardiac surgery
2. Non-cardiac surgery
a. General surgery
b. Vascular surgery
c. Carotid artery surgery
The factors contributing to the mortality/morbidity should be understood better in
order to understand the sequence in which the preoperative assessments are made. The
following are some of the important factors, which contribute to the adverse outcome
after surgery in patients with cardiac disease.
Previous MI:
There has been a great deal of interest in this area because the incidence of
perioperative MI has been quoted in the region of 5-8 %. The group from Loyola
University reported an incidence of perioperative MI of 4.3% at 0-3 months, 0 at 4-6
months and 5.7% at more than 6 months with an intermediate of 3.3%.
However, there has been a consensus that good control of congestive heart failure,
dysfunctional ventricles, and arrhythmia have generally reduced the morbidity and
mortality in cardiac patients undergoing non cardiac surgery.
Angina:
 Presence of angina of any form generally indicates higher risk in terms of cardiac
complications like sudden death and MI 1979, McPhail
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Congestive cardiac failure (CCF):
Patients with clinical or radiological evidence of CCF have a poor prognosis. In fact,
patients with poor left ventricular function have a high mortality - 33% in the first year
and nearly 75% in the second. In some of the recent studies, there are suggestions to
place these patients under high-risk group .Caution should be exercised about the
possibility of missing CCF because of its atypical presentation and appropriate
treatment should be initiated if needed. Prause and others indicate that if applied
correctly, the ASA and Goldman's risk index increase the prediction of perioperative MI .
Arrhythmias:
Arrhythmias are usually common in the elderly patients and are indicators of
underlying IHD. If they are coupled with dysfunctional ventricle, it is dangerous.
Arrhythmias are a matter of great concern during vascular surgery especially of
carotids. Most of the antiarrhythmic drugs are either myocardial depressants or have
local anesthetic properties. Therefore, they may enhance the effects of general
anesthetics, local anesthetic agents and muscle relaxants.
Hypertension:
The Framingham study has established the association between hypertension
and IHD. The clinical importance of preoperative hypertension as a risk factor for
Perioperative MI has become controversial. However, the possibility of enhanced
atherosclerosis in patients with hypertension must be kept in mind.
Diabetes mellitus:
Coronary artery disease as a major cause of death in adult diabetics is known. In a
multicentric European study have concluded that diabetics have higher incidence of
cardiac complications during noncardiac surgery. The same authors have recommended
tight control of blood sugar and prevention of ketoacidosis in order to prevent diabetes-
induced cardiac complications.
Renal failure:
Renal failure is a fairly common problem in patients with JHD. The possibility of renal
failure should be kept in mind when dealing with diabetics with severe peripheral
vascular disease. It may be worthwhile to remember that various contrast; used in
diagnostic radiology have deleterious effects on the kidneys. It is also important to keep
the patients waiting for such diagnostic procedures well hydrated to avoid deterioration
of renal function following the use of contrast.
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Cerebrovascular disease:
Cerebrovascular disease is a manifestation of the genera! Atherosclerotic process.
Patients with previous cerebrovascular events have to be questioned for in-depth
details about the event. Association of hypertension and diabetes in the presence of
peripheral vascular disease is ominous. Auscultation of the carotid arteries during the
routine clinical exam of the patients can be very helpful. Carotid Doppler examination
may be considered in cases with a high suspicion of cerebrovascular disease.
Clinical History:
The time spent during preoperative interview with the patients is worth. The
knowledge gained from the history car guide us to take appropriate decisions regarding
the tests to be ordered, premedication and anesthetic technique to be applied Variants
of angina and the occurrence of angina related to the routine activity of the patient can
give us fairly good idea about his cardiopulmonary reserve. The occurrence of silent
ischemia in diabetics should be kept in mind .It is also worthwhile to obtain the history
of drug allergies if any of the patient.
There are other concomitant diseases such as valvular heart disease, peripheral
vascular disease and chronic obstructive airway disease etc. that have to be kept in
mind while executing the anesthesia. The other most important aspect of cardiac
patients is the multiple drugs that the patients often receive”. These include beta-
blockers, calcium channel blockers, diuretics digoxin etc. Close attention must be given
to the possible drug internet ions to prevent avoidable complications.
Physical Examination:
Physical examination includes examination of the heart and looking for the signs of
concomitant xanthomas etc Cardiac-examination should include signs and symptoms of
heat failing arrhythmia, and vascular disease etc. Signs of heart rate of great importance,
because the presence of heart failure of recent occurrence of CHF increases morbidity
and mortality. Examining other systems such as respiratory and central nervous system
is also very important. The incidence of other systems involvement in patients suffering
from IHD is fairly high.
Preoperative Cardiac Tests:

There are certain routine cardiac tests that are performed before one undertakes
anesthesia in patients who suffer from cardiac ailments, especially IHD. We may need to
discuss with several specialists such as, cardiologists, chest physicians, etc. There are
certain systems of risk stratification such as ASA grading, Goldman's cardiac risk index,
Lewis risk index, Jeffrey, and Carliner risk index. The most important fact is that there is
a need to recognize high-risk group. Prause in a discussion on the validity of, these
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scores concludes that perioperative morbidity can be predicted with the ASA grade to a
lesser degree, the Goldman's index. Teplick comments that elaborate testing may not be
necessary even if patients with IHD are scheduled for high-risk surgery. The American
College of cardiology has proposed guidelines on preoperative cardiovascular
evaluation for noncardiac surgery and following these guidelines allows very little scope
for missing high-risk patients. The routine tests that are performed after obtaining
clinical history find performing physical examination are as follows:
1. Laboratory tests
2. Radiological examination
3. Electrocardiogram
4. Exercise stress testing (tread mill test-TMT)
5. Echocardiography
6. Nuclear imaging
7. Myocardial perfusion imaging
8. Magnetic resonance imaging
Laboratory Tests:
The necessary laboratory tests in-patients with IHD are those, which affect the oxygen
transfer, like Hb% and PCV. The other tests that are necessary are those relevant to the
systemic disease that the patient has, for e.g., pulmonary function tests in patients with
COPD, thyroid function test in those suffering from thyroid disease, renal parameters in
patient with known or dysfunction. There is a strong correlation between high
cholesterol level and IHD (Cohn et al 1976).
Therefore, it may be relevant to subject patients with abnormal cholesterol levels to
further tests. The most sensitive laboratory test reflecting myocardial ischemia are
elevated levels of cardiac enzymes viz., CFK M and B, Troponin T. These tests are useful
if acute myocardial ischemia is suspected.
Chest Radiography:
Routine chest-x ray is immensely useful and it is also cost effective, although there is
some controversy regarding this. Chest x ray can be specific in patients with IHD, heart
size being small in patients with good LV function. Chest radiograph can be a good
indicator in presence of heart failure; one would expect to see cardiomegaly in them. In
acute, heart failure, other drugs such as prominent hilar shadows, venous congestion
can be seen; this kind of pulmonary edema picture can be seen in acute left ventricular
failure following anteroseptal myocardial infarction and acute VSD.
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Electrocardiogram (ECG):
Although in up to 50%of the patients with IHD, the resting ECG may be normal, the role
of preoperative ECQ |n developing countries like ours should not be undermined. ECG is
a very cost-effective investigation that gives information about ischemic injury and
infarction. Comparison of the current and old traces of ECG helps us to detect changes.
In case of doubtful or ambiguous changes, it may be helpful to discuss with the
cardiologists .
Exercise Stress Testing:

As early as 1908, Einthoven has described alteration of with exercise. After several
modifications and advancements, it has reached the present state of computerized
testing. The basic physiology of stress testing is alteration in the ECG following raise in
the myocardial oxygen requirement subsequent to exercise. The "target heart rate" for
an individual is calculated using the patient's body weight and the height. If the patient
develops changes in the ECG before attaining the target heart rate, or during the
recovery phase, the stress test is said to be positive. The data that is useful for the
anesthesiologist is the target heart rate, beyond which the patient is likely to sustain
ischemia. It may be pertinent to note that even those who are physically active and who
are in the high risk group, should prove their ability to perform the tread mill test
without or^ minimal changes in the ECG. Those who out of physical disability can not
perform the TMX can be assessed by pharmacological means i.e., by Dobutamine stress
testing. Other drugs that are available are dipyridamole (an indirect coronary
vasodilator) and adenosine (a direct coronary vasodilator). Whatever, be the type of
stress test, the positivity is determined by the changes in the ST - T segments. The
changes may be in the form of ST depression ST elevation, depression of the J point, and
rarely changes in the P wave. The changes in the ECG can occur during TMT or after. The
changes are significant and signify ischemia regardless of the stage.
Echocardiography:
Echocardiogram has become an important tool in not only the preoperative period to
investigate the patient but also to monitor the patients during the surgery.
Echocardiography can noninvasively assess the wall motion abnormalities, valvular
function, and global ventricular function. Recently, transoesophageal echocardiography
(TEE) has revolutionized the diagnosis and preoperative monitoring of certain
otherwise difficult parts of the heart, easy. In the recent times there are doubts raised
about the role of Swan Ganz catheter and also suggestions are made about likely
replacement of all other monitors by Transoesophageal echocardiography. This also
brings up the need for us to learn and/or update our knowledge of echocardiography. In
the author's opinion, in the near future, this may not only become a part of the MD
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curriculum, but may also become a daily necessity. The indications for preoperative
echocardiac examination are:
1. IHD patients with hypertension of long duration.
2. IHD patients with diabetes of long duration.
3. Unexplained breathlessness in a preoperative patient.
4. Patients with known dysfunction of the ventricles, with or without recent
congestive heart failure.
5. Any of the above patients scheduled for surgery during which there is a likely
massive fluid shift.
There is another modification of echocardiography, which is the stress
echocardiograph. In the stress echocardiography, the changes in the wall motions
secondary to exercise arc analyzed. Some of the patients develop wall motion
Abnormality only after exercise and not during rest. These patients need to be further
subjected to invasive tests such as coronary angiogram etc.
Nuclear Imaging:
Nuclear imaging is a technique where in a radioactive dye is injected in to the patient
and its concentration is imaged. There are different types of cameras, which can
calculate hemodynamic values such as ejection fraction, cardiac output, pulmonary
transit time and global LV function. Nowadays, most of the measurements are made by
tomography, using single-photon or positron emission.
Myocardial Perfusion Scanning:

This test is similar to nuclear imaging but the details available are related to the
regional perfusion of the heart. This procedure gives us an idea about the severity of the
coronary artery block and the need for revascularization. If a patient has proven
coronary artery disease, thallium 201 scan can tell us how significant the disease is and
also the likely therapeutic benefit that the patient may have. This is usually performed
before undertaking coronary revascularization, angioplasty or coronary artery bypass
graft surgery. Lette and his coworkers have shown that, by using scintigraphic indices,
patients can be stratified into various subgroups and surgery can safely be performed in
the low risk and the intermediary groups.
Magnetic Resonance Imaging:

Magnetic resonance imaging (MRI) is a useful tool to have a three-dimensional picture
of the chambers of the heart and its contents. MRI can help in the accurate assessment
of LV function. Ischemic insults to the heart can be very accurately assessed. The
disadvantage of this procedure is its prohibitive cost.
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Guidelines for preoperative testing:
The algorithm as proposed by Eagle et al 1996, based on the expert’s opinion (figure
land 2) is useful in deciding upon the approach that one has to take while dealing with
patients with IHD. Exercise tolerance and anginal patterns are the most important
determinants of perioperative risk and the need for invasive monitoring. McPhail and
colleagues demonstrated that patients undergoing major vascular surgery, who could
exercise up to 85% of their peak heart rate, were at lower risk even if their stress test
was positive. An excellent exercise tolerance even in the presence of positive stress test
and stable angina suggests that the heart can be stressed to a great extent before it
becomes ischemic. A patient who can walk a mile without angina has a far less risk, than
the one who gets angina on minimal exercise and who is a high-risk patient. This is
where the patient’s life style (as obtained by the history) can guide of the investigations
that the patient is likely to need.
The surgical procedure itself has a significant impact on the perioperative risks and the
amount of preoperative information that is required to safely perform an anesthetic. For
surgical procedures, which are not associated with significant risk, the preoperative
investigation charges should not exceed the cost of the operation itself. For e.g.,
outpatient procedures are shown to have lesser morbidity and mortality; therefore, an
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outpatient surgical patient is less likely to need elaborate perioperative interventions/
investigations. On the other hand, a patient with multi valvular disease or severely
compromised ischemic heart disease is likely to need extensive perioperative care and
monitoring, if he has to undergo a major intra-abdominal, vascular or intrathoracic
surgery. Open-heart surgery, vascular surgery, carotid artery surgery and general
surgery carry different grades of risks. In the present day anesthesia, it is not impossible
to manage major cases with reduced morbidity and avoid mortality.
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- PERIOPERATIVE RECOGNITION AND
Chapter 32
TREATMENT OF MYOCARDIAL ISCHEMIA

The pattern of cardiovascular disease in the general population of developed and
developing countries has changed considerably in the last two decades. Ischemic heart
disease has become the hallmark of our overfed and under exercised society and is the
most important single preexisting medical condition affecting patients presenting for
anesthesia. Regional or global imbalances in myocardial oxygen supply and demand
result in the production of myocardial ischemia. Early recognition of myocardial
ischemia in patients in perioperative period can enable anesthesiologist to prevent the
morbidity and mortality by appropriate pharmaceutical interventions.
INCIDENCE OF PERIOPERATIVE ISCHEMIA

Preoperative Ischemia
Historically, the efforts of prevent myocardial ischemia in preoperative period have
been directed towards careful control of the readily obtainable hemodynamic
determinants of myocardial oxygen demand such as heart rate and blood pressure. The
recent evidence demonstrates that most ischemic episodes that occur during daily
activities are not preceded by increases in heart rate, or rate pressure product and are
clinically silent. Knight et al; monitored 50 patients of IHD with Holier monitoring for 24
h. before elective surgery and demonstrated that 21 patients had ECG evidence of
ischemia despite maximal therapy. Only 23% of these ischemic episodes were preceded
by an increase in heart rate of 20% or more.
Other studies have examined the incidence of myocardial ischemia upon arrival in the
operating room in patients undergoing coronary revascularization. The incidence varies
from 0.3 to 27%; a large proportion of the episodes were hemodynamically unrelated.
Intraoperative Ischemia
A large percentage of intraoperative ischemic events are not preceded by changes in
heart rate and blood pressure.
Defining tachycardia as an increase in heart rate of 10 beats/ minute, hypotension as
20% decrease in systolic pressure, the authors found that 43% of patients suffered
intraoperative ischemic event. Of these ischemic episodes 74% occurred while heart
rate and blood pressure were in patients 'in-hospital resting range'. Other recent
studies have confirmed that mast intraoperative ischemic events are unrelated to
hemodynamic perturbations, suggesting that decreases in myocardial oxygen supply
may be important in the genesis of intraoperative ischemia.
Though the reported incidence of intra operative myocardial ischemia is variable, it is
clear that a large portion of these episodes (> 50%) occur without readily measurable
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changes in myocardial oxygen consumption. This supports the conclusion that ischemia
seen in the intraoperative period consists of not only hemodynamically related episodes
but also hemodynamically unrelated silent episodes as well.
OUTCOME AFTER MYOCARDIAL ISCHEMIA
The most feared consequence of perioperative ischemia is postoperative myocardial
infarction (PMI). Slogoff el al has shown that the risk of PMI was 6.9% in patients who
had perioperative ischemia compared to 2.5% who did not have ischemia. The risk of
PMI was also correlated with the severity of ischemia. In one study, patients who had ST
segment depressions greater than 2 mv had a 9.3% incidence of PMI, whereas those
who had ST segment depressions between 1.0 and 1.9 mv had a 6-2% incidence.
DIAGNOSING MYOCARDIAL ISCHEMIA

Electrocardiography (ECG):
The gold standard for diagnosis of myocardial ischemia is the presence of ECO changes.
ECG changes occur relatively late in the temporal sequence of myocardial ischemia after
deterioration of ventricular diastolic and systolic function. For ECG monitoring to be
effective in detecting ischemia, the appropriate leads must be monitored. Simultaneous
monitoring of leads II and V is commonly used because of the high sensitivity of this
combination in detecting myocardial ischemia, Monitoring of leads II and V. will not
detect true posterior ischemia, and this for this reason, use of an esophageal ECG lead
has been suggested to monitor right ventricular and posterior left ventricular ischemia.
Pulmonary Capillary Wedge Pressure (PCWP)
 The PCWP trace of the pulmonary artery catheter has been described as a tool to
make early diagnosis of the left ventricular (LV) ischemia. Similar observations
have been made regarding the CVP trace and RV ischemia. Reduction in LV
distensibility occurs in the early stages of LV ischemia because of diastolic
dysfunction. In particular, LVEDP is elevated. Under these circumstances, left
atrial pressure (LAP) will be elevated to maintain LV diastolic filling. Movement
of the left atrium to a steeper portion of its pressure-volume relationship will
result in magnification of the normal LAP waveforms. In addition, dilation of the
LA may result in a more forceful atrial contraction and production of an enlarged
A wave. The peak of this A wave will reflect LVEDP. LV ischemia, which produces
LV dilation or papillary muscle dysfunction, may cause mitral regurgitation with
generation of a prominent V wave.
 The PCWP trace is a reflection of LAP. However, because the PCWP waveform is
transmitted through the complaint pulmonary venous system, it is a damped
version of the LAP. In particular, the left atrial A wave may be poorly seen. As a
result, it has been demonstrated that mean PCWP reflects mean LV diastolic
pressure and may underestimate LVEDP by 10 to 15 mm Hg during ischemia.
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 Changes in PCWP and the PCWP waveform have poor sensitivity and specificity
in detecting episodes of myocardial ischemia. This is true for a number of
reasons
o PCWP does not necessarily reflect LVEDP as previously described.
o When only a small region of LV wall develops diminished distensibility with
an ischemia episode, the distensibility of the LV as a whole changes only
slightly and subsequent changes in LVEDP as reflected by the PCWP are
difficult to detect.
o The quantitative change in PCWP and the qualitative change in the PCWP
waveform necessary to define an ischemic event have not been systematically
defined.
o Acute elevations in after load in the absence of ischemia can produce
elevations in PCWP.
Because PCWP trace changes are not seen in all episodes of myocardial ischemia, they
cannot be relied upon as the sole indicator ischemia. For this reason, it is important to
emphasize that suspicious ECG or TEE changes cannot be ignored simply because there
is no change in the value of the PCWP or the PCWP waveform.
Transesophageal Echocardiography
 Regional wall motion abnormalities (diminished inward excursion and
thickening) are known to occur as a result of ischemia, and these wail motion
and thickening abnormalities are known to precede ECG changes. The
development of severe hypokinesia, akinesia, or dyskinesis is more specific for
ischemia than mild hypokinesia Changes in wall thickening are more sensitive
for detecting ischemia than changes in wall excursion. In the instance of
complete coronary occlusion, wall motion abnormalities and ECG changes occur
within 60 seconds each other. For cases in which ischemia is less severe, RWMA
may precede ECG changes by several minutes. In fact, numerous studies have
shown intraoperative TEE qualitative analysis of regional wall excursion and
thickening to be a more sensitive detector of myocardial ischemia than ECG
changes and to be capable of detecting ischemia before ECG changes.
 Recent data demonstrate a lack of concordance between ischemia detected by
ECG and that detected by TEE. There are both TEE-detected ischemic episodes
not detected by ECG and ECG-detected ischemic episodes not detected by TFE.
This may be due to several factors:
 Normally, the TEE probe is placed at the mid-left ventricular level (level of the
papillary muscles), at which wall segments in the distribution of all three
coronary arteries can be monitored- Because a short -axis view of the left
ventricle can only be obtained at one level at a time, ischemic changes occurring
in the basal or apical ventricular levels will be missed. Biplane and multi plane
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probes allow visualization of the apex and base of the heart. Recent evidence
demonstrates better concordance between ECG and TEE detected ischemia when
biplane TEE is used and RWMA are detected in both the short-axis and long-axis
views.
 Ischemic episodes may be missed because qualitative wall motion analysis is
difficult for patients with preexisting wall motion abnormalities. Likewise, all
RWMAs (particularly in areas tethered to scar) may not be ischemic in origin.
Changes in after load may unmask areas of previous scarring. Ventricular pacing
or a bundle-branch block may make detection of RWM A more difficult because
of asynchronous contraction. Stunned myocardium may exhibit continued
RWMA despite adequate perfusion.
 ECG may detect ischemia with small areas of subendocardial ischemia
undetectable by TEE.
 These observations, combined with the fact that no evidence exists to support
the contention that early detection and treatment of ischemia alters outcome,
temper enthusiasm for TEE as the ideal ischemia monitor.
PREDICTING MYOCARDIAL ISCHEMIA
The ability to predict hemodynamic alterations that are likely to result in myocardial
ischemia in individual patients would allow prompt treatment and avoidance of events
initiating ischemia. Unfortunately, the diverse nature of myocardial oxygen imbalance in
patients leaves the anesthesiologists with no predictor of myocardial ischemia that is
reliable in all circumstances. The indices used in the next sections all have limited
usefulness.
Rate-Pressure Product and Triple Index

The RPP is the product of heart rate and systolic blood pressure, where the TI is the
product of heart rate, systolic blood pressure and PCWP. The RPP has been shown to
provide a useful assessment of MVO2 and to predict ischemia in patients undergoing
stress testing. Most patients experience the onset of ischemia at an RPP of 20,000.
However, its usefulness in assessing MVO2 and predicting ischemia in anaesthetized
anesthetized patients not reliable. For patients anaesthetized with halothane, RPP does
not provide a good assessment of MVO2 because halothane induced reductions in MVO2
are not reflected in the RPP. Of greater importance is the fact that RPP is a poor
predictor of myocardial ischemia in anesthetized patients. Episodes of hypertension and
tachycardia leading to ischemia will be predicted by an RPP greater than 12.000 in
patients with coronary artery disease. However, under anesthesia, it is possible for a
patient to have a combination of hemodynamic Parameters (tachycardia and
hypotension) particularly deleterious to myocardial oxygen delivery that will not result
in an elevated RPP. It has been demonstrated in animals that RPP does not correlate
with the onset of myocardial ischemia when a wide variety of heart .ales and systolic
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blood pressure are examined. Similarly, RPP was not a useful predictor of myocardial
ischemia in patients undergoing coronary revascularization with halothane anesthesia,
because tachycardia and hypotension were the hemodynamic alterations most often
associated with intraoperative ischemia.
The TI is subject to the same criticisms as the RPP. The addition of PCWP to the product
adds the variable of wall radius to the assessment of MVO2. However, the TI still fails to
account for large reductions in myocardial oxygen delivery in the genesis of ischemia.
Myocardial Supply-Demand Ratio (DPTI: SPTI)

Efforts to account for beat-to-bat variations in both myocardial supply and demand in
the genesis of ischemia led to development of the supply-demand ratio. Supply is
defined as the diastolic pressure time index (DPTI). DPTI = (mean diastolic pressure -
left ventricular end diastolic pressure) x duration of diastole. Demand is defined as the
systolic pressure time index (SPTI). SFTI = mean arterial pressure x duration of systole.
Ratios below 0.5 have been found to result in development of subendocardial ischemia.
Unfortunately, use of this ratio is unreliable for several reasons.
Increases in MVO2 due to increased contractility are not reflected in blood pressure and
heart rate changes and therefore are not accounted for by SPTI.
A higher ratio will be needed in the presence of anemia to compensate for the reduced
oxygen carrying capacity of blood. The presence of pressure drops across coronary
stenoses makes the DPTI an unreliable index of distal coronary perfusion. Use of the
ratio is cumbersome because it requires calculation of the areas under the diastolic and
systolic pressure curves, respectively.
Mean Arterial Blood Pressure- Heart Rate Quotient

Recent animal work demonstrates that ischemia occurs in the distribution of a critical
coronary stenosis and in collateral-dependent myocardium when the pressure rate
quotient (PRQ), defined as MAP/HR. is less than 1. This relationship seems to be valid
over a wide range of pressures and heart rates. An increase in heart rate can C-JSC or
worsen ischemic dysfunction at any mean arterial blood pressure; however, the
absolute heart rate at which ischemia occurs is dependent on the preexisting mean
arterial pressure. In other words, higher heart rates are tolerated without ischemia at
higher mean arterial pressures. For patients undergoing coronary revascularization,
PRQ < 1.0 has poor sensitivity and specificity in predicting myocardial ischemia as
detected by both ECG and TEE.
In summary
 The combination of hypertension and tachycardia may result in myocardial
ischemia by increasing myocardial oxygen demand.
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 The combination of hypotension and tachycardia is particularly detrimental to
myocardial oxygen balance because it reduces both the time and the pressure
.gradient available for myocardial oxygen.
 Tachycardia, in and of itself, is detrimental to myocardial oxygen balance.
Experimentally, tachycardia causes or worsens ischemic dysfunction at any given
mean arterial blood pressure. Clinically, tachycardia is associated with the
development of ischemia in patients undergoing coronary revascularization
whereas hypertension per say is not a risk factor. In particular, heart rates
greater than 110 beats per minute are associated with a dramatically increased
incidence of intraoperative ischemia in patients undergoing coronary
revascularization.
TREATMENT OF ISCHEMIA
Because the genesis of myocardial ischemia is multifactorial, treatment must be aimed
at the specific causes at work in each instance.
Tachycardia
 No single value of heart rate is uniformly detrimental to myocardial oxygen
balance in a given patient. As already discussed, the heart rate at which ischemia
is likely to occur will vary with mean arterial blood pressure and the other
determinants of myocardial oxygen balance. When an increase in heart rate
results in ischemia or is likely to result in ischemia, immediate therapy is
necessary.
 Immediate steps should be taken to eliminate inadequate anesthetic depth as a
cause. Efforts to ensure that preload is adequate also must be taken. This is
particularly important for patients with diminished ventricular distensibility, for
when a higher-than-normal end-diastolic pressure will be necessary to ensure an
adequate ventricular end-diastolic volume. When these measures fail, treatment
with a beta-blocker may be necessary in patients with and without preoperative
beta-blocker therapy. Many patients taking beta-blockers preoperatively will
have plasma concentrations that are too low to blunt the hemodynamic
responses to surgery and will require supplemental beta-blockade. Propranolol
in incremental doses of 0.5 to l.0mg to a total of 0.1 mg/kg may be used for
patients without severe, ventricular systole dysfunction. For patient with a
history of bronchospasm or reactive airway disease, a beta-1 -selective agent
such as metoprolol is useful. Incremental doses of 2.5 to 5.0 mg to a total of 0.5
mg/kg can be used; because elevations in PCWP will reduce coronary perfusion
pressure (CPP), concomitant therapy with nitroglycerin 0.5 to l.0 mg/kg/min is
indicated in the presence of an elevated PCWP.
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 In some instances, the ultra-short- acting beta-blocker esmolol may be useful.
Esmolol has an elimination half-life of 9 minutes due to metabolism by red-cell
esterase and is relatively beta-1-selective. Esmolol is started with a bolus of 0.5
mg/kg given over several minutes followed by an infusion of 50 mg/kg/min and
titrated up to 300 mg/kg/min as necessary. Esmolol is useful for patients with
poor ventricular function or bronchospastic disease, because if it is not tolerated,
therapy can be quickly terminated. Furthermore, unlike longer acting beta
blockers, esmolol can be used aggressively in the pre-CPB period without fear
that it will compromise termination of CPB.
Hypotension
The extent of hypotension that can be tolerated before ischemia develops is dependent
on several variables. For example, a reduction in arterial blood pressure may reduce
MVO2 by reducing after load, but at the same time, it may reduce proximal perfusion
pressure which drastically reduces myocardial blood flow distal to a stenosis.
Furthermore, as discussed previously, at higher heart rates, lesser degrees of
hypotension will be tolerated. The source of hypotension must be quickly and
accurately determined. Determination of cardiac output and systemic vascular
resistance (SVR) will help direct therapy.
When hypotension is due to a reduction in cardiac output, heart rate and preload should
be optimized. If these measures fail to correct the fall in cardiac output, any inhalational
anesthetic agents should be discontinued to eliminate their negative inotropic
properties. A fall in SVR can be treated with an alpha-adrenergic agonist such as
phenylephrine in incremental doses of 40 to 100 mg. It should be kept in mind that
dynamic stenosis and should therefore be titrated carefully. Because elevation in PCWP
will reduce CPP, concomitant therapy with nitroglycerin 0.5 to 1.0 mg/kg/min is
indicated in the presence of an elevated PCWP.
Hypertension
Hypertension is classically associated with tachycardia in the genesis of myocardial
ischemia. Treatment, in this instance, is directed toward deepening of anesthesia. If
hypertension is persistent despite adequate anesthetic depth, vasodilator therapy is
warranted sodium nitroprusside is a readily titrable, potent arteriolar dilator and can
be used effectively to treat hypertension. An infusion can be started at 0.25 mg/kg/min
and titrated upward. However, because sodium nitroprusside is a potent arteriolar
dilator, it has the potential to induce a coronary steal in the presence of the appropriate
anatomy.
Nitroglycerin dilates large coronary vessels and not arterioles and therefore is not
implicated in the steal phenomenon. Nitroglycerin has its greatest dilating effect on the
venous beds and arterial dilatation occurs only at higher doses. Despite this, when used
in appropriate doses, nitroglycerin and nitroprusside have been shown to be equally
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effective in treatment of hypertension associated with coronary artery bypass surgery.
Both agents have comparable effects on heart rate, cardiac output, and PCWP. With
comparable reductions in systolic blood pressure, nitroglycerin causes less reduction in
diastolic blood pressure than does nitroprusside. Therefore, CPP may be better
preserved with nitroglycerin than with nitroprusside. For these reasons, nitroglycerin
may be the preferred agent for treatment of hypertension associated with myocardial
ischemia. For treatment of hypertension, nitroglycerin is started at 0.5 mg/kg/min and
may have to be increased up to 20 mg/kg/min.
Dynamic Stenosis
Evidence of myocardial ischemia may occur with little or no initial change in heart rate
or blood pressure. In these instances, acute reductions in coronary blood flow may
occur due to vasoconstriction in the area of a coronary stenosis or due to true coronary
spasm in an area free of a stenosis. The mainstays of therapy are nitroglycerin and
calcium channel blockers to reduce coronary vasomotor tone. Nitroglycerin can be
started at 0.5 mg/kg/mi n and titrated upward. When an elevated PCWP accompanies
one o7 these episodes nitroglycerin is effective in reducing PCWP through both veno
dilation and treatment of the underlying ischemia. Nifedipine is a calcium channel
blocker and systemic vasodilator that can be administered sublingually in a 10-mg dose
to reduce coronary vasomotor tone. Intravenous Verapamil 7.5 mg also has been used
to terminate an episode of intraoperative coronary vasospasm.
Care must be taken to avoid systemic hypotension with administration of these agents.
CPP is improved when the pressure drop across the stenosis diminishes with
vasodilation in the area of the stenosis and when veno-dilation reduces PCWP.
However, extreme diastolic hypotension will offset any potential improvement of CPP.
For this reason, phenylephrine augmentation of diastolic blood pressure may be
necessary to preserve CPP.
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Chapter 33 - VASOPRESSORS AND INOTROPES IN CLINICAL PRACTICE
INTRODUCTION
Cardiovascular instability is one of the most common life-threatening clinical situations
that an anesthesiologist comes across in clinical practice either in the operation theatre
or in the intensive care unit. Vasoactive medications are drugs that can often prove life
saving in such situations. However, used without propel indication, these medications
may not only be useless but may even be positively harmful.
Vasopressors and inotropes are two broad categories of drugs used to treat
cardiovascular instability. A vasopressor is a drug that brings about an increase in blood
pressure by causing constriction of the blood vessels. An inotrope, on the other hand, is
a drug that directly increases the force of contraction of the myocardium, resulting in an
improvement of cardiac output, tissue perfusion and blood pressure.
This article will begin with a classification of vasopressors and inotropes that are
commonly used in clinical practice and describe their relevant pharmacological effects.
It will then review the pathophysiology of clinical conditions where such drugs are used
in order to provide the rationale for the choice of such medications. Guidelines for the
easy administration of such drugs will then be provided.
CLASSIFICATION OF VASOPRESSORS AND INOTROPES

Sympathomimetics are drugs that cause stimulation of the sympathetic nervous system
through agonistic effects on the α and β-receptors of the sympathetic nervous system.
They are classified as naturally occurring (endogenous) catecholamines, synthetic
catecholamines and synthetic non catecholamines. Synthetic non catecholamines are
further categorized as direct and indirect acting drugs. While stimulation of a-receptors
increases blood pressure, stimulation of the b1-receptors causes an increase in heart
rate and myocardial contractility.
Inotropes are drugs that bring about an increase in cardiac output and tissue perfusion-
by primarily increasing the force of myocardial contraction. Sympathomimetic agents
and inotropes that are commonly used in clinical practice are listed in Table I.
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Table I: Classification of commonly used sympathomimetic
agents and inotropes
Sympathomimetic agents
 Natural (endogenous) catecholamines Adrenaline
Noradrenaline
Dopamine
 Synthetic catecholamines Dobutamine

Isoprenaline
 Synthetic non catecholamines

Indirect-acting Ephedrine
Mephentermine
Direct-acting Phenylephrine
Inotropes
Cardiac glycosides Digoxin
Selective phosphodiesterase inhibitors Amrinone
Milrinone
Other agents Calcium
Adrenaline
 Adrenaline is an endogenous catecholamine with both α and β adrenergic effects.
It is a potent stimulator of the a-adrenergic receptors. Adrenaline activates the
β1 and β2 adrenergic receptors as well. However, the α effects predominate at
the higher dose range.
 The clinical uses of adrenaline include its application in the treatment of life-
threatening allergic reactions (e.g., anaphylactic shock where it effectively
counteracts the vasodilatation and bronchospasm associated with the condition),
as a continuous infusion to increase myocardial contractility (inotropic action)
and during cardiopulmonary resuscitation.
 The cardiovascular effects of adrenaline depend on the dose and manner in
which it is administered. When administered intravenously as an infusion of 1 to
2 mg/minute in a 70-kg adult, it stimulates mainly the b2 receptors in the
peripheral vasculature. Stimulation of β1 receptors occurs at doses of 4
mg/minute while at 10 to 20 mg/minute, stimulation of both a and b receptors
occurs with a effects predominating in most vascular beds including cutaneous,
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splanchnic and renal circulations. The concomitant administration of a
vasodilator can offset this adrenaline-induced vasoconstriction of the splanchnic
and renal vascular beds. A single intravenous bolus injection of 2 to 8 mg in a 70-
kg adult produces transient increase in heart rate and blood pressure lasting
about 1 to 5 minutes. Adrenaline is usually administered as a continuous infusion
for its cardiovascular effects in a dose ranging between 0.05 to 0.2 mg/kg/
minute.
Noradrenaline
Noradrenaline is an endogenous catecholamine that is released from postganglionic
sympathetic nerve endings. Because of its potent a-receptor stimulating effect (along
with lack of b2 effect), it produces intense arterial and veno constriction in all vascular
beds. Like adrenaline, it has a β1 stimulating effect that tends to increase heart rare and
cardiac output. Noradrenaline has no effect on bronchomotor tone because of its lack of
b2 effect on bronchial smooth muscles. It needs to be noted that the intense
vasoconstriction produced by α-receptor stimulation causes an increase in systemic
vascular resistance as reflected by an increase in systolic, diastolic and mean arterial
pressures and a reduction in venous return. This, along with the baroreceptor-mediated
reflex decreases in heart rate and cardiac output, more than offsets the direct β1-
mediated effect of increase in heart rate and cardiac output produced by noradrenaline.
Noradrenaline is administered as an intravenous infusion in a dose of 4to 16 ms/minute
(in a 70-kg adult) to treat refractory hypotension unresponsive to other vasopressors.
Noradrenaline is also administered as a continuous infusion for its cardiovascular
effects in a dose ranging between 0.05 to 0.3 mg/kg/minute.
Dopamine
Dopamine is a naturally occurring neurotransmitter in die central and peripheral
nervous systems. Dopamine-1 receptors are located postsynaptically and are
responsible for vasodilatation of renal, mesenteric, coronary and cerebral blood vessels.
Dopamine-2 receptors situated pre-synaptically inhibit the release of noradrenaline.
Dopamine produces dose-dependent effects on the cardiovascular system. In the dose
range of 0.5 to 3 mg/kg/minute, dopamine-1 receptors are stimulated resulting in renal
vasodilatation, increased urine output and mild increase in blood pressure. b1 receptor
stimulation at doses ranging from 3 to 10 mg/kg/minute causes a positive inotropic
effect reflected as in increase in blood pressure and cardiac output. Doses of 10 to 20
mg/kg/minute produce intense vasoconstriction and increase in blood pressure
through its a-receptor stimulating effect.
Dopamine is used clinically to increase cardiac output in patients with low blood
pressure, increased atrial filling pressures and low urine output. It is unique among the
catecholamines in its ability to simultaneously increase myocardial contractility, blood
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pressure, renal blood flow, glomerular filtration rate and urine output. The
vasodilatation of renal blood vessels and diuresis seen with low doses of dopamine (3 to
3 mg/kg/minute) has lead to a mistaken belief among clinicians that a "renal dose
dopamine" regime can prevent the development of acute renal failure in perioperative
patients (or in critically ill patients in the intensive care unit) who are at a high risk of
developing renal failure. However, there is no evidence in literature to support such an
effect. In the absence of data confirming the efficacy of dopamine in preventing acute
renal failure in patients at risk as detailed above, the use of renal dose dopamine cannot
be recommended.
Dobutamine
Dobutamine is a synthetic catecholamine that acts as a selective βl adrenergic agonist. It
is used as a continuous intravenous infusion in a dose of 2 to 10 mg/kg/minute.
Dobutamine produces a dose-dependent increase in cardiac output. It decreases atrial
filling pressures without associated significant increases in systemic vascular
resistance, blood pressure and heart rate. In contrast to dopamine, dobutamine does not
have any clinically important vasoconstrictor activity. Increased cardiac output is
usually accompanied by a baroreceptor-mediated decrease in systemic vascular
resistance explaining why blood pressure remains unchanged. For this reason,
dobutamine may be ineffective in patients who need increased systemic vascular
resistance rather than augmentation of cardiac output to increase blood pressure. While
dopamine increases renal blood flow through its action on the dopamine-1 receptor,
dobutamine has no such salutary effect on renal perfusion. Dobutamine, unlike
dopamine, has the advantage of being a coronary vasodilator.
The divergent cardiovascular effects of dopamine and dobutamine provide an
opportunity for the clinician to combine the two medications in order to obtain an
overall beneficial effect on cardiovascular function. Infusions of a combination of
dopamine and dobutamine produces a greater improvement in cardiac output at lower
doses than can be achieved by either drug alone. Dopamine can potentially distribute
the increased cardiac output to the renal and mesenteric vascular beds while
dobutamine could provide additional after load reduction by dilating the cutaneous and
skeletal vessels. The combination of dopamine with dobutamine could thus increase
coronary perfusion and cardiac output while at the same time decreasing after load a
pharmacological "intra-aortic balloon pump".
Isoprenaline
Isoprenaline is a powerful inotropic and chronotropic agent whose actions are mediated
via the activation of β1 and β2 adrenergic receptors. In clinical doses, isoprenaline is
devoid of a-effects. β1 effects cause an increase in heart rate, myocardial contractility
and cardiac automaticity while b2 effects result in a decrease in systemic vascular
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resistance due to vasodilatation in the skeletal muscles. The net effect of these changes
is an increase in cardiac output that is usually sufficient to increase systolic blood
pressure. The mean arterial pressure may decrease due to decrease in systemic vascular
resistance and associated decreases in diastolic blood pressure.
The clinical use of this drug is currently limited to its use as an intravenous
infusion of 1 to 5 mg/minute in a 70 kg adult for the treatment of significant
bradycardia in the presence of complete heart block. Even in such situations, a
transvenous or external pacemaker is referred over pharmacological pacing.
Ephedrine
Ephedrine is primarily an indirect-acting synthetic non catecholamine. It
stimulates both α and β adrenergic receptors through the release of endogenous
noradrenaline. It also has some direct stimulating action on adrenergic receptors.
The cardiovascular effects of ephedrine are similar to that seen with adrenaline
but are less intense and last about ten times longer. Intravenous administration of
ephedrine causes increase in systolic and diastolic blood pressure, heart rate and
cardiac output. Renal and splanchnic blood flows are decreased while coronary and
skeletal muscle blood flows are increased. Systemic vascular resistance is altered
minimally because vasoconstriction in some vascular beds is offset by vasodilatation in
other areas.
The clinical use of ephedrine is to increase blood pressure in the presence of
sympathetic nervous system blockade produced by regional anesthesia or hypotension
due to intravenous/inhaled anesthetics. Uterine blood flow is not greatly altered when
ephedrine is administered to treat hypotension under regional anesthesia. This is in
contrast to other vasopressors that produce generalized vasoconstriction including
vessels in the uterine circulation. This sparing effect of ephedrine on uterine perfusion
may reflect more selective a-mediated vasoconstriction on systemic vessels than uterine
vessels.
Ephedrine is administered as intravenous bolus injections of 3 to 6m g (in a 70-
kg adult) to achieve the desired elevation of blood pressure. It is not administered as an
infusion.
Mephentermine
Mephentermine, like ephedrine, is an indirect-acting synthetic non-
catecholamine. It stimulates both α and β adrenergic receptors through the release of
endogenous noradrenaline. Its cardiovascular effects are similar to that of ephedrine
but the drug does not have the sparing effect on uterine blood flow.
Mephentermine is administered as intravenous bolus injections of 3 to 6 mg (in a
70-kg adult) to achieve the desired elevation of blood pressure. Like ephedrine,
mephentermine is also not administered as an infusion.
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Phenylephrine:
Phenylephrine is a synthetic non-catecholamine that stimulates principally al
receptors by a direct effect. The cardiovascular effects of phenylephrine include a dose-
dependent increase in blood pressure accompanied by decrease in cardiac output. The
latter effect may be mediated through a baroreceptor-mediated reflex bradycardia in
response to an increase in blood pressure. Renal, splanchnic and cutaneous blood flows
are decreased while coronary blood flow is increased.
Phenylephrine is used as an intravenous bolus injection of 50 to 200 mg to treat
decreases in blood pressure resulting from sympathetic nervous system blockade
following regional anesthesia or peripheral vasodilatation that accompanies
administration of intravenous/inhaled anesthetics. Phenylephrine is said to be
particularly useful in patients with coronary artery disease and in patients with aortic
stenosis as this drug increases coronary perfusion pressure without increasing heart
rate.
Digoxin
Digoxin is one of the digitalis group of cardiac glycosides that is used to treat
cardiac failure (positive inotropic effect) or slow the ventricular response rate in
patients with supraventricular tachydysrhythmia (paroxysmal atrial tachycardia, atrial
fibrillation or atrial flutter). Digoxin brings about a positive inotropic effect by causing
an increase in intracellular calcium.
The average digitalizing dose ranges from 0.03 mg/kg in adults to 0.06 mg/kg in
infants and children. This works out to around 2 mg in a 70 kg adult. Half to two-thirds
of the calculated dose can be administered intravenously over 30 minutes the beneficial
effect becoming apparent within 5 to 30 minutes. The remainder of the calculated dose
is administered as 0.25 mg doses intravenously every 6 hours to obtain full
digitalization within 24 hours. The therapeutic blood level of digoxin is 0.5 to 2
nanogram/ml. The drug has a narrow therapeutic window with levels > 3 nanogram/
ml being definitely indicative of toxicity.
Amrinone
Amrinone is a selective phosphodiesterase inhibitor (PDE III isoenzyme fraction)
that causes positive inotropic and vasodilator effect manifesting as an increase in
cardiac output and decreased left ventricular end diastolic pressure. Heart rate may
increase and blood pressure may decrease. Amrinone thus has an "inodilator" action on
the cardiovascular system that finds clinical use in patients with cardiogenic failure,
resulting from systolic dysfunction (vide infra).
Amrinone is degraded in the presence of dextrose and light. Hence, it should not be
infused in dextrose-containing solutions and the infusion must be protected from light.
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Administered as a single intravenous dose of 0.5 to 1.5 mg/kg, amrinone increases
cardiac output within 5 minutes, with persistent positive inotropic effect lasting upto 2
hours. The initial intravenous bolus is followed by a continuous intravenous infusion of
2 to 10 mg/kg/minute for sustained effect during the infusion and for several hours
after discontinuation of the drug. The recommended maximum daily dose of amrinone
is 10 mg/kg including the initial loading dose, which may be repeated 30 minutes after
the first injection.
Milrinone
Like amrinone, Milrinone also has positive inotropic and vasodilating effects. The
"inodilator" action of Milrinone on the cardiovascular system finds clinical application
in die management of patients with cardiogenic failure resulting from systolic
dysfunction (vide infra). It is administered as an intravenous bolus of 50 mg/kg followed
by a continuous of 0.5 mg/kg/ minute.
Calcium
Calcium is an intracellular ion that increases the force of myocardial contraction.
Intravenous administration produces an intense positive inotropic. Affect that lasts for
10 to 20 minutes. The cardiovascular effects include an increase in stroke volume and
decrease in left ventricular end-diastolic pressure, heart rate and systemic vascular
resistance.
The drug finds clinical application in low cardiac output states following open-
heart surgery where it is administered intravenously in a dose of 5 to 10 mg/kg to
improve myocardial contractility and stroke volume. A10% solution of calcium chloride
contains three times more elemental calcium than an equal volume of 10% calcium
gluconate (27 mg/ml versus 9 mg/ ml). Though the availability of ionized calcium is
prompt in the presence of normal liver function regardless of the intravenous
preparation administered, calcium chloride is still preferred in an emergency for its
prompt clinical effects.
Calcium is also indicated in the emergency management of cardiac arrest resulting from
hyperkalemia, hypocalcaemia or overdose of calcium channel blockers.
PATHOPHYSIOLOGIC RATIONALE FOR USE OF

VASOPRESSORS AND INOTROPES IN CLINICAL CONDITIONS
Septic shock
Septic shock is a condition associated with severe sepsis characterized by
features of inadequate tissue perfusion including lactic acidosis, oliguria and altered
mental status. Proinflammatory mediators released in a variety of infections causes
vasodilatation and increased vascular permeability. In the early stages of septic shock,
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vasodilatation reduces systemic vascular resistance and at the same time increases
venous return and maintain cardiac output (warm, normotensive stage of septic shock
with bounding pulse, normal blood pressure and normal/increased cardiac output). In
early septic shock, blood volume is often normal and "inadequate" tissue perfusion is
the result of abnormal distribution of blood flow. As septic shock progresses, circulating
blood volume becomes less because of the combined effect of peripheral venous pooling
and increased vascular permeability. This results in hypotension, especially if the
patient has decreased cardiovascular reserve, producing the more common clinical
presentation of septic shock accompanied by hypotension and evidence of decreased
tissue perfusion as described above (cold, hypotensive stage of septic shock).
The primary pathophysiology of septic shock thus centres around intense vasodilatation
and increased vascular permeability. Vasopressors are useful in combating
vasodilatation seen in septic shock. Like in any other form of shock, the first objective is
to normalize circulating blood volume through volume resuscitation. If blood pressure
remains low, or clinical signs of tissue hypoperfusion are present (a evidenced by slow
capillary refill, oliguria, intolerance to tube feeds and altered sensorium), vasoactive
drugs are administered. Dobutamine and noradrenaline are currently the drugs of
choice for the treatment of septic shock. Dobutamine is started at a dose of 2.5
mg/kg/minute and increased in a stepwise manner until adequate circulation is
restored, no further benefit is achieved or a dose of 10 mg/kg/minute has been reached.
At this point, noradrenaline is added, starting with a dose of 0.1 mg/kg/minute and
increasing up to 15 mg/minute. If a combination of dobutamine and noradrenaline at
usual doses fails to improve cardiovascular function, consider increasing the dose of
dobutamine or noradrenaline. Dopamine and adrenaline at this stage may increase
blood pressure but at the expense of splanchnic blood flow.
Alternative drugs that might find a place in the years to come include vasopressin and
angiotensin. Blood levels of vasopressin have been found to be low in septic shock and
may be contributory to the vasodilatation seen in this condition.1 Administration of
vasopressin in a dose ranging from 0.01 to 0.04 units/minute to patients in septic shock
has been shown to reduce the requirements of other vasopressors such as
noradrenaline.2 Vasopressin increases blood pressure and systemic vascular resistance.
It has an advantage in that it produces vasodilatation of cerebral and coronary
vasculature. Though vasopressin improves blood pressure and tissue perfusion in septic
shock, it still remains to be seen whether this translates into improved clinical
outcomes.
Cardiogenic shock
Cardiogenic shock is characterized by an inappropriately low cardiac output in the face
of normal or high atrial filling pressures. In addition to clinical signs of tissue
hypoperfusion (slow capillary refill, oliguria, intolerance to tube feeds and altered
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sensorium), patients present with crepitation' in lung bases, elevated jugular venous
pulse, lender hepatomegaly and peripheral edema. Cardiogenic shock can result from
systolic dysfunction (decreased ability of the ventricle to achieve normal stroke volume
for a given after load) or diastolic dysfunction (characterized by increased left
ventricular stiffness as a result of myocardial ischemia.
Management of cardiogenic shock includes optimization of cardiac filling pressures
using smaller boluses of 50 to 100 ml until clinical manifestations of fluid overload
become evident. At this point, drugs with positive inotropic effect such as dobutamine
or digitalis are considered. Patients in cardiogenic shock are often vasoconstricted due
to intense sympathetic activity. Such patients usually benefit from an "inodilator" drug
such as amrinone or milrinone that has combined inotropic and vasodilator action.
Nonpharmacologic measures such as the use of an intra-aortic balloon pump are also
helpful.
Anaphylactic shock
The release of histamine and other similar mediators in anaphylactic shock produces
marked vasodilatation, depressed systolic function. increased vascular permeability and
bronchospasm. As in other forms of shock, the initial therapy is volume resuscitation.
Adrenaline in a dose of 0.05 to 0.1 mg intravenously every 1 to 5 minutes is useful in
counteracting the vasodilatation and bronchospasm that is associated with this
condition.
Hypovolemic shock
Hypovolemic shock is a condition where the primary pathology is decreased blood
volume. It could be the result of blood loss (trauma, haemorrhage, major surgery) or
excessive fluid losses (diarrhea, vomiting, diuresis). Volume resuscitation forms the
mainstay of treatment. Vasoactive drugs are indicated only for short periods until
volume resuscitation is complete in order to protect vital organs such as the brain, heart
and kidneys. Dopamine in a dose of 1 to 10 mg/kg/ minute or adrenaline 1 to 10
mg/minute is titrated to achieve the desired blood pressure. If higher doses are needed,
add noradrenaline in a dose of 2 to 20 mg/minute. Vasopressors are discontinued as
soon as volume resuscitation and surgical control of bleeding is accomplished.
Hypotension following spinal or epidural anesthesia is the result of extensive
sympathetic blockade causing vasodilation. The situation is akin to a sudden increase in
the size of the container (vascular system) in the presence of unaltered contents (blood
volume) - a "relative hypovolemia". The treatment is aimed at restoring volume status
(by filling the container) and using vasopressors (to shrink the container). The drugs
that are commonly used include ephedrine and mephentermine in boluses of 3 to 6 mg
until adequate blood pressure is established. Ephedrine has an edge over
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mephentermine in obstetric patients undergoing procedures under regional anesthesia
as it maintains uterine blood flow.
GUIDELINES FOR EASY ADMINISTRATION OF DRUGS

As a general rule, vasoactive drugs are made up in 5% dextrose in water as the acidic
environment prevents oxidation of the drug and affords better drug stability. Amrinone
and milrinone are an exception to this rule.
As vasopressors and inotropes are often required in an emergency, clinicians need to
have a user-friendly formula for easy administration of such drugs. One such formula
for preparing an infusion of dopamine (or dobutamine) is to multiply body weight (in
kg) by 3 to obtain the number of milligrams of the drug to be added to 5% dextrose in
water to make a total volume of 50 ml. Infusion of this solution at a rate of 1 ml/hour
will result in the patient receiving 1mg/kg/minute. Working out an example for a 60 kg
individual, addition of 180 mg of dopamine to 5% dextrose in water to make a total
volume of 50 ml will result in a solution containing 3.6 mg/ml (or 3600 mg/ml).
Administration of this solution at a rate of 1 ml/hour will result in the patient receiving
1 mg/kg/minute. Controlling the rate of drug administration becomes easy as the rate
of infusion (in ml/hour) is numerically the same as the dose (in mg/kg/minute) that the
clinician wishes to administer.
A similar formula for adrenaline (or noradrenaline) is to add 0.15 mg/kg of the drug to a
total volume of 50 ml of 5% dextrose in water. Administration of the infusion at a rate of
1 ml/hour is equivalent to administering the drug at 0.05 mg/kg/minute (or 50
nanogram/kg/minute).
SUMMARY:
Vasopressors and inotropes constitute two classes of drugs that are used to treat
cardiovascular instability under anesthesia or in the intensive care unit. Sound
knowledge of the pharmacological basis of action of these drugs and proper
understanding of the altered pathophysiology in a variety of clinical situations helps the
anesthesiologist or Intensivist to choose the appropriate drug for a particular clinical
situation. It is hoped that this article will provide the reader with the rationale for
choosing a particular drug for treating cardiovascular instability in clinical practice.
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Chapter 34 - HYPERTENSION
Introduction: Hypertension is a common clinical problem faced by the anesthesiologist.
 Leading cause of death and disability
 Most frequent pre op abnormality
 Prevalence 20-25%
 Hypertension affects the anesthesiologist’s choice of drugs, monitoring and post
operative planning.
Definitions:
* Joint National Committee on prevention, detection, evaluation and treatment of high
BP (6th report) has recently defined
** Hypertensive patients as anyone with a systolic BP of 140mm Hg or greater, anyon
with a diastolic BP of 90mm Hg or greater or anyone currently taking antihypertensive
medicine.
 Further classified hypertension by the levels of SBP and DBP as follows:
SBP (mmHg) DBP (mmHg)
Optimal < 120 And < 80
Normal < 130 And / or < 85
High normal 130-139 Or 85-89
> 140 > 90
Hypertension
Stage I (mild) 140-159 Or 90-99
Stage II (mod) 160-179 Or 100-109
Stage III (Severe) 180 (180-200) Or > 110 (110-119)
Stage Iv (V severe) > 210  120
When SPB and DBP fall in different categories, the higher category should be
used to classify the individual’s B.P.
WHO: Has defined hypertension as a single sitting BP exceeding 160/95 mmHg,
values less than 140/90 mmHg are considered as normotensive; values between
140/90 mm Hg and 160/95 mmHg are considered as borderline hypertension.
 Accelerated or severe hypertension – a recent, sustained and progressive
increase in blood pressure, usually with diastolic BP in excess of 110-115 mmHg,
renal dysfunction is often present.
 Malignant hypertension – true medical emergency. Severe hypertension (>
200/140 mmHg) associated with papilledema and frequently, encephalopathy.
 HTN in children is defined as average systolic or diastolic pressures equal to or
greater than 95th percentile for age on at least 3 occasions.
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 Specific guidelines for BP measurement to get an accurate and repeatable
measurement.
 Abstinence from Caffeine and tobacco for at least the previous 30 min.
 The allowance of at least 5 min of rest before measurement
 The use of appropriate size of cuff (cuff’s rubber bladder should extend half way
around the extremity and width of cuff should be 20.50% greater than the
diameter of extremity.
 The use of at least 2 measurements before reaching a diagnosis.
Classification and pathophysiology:
Idiopathic / essential HTN Secondary HTN

80-95% case Renal disease
Associated with abnormal baseline Primary hyperaldosteronism
elevations of cardiac output, SVR or both. Cushing’s syndrome
Evolving pattern (initially CO , SVR Pheochromocytoma
normal  CO normal SVR ) Acromegaly
ECF vol / plasma renin activity  low, Pregnancy
Normal or high Oestrogen therapy
Altered CBF autoregulation, altered Drug induced
diastolic function, concentric LVH.
Mechanisms responsible for changes observed in HTN patients:

a. Vascular hypertrophy
b. Hyperinsulinemia
c. Abnormal  in intracellular Ca+2 ( arteriolar tone)
d. Increased intracellular Na+ (impairs renal Na+ excretion)
e. Sympathetic nervous system over activity and enhanced responses to
sympathetic agonists (exaggerated responses to vasopressors).
f. Over activity of the renin-angiotensin-aldosterone system CRAA).
Fundus:
 Grade I: Arteriolar narrowing leading to copper wire and silver wire
appearance.
 Grade II: Arteriovenous nipping where arteries excess the vein.
 Grade III: Grade II changes (+) superficial flames shaped and deep dot like
hemorrhages and cotton wool exudates.
 Grade IV: Grade III (+) papilloma.
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Preoperative evaluation:
Objectives:
1. To treat the HTN if not on treatment.
2. To know the adequacy of control of HTN – if patient is on treatment.
3. To differentiate essential and secondary HTN.
4. To detect associated end organ damage.
5. To decide whether the patient can be taken up for surgery or not.
6. To decide what further investigations have to be done.
History: The patient should be asked about
a. Duration of HTN and severity
b. Regimen of treatment
c. Regularity of treatment
d. Symptoms suggestive end organ damage
CVS:
 Myocardial ischemia – chest pain
 Cardiac failure  exercise in tolerance, shortness of breath (nocturnal), nocturia
dependent edema.
a. CNS: impaired cerebral perfusion  TIA, stroke  postural light head
ache  syncope, amaurosis (eye)
b. Peripheral vascular disease  claudication pain
c. Renal  weakness, lethargy, pedal edema, puffiness of face.
a. Symptoms of adverse effects of current anti HTN treatment
1. Ht, wt, body habitus
2. Presence / absence of pallor, icterus, clubbing, cyanosis lymphadenopathy, pedal
edema
3. Presence / absence of thyroid enlargement
4. Pulse rate: rate, rhythm, volume
5. Blood pressure: both arms, sitting and supine
6. JVP
1. Ophthalmoscopy: visible changes in the retinal vasculature usually parallel the
severity and progression of atherosclerosis and hypertensive damage in organic
parasternal.
2. CVS examination: ventricular lift / Heave (LVH) raised JVP, S3 gallop / SF (RVH)
pulmonary rates)
3. CNS: presence / absence of carotid bruits
4. Resp. system: B/L basal rates  CCF
5. P/A: abdominal mass, bruits, hepatojugular, reflex, ascitis etc.
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Laboratory investigations:
 Hb%
 TC, DC, ESR
 RBS/PLBS
 Blood urea and serum creatinine
 Serum electrolytes Na+, K+, Ca+2, Mg+2
 Coagulation profile
 Serum cholesterol
 ECG – shows evidence of ischemia, infarction, conduction abnormalities, LVH, LV
strain
 Chest radiograph – cardiomegaly, LVH, pulmonary vascular congestion
 Echocardiography – LVH, RWMA, RF and valve abnormal.
Preoperative anti HTN treatment:

Drug therapy has been shown to
a. Reduce progression of HTN
a. Incidence of stroke, congestive failure, CAD and renal damage.
b. Reverse concomitant pathophysiological changes LVH, altered cerebral
autoregulation.
– If preoperative BP exceeds 180mmHg SBP or 110mmg Hg DBP
Elective surgery delayed – to control HTN and detailed evaluation and
treatment.
– Mild HTN – require single drug therapy ( blockers, ACE inhibitors Ca+2 Ch.
Blocker / diuretic)
 Concomitant illnesses influence drug selection indicated agents
1. Type I DM – ACE inhibitors
2. Type II DM – diuretics
3. Heart failure – ACE inhibitors
4. Renal insufficiency – ACE
5. Myocardial infarction -  blockers and/or ACE inhibitors
6. Hyperthyroidism - -blockers
7. Dyslipidemia - -blockers
8. Atrial tachycardia - -blocker, Ca+ cha. blockers
9. Isolated sys. HTN – diuretics, Ca+ cha. Blockers
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Agent:
CI in
 Blockers – bronchospastic diseases, depression, DM (type I and II) heart blocks,
heart failure.
 Ca+ cha. blockers – heart block
 Thiazide diuretics – gout
 ACE inhibitors and angiotensin II – renovascular disease receptor blockers.
 Moderate to severe HTN – require a second or third drug.
Oral anti HTN agents:
Thiazide – chlorothiazide, hydrochlorothiazide, chlorthalidone,

Diuretics
indapamide, metolazone
Potassium sparing – spironolactone, triamterene, amiloride
Loop – furosemide, bumetanide, ethacrynic acid, torsemide
Sympatholytics:
Adrenergic Beta – acebutolol, atenolol, propronolol, timolol,

receptor metoprolol, bisoprolol, pindolol, nadolol
blockers
Alpha (DPT) – 1 doxazosin, prazosin, terazosin
1 - 2 Phenoxybenzamine
Alpha and beta – labetalol, carvedilol
Central 2 – Agonist’s  clonidine, methyldopa, guanabenz,

guanfacine
Post ganglionic blockers  Guanithidine, reserpine
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Vasodilators:
Calcium channel Benzothiazepines – diltiazem

blockers
Phenylakylamines – Verapamil
Dihydropyridine – amlodipine, nifedipine,

nicardipine, felodipine, nisoldipine
ACE inhibitor  captopril, enalapril, lisinopril, ramipril etc.
Angiotensin- receptor antragonists  losartan, valsartan,

telmisartan etc
Direct vasodilator  hydralazine, Minoxidil
Indications:
ACE inhibitors:
 Type I DM
 Heat failure
 Renal insufficiency
 MI
-blockers:
 Dyslipidemia
-blockers:
 MI
 Hyperthyroidism
 Atrial tachycardia
Ca+ channel blockers:

 Atrial tachycardia
 Isolated sys HTN
Diuretics:
 Type II DM
 Isolated sys HTN
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Preoperative management:
 Degree of pre operative HTN that is acceptable for patients scheduled for elective
surgery
 Untreated or poorly controlled HTN patient is more prone for episodes of
myocardial ischemia stroke, arrhythmias or both HTN and hypotension.
 Patients should ideally undergo elective surgery only when rendered
normotensive – this approach not always feasible or necessarily desirable
because of altered cerebral autoregulation.
o Excessive reductions in BP can compromise cerebral perfusion.
 Decision whether to delay or to proceed with surgery is individualized based on
a. Severity of the preoperative BP elevations
b. Likelihood of coexisting myocardial ischemia, ventricular dysfunction, cerebral
or renal complications.
c. Surgical procedure – whether major surgically induced changes in cardiac
preload or after load are anticipated.
 Anti HTN treatment should be continued up to time of surgery except ACE
inhibitors withheld on the morning of surgery due to increase incidence of intra
op hypotension but withholding -  risk of marked perioperative HTN and need
for parenteral anti HTN agents.
 Surgical procedures on patients with sustained preoperative DBP higher than
110mmHg – especially those with evidence of end-organ damage should be
delayed until BP is better controlled over the course of several days.
Premedications:
Anxiolytics:
 Reduce preop anxiety and is highly desirable in HTN patients – night and
morning
 Midazolam, diazepam
Anti HTN treatment: continued as class to schedule as possible.
Central 2 agonists: useful adjunctive clonidine (0.2mg)
Augments sedation,  intraoperative anesthetic req.  perioperative HTN
But associated with profound intra op hypotension and bradycardia.
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Anti regurgitation prophylaxis:
Intra-op management / goals:

a. Maintain a stable BP range appropriate for that patient.
b. Arterial BP should generally kept within 10-20% of preop value.
c. Patients with borderline HTN: may be treated as normotensive patients.
d. Patients with long standing or poorly controlled HTN have altered
autoregulation of CBF; higher than normal mean blood pressures may be
required to maintain adequate CBF.
e. Have some element of coronary artery disease and cardiac hypertrophy,
excessive blood pressure elevations are undesirable HTN especially in
association with tachycardia can precipitate or exacerbate myocardial ischemia,
ventricular dysfunction or both.
f. If marked HTN (>180 / 120mmHg) is present preoperatively arterial BP should
be maintained in the high-normal range (150-140/90-80 mmHg).
Monitoring:
a. Pulse oximetry
b. O2 sati
c. Urine output
d. ECG for ischemia
e. BP
f. Direct intra-arterial pressure monitoring reserved for patients with hide swings
in blood pressure. For those undergoing major surgical procedure associated
with rapid or marked charges in cardiac preload or after load.
Induction: induction and intubation – are periods of hemodynamic instability for HTN
patients.
 Irrespective of pre operative BP control – many patients with HTN display an
accentuated hypotensive response to induction followed by an exaggerated
hypertensive response to intubation.
 Hypotensive response to induction due to
1. Additive circulatory depressant effects of anesthetic agents and anti HTN agents.
2. Most anti HTN agents and anesthetic agents are vasodilators, cardiac
depressants or both.
3. Many HTN patients are volume depleted.
4. Sympatholytic agents also alternate the normal protective circulatory reflexes,
reducing sympathetic tone and enhancing vagal activity.
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Intubation: Laryngoscopy duration should be as short as possible.
 Should be performed under deep anesthesia.
 Alternate hypertensive response to:
1. Depending anesthesia with volatile agent for 5-10 minutes
2. Administering a bolus of opioid (fentanyl 2.5-5g/kg Remifentanyl 0.5-1g/kg,
sufentanil 0.25-0.5g/kg, carfentanyl 15-25g/kg).
3. Lidocaine 1.5mg/kg IV/intratracheal
a. adrenergic blockade / esmolol 0.3-1.5mg/kg,. propranolol 1-3mg,
labetalol 5-20mg.
4. IV nitroprusside / nitroglycerin 0.5-1g/kg with invasive BP monitoring
5. Using topical airway anesthesia
Choice of anesthetic agents:
A. Induction agents: barbiturates, benzodiazepines, propofol and etomidate,
ketamine CI for elective procedures – sympathetic stimulating properties
blunted or eliminated by co-administration of a small dose another agent –
benzodiazepine / propofol.
B. Maintenance agents:
 Volatile agents alone / with nitrous oxide
 Balanced technique  opioid + N2O + muscle relaxant
 TIVA
 For any techniques addition of volatile agent / IV vasodilator – satisfactory intra
op. BP control.
 Sufentanil – greatest autonomic suppression and control over BP.
A. Muscle relaxants: any muscle relaxant except pancuronium (large dose)
pancuronium  induced vagal blockade and neural release of catecholamines –
exacerbate HTN
 May be useful in offsetting excessive vagal tone induced by opioids or surgical
stimulation.
 Hypotension following large (intubating) doses of tubocurarine, metocurine,
atracurium or mivacurium may be accentuated in HTN patients.
A. Vasopressors:
 Exaggerated response to both endogenous catecholamines (intubation or
surgical stimulation) and exogenously administered sympathetic agonists.
 If vasopressor needed to treat hypotension – direct acting agent phenylephrine
(25-50g) or ephedrine (5-10mg) (when vagal tone is high).
 Patients on sympatholytics  response to vasopressors (especially ephedrine)
Intraoperative HTN: characterized by systemic vasoconstriction with intravascular

hypovolemia.
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 Intraoperative HTN not responding to an increase in anesthetic depth especially
with volatile agent is treated with a variety of parenteral agents.
 Reversible causes
o Inadequate depth of anesthesia
o Hypoxemia Should always be excluded before
o Hypercapnia initializing anti HTN treatment –
o Inadequate analgesia exogenous catecholamines
o Inadequate muscle relaxation
 Selection of a hypotensive agent depends on
o Severity, acuteness and cause of HTN
o Baseline ventricular function
o Heart rate
o Presence of bronchoplastic pulmonary. disease
 adrenergic blockade alone or a supplement good choice
Onset Duration
For patient with good Esmolol IV 0.5mg/kg over 1min 12-20min
LV function  HR CI in /min
bronchospastic 50-
disease 300g/kg/min
Labetalol 5-20mg 1-2min 4-8hr
Propanol 1-3mg 1-2min 4-6hr
Ca+2 channel blockers Nicardipine 0.25-0.5mg 1-5min 3-4 hr
Myocardial ischemia Nifedipine 10mg 5-10min 4h
 reflex tachycardia (S/L)
Mod to severe HTN – Nitroprusside 0.5- 30-60 1-5min
most rapid 10g/kg/min sec
Nitroglycerine 0.5- 1min 3-5min
10g/kg/min
Sustained control of Hydralazine 5-20mg 5-20min 4-8hr
BP  delayed onset Phentolamine 1-mg 1-10min 20-40mm
reflex tachycardia Enalaprilat 0.625-1mg 6-14min 4-6h
Fenoldopam 0.1-0.6 5 min 5 min
g/kg/min
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Reversal with neostigmine + glycopyrrolate
Extubation done in deeper planer of anesthesia
 Precautions to blunt sympathetic response taken.
 Smooth gentle
Regional anesthesia: SA/EA Adv / disadvantages
 High sensory levels of anesthesia and ass sympathetic N.S denervation can
unmask unsuspected hypovolemia (present in patients with chronic HTN).
 Sudden fall in BP may precipitate IHD.
 In chronic HTN-cerebral autoregulation curve shifted to right – CBF is more
dependent on perfusion pressure than in normotensive – can’t tolerate sudden
fall in BP.
Post operative HTN: Can lead to MI, cardiac dysrrhythmias, CCF, stroke, formation of
wound hematoma disruption of suture lines.
 Continuous monitoring during post op period.
Treatment:
1. Underlying curve should be corrected.
2. Pain (analgesics) bladder distress (catheterization) volume overload, resp.
abnormalities.
3. Nicardipine for sustained HTN and in presence of bronchospasm or MI.
4. Hydralazine 2.5-10mg IV every 10-20min
5. Nitroprusside
6. Labetalol
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Chapter 35 - CONGENITAL HEART DISEASES
Congenital Malformation Syndromes Associated with Congenital Heart Disease:
Syndrome Features
Chromosomal Disorders
21-Trisomy (Down syndrome) Endocardial cushion defect, VSD, ASD
22p-Trisomy (cat eye syndrome) Miscellaneous, total anomalous pulmonary
18-Trisomy venous return
9-Trisome VSD, ASD, PDA, coarctation of aorta, bicuspid
XXXXY aortic or pulmonary value
Penta X CSD. ASD, PDA, coarctation of aorta, bicuspid
Triploidy aortic or pulmonary valve miscellaneous
XO (Turner’s syndrome) PDA, ASD
Fragile X PDA, VSD
Duplication 3q2 VSD, ASD, PDA
Deletion 4p Bicuspid aortic valve, coarctation of aorta
Deletion 9p Mitral valve prolapsed, aortic root dilatation
Deletion 5p (cri du chat Miscellaneous
syndrome) VSD, PDS, ASD
Deletion 10q VSD, TOF. Conotruncal lesions
Deletion 13q VSD
Delection 18q VSD
Syndrome Complexes
CHARGE association (coloborma, VSD, ASD, PDA, TOF, endocardial cushion defect
heart, atresia choanae, Aortic arch anomalies, Conotruncal anomalies
retardation, genital and ear Peripheral pulmonic stenosis
anomalies) VSD, TOF, ASD, PDA
DiGeorge’s sequence, CATCH 22 TOF, VSD
Alagille’s syndrome Miscellaneous
(arteriohepatic dysplasia) Pericardial thickening, constrictive pericarditis
WATER association (vertebral, Complex cyanotic heart lesions with decreased
anal, tracheoesophageal, radial, pulmonary blood flow, transposition of great
and renal anomalies) arteries, anomalous pulmonary venous return,
FA/S (facio-auriculo-vertebral dextrocardia, single ventrick, common
spectrum) atrioventricular valve
CHILD (congenital hemidysplasia
with ichthyosiform
erythroderma, amb defects)
Mulibrey nanism (muscle, liver.
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Brain, eye)
Asplental syndrome
Polysplenia syndrome
Tertogenic Agents
Congenital rubella PDA, peripheral pulmonic stenosis
Fetal hydantion syndrome VSD. ASD, coarctation of aorta, PDA, ASD, VSD
Fetal alcohol syndrome Coarctation of aorta, hypoplastic left side of the
Fetal valproate effects heart, aortic stenosis, pulmonary atresia, VSD
Maternal phenylketonuria VSD, ASD, PDA, coarctation of aorta
Retinoic acid embryopathy Conotruncal anomalies
Otbers
Alpert’s syndrome VSD
Autosomal dominant polycystic Mitral valve prolapse
kidney disease PDA
Carpenter VSD, PDA
Conradi PDA, coarctation of aorta
Crouzon Pulmonary hypertension, pulmonic stenosis
Cutis laxa VSD
de lange Single atrium, VSD
Ellis-van creveld ASD, VSD: 1st degree heart block
Holt-Oram Hypertrophic cardiomyopathy, VSD, Conotruncal
Infant of diabetic mother anomalies
Kartagener Dextrocardia
Meckel-Gruber ASD, VSD
Noonnan Pulmonic stenosis, ASD, cardiomyopathy
Pallister-Hall Endocardial cushion defect
Rubinstein-Taybi VSD
Scimitar Hypoplasia of the right lung, anomalous
pulmonary venous return to the inferior vena
cava
VSD, PDA
ASD, TOF
VSD, ASD, PDA
Supravalvular aortic stenosis, peripheral
pulmonic stenosis
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 Conotruncal = TOF, pulmonary atresia, trunks arteriosus, transposition of the
great arteries.
 VSD = ventricular septal defect: ASD = atrial septal defect: PDA = patent ductus
arteriosus; TOF = tetralogy of fallot.
o Incidence 0.7 to 1 of 30% of congenital diseases 10-15% have association
anomalies of other systems 10-15% survive to adulthood.
INTRODUCTION:
CHD occur in 7-10 per 1000 live births i.e. 0.7 – 1%. It is the commonest form of
congenital disease and accounts for 30% of the total congenital disease. The causes of
CHD are idiopathic, genetic or environmental.
10-15% of affected children have associated congenital anomalies of the skeletal,
genitourinary or gastrointestinal systems.
10-15% of patients with CHD survive untreated to adulthood. Non-cardiac
congenital anomalies make it likely that these patients will present for anesthesia for
non-cardiac surgery.
Incidence of common congenital heart defects Acyanotic
lesions:
1. Ventricular septal defect - 35% VSD
2. Atrial septal defect - 9% ASD
3. Patent ductus arteriosus - 8% PDA
4. Pulmonary stenosis - 8% PS
5. Aortic stenosis - 6% AS
6. Coarctation of aorta - 6% COA
7. Atrioventricular septal defect - 3% AVSD
Cyanotic lesions:
 Tetralogy of fallot - 5 % TOF
 Trans position of the great arteries - 4% TGA
Classification:
A simple classification of CHD based primarily on the pathophysiology.
I. Lesions that have L  R shunting and causing increased PBF
a. Atrial septal defect.
b. Ventricular septal defect,
c. Patent ductus arteriosus.
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II. Lesions that have R  L shunting and causing decreased PBF
a. Tetralogy of fallot
b. Pulmonary atresia
c. Tricuspid atresia
III. Lesions that primarily obstruct blood flow.
a. Aortic stenosis
b. Pulmonic stenosis
c. Coarctation of aorta.
Atrial septal defect:

ASD can occur in any portion of the atrial septum depending on failure to
develop in embryonic septal structure. The types of ASD are ostium secundum in the
region of fossa ovalis, ostium primum in the lower part of the atrial septum and sinus
venosus in upper atrial septum.
Ostium secundum defects make up 75% of ASD, ostium primum 15% and sinus
venosus 10%.
Pathophysiology:
The consequences of ASD are the result of the shunting of blood from our atrium
to the other.
The direction and magnitude of shunting are determined by the (a) size of the
defect and the (b) relative compliance of the ventricles. A small defect less than 0.5 cm
in diameter is associated with a small shunt and no hemodynamic sequelae. A size
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defect more than 2 cm in diameter is associated with a large shunt and hemodynamic
consequences.
In large defects oxygenated blood flows from the left to right atrium. This blood
is added to the venous return to the right atrium and is pumped by the right ventricle to
the lungs. The ratio of pulmonary to systemic blood flow is between 2:1 and 4:1.
The large blood flow through the right side of the heart results in enlargement of
the right atrium and ventricle and dilatation of the pulmonary artery. PVR remains low
throughout childhood and begin to increase in adulthood and result in reversal of the
shunt.
A child with ASD is most often asymptomatic. Exercise intolerance, easy
fatigability and recurrent pneumonia are manifested with large L  R shunts.
Auscultatory sings:
– Accentuated 1st heart sound.
– Splitting of the second sound
– Ejection systolic murmur in pulmonary area. ESM – pulmonary area
– Low pitched mid-diastolic MDM rumbling murmur at apex. Apex.
Diagnosis:
X-ray chest: show marked Cardiac enlargement caused by prominence of both
ventricle and atria. The pulmonary artery is large and pulmonary vascularity is
increased.
ECG:
1. Signs of biventricular hypertrophy.
2. Right ventricular conduction delay
3. Tale P waves (right atrial hypertrophy)
4. Prolongation of PR interval
5. Right axis deviation RAD
Echocardiogram:
Shows characteristic of RV volume overload and abnormal motion of the
ventricular septum.
Confirms the presence of the defect and allows measurement of the shunt ratio
and pulmonary pressures.
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Prognosis and complications:
ASD are well tolerated during childhood. Pulmonary hypertension, atrial
dysryhtmias, tricuspid or mitral insufficiency and heart failure are late manifestations.
Treatment:
Surgery is advised for all symptomatic patients and asymptomatic patients with
Qp: Qs ratio of 2:1.
Ventricular septal defect:

VSD is the most common congenital cardiac abnormality. Defects may occur in
any portion of the ventricular septum and majority 70% are of membranous type and
20% in the muscular portion. Five types of VSD are (1) infundibulo-ventricular, (2) in
fundibular, (3) atrioventricular canal type, (4) muscular and (5) malignant.
25-40% of defects close spontaneously by the time the child is 2 years old and
90% eventually close by the time the child is 10 years.
Pathophysiology:
The size of the defect and PVR determine the magnitude of PBF resulting L  R
shunt across the defect. The PVR continue to fall in the 1st few weeks after birth, and the
size of the L  R shunt increases. With continued exposure of the pulmonary vascular
bed to high systolic pressure and high flow, pulmonary vascular obstructive disease
develops. When the ratio of pulmonary to systemic resistance approaches 1:1 the shunt
becomes bidirectional and the patient becomes cyanotic. If the shunt is large Qp: Qs >
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2:1 left atrial and ventricular volume overload occurs and pulmonary hypertension
develops. The main pulmonary artery, left atrium and left ventricle are enlarged.
The clinical presentation of patients with VSD varies according to the size of the
defect and the PBF. Large VSD with excessive PBF and pulmonary hypertension are
responsible for dyspnea, feeding difficulties, poor growth, perspiration, recurrent
pulmonary infections and cardiac failure.
Auscultatory sings:
Pan systolic murmur heard in left 3rd or 4th intercostals space and second heart
sound is split.
Diagnosis:
Chest X-ray: show pulmonary artery enlargement, cardiomegaly and increased
pulmonary vascularity.
ECG: shows biventricular hypertrophy broad p waves which may be notched or peaked.
Echo: shows the position and size of VSD.
Prognosis and complications:
A significant number of small defects close spontaneously. Adults with
unoperated VSD show an increased incidence of arrhythmia, sub aortic stenosis and
exercise intolerance.
Tetralogy of fallot:
TOF is the most common cyanotic CHD and consists of
1. Large VSD
2. Aorta that over side the left and right ventricles.
3. Obstruction to sight ventricular outflow
4. Right ventricular hypertrophy.
Without surgical intervention, most patients die in childhood. The rate of survival is
66% at 1 year of age, 40% at 3 years 11% at 20 years, 6% at 30 years and 3% at 40
years.
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Pathophysiology:
Obstruction to pulmonary artery outflow results in a pressure gradient that

favors blood flow across the VSD from the RV to the LV. The resulting R  L shunt
combined with obstruction to ejection of the stroke volume from the RV leads to
marked decrease in PBF and development of hypoxemia. Any event that increase PVR or
decrease SVR increases the shunt and increased arterial hypoxemia.
Clinical features: Most patients with TOF have cyanosis from birth. In childhood such
patients have sudden hypoxic spells characterized by tachypnea and hyperpnoea
followed by worsening cyanosis and in some cases loss of consciousness, seizures, CVA.
Such spells do not occur in adolescents or adults with TOF have dyspnea and
limited tolerance of exercise. They may have complications of chronic cyanosis 
erythrocytosis, hyperviscosity, abnormalities of hemostasis, cerebral abscess or stroke
and endocarditis.
Squatting is a common feature of children with TOF. Squatting increase the SVR
by kinking the large arteries in the inguinal area and decrease R  L shunt which leads
to increase PBF and improvement in arterial oxygenation.
A systolic thrill is felt along the left sternal border. A systolic murmur along the
left sternal border caused by obstruction of right ventricular outflow.
Hypercyanotic attack / “TET” spell:

About 35% of children with TOF develop hypercyanotic attacks or TET spells.
These attacks are associated with crying or exercise. The mechanism for the attack is a
sudden reduction in PBF due to either spasm of the infundibular cardiac muscle or
decrease in SVR. Recurrent hypercyanotic attacks are indication for surgical correction
of TOF.
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Treatment of hypercyanotic attacks:
o adrenergic antagonists
o Esmolol – 300-500 g/kg
o Propranolol – 0.1-0.2 g/kg is effective when attack is due to spasm of
infundibular cardiac muscle.
o Phenylephrine – 5-10 g/kg when cause is decrease SVR.
Cerebrovascular accidents: CVA is common in children with severe TOF. Cerebral
vascular thrombosis or severe arterial hypoxemia may be the cause.
Cerebral abscess: Is suggested by the abrupt onset of headache, fever and lethargy
followed by persistent emesis and appearance of seizure. The likely cause is bacterial
seeding into areas of cerebral infarction.
Diagnosis:
Chest X-ray: Shows “boot: shaped appearance of the heart due to the / absence of the
normal pulmonary artery shadow, / RV hypertrophy and / oligemic lung fields.
ECG: Shows right axis deviation RAD, RVH and RV hypertrophy.
Echo: Provides information of extent of aortic over side of the septum, the location and
degree of the right ventricular outflow treat obstruction, size of pulmonary arteries and
side of aortic arch.
Pre-operative evaluation:
Each patient with CHD presenting for cardiac or Non-cardiac surgery deserves an
in-depth pre-operative evaluation.
The primary goals of the pre-operative evaluation are
1. Developing a detailed understanding of the Childs cardiac anatomy and its
physiologic consequences.
2. Ascertaining anesthetic problems pertaining to the Childs non-cardiac medical
condition.
3. Educating the child and family concerning the expected course of the planned
anesthetic.
4. Reducing the anxiety and fear relating to the operative procedure.
History: A thorough history is the most important part of the pre-operative evaluation.
A complete (a) description of symptoms, (b) associated anomalies, (c) activity level, (d)
feeding pattern (e) past and current medical and surgical treatment.
History of physical limitation with increase fatigability, decrease activity,
shortness of breath and frequent hyper cyanotic episodes suggest limited cardio-
respiratory reserve. In infant’s presence of dyspnea, diaphoresis, or irritability during
feeding suggest cardio-respiratory compromise.
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Cyanosis: CHD is a leading cause of central cyanosis. Cyanosis occurs in lesions when
the PBF is decrease or when there is decrease mixing between separated systemic and
pulmonary blood.
Cyanosis seen in the lips and nail beds, may be present at rest or with exertion.
Clinically recognizable cyanosis indicates the presence of more than > 5 gms/dl of
reduced hemoglobin.
Hypoxemia:
Hypoxemia is caused by decrease pulmonary perfusion with R  L shunts or by
pulmonary hyperperfusion. Hypoxemia results in polycythemia limitation of exercise
capacity and a tendency to vascular thrombosis.
Polycythemia is the main adaptive response to chronic hypoxemia and is
necessary to provide adequate tissue oxygenation Red cell mass increase up to three
times normal and blood volume may exceed 100 ml / kg blood viscosity is increase and
associated with an increase risk of thrombosis and intracranial hemorrhage.
Symptoms of hyperviscosity are headache, fatigue, paresthesia, dizziness,
depressed mental state are common with hematocrit above 65%.
Congestive cardiac failure:

CCF occurs most commonly in cardiac shunt lesions when the pulmonary to
systemic blood flow ratio exceeds 2:1 CCF will increase endogenous catecholamine
production and redistribute co to essential organs, resulting in increase HR and
decrease skin temperature.
 Cyanosis
 Hypoxemia – polycythemia
 CCF
 Pulmonary HTN
 Association medical problems
Pulmonary hypertension:
L  R shunts which result in increase PBF prevent the normal postnatal
decrease in PBF, PVR and pulmonary artery pressure. E.g. VSD and PDA. These lesions
produce pH and right ventricular hypertrophy.
Associated medical problems:
In addition to the cardiac lesions other congenital defects or diseases are
associated with CHD 25% of infants born with diaphragmatic hernia or omphalocele
have cardiac malformation 40% of children with trisomy 21 down syndrome have CHD.
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II. Physical examination:
The examination of the children with CHD should focus on the cardio-respiratory
system and any abnormalities that pertain to the planned surgical procedure.
Pulse and blood pressure noted in all four extremities. Children with CHD are at
increase risk for an abnormal origination of the arterial supply to the extremities and
for stenosis of peripheral vessels.
Examination of the patient’s airway for macroglossia, hypoplastic mandible and
protuberant teeth which are signs of difficult airway.
 Hb
 Coagulation
 Ser. Electrolytes
 ABG
 Chest X-ray
Laboratory studies:
Hemoglobin: The relative hypoxemia lead to the development of hemoglobin levels of
20 G/dl or higher. Increase in Hb lead to significant increase in viscosity in low flow
vessels such as capillaries and veins.
When the Hb reaches 20 g/dl peripheral sludging of blood reduces peripheral O2
delivery which in turn leads to development of acidosis. As compensation 2, 3 – DPG
levels increase, which allow the unloading of peripheral O2 by a rightward shift in the
ODC.
The potential for peripheral sludging acidosis and organ thrombosis with Hb
concentrations above 20 g/dl. Consideration is given to pre-operative erythropheresis.
Coagulation: Prothrombin time, partial thromboplastin time, fibrinogen concentration
and platelet count with CHD. Polycythemia children have a constricted plasma volume
leading to reduced levels of clotting factors.
Serum electrolytes: Pre-operative evaluation of electrolytes is recommended for all
children receiving digitalis or diuretics.
Blood gases: Pre-operative blood gases for the child with respiratory compromise or
severe cyanosis. PaO2 of 30-40 mm Hg or SPO2 less than 70% indicates risk for
development of metabolic acidosis.
Chest x-ray: The chest x-ray is analyzed for heart size position and shape, pulmonary
artery position, pulmonary arterial vascularity aortic contour, pulmonary congestion,
and areas of consolidation.
Cardiac grid: A hemodynamic profile or cardiac grid is a tool that can be useful in
sorting out the complex physiologic needs resulting from the anatomic lesions.
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The purpose of the grid is to show how five hemodynamic factors – heart rate,
pre-load, SVR, PVR and contractility can be best manipulated to ensure intraoperative
stability.
Preload PVR SVR HR Contractility
L  R ASD    N N
VSD    N N
R  L TOF     
Methods for intraoperative modifications of hemodynamic factors:

1. Preload: Increase – Volume loading capacitance vessel constriction peep.
2. Decrease – Phlebotomy, non-replacement of volume capacitance vessel
dilatation.
3. SVR: Increase – Arteriolar constriction ketamine, nitrous oxide.
4. Decrease – Arteriolar dilatation, isoflurane, histamine releasing agents.
PVR:
Increase:  PCO2 or acidosis
 PO2
PEEP
Decrease:  PO2
 PCO2
Heart rate:
Increase: Anticholinergics
Muscle relaxants
Decrease: -blockers,
Calcium channel blockers
Fentanyl, cardiac glycosides
Contractility:
Increase: Inotropes
Calcium, cardiac glycosides
Decrease: -blockers, calcium channel
blockers, inhalation agents.
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Fasting interval:
Children with CHD can ingest clear fluids up to 2 hours prior to induction of
anesthesia. This reduces the need for pre-operative intravenous hydration.
Medications: Children with CHD should receive all of their cardiac medications on the
day of surgery except anticoagulants and diuretics.
SBE prophylaxis:
Antibiotic prophylaxis for SBE is indicated for patients with CHD undergoing
many non-cardiac procedures.
Surgical procedures that do and do not require endocarditis prophylaxis:
Endocarditis prophylaxis Endocarditis prophylaxis not
recommended recommended
Dental procedures known to induce Dental procedures not likely to induce
gingival or mucosal bleeding, including gingival bleeding, such as simple
professional cleaning. adjustment of orthodontic appliances or
Tonsillectomy or adenoidectomy fillings above the gum line.
Surgical operations that involve intestinal Injection of local intraoral anesthetic
or respiratory mucosa (except intraligementary injections)
Bronchoscopy with a rigid bronchoscope Shedding of primary teeth
Sclerotherapy for esophageal varices Tympanostomy tube insertion
Esophageal dilatation Oral endotracheal intubation
Gallbladder surgery Bronchoscopy with a flexible
Cystoscopy bronchoscope with or without biopsy
Urethral dilatation Cardiac catheterization
Urethral catheterization if urinary tract Endoscopy with or without
infection is present gastrointestinal biopsy
Urinary tract surgery if urinary tract Cesarean section
infection is present In the absence of infection for urethral
Prostatic surgery catheterization, dilatation and curettage,
Incision and drainage of infected tissue uncomplicated vaginal delivery,
Vaginal hysterectomy therapeutic abortion, sterilization
Vaginal delivery in the presence of procedures, or insertion or removal of
infection intrauterine devices
From Dajani AS, Bisno AL, Chung KJ, et al: Prevention of bacterial endocarditis:
Recommendations by the American Heart Association. JAMA 264:2919 1990; reprinted
with permission of the American.
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Recommendations for prophylaxis against SBE:
Ampicillin - 50 mg/kg IV 30 min before procedure.
Then 25 mg/kg 6 hr after initial dose.
Clindamycin - 10 mg/kg IV 30 min before procedure.
Then 15 mg/kg 6 hr after initial dose
High risk patients:

Ampicillin - 50 mg/kg IV 30 min before procedure.
Gentamycin - 2 mg/kg IV 30 min before proceure
Repeat drugs after 8 hour
Vancomycin - 20 mg/kg IV 1 hour before procedure.
Preanesthetic medication:
The premedicant should produce a sedate and co-operative child at the time of
separation from the parents, plus maintenance of airway reflexes, a smooth induction of
anesthesia and decrease anesthetic requirement.
Premedication recommendations for children with congenital heart disease over 1

year of age:
Drug Dose Minutes prior to
induction to be
given
Oral premedicant combinations
Meperidine 3 mg/kg (maximum 100 mg) 60-90
Pentobarbital 4 mg/kg (maximum 100 mg)
Or
Meperidine 1.5 mg/kg (maximum 100 mg) 30-60
Diazepam 0.15 mg/kg (maximum 10 mg)
Or
Meperidine 2-3 mg/kg (maximum 100 mg) 60
Diazepam 0-1 mg/kg (maximum 10 mg)
Pentobarbital 2-4 mg/kg (maximum 100 mg)
Or
Fentanyl 15-20 g/kg 30-45
oral/transmucosal)
Or 0.5-0.75 mg/kg (maximum 5 20-30
Midazolam mg)
Intramuscular premedicant combinations
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Scopolamine 0.01 mg/kg (maximum 0.4 mg) 60
Morphine 0.2 mg/kg (maximum 10 mg)
Or
Atropine 0.02 mg/kg (maximum 0.4 mg) 60
Morphine 0.2 mg/kg (maximum 10 mg)
Or
Midazolam 0.08 mg/kg (maximum 5 mg) 10
Nasal premedication
Midazolam 0.2-0.3 mg/kg (maximum 5 mg) 10
Or
Ketamine 1-5 mg/kg 5-15
Or
Sufentanil 0.3-3 g/kg 10
Rectal premedication
Midazolam 0.3-1.0 mg/kg 20-30
Under 6 months of age only atropine should be used; between 6 months and 1
year atropine in combination with a sedative can be used. For all children
premedication recommendations should be modified based upon the severity of the
illness, airway patency, and any associated problems.
Age > 1 year
Fentanyl:
Oral / transmucosal – 15 to 20 g/kg (30-45 min)
Diazepam (elimination):
Oral 0.1 mg/kg (max 10 mg) 60 min.
Midazolam:
Nasal 0.2 to 0.3 mg (max 5 mg) 10 min
Oral 0.5 to 0.75 mg/kg (max 5 mg) 20-30 min
IM 0.08 mg/kg (max 5 mg) 10 min
Rectal 0.3 – 1 mg/kg 20-30 min
Pre-operative preparation: For every operative procedure minimal pre-operative
preparation includes checking for the presence of a functional suction apparatus, an
operational anesthetic machine with circuit, airway and intubation equipment and
availability of drugs. In addition cardiac resuscitative drugs and a defibrillator with
appropriate sized paddles present.
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Venous access:
Special precautions are taken whenever an IV catheter is placed in the presence
of intracardiac shunt to prevent the inadvertent introduction of air into the venous
circuit children with R  L shunts are at risk for systemic air embolization with
introduction of air into vein.
Monitoring:
Standard monitoring for children with CHD undergoing non-cardiac surgery.
1. Pulse oximeter
2. Precordial stethoscope
3. NIBP
4. ECG
5. ETCO2
6. Temperature
7. CVP
8. TEE
9. Urinary catheter
TEE: The use of TEE for non-cardiac procedures is reserved primarily for operations in
which the child is placed at risk for embolization arising from the surgical field.
Accuracy of Capnography and pulse oximetry:

ETCO2: Children with CHD are susceptible to abnormal pulmonary ventilation perfusion
ratios resulting in increase dead space or shunt. These abnormalities alter the arterial to
ETCO2 difference. In present of R  L shunts ETCO2 underestimates PaCO2 due to large
dead space ventilation.
Pulse oximeter: Have limited accuracy at oxyhemoglobin saturation below 70%.
Fluid management:
Fluid management is individualized for each patient on his age, cardiac
physiology, specific fluid needs, pre-operative deficit and expected third space fluid and
blood losses associated with surgical procedure.
The choice of fluid for perioperative management – Isolyte-P.
Care must be taken not to fluid overload a child with borderline myocardial
dysfunction. The ultimate goal of fluid management is to produce a hemodynamically
stable child during the anesthetic while maintaining a flow of 0.5-1 ml/kg/hr.
Speed of anesthesia induction:
R  L shunts: Slows the rate of rise in alveolar concentrations of inhalation anesthetic
drugs and prolongs induction and emergence from anesthesia.
IV induction agents have a more rapid onset of action science the agent more
rapidly reach the systemic circuit.
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L  R shunts:
Have a relative over perfusion of the pulmonary circuit. The blood from the lungs
which already contains anesthetic agent is recirculated thereby acquiring additional
anesthetic. The result is a higher peak anesthetic concentration in the blood and a rapid
inhalation anesthetic induction.
IV induction agents have a slower onset of action as a result of a delay in
reaching the brain during the period of recirculation through the pulmonary circuit.
General anesthesia with tracheal intubation and IPPV used to avoid the potential
complications of transient hypoxemia or hypercapnia. Regional anesthetic technique
used wherever possible and suitable.
Breathing system:
Jackson Rees circuit (Below 20 kg) Fresh gas flow twice the MV
Bain circuit 70 ml/kg for controlled
Closed system 2-4 L/min fresh gas flow
Induction:
Inhalation induction for patients with good cardiac reserve.
Halothane: Used in children with CHD for mask induction because of its easy acceptance
and has minimal effect on PVR and SVR and ability to titrate anesthetic depth.
Sevoflurane: Produces less myocardial depression than halothane which make it a
valuable induction agent for children.
IV Induction:
Thiopental – 2-5 mg/kg.
Fental – 1-3 mg/kg
Midazolam – 0.05 – 0.1 mg/kg
Ketamine – 1-2 mg/kg IV for cyanotic heart disease because it  SVR and Co.
Narcotic induction:
Fentanyl – 25-50 g/kg
Sufentanil – 5-10 g/kg
In children with minimal cardiac reserve and suited for longer surgical
procedures where early extubation is not required.
Relaxants:
Succinylcholine – 1.5 – 2 mg/kg used for rapid sequence intubation.
Vecuronium – 0.07 – 0.1 mg/kg
Atracurium – 0.3-0.5 mg/kg.
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Pancuronium – 0.1 – 0.15 mg/kg
Pancuronium is the muscle relaxant of choice when given with high dose
narcotics.
Maintenance:
N2O + O2 + Relaxant + Halothane + IPPV controlled ventilation is used in all
patients. PaCO2 is maintained between 30-40 mm Hg. In TOF excessive positive
pressure ventilation is avoided as it may lead to increase R  L shunt across a VSD and
decrease PaO2.
N2O is avoided in patients with pulmonary hypertension as it increase PVR

and increase the R  L shunt.
Reversal:
Neostigmine – 0.05 mg/kg.
Glycol-P – 4-8 mg/kg.
Regional anesthetic serve as useful adjuvants to GA in children with CHD the
advantages of regional techniques are reduced requirement for general anesthetic
agents and post-operative analgesia.
Peripheral nerve or plexus blocks are safe with exception of coarctation of aorta
use of local anesthetics in children with CHD is safe. Peripheral vasodilatation in
patients with polycythemia have benefit of improved microcirculatory flow and
decrease venous thrombosis.
Spinal and epidural anesthesia are tolerated with limited changes in HR or BP in
children less than 5 years of age.
Patients with chronic cyanosis are at risk for coagulation abnormalities and are
evaluated prior to regional anesthesia
Post-operative pain:
Post operative pain relief is considered as part of the anesthetic plan.
Day care surgery: Regional blockade such as caudal blocks in pediatric patients for
genitourinary surgery.
Injection Sensorcaine 0.25% - 1 ml/kg.
Injection morphine – 0.05 – 0.075 mg/kg.
NSAID: Provide effective analgesia for mild to moderate post-operative pain.
Ketorolac – 0.5 mg/kg IV 6th hrly
Ibuprofen – 8-10 mg/kg orally 6th hrly
Acetaminophen – 15 mg/kg orally
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Diclofenac – 1-3 mg/kg/day oral or rectally.
In patient surgery:
Epidural analgesia – injection Sensorcaine 0.1% with fentanyl 2 g/ml.
Morphine – 30 g/kg/hour
Systemic analgesics: PCA is a method of giving patients small doses of opioids at
frequent interval to minimize the side effect and used in patients above 6 years.
Loading dose: Morphine – 0.03 mg/kg
Pethidine – 0.3 mg/kg
PCA dose: Morphine – 0.02 – 0.03 mg/kg

Pethidine – 0.2 – 0.3 mg/kg.
Intermittent opioid administration:

Alternative to PCA in young patients unable to understand and effectively use
PCA.
Morphine – 100 g/kg.
CHD AND PREGNANCY:

CHD has overtaken RHD as the most common type of heart disease seen with
pregnancy. If either parent has a congenital heart abnormality the chance of the child
having a cardiac abnormality ranges from 2-50%.
Women with a L  R shunt tolerate surgery, pregnancy, labour and delivery
well. Women with a R  L shunt are fetal mortality. The risk to the fetus is in
proportion to the degree of maternal hypoxemia with a 50% risk of fetal death if
maternal oxygen saturation is less than 85%.
L  R shunts: pregnancy creates an additional burden by increase intravascular blood
volume, heart rate, and cardiac output. Parturient with small shunts who are
asymptomatic prior to pregnancy tolerate this additional stress. Patient’s with large
shunts develop symptoms of congestive heart failure.
Should receive antibiotic prophylaxis during surgery for SBE. Avoiding systemic
hypotension which may cause shunt reversal. Conditions that increase PVR such as
hypoxemia, hypercarbia and acidosis are avoided. Avoid aortocaval compression by left
uterine displacement.
Lumbar epidural anesthesia is most appropriate as it is free from major changes in
vascular resistance.
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R  L shunt:
A few women with these lesions reach child bearing age and are associated with
high maternal and fetal mortality. Pregnancy results in up to 50% maternal mortality
and 80% fetal loss. Pregnancy in these women is inadvisable.
The decrease SVR in pregnancy promotes increase R – L shunting and cyanosis.
Prime importance is to avoid myocardial depression and to maintain normal
SVR, venous return and blood volume.
Labour and delivery:
Epidural anesthesia is chosen as it allows a more gradual onset of the block. Slow
incremental dosing of the epidural anesthetic to provide a slow onset of hemodynamic
changes. Epidural opioids are used which improve the quality of block and allow use of
lower concentrations of local anesthetic.
General anesthesia is preferable during caesarean section as it allows optimal
airway management and titration of drugs to maintain vascular resistance and volume.
CONCLUSION:
Patients with CHD undergoing noncardiac surgical procedures require that their
anesthesiologists appreciate their unique cardiac physiology and formulate a plan based
on the principles dictated by that physiology.
Control of the hemodynamics within the physiologic limits imposed by the
cardiac lesion can be achieved with a variety of anesthetic techniques.
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Chapter 36 - JUGULAR VENOUS PRESSURE – WAVES
Wave- type Cause

‘a’ wave - Atrial Systole, increase pressure due to closure at atrial end
‘X’ - Fall of atrial pressure in later part of systole
‘C’ Bulge of A- V valve during IMC
‘X1’ Atrial relaxation and pull of A-V ring
‘V’ Gradual atrial filling
‘Y’ A-V valve opening, atrial flow to ventricle
PULSE
Pulse is the expansion and elongation of the arterial walls, passively produced by
the pressure – changes during systole and diastole of the ventricles.
Velocity of the pulse:

The pulse wave velocity is most rapid in the least distensible arteries.
In the aortic- arch: Pulse wave travels; 3-5 mts/sec
In subclavian artery: Pulse wave travels; 7-10 mts/see
In small, non distensible, peripheral-arteries; - 15-30 mts/see
Recording of Radial – Pulse:
a – Primary-wave / percussion-wave
c – Pre-dicrotic wave d – Dicrotic wave
D – Dicrotic notch e – Post-dicrotic wave
 The upstroke is abrupt and without any recording wave on it.
 Near the middle of the down stroke, there is a sharp depression called, dicrotic
notch. This is immediately followed by dicrotic wave.
 The wave form, from beginning to dicrotic-notch is called the “Primary-wave or
percussion wave. It corresponds to the ventricular systole
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 Dicrotic- notch: Is produced to sharp fall of pressure caused by the rolling back
of aortic blood towards left ventricle at the beginning of the diastole.
 Dicrotic – wave: is produced by the return of the same blood column, reflected
back by the closed. Semi lunar – valves.
Significance:
 A large Primary-wave is due to;
1) Large stroke-volume
2) Slow – heart – rate
3) Low – peripheral resistance.
 A small primary wave is due to:
1Small output
2) Rapid heart rate
3) High peripheral resistance
4) Stiffness of the vessel.
Special verities of pulse:

Anacortic pulse: Is a slow rising, twice beating-pulse, where both the waves are felt
during systole. The waves that are felt are “Anacortic – waves” or percussion-waves.
Conditions: best felt in carotid artery in aortic stenosis.
Dicrotic – pulse: Is a twice beating pulse, where the percussion wave is felt during
systole and the second dicrotic wave is felt during diastole. It is seen when the
peripheral- resistance and diastolic-pressures are low.
Conditions: - Typhoid fever
- CCF
- Cardiac tamponade
- Following Open-Heart Surgery
Pulsus - Bisferiens: is a rapid, rising, twice beating pulse where both the waves are felt
during systole. Hence the percussion – wave is felt first, followed by a small – wave.
Conditions:
Idiopathic hypertrophic sub aortic stenosis.
Severe AR with AS.
Pulsus – Parvus: is a slow rising pulse like the anacortic pulse but the anacortic wave is
not felt.
Condition: A.S.
Pulsus – alternans: Characterized by strong and weak beat, occurring alternately.
Conditions:
LV failure
Toxic myocarditis
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Paroxysmal – Tachycardia.
Pulsus – Bigeminus [Coupling]: Is the coupling of the pulse waves in pairs followed
by a pause.
Conditions:
Alternate premature beats
A-V block
Sinoatrial block
Thready pulse:
The pulse rate is rapid and is the pulse – wave is small, disappears quickly.
Condition: Cardiogenic shock. Signifies low LV ejection of blood.
Water – hammer – pulse: Is a large bounding pulse associated with increased stroke
volume of the left-ventricle and decrease in peripheral resistance, leading to a wide
pulse pressure. Best felt in radial pulse
Conditions:
High output states
Anemia
Thyrotoxicosis
Cirrhosis of liver
A-V fistula
Cardiac – conditions
AR
PDA
Aorto pulmonary – window
Pulsus – paradoxus:
Normally systolic BP falls by 3-10 mm Hg, during inspiration. This is because
negative intrathoracic pressure and expansion of the lung causes, pooling of the blood
in the pulmonary-vasculature,  VR to Lt Atrium and ventricle  CO  BP.
When SBP falls more than 10 mm of Hg during inspiration, the pulse is
erroneously called “Pulsus – paradoxus”.
Conditions:
Superior – venacaval obstruction
Cardiac – tamponade
Severe – CCF
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Chapter 37 BLOOD – PRESSURE
It is the lateral pressure exerted by the blood on the vessel wall.
SBP: Max pressure during systole. DBP: Min pressure during diastole.
Pulse pressure: Diff between systolic and diastolic BP.
Mean arterial pressure (MAP) = Diastolic BP + 1/3 PP.
Or MAP = (SBP + 2DPB) / 3
Normal value of BP is 120/80 mm of Hg.
Cut off Values to determine hyper or hypotension:

High values:
1. < 140 mm of Hg – Normal
SBP 2. Between 140-159  Borderline
3. SBP > 160 mm of Hg  High
1. < 85 mm of Hg is normal
DBP
2. DBP between 85-89 mm Hg  high – normal
3. DBP > 90 mm of Hg  high.
Low values: SBP < 100 mm of Hg
DBP < 50 mm of Hg
Height of SBP indicates:

1. The extent of work done by the heart
2. The force with which the heart is working
3. The degree of pressure which the arterial wall has to withstand.
Height of DBP Indicates:

1. The constant blood pressure against which, heart has to work.
2. Or is the measure of peripheral resistance.
Fall in BP leads to:

 Fall of perfusion pressure (Eg. Hypovolemia, MI)
 Anoxia in vital organs like brain
 Reduced filtration by the kidney leads to death
Increased BP – Results in:

 Cerebro vascular accidents (CVA)
 Heart failure
 Atherosclerotic complications.
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Factors controlling the BP:
1. Pumping action of the heart
2. Cardiac – output
3. Peripheral – resistance
4. Blood volume
Regulation of Blood Pressure:

Through vaso motor center (VMC)
It has 2 parts
1. Pressor centre – Causes rise of BP
2. Depressor centre – Causes fall of BP
Vasomotor reflexes:
Depressor – Reflex: Rise of BP stimulates baroreceptors of carotid and aortic
sinuses, and causes flowing of the heart and arteriolar dilation.
Vasodilatation is due to inhibitions of vasoconstrictor effect of sympathetic
system.
Pressor – reflex: Diminution of BP fails to stimulate baroreceptors and the
parasympathetic inhibitory tone over the heart and blood vessel is withdrawn. BP is
raised reflex through over activity of sympathetic system. This is due to stimulation of
pressure or vasoconstrictor centre.
CONTROL OF VASOMOTOR CENTRE
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Chapter 38 - CORONARY – CIRCULATION
Blood supply of the heart is derived from left and right coronary arteries that arise from
sinuses of valsalva at the root of aorta. These coronary arteries and their branches
travel through the epicardial surface and serve as conductance vessels offering little
resistance to blood – flow. Small coronary arterioles ramify throughout cardiac muscle
and impose variable resistance to blood flow and thus regulate distribution of coronary
flow. Coronary artery disease involves large epicardial coronary arteries and not
arterioles.
RIGHT CORONARY ARTERY (RCA)Supplies
1. Right atrium.
2. Inter atrial septum.
3. Right ventricle.
4. Posterior one third of inter ventricular septum.
5. S.A node in 60% of individuals. A.V node in 90% of individuals. Branches also
supply the bundle of His.
Occlusion of right coronary artery can lead to infarction of S.A node and atrial
dysrrhythmias. Infarction of A.V node leads to third-degree heart block.
Left coronary artery:

Divides into left anterior descending artery and circumflex coronary artery.
1. Left anterior descending artery (LAD) supplies anterolateral aspects of the left
ventricle, right bundle branch, anterior fascicle of left bundle branch and
Anterior 2/3rd of inter ventricular septum.
2. Circumflex coronary artery (CCA) supplies, lateral aspects of left ventricle.
 Posterior fascicle of left bundle-branch is supplied by all three main coronary
arteries.
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 Anterior-papillary muscle is supplied by left-coronary artery.
 Posterior papillary – muscle receives blood supply, from both left and right
coronary arteries.
 Collateral blood supply to papillary muscles is well developed.
Applied:
1. Severe ischemia may produce dysfunction of papillary muscles leading to acute
mitral regurgitation.
2. Incomplete – obstruction usually due to spasm of the coronary artery causes –
angina pectoris.
3. Thrombosis of the coronary artery leads to myocardial infarction and ventricular
fibrillation.
 Resting coronary blood flow about 80ml/100gm/min.
 During exercise this may raise up to 250ml/100gm/min or more.
 Resting myocardial oxygen consumption is 8ml/100gms/min.
Unique features of coronary blood flow:

1. No anastomosis exists between left and right coronary arteries.
2. Blood-flow to left-ventricle is interrupted during systole due to mechanical
compression of vessels by myocardial contraction.
3. Cardiac muscle shows almost maximum O2 extraction at rest. Hence during
exercise, demand for increased O2 supply can be met only by increasing the
coronary blood flow. Such increase can be severely limited by coronary artery
disease. Moreover cardiac muscle has limited capacity for anaerobic metabolism
and therefore cannot incur “oxygen-debt”.
4. The subepicardial portions of myocardium are better supplied than
subendocardial part. The subendocardial region of left ventricle is the most
common site for myocardial infarction.
Autoregulation of coronary blood flow:

Between 60 to 140mm of Hg, of mean arterial pressure in the aorta, the coronary
flow remains unchanged due to autoregulation which is independent of nerves.
Theories proposed to explain autoregulation are
1. The tissue-pressure theory
2. Myogenic theory
3. Metabolic theory
Major determinants of coronary flow:

1. Coronary – perfusion pressure (CPP)
2. Myocardial – extra vascular compression
3. Myocardial – metabolism
4. Neurohumoral control
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1. Coronary perfusion pressure (CPP):
Coronary blood flow is directly proportional to CPP, diastolic blood pressure, (i.e.
L.V.E.D.P) and perfusion time (duration of diastole).
And inversely, related to coronary vascular resistance (C.V.R.)
Coronary vascular resistance (C.V.R.) is influenced by local metabolic factors,
such as oxygenation of cardiac muscle, viscosity of blood, activity of autonomic nervous
system (ANS) and patency of coronary arteries.
In the presence of coronary atherosclerosis changes in coronary vascular
resistance cannot occur and coronary blood flow becomes entirely pressure dependent.
2. Resistance due to extra-vascular compression increases with BP, heart rate,
contractility and preload.
3. Myocardial metabolism:
Whenever there is myocardial hypoxia there is coronary vasodilatation leading
to correlation of hypoxia, vasodilatory substances are released by myocytes in
proportion to their level of work. Vascular-endothelium also produces vasoregulators.
Some of the mediators of vascular tone that have been proposed, include, adenosine,
ATP, prostaglandins, nitric-oxide (NO), endothelin, O2, K+ etc.
4. Neural control:
Coronary arteries receive innervations from parasympathetic (vagus and cardiac
plexus at the base of aorta) and sympathetic fibres (Stellate ganglion).
1 – Receptor predominate in conductance vessels
1 – Receptor predominates in resistance vessels.
Parasympathetic stimulation causes vasodilatation.
Sympathetic – stimulation induces coronary dilatation secondary to  metabolic
demand, unopposed 1 – adrenergic stimulation may produce coronary spasm.
5. Humoral control:
– Vasopressin (A.D.H) in high concentrations can cause vasoconstriction.
– Atrial natriuretic peptide (ANP) can cause endothelium dependent coronary
dilatation.
– Vasoactive intestinal peptide (VIP), neuropeptide-Y, calcitonin generated peptide
cause vasoconstriction.
– Angiotensin II causes coronary vasoconstriction.
– PGI2 (Prostacyclin) –synthesized in vascular endothelium induces, vasodilatation
and inhibits platelet aggregation.
– Thromboxane (TxA2) causes vasoconstriction and platelet aggravation.
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I. Tachycardia and coronary flow:
During tachycardia, diastole is shortened and C.B.F. falls. The rise of metabolism
during tachycardia, by virtue of O2 lack causes coronary – vasodilatation. Despite this, in
elderly people, or people with C.H.D. tachycardia may be dangerous.
II. Blood pressure and coronary flow:

Very low – diastolic pressure (e.g. aortic incompetence) decreases coronary
perfusion pressure (CPP)  C.B.F.
In severe M.I. – severe cardiogenic shock and hypotension  insufficient
coronary filling due to  C.P.P.  further infarction.
High BP  wall tension  C.B.F.
III. Atherosclerosis of coronary artery (C.H.D):

Blood supply distal to the region of partial occlusion falls, but may still remain
sufficient provided the person is at rest, when the person undertakes muscular work,
the reduced blood supply becomes insufficient to meet the demands as the hardened
arteries fail to dilate and chest-pain called angina-pectoris develops.
IV. Reactive hyperemia:

When there is temporary occlusion of a branch of coronary artery, the part distal
to the occlusion suffers from anoxia. When the occlusion is removed, a marked,
vasodilatation occurs. This is called reactive hyperemia. It may be due to accumulation
of metabolites in the ischemic area.
Coronary steal:
If one of the branches of coronary artery is tightly occluded by a stenotic lesion
administration of a pharmacologic vasodilator or endogenous release of local
vasodilators may cause preferential vasodilatation of normal vessel because the stenotic
vessel is already maximally dilated. There is relative  in blood flow to normal area of
heart and a relative decrease in flow to ischemic area. There are two kinds of steal;
transamural and inter coronary steal.
Coronary reserve:
The difference between resting coronary blood flow, and peak flow, during
relative hyperemia represents autoregulatory coronary flow reserve.
Subendocardial / subepicardial or inner / outer blood flow ratio is often used as a
measure of adequacy of myocardial blood flow. Normal ratio is 1:1. The ratio close to 1
indicates, appropriate matching of myocardial O2 supply to O2 demand.
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Effect of anesthetics on coronary circulation:
Volatile anesthetics:
In vitro-volatile anesthetics are coronary vasodilators. In vivo, they cause
reduction in MVO2 which leads to coronary vasoconstriction, via metabolic
autoregulation. They also make reduction in coronary perfusion pressure  in O2
extraction are seen. Isoflurane induced coronary arteriolar-vasodilatation may result in
coronary artery steal and regional myocardial ischemia.
N2O redistributes transamural coronary blood flow  preferentially to
subepicardium ( I/O ratio).
Transmural steal: this occurs in the myocardium, diverting blood from the
subendocardial to the subepicardial areas. This is because lower limit of autoregulation
perfusion pressure is greater for the subendocardial layers than for the subepicardial
layer, subendocardial – blood-flow may be reduced when subepicardial B.P. is
preserved.
Drugs causing coronary steal
– Isoflurane
– Dipyridamole
– Nitroprusside
– Adenosine
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Chapter 39 - INTRA-AORTIC BALLOON PUMP (IABP)
Intra-aortic balloon counter pulsation is the simplest and most commonly used
form of cardiac assist device. The concept of mechanical support of the failing left
ventricle was first proposed by Clause (1961), but it was moulopoulos in 1962 who
devised the modern intra-aortic balloon pump (IABP).
This device produces diastolic counterpulsation with compressed gas driven,
volume displacement of an elongated catheter mounted balloon, which is electronically
gated to the patient’s ECG. It is introduced from the common femoral artery into the
descending thoracic aorta. The inflation is timed with the dicrotic notch of the arterial
pressure and deflation is done just before isometric left ventricular contraction thus
reducing the after load.
Previously, it used to be introduced surgically via the common femoral artery.
Another route of insertion is the trans-thoracic approach where it is inserted through a
tetra fluroethylene graft stitched to ascending aorta. The device has become popular
with the advent of the percutaneous approach but it has been shown that the incidence
of complications is more with the percutaneous approach than the surgical approach.
Advantages of IABP:
 Physiologically effective
 Relative ease and safety to use
 Scope of clinical applicability
 Useful when rapid reversibility of cardiac damage is expected. Unloading of left
ventricle also assists the right ventricular function.
CRITERIA FOR MECHANICAL SUPPORT OF CIRCULATION

Severe left ventricular dysfunction (cardiac index less than 1.7 L/mt/m2, systolic BP less
than 100 mm Hg, systemic vascular resistance more than 1200 dynes, sec. cm5 mean
atrial pressure more than 20 mm Hg, heart rate more than 80 beats / minute) despite
maximum inotropic support. Maximum inotropic support means a combination of two
or more of the following:
1. 10 mcg/ kg / min of dopamine
2. 10 mcg/kg/min of dobutamine
3. 10 mcg/kg/min of amrinone
4. 0.2mcg/kg/min of Adrenaline.
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INDICATIONS FOR IABP:
1. Post cardiotomy cardiogenic shock
2. Acute myocardial infarction
I. Cardiogenic shock
II. VSD with progressive LV failure and shock
III. A/c papillary dysfunction causing acute mitral regurgitation, LV failure
and cardiogenic shock.
3. Myocardial ischemia refractory to medical therapy
i. Unstable pre infraction angina.
ii. Unstable post infraction angina
iii. Refractory ventricular tachyarrhythmias.
4. Post of cardiogenic shock
5. Preop prophylaxis –
i. Severe LV dysfunction
ii. Critical left main coronary stenosis with occlusion of dominant right
coronary or unstable angina.
iii. Combined severe valvular and coronary artery disease with severe LV
dysfunction or unstable angina.
6. Failed coronary angioplasty with unstable myocardial ischemia.
PHYSIOLOGICAL CHANGES WITH IABP:

1. Increases aortic diastolic pressure thus improving the coronary perfusion,
producing an increase in cardiac output.
2. Increases coronary perfusion pressure by:
a. Reducing after load with increased forward flow.
b. Reducing intra myocardial wall tension.
c. Reducing myocardial oxygen consumption.
Diastolic pressure time index,(DPTI) which is a measure of myocardial oxygen supply is
increased so the endocardial viability ratio is improved thus useful in myocardial
salvage after acute myocardial infarction.
ENDOCARDIAL VIABILITY RATIO = DPTI / TTI (total time index) normal is 1. Ratio <
0.7 indicates subendocardiac ischemia
Applications:
1. Complicated myocardial ischemia
2. Cardiogenic shock
3. In cardiac surgery – Standby
4. Elective balloon pumping
5. In postoperative cardiac critical care unit.
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6. In cardiac catheterization
7. In septic shock
8. In pediatrics
9. Pulmonary artery balloon pumping
10. Trauma and hemorrhagic shock.
Complications: 8-30% incidence

1. Limb ischemia
2. Infection
3. Coagulopathy
4. Haemorrhage
5. Aortic dissection
6. Aortic or iliac artery perforation
7. Renal artery embolism or thrombosis
8. Mesenteric infarction
9. Spinal cord ischemic injury
10. Balloon rupture with gas emboli
11. Air embolism
12. CVA
To reduce the incidence of vascular complications:

A. Heparinized the patient within 2-4 hours and maintain ACT at 1-1 ½ times the
normal.
B. Use longer introducer sheath 16 inches
C. Abdominal aortogram to delineate aorto-ilio-femoral artery anatomy to select
the preferred side.
D. Use central lumen wire guided IABP.
LIMITATIONS OF IABP
1. Not useful when the left ventricle is not able to eject blood into aorta.
2. Not very effective in irregular and fast cardiac rhythms, because there is
insufficient time for the gas to fill the empty the balloon.
CONTRAINDICATIONS
1. Aortic insufficiency – The incompetent aortic valve allows the ventricle to
distend during diastole thus reducing coronary perfusion pressure.
2. Sepsis
3. Severe vascular disease – technically difficult, and prone to thrombosis. Risk of
rupture of abdominal aneurysm.
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Chapter 40 - CPCR – CONTROVERSIES
CRCP is a clinical situation which produces so dramatic results, that a few minutes of
treatment makes the difference between life and death. There is no role for a single
improper step or delay. So also, any modification which offers a very minute advantage
may be important. Thus, it is natural that the intricate details of the procedure are the
subject of intense research and arguments.
Let us now discuss certain controversial points
CARDIAC PUMP versus THORACIC PUMP -

As mechanism of External Cardiac massage.
It has long been held that a closed chest massage compressed the heart between
the sternum and the spine, thereby increasing ventricular pressure; which is
transmitted to vessels and not backwards due to a closed mitral valve, on release, the
ventricle refills passively. This cardiac pump mechanism was questioned on several
grounds. In 1976, Criley found during angiography that if the patients who developed an
arrest coughed immediately, the peripheral perfusion was maintained. This led the John
Hopkin’s Researchers to investigate the matter and they found that an increase in
intrathoracic pressure increased peripheral perfusion. Ineffectiveness of ECM in flail
chest patients was also an argument in favor of this thoracic pump mechanism.
Here heart acts as a passive conduit between two vascular beds and an increase
intrathoracic pressure drives blood from a low pressure pulmonary circulation to a high
pressure systemic circulation. This increased intrathoracic pressure compresses
systemic veins more than arteries (being more collapsible) and since they have valves at
thoracic inlet there is no back pressure along them. This creates an arterio-venous
pressure gradient which is essential for organ perfusion (since I.V.C. has no valves, the
back pressure reduces the perfusion of lower ½ of body during ECM). This has been
supported by experimental evidence of open mitral valve on cineangiography and equal
pressures in all 4 chambers. More time spent in compression was assumed to increase
intrathoracic pressure and hence a low rate with increased compression duration was
adopted (60/min). But this increased intrathoracic pressure is likely to decreases
coronary and cerebral perfusion. So also various techniques like SCV-CPP, IAC-CPR,
abdominal binding etc. were not found to give superior results in arrested humans.
During manual CRP in dogs it was found that LV and aortic pressures were
higher than the rest and mitral valve was closed during compressions. This rekindled
interest in cardiac pump mechanism. Echo evidence showing deformation of heart on
ECM (being more anteriorly) brought forth the argument that a HIGH IMPULSE
(increased force and velocity) CRP was needed to compress the chamber, rather than
the displacement which occurs at low impulse. Moreover increased rate naturally
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increased the C.O. and rate of 120 or more was suggested and was supported by
experimental evidence of better prognosis.
Ultimately which of these mechanism is active in a person is decided by heart
size, thoracic size and compliance, force and rate of compression, compression /
relaxation ratio etc. In order to strike a compromise AHA recommends a rate of 80-
100/min with 50:50 ratios. Alternation of compression and ventilation (5:1 or 15:2) is
still the method of choice.
Pediatrics-more of heart being behind sternum, cardiac pump may be more
important.
SITE OF COMPRESSION:
The site of compression in children for ECM has been subjected to change
recently, midsternal was earlier used assuring that in children, heart is higher and lower
compression will cause liver injury. Recent experimental data shows that there is no
such variation in position of heart in children. Both these positions have their own
advantages.
CAB OR ABC?
C-A-B sequence for basic life support has been put forward by a Dutch group in
cases of witnessed cardiac arrest. They argue that the partially oxygenated blood
(patient may even be gasping) could be delivered to vital organs, buying precious time.
But this has not been universally accepted, though a thump on the chest is practiced
widely.
THE DEMISE OF POLYPHARMACY
An area where changes are made every now and then is DRUGS. There is a trend
towards fewer drugs. The parts of disagreement are
a. Route of administration – intracardiac has been and is still the choice with many
practitioners. High rate of complications have made the AHA to supercede this
with I.V. route. Transpulmonary instillation is now thought to be less effective
even with higher doses.
b. Sodium bicarbonate – countless are the pages that are written, both for and
against NaHCO3, but is still used wide as the last resort. It is used on the ground
that it neutralizes the metabolic acidosis occurring as a result of anaerobic
metabolism. But it leads to following side effects – hypernatremia,
hyperosmolarity (ventricular haemorrhage in infants), liberate CO2, paradoxical
CSF acidosis, alkalosis, shift of ODC to left neutralize adrenaline in the IV line.
After lot of arguments AHA has finally discontinued its routine use in CPCR (as
per 185 guidelines). Its use is reserved for prolonged arrest, preexisting acidosis,
Hyperkalemia etc.
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THAM and carbicarb (NaHCO3 + Na2 CO3)
a. Are prescribed on the ground of fewer side effects, but many do not favor
any buffers in arrest.
c. Ca++ - was a universal cardio tonic used, but has been found to cause muscle
necrosis and promote cellular autolysis in ischemic organs. AHA has limited its
use to situations like hypo Ca++, Hyper Mg++, Ca channel blocker toxicity, some
EMD cases etc.
d. Adrenaline – its role as the ultimate drug in cardiac arrest has been questioned
by countless studies comparing it with other stimulants and noradrenaline. But
still none has been proved superior to it. A higher dose (0.1-0.2mcg/kg as against
classical 0.01 µgms/kg schedule) was found to get unanimous approval.
5-10 mcg/kg for every 5 min’ arrest time is the accepted regimen now.
COLLOID VERSUS CRYSTALLOID:

Controversy has been discussed too many times. Suffice is to say that a
crystalloid may be sufficient as the 1st time of management and colloids. Hypertonic
dextran is advocated by several groups as it suddenly expands intravascular volume.
DEFIBRILLATION:
There is a trend towards early usage of electrical defibrillation. 3 rapid shocks
without pause has been claimed to be more effective than the classical method; though
not proved beyond doubt.
Early usage of bretylium (a clinical defibrillation routinely is being advocated.
Though it increases defibrillation threshold, it decreases post-resuscitation
arrhythmias.
EARLY INTUBATION:
Is the choice of WFSA, but AHA say s it will interfere with ECM and should be
reserved for prolonged arrests.
ROLE OF TAYMEN: Or trained paramedic has been often disputed – whether to
allow them to do intubation and defibrillation. This they are being increasingly involved
in the early management. The development of ECTA, EDTA, esophageal Combitube and
automatic defibrillators are evidence of recognition of this role.
CEREBRAL PROTECTION: is an area of intense research and conflicting reports.
The use of high dose barbiturates is now condemned and even the low dose regimen is
controversial, though many drugs offer theoretical advantage and have their
proponents – none have been recognized for routine clinical use.
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Chapter 41 - CORONARY CIRUCLATION
Blood supply to heart is derived from the coronary artery which divide into left and
right.
They arise from Sinuses of Valsalva at the root of aorta. Coronary are perfused during
diastole.
Right Coronary Artery:
TOTAL 6 BRANCH
Right coronary artier supplier
1. Right Atrium
2. Right Ventricle
3. Inter atrial Septum
4. Post 1/3rd of Inter ventricle Septa
5. SA (60% of Individual)
6. AV node (85% to 90%)
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Left Coronary Artery:
Left Coronary Artery Divide into:

a). Left Anterior Descending Artery
b). Left Circumflex Artery
LCA SUPPLIER
1. Left Atrium
2. I.V. Septum (anterior 2/3rd)
3. Left ventricle (Septa anterior, & Lateral wall)
4. SA Node (LAD 40%)
5. Left Circumflex Artery (10-15%)
LAD- Supplier Septum & anterior wall

LCX - Lateral wall
Bundle of His = Dual blood supply by post descending artery & LAD
Anterior papillary muscle = Supplied by Diagonal br. G LAD +
Marginal Br. Of Circumflex
Posterior Papillary muscle = one supply Post Descends artery = Ischemia
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Major Determinants of Coronary Flow
1). Coronary perfusion Pressure (CPP)
2). Myocardial O2 balance
3). Myocardial Metabolism
4). Neural Control
1) Coronary Perfusion pressure

CPP = Arterial Diastolic Pressure – LVEDP
2) Myocardial O2 balance
- It is most important determinant of Myocardial blood flow
- The myocardium normally extracts 65% of O2 is arterial blood
Factor affecting myocardial O2 supply demand balance

Supply Demand
1. Heart Rate 1. Basal requirements

2. CPP 2. Heart Rate
3. Arterial O2 content 3. Wall Tension (after load, preload)
4. Coronary vessel diameter 4. Contractility
Myocardial extra vascular compression
3). Myocardial Metabolites:
- When ever myocardial hypoxia there will be coronary vasodilation leading to

correction of hypoxia. It may be due to vaso-regulator produced by vascular
endothelium like adenosine, ATP, NO Prostaglandin, O2, K+ etc.
4). Neural Control:

Coronary artery receives: Para sympathetic
Sympathetic in values
Para sympathetic: By vagus & Cardiac plexus at the base of the aorta.
Sympathetic from: Stellate ganglion (C6,7,8, T1)
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Both α1& β2 present in the coronary arteria.
α1 = located on large epicardial vein
β2 = are mainly found on small intra mucous and subendocardial vessels.
 Angiotensin II : Causes coronary Vaso constriction
 Thromboxane (TXA2) : Vasoconstriction & platelet aggregation
 PGI2 (Droxtacyctin): Synthesized in vascular endothelium induces vasodilator &
inhibit platelet aggregation.
Coronary steal:
Coronary steal is an important phenomenon that may affect the coronary blood flow, to
the ischemic myocardium.
Coronary steal phenomenon in the above fig.
Say (n) Coronary artery A divide into B – Completely occlude

C – partially stenosed occluded
C – (n) supplies an area of myocardium, but now has to provide collaterals
D to sustain the area of myocardium normally.
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2 main branches B & C
B – Supplies the area of myocardium B1 &
C – Supplies the area of myocardium C1
B – Completely Occluded
C – Partially Occluded
 Due to diseased artery B,
 C –gives collateral (D) to the myocardium B in addition to normal vessels to
myocardium C1.
 Myocardium B1 is now depended for its blood supply on collateral D arising
from C.
 The functional Dynamics of this arrangement under resting condition are that
both the (n) artery C and the collateral D are of normal caliber with both the
areas of myocardium B1 & C1 being perfused well. The patient will have no
ischemic symptoms.
 However the functional dynamics changes markedly in conditions of execution /
exercise that includes vasodilation of the vessels, the (n) artery C can vasodilate,
collateral artery D-Cannot. As the flow access the proximal stenosis is fixed,
there is no scope for both C & D to get adequate blood supply. In this C-will steal
blood from the collateral D rendering the B myocardium more ischemic. The
patient may have myocardial ischemia.
 Reducing the level of execution reduces the O2 requirement, there by restoring
basal function, dynamic restoring blood supply to myocardium B.
Condition pre-disposing to the steal phenomenon as

1). An inflow restricted (stenotic) vessel supplies two parallel vascular beds.
2). One of the vascular bed can dilate, but the other is already maximally dilated.
3). Both beds are exposed to vasodilating stimuli.
Drugs causing coronary steal
1. Isoflurane – I ANDI
2. Dipyridamole – D
3. Nitroprusside – N
4. Adenosine – A
Two kinds of steal:

 Inter coronary (all the above are exception) (Collateral)
 Transmural
Transmural steal: occurring in the myocardium, diverting blood from the sub
endocardial to the subepicardial areas. This is because the lower limit of autoregulation
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perfusion pressure is greater for the subendocardial layer. Subendocardial blood flow
may be reduced when subepicardial blood flow is preserved.
Effects of anesthetic agents on coronary circulation:

Most volatile anesthetic agents are vasodilating effect on coronary arteries.
They also  CPP  CBF
Isoflurane induced coronary arterial validation may result in coronary artery steal and
regional myocardial ischemia.
N2O redistribute transmural coronary blood flow preferentially to subepicardium.
Relationship of ECG with coronary artery

ECG Lead Coronary artery involved Areas myocardial
II III AVF Rt. Coronary Artery RA, RV, SA & AV Nod
I avL Circumflexed corrugating Lateral of LV
V3 – V5 Left anterior descends artery Anterolateral aspect of LV
CORONRY ARTERY
Root of Aorta
Epicardial – Right & Left coronary artery

Intramyocardial – Resistant arteries 10 – 250 micros diameter
Subendocardial
Collaterals develop = intra-myocardial plexus
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Chapter 42 - Discuss the etiology, C/F inv & Anesthetic
management of pericardial effusion?
Definition:
Accumulation of Fluid in the pericardial cavity is called pericardial effusion.
Etiology
 Common causes Less common
Tuberculosis Rheumatic fever
Viral – Coxsackie B Virus Uremia
Acute myocardial infraction Malignant disease
Trauma SLE &
It can accommodate 2000ml
C/F
 Apical impulse may not be palpated
 Increases in Cardiac dullness on percussion
 Heart sounds are faint or muffled.
 A pericardial rub may be audible
 Ewart’s sign = area of dullness and tubular breathing at the angle of left scapula,
resulting from compression of lung.
Investigations
Chest X-ray
 Enlarged cardiac silhouette
 Water-bottle appearance of heart shadow
 Lucent pericardial future
ECG
 Low voltage QRS Complex
 T wave may be inverted
Echocardiography: To confirm the diagnosis

 Diagnostic Paracentesis
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Management:
1. Therapeutic Paracentesis.
2. Anti inflammatory drugs like aspirin or Indomethacin
3. Rx of underlying Law
Anesthetic Management
Pre-operative preparation
 The presence of pericardial effusion that is hemodynamically significant can
result in life threatening hypotension.
 Pericardiocentesis performed with local anesthesia is often preferred, so that the
CO is increased.
 After hemodynamic status has been improved by percutaneous
pericardiocentesis, it may be acceptable for anesthesia.
General Anesthesia is preferred

1. Ketamine or benzodiazepine plus nitrous oxide are acceptable
2. Muscle relaxants like Pancuronium, is useful
3. Intra arterial & CVP monitoring is useful
4. Intraoperative cardiac art is maintained
5. Avoid increase SVR & Myocardial contractility
6. Fentanyl can be used as analgesia
7. If decrease CO then IV Infusion of Isoproterenol, dopamine or dobutamine
8. Reversal with inj. Neostigmine and glycopyrrolate is 0.05 & 0.01 doses
respectively.
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Chapter 43 - What is cardiac tamponade, C/F, Inv, Rx
and anesthetic management?
Definition:
Cardiac tamponade result from the accumulation of fluid in the pericardium in an
amount sufficient to cause compression of the heart and impair diabetic filling.
The minimum amount of fluid required for tamponade depends on the speed of
accumulation (about 250 ml is rapidly developing effusion and > 2000ml in slowly
developing effusions)
Etiology
 Refer pericardial effusion
 Hemopericardium
C/F
1. Dyspnoea & orthopnea
2. Pulses Paradoxus or Paradoxical are in the hall mark of tamponade
3. Hypotension
4. Raised JVP
5. Increase in cardiac dullness to percussion
6. Faint heart sound
7. Tender hepatomegaly
Rest refer pericardial effusion notes:
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Chapter 44 - Pace Makers
Cardiac pacing is valuable techniques for treating arrhythmias
Principles of Pacing: Capture
Threshold for capture

Sensing
Threshold for Sensing
Capture
 In cardiac pacing brief electric pulses are used to depolarize the heart.
 Each pulse directly depolarizes only a small volume of the myocardium
 When sufficient myocardium has been depolarized a self propagating wave front
of activation, spreads from the site of stimulation.
 At this point the stimulus is said to have captured the heart.
Threshold for capture

 The threshold for capture is a function of the duration of the stimulus, being
greater as the police width is shortened.
 It also depends on the degree of contact between the pacing electrode and the
heart.
Sensing
 The modem cardiac pace maker not only stimulates the heart but also capable of
sensing the spontaneous heartbeats.
Threshold for Sensing

 For sensing to occur, the spontaneous beat must produce a signal whose
amplitude exceeds the present sensing threshold of the pacemaker.
 Single chamber pacemakers: Single Chamber pacemakers are usually inhibited
from delivering stimuli whenever the native ventricle rate exceeds the present
rate of the pacemaker.
 Dual chamber pacemakers
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 Spontaneous ventricular beats inhibit ventricular stimuli
 Spontaneous atrial beat inhibit atrial stimuli, but trigger the delivery of
ventricles stimuli after a present atrio ventricular (AV) interval.
 This cause AV synchrony to be maintained, which is desirable during sinus
rhythm, but problematic if patient develops atrial flutter / fibrillation.
Types of Pacemakers:
 It has a five letter nomenclature. A code has been devised to identify the
different types of pacemakers. The protocol is
First letter
The first letter indicates the chambers that are paced.
1. A for atrium
2. V for Ventricle
3. D for Dual Chamber Spacing
4. S for single chamber pacing which may be applied to either atrium or ventricle
Second Letter
The Second letter indicates the chambers that are sensed. D is used if the pacemaker is
incapable of sensing.
Third letter
The third letter indicates the type of response of the pacemaker makes to a denied
signal. It indicates whether the pacemakers stimuli are inhibited (1) or triggered (T) as
both (D) by sensed spontaneous beats.
Fourth Letter
Was originally used to describe programmable functioning of general, but is now used
to designate the presence of rate adaptive abilities e.g. It varies with metabolic
demands like exercise.
Fifth Letter
The fifth letter indicates the presence of anti tachycardia pacing capabilities but now
incorporated into automatic implantable deliberators.
Final nomenclature
1). Ventricular demand pacemakers are therefore labels VVI (or) SSI
2). Dual chamber pacemakers that pace and sense in both chamber one labeled
DDD.
3). Temporary dual chamber pacing systems usually are incapable of sensing a trial
activity, they are labeled DVI.
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Choice of Pacing Mode
AAI: Used in SA node disease with no evidence of atrio ventricular (AV) node or bundle
of His
Rapid adaptive pacing system

It is useful in conditions in which the heart rate does not respond to increased metabolic
demand
E.g. : 1. SA node disease

2. AV node disease
3. Fascicular disease
Complications of pacing
Pacemaker syndrome
Symptoms
Manifests are symptoms associated with ventricular pacing including
1. Syncope
2. Weakness
3. Orthopnea
4. DND
5. Pulmonary edema
Pathophysiology features
1. Hypotension due to reduced cardiac output due to reduced atrial
contribution to the LV filling.
2.  in atrial presence due to contraction of atria against closed metal and tricuspid
values when ventricle is paced (VVI)
3. Activation of baroreceptor from inappropriate atrial stretch can lead to reflex
peripheral vasodilatation.
Life of Pace Maker

1. Lithium batteries – 8 – 20 Years
2. Dual chamber – 7 – 10 years
Dual chamber pacing: (DDD pacing)

This has the following advantages
1. Maintenance of AV synchrony
2. Reduction in the incidence of pacemaker syndrome
3. AV synchrony is maintained
4. Useful in hypertrophic cardiomyopathy
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Indications for pacing
Temporary Pacing
1. Rate or rhythm related hypoperfusion
2. High risk lethal bradycardia
3. Prevention of tachycardia
4. Re of re-entrant tachycardia
5. Diagnostic aid
INDICATION:
PERMANENT PACING
1. Acquired complete heart block
2. Second degree AV Block
3. Atrial flutter (or) fibrillation, SVT
4. Persistent advanced second degree
6. Bifascicular block
7. Sinus Bradycardia
SITE OF PACING
1. Internal Jugular (most commonly used)
2. Ante cubital vein
3. External jugular
4. Femoral veins
POSITIONING
1. Fluoroscopy – guided
COMPLICATION OF TEMPORARY PACING

1. Inadvertent Puncture of an artery
2. Pneumothorax
3. Air embolism, perforation of the heart
4. Catheter embolism, hematoma
5. Ventricular perforation
6. Arrhythmias
7. Infection
OTHER TYPES OF PACING

1. Epicardial pacing
2. Transesophageal pacing
3. Transthoracic pacing
4. Transcutaneous pacing
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MALFUNCTION OF PACEMAKER
1. Failure to produce stimuli
2. Battery failure
3. Disconnected lead & lead
4. Battery faith
5. Undesired stimulation
6. Failure to sense
7. Lead dislodgment
Surgery in patients with artificial pacemaker

Pre-operative valuation
1. Determine the reason for pacing
2. Ask H/O vertigo (or) syncope
3. Check HR, AV synchrony
4. ECG – Ventricular synchronous
5. Chest x ray: to confirm & evaluate the intactness of pacemaker
Management of Anesthesia
1. Monitor to confirm function of pulse generation
2. Availability of equipment & drugs to maintain intensive HR, if pacemaker fails
3. ECG monitoring contours
4. Continuous peripheral pulse monitoring
5. Place the ground plate for electrocuted as far as possible from pulse generator.
6. Drug Atropine, isoproterenol should be available
 Succinylcholine: Inhibits the normally functioning pacemaker by causing.

Contraction of skeletal muscle groups. Myo-potentials are interpreted as intrinsic R-
ware by the pulse generator. This can be either reduced by very non-depolarizing
muscle relaxes can pre treat with NDM before administrating depolarizing muscle
relaxant.
 K or K leads to transverse pacing failure.
 Arterial hypoxia.
 MI
 Catecholamine release.
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2011

Dr Azam's Notes in Anesthesiology

Dr Azam’s Notes in Anesthesiology

www.DrAzam.com Cardiovascular System

Graphic representation of data is an excellent form of data compression; figures or

I constructed parts of Dr Azam’s Notes in Anesthesiology for Postgraduate students

Dr Azam’s Notes is aimed primarily at trainees in Anesthesia though more experienced

The format is designed to provide easy access to information presented in a concise

www.DrAzam.com Cardiovascular System

Anesthesiology is an ever-changing field. Standard safety precautions must be followed,

However, in view of the possibility of human error or changes in medical sciences,

www.DrAzam.com Cardiovascular System

To Mohammed Shafiulla, my father, my oxygen,

I also would like to thank my mom (Naaz Shafi), my wife

I also thank my Colleagues Dr Rajshekar Reddy & Dr

Finally, I would like to thank my teachers. The dream begins

www.DrAzam.com Cardiovascular System

01. Dr. Rajshekar Reddy – UAE

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CHAPTER 1 CARDIOVASCULAR SYSTEM PHYSIOLOGY .................................................................................... 25

CELLULAR CARDIAC PHYSIOLOGY:............................................................................................................................. 25

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CHAPTER 2 ADULT, PEDIATRIC AND NEWBORN RESUSCITATION ................................................................... 55

OVERVIEWS CARDIOPULMONARY RESUSCITATION (CPR): ............................................................................................. 55

CHAPTER 3 “ANESTHETIC MANAGEMENT OF HYPERTENSIVE PATIENTS” ....................................................... 87

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CHAPTER 4 ANESTHESIA FOR PATIENT WITH MS AND MR ........................................................................... 117

INTRODUCTION .............................................................................................................................................. 117

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AORTIC STENOSIS ........................................................................................................................................... 159

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CHAPTER 7 MANAGEMENT OF PERIOPERATIVE ARRYTHMIAS ..................................................................... 182

MANAGEMENT OF PERIOPERATIVE ARRYTHMIAS ......................................................................................... 182

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RISK FACTORS FOR DEVLEOPMENT OF IHD: ................................................................................................... 204

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CHAPTER 9 - ANESTHESIA FOR OPEN HEART SURGERY ................................................................................ 241

CHAPTER 10 ANESTHESIA PROTOCOL FOR ADULT CARDIAC SURGERY ........................................................ 251

DUTY OF ANESTHESIOLOGIST ................................................................................................................................. 251

CHAPTER 11 PROTOCOL FOR OFF-PUMP CABG ............................................................................................ 266

CHAPTER 12 - CARDIAC INTENSIVE CARE ..................................................................................................... 267

REGIONAL ANESTHESIA:........................................................................................................................................ 267

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CHAPTER 13 - CLINICAL PRACTICE OF CARDIAC ANESTHESIA ....................................................................... 270

ACUTE TREATMENTS FOR SUSPECTED INTRAOPERATIVE MYOCARDIAL ISCHEMIA ............................................................... 271

CHAPTER 14 - PAEDIATRIC INTENSE CARE UNIT ........................................................................................... 273

PEDIATRIC ICU INFUSIONS ............................................................................................................................. 275

CHAPTER 16 - PATIENT DUCTUS ARTERIOSUS (PDA): ................................................................................... 292

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CHAPTER 17 - ANESTHESIA FOR VASCULAR SURGERY .................................................................................. 318

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CHAPTER 18 - DELIBERATE HYPOTENSION ................................................................................................... 338

SYNONYMS: ....................................................................................................................................................... 338

CHAPTER 19 - SHOCK ................................................................................................................................... 349

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CHAPTER 20 - CARDIOMYOPATHIES ............................................................................................................. 375

CHAPTER 21 - CARDIO PULMONARY BY PASS (CPB) ..................................................................................... 385

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CHAPTER 22 - CARDIOVASCULAR MONITORING .......................................................................................... 423