CARDIOLOGY

Dr. A. Woo Stephen Juvet, Daniel Kreichman and Manish Sood, chapter editors Katherine Zukotynski, associate editor
BASIC CLINICAL CARDIOLOGY EXAM . . . . . . 2 Cardiac History Functional Classification of Cardiovascular Disability Cardiac Examination CARDIAC DIAGNOSTIC TESTS . . . . . . . . . . . . . ECG Interpretation - The Basics Hypertrophy and Chamber Enlargement Ischemia/Infarction Miscellaneous ECG Changes Ambulatory ECG (Holter Monitor) Echocardiography (2-D ECHO) Coronary Angiography Cardiac Stress Tests and Nuclear Cardiology Tests of Left Ventricular (LV) Function ARRHYTHMIAS . . . . . . . . . . . . . . . . . . . . . . . . . . . Mechanisms of Arrhythmias Altered Impulse Formation Altered Impulse Conduction Other Etiologic Factors Clinical Approach to Arrhythmias Bradyarrhythmias Conduction Delays Tachyarrhythmias Supraventricular Tachyarrhythmias (SVTs) Ventricular Tachyarrhythmias (VTs) Pre-excitation Syndromes Pacemaker Indications Pacing Techniques 6 CARDIOMYOPATHIES . . . . . . . . . . . . . . . . . . . . . Dilated Cardiomyopathy (DCM) Hypertrophic Cardiomyopathy (HCM) Restrictive Cardiomyopathy (RCM) Myocarditis 32

12

VALVULAR HEART DISEASE . . . . . . . . . . . . . . . 36 Infective Endocarditis (IE) Rheumatic Fever Aortic Stenosis (AS) Aortic Regurgitation (AR) Mitral Stenosis (MS) Mitral Regurgitation (MR) Mitral Valve Prolapse Tricuspid Valve Disease Pulmonary Valve Disease Prosthetic Valves PERICARDIAL DISEASE Acute Pericarditis Pericardial Effusion Cardiac Tamponade Constrictive Pericarditis
. . . . . . . . . . . . . . . . . . . 45

SYNCOPE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

47

EVIDENCE-BASED CARDIOLOGY . . . . . . . . . . . 48 Congestive Heart Failure (CHF) Ischemic Heart Disease (IHD) Atrial Fibrillation (A fib)

COMMONLY USED CARDIAC . . . . . . . . . . . . . . . 49 ISCHEMIC HEART DISEASE . . . . . . . . . . . . . . . . 19 MEDICATIONS -blockers Background Calcium Channel Blockers (CCB) Angina Pectoris Angiotensin Converting Enzyme (ACE) Inhibitors Acute Coronary Syndromes Angiotensin II Blockers Unstable Angina/Non ST Elevation Diuretics Myocardial Infarction (MI) Nitrates Acute ST Elevation MI Anti-Arrhythmic Sudden Death Anti-Platelet HEART FAILURE . . . . . . . . . . . . . . . . . . . . . . . . . . Compensatory Responses Systolic vs. Diastolic Dysfunction Sleep-Disordered Breathing High-Output Heart Failure Acute Cardiogenic Pulmonary Edema Cardiac Transplantation
............................. 27 REFERENCES

52

MCCQE 2006 Review Notes

Cardiology C1

BASIC CLINICAL CARDIAC EXAM

CARDIAC HISTORY
coronary artery disease: chest pain (CP) (location, radiation, duration, intensity, activities associated with onset; alleviating factors (associated with rest, NTG) heart failure: fatigue, presyncope left-sided symptoms: decreased exercise tolerance, shortness of breath on extertion (SOBOE)/chest pain on exertion (CPOE) right-sided symptoms: paroxysmal nocturnal dyspnea (PND)/orthopnea, SOB at rest, ascites, Arrhythmia: presyncopal/syncopal episodes, palpitations Baseline function: exercise tolerance (# flights of stairs/blocks), need for nitroglycerin (NTG), symptoms during low impact activities/daily activities (combing hair, showering) or at rest

FUNCTIONAL CLASSIFICATION OF CARDIOVASCULAR DISABILITY

Table 1. Canadian Cardiovascular Society (CCS) Functional Classification
Class I II III IV Function ordinary physical activity does not cause angina; angina only with strenuous or prolonged activity slight limitation of physical activity; angina brought on at > 2 blocks on level (and/or by emotional stress) marked limitation of physical activity; angina brought on at 2 blocks on level inability to carry out any physical activity without discomfort; angina may be present at rest

Table 2. New York Heart Association (NYHA) Functional Classification

Class I II III IV Function ordinary physical activity does not evoke symptoms (fatigue, palpitation, dyspnea, or angina) slight limitation of physical activity; comfortable at rest; ordinary physical activity results in symptoms marked limitation of physical activity; less than ordinary physical activity results in symptoms inability to carry out any physical activity without discomfort; symptoms may be present at rest

CARDIAC EXAMINATION
General Examination Skin peripheral vs. central cyanosis, clubbing, splinter hemorrhages, Oslers nodes, Janeway lesions brownish-coloured skin hemochromatosis Eyes conjunctival hemorrhages, Roth spots, emboli, copperwire lesions, soft/hard exudates Blood Pressure (BP) should be taken in both arms with the patient supine and upright be wary of calcification of the radial artery in the elderly as it may factitiously elevate BP (Oslers sign) orthostatic hypotension - postural drop > 20 mm Hg systolic or > 10 mm Hg diastolic increased HR > 30 bpm (most sensitive - implies inadequate circulating volume) patient unable to stand - specific sign for significant volume depletion wide PP: increased cardiac output (CO) (anxiety, exercise, fever, thyrotoxicosis, AR, HTN), decreased total peripheral resistance (TPR) (anaphylaxis, liver cirrhosis, nephrotic syndrome, AVM) narrow PP: decreased CO (CHF, shock, hypovolemia, acute MI, hypothyroidism, cardiomyopathy), increased TPR (shock, hypovolemia), valvular disease (AS, MS, MR), aortic disease (e.g. coarctation of aorta) pulsus paradoxus (inspiratory drop in SBP > 10 mmHg ): cardiac tamponade, constrictive pericarditis, airway obstruction, superior vena cava (SVC) obstruction, COPD (asthma, emphysema) The Arterial Pulse remark on rate, rhythm, volume/amplitude, contour amplitude and contour best appreciated in carotid arteries pulsus alternans - beat-to-beat alteration in PP amplitude with cyclic dip in systolic BP; due to alternating LV contractile force (severe LV dysfunction) pulsus parvus et tardus slow uprising of the carotid upstroke due to severe aortic stenosis (AS) pulsus bisferiens a double waveform due to AS + AR combined spike and dome pulse double carotid impulse due to hypertrophic obstructive cardiomyopathy (HOCM) C2 Cardiology MCCQE 2006 Review Notes
pulse pressure(PP) (PP = systolic BP (SBP) - diastolic PB (DBP))

BASIC CLINICAL CARDIAC EXAMCONT. ...

Precordial Inspection observe for apex beat, heaves, lifts Precordial Palpation apex - most lateral impulse PMI - point of maximal intensity location: normal at 5th intraclavicular space (ICS) at midclavicular line (10 cm from midline), lateral/inferior displaced in dilated cardiomyopathy (DCS) size : normal is 2-3 cm in diameter, diffuse > 3 cm duration: normal is <1/2 systole (duration > 2/3 systole is considered sustained) amplitude (exaggerated, brief - AR, MR, L to R shunt) morphology (may have double/triple impulse in HOCM) abnormal impulses palpable heart sounds (e.g. S1 in MS, P2 = pulmonary artery (PA) pulsation, S3, S4) left parasternal lift (right ventricular enlargement (RVE), left atrial enlargement (LAE) , severe left ventricular hypertrophy (LVH)) epigastric pulsation (RVH especially in COPD) thrills (tactile equivalents of murmurs) over each valvular area Clinical Pearl Left parasternal lift - DDx - RVH (with pulmonary hypertension (HTN), LAE (secondary to severe MR), severe LVH, rarely thoracic aortic aneurysm. Auscultation - Heart Sounds S1 composed of audible mitral (M1) and tricuspid (T1) components may be split in the normal young patient if S1 is loud short PR interval high left atrial (LA) pressure (e.g. early MS) high output states or tachycardia (diastole shortened) if S1 is soft first degree AV block calcified mitral valve (MV) (e.g. late MS) high LV diastolic pressures (e.g. CHF, severe AR) occasionally in MR if S1 varies in volume AV dissociation (complete AV block, ventricular tachycardia (VT)) AFib S2 normally has 2 components on inspiration: A 2 and P 2 normal splitting of S2 (A2 < P2) should vary with respiration Exp. S2 A2 P2 S2 P2 A2 Insp. A2 P2 normal increased venous return to right side of heart with inspiration results in delayed closure of pulmonary valve (PV) (widens split) A2 P2 wide fixed splitting atrial septal defect (ASD) A2 P2 widened splitting (delayed RV or early LV emptying) right bundle branch block (RBBB), pulmonary HTN, MR, ventricular septal defect (VSD) S2 paradoxical splitting (delayed LV or early RV emptying) left bundle branch block (LBBB), tight AS, systemic HTN, LV fib, paced rhythm, tricuspid regurgitation (TR), Wolfe Parkinson White (WPW)

soft S2 aortic (A 2 ) or pulomonic (P2 ) stenosis loud S 2 systemic (A 2 ) or pulmonary HTN (P2 ) soft heart sounds low cardiac output obesity emphysema pericardial effusion ("muffled" = tamponade) S3 (see Figure 1): volume overloaded ventricle occurs during period of rapid ventricular filling low frequency - best heard with bell at apex causes may be normal in children and young adults (age < 30) LV failure (systolic dysfunction, acute MI) rapid ventricular filling (MR or high output states), RV S3 (TR, MS, RV failure) DDx - split S 2 , opening snap, pericardial knock, tumour plop S4 (Figure 1): pressure overloaded ventricle (decreased capacitance, increased contribution of atrial kick to ejection fraction (EF)) occurs during atrial contraction best heard with bell at apex always pathological (associated with diastolic dysfunction), ischemia (ventricular relaxation needs ATP), hypertrophy (HTN, AS, HCM), RCM, RV S 4 (pulmonary HTN, PS) DDx - split S 1 , ejection clicks, prolapse clicks MCCQE 2006 Review Notes Cardiology C3

BASIC CLINICAL CARDIAC EXAMCONT. ...

Extra Sounds opening snap - early-diastolic (see Figure 1) - MS (A 2 -opening snap (OS) interval shortens as MS worsens) ejection clicks (AS, PS) non-ejection mid-systolic clicks (mitral and tricuspid valve prolapse (MVP/TVP)) pericardial (friction) rub: pericarditis, triphasic - ventricular systole, ventricular diastole and atrial systole ("scratchy" sound, like velcro) tumour plop Auscultation - Murmurs Classification: timing (systolic/diastolic), location, radiation, intensity (grade murmurs I-VI), shape, pitch (quality), variation with respiration or maneuvers presence or absence of accompanying thrills, association with extra heart sounds Clinical Pearl Inspiration augments all right-sided murmurs and sounds, except pulmonary ejection click. Expiration augments AR (heard best on full exhalation, sitting leaning forward). postural maneuvers left lateral decubitus (LLD) for MS, S3, S4 squatting to standing position (MVP, hypertrophic obstructive cardiomyopathy (HOCM)) passive leg elevation (MVP, HOCM) Table 3. Maneuvers for Auscultation of Heart Murmurs
Maneuvers Quiet inspiration Transient arterial Sustained abdominal occlusion (using 2 pressure sphygmomanometers) Fist clenching Standing to squatting Passive leg elevation Valsalva

Physiological Effect

8venous return
8right-sided murmurs 8TR 8PS

8systemic arterial
resistance 8left-sided murmurs 8MR 8VSD

8venous return 8systemic arterial

resistance 9HCM 9MVP

9venous return 8systemic arterial

resistance

Effect on Intensity of the Mummer

9 AS

systolic ejection murmurs (see Figure 1) diamond-shaped, crescendo-decrescendo outflow obstruction: AS, HOCM, PS high output or "flow" murmurs anemia thyrotoxicosis pregnancy arteriovenous fistula children fever pansystolic murmurs (see Figure 1) require a sustained pressure difference throughout systole MR TR VSD high-pitched diastolic decrescendo murmurs (see Figure 1) AR PR low-pitched diastolic murmurs (mid-diastolic rumble) (see Figure 1) MS TS severe AR may produce Austin Flint murmur high flow murmurs (result from 'relative' stenosis) MR, persistent ductus arteriosus (PDA), VSD (increased left atrial (LA) filling) ASD (increased right atrial (RA) filling) continuous murmurs (see Figure 1) PDA mammary souffle - goes away with pressure on stethoscope coronary arteriovenous fistula venous hum due to high blood flow in the jugular veins heard in high output states C4 Cardiology MCCQE 2006 Review Notes

BASIC CLINICAL CARDIAC EXAMCONT. ...

S1 S2 S3 S1 S1 S2

S3
S1 S2 S4 S1

Pansystolic Murmur
S2 S1

S4
S1 S2 OS S1

High Pitched Diastolic Murmur

S2 OS S1

Opening Snap
S1 S2

Low Pitched Diastolic Murmur

S1 S2 S1

Systolic Ejection Murmur Figure 1. Heart Sounds and Murmurs

Continuous Murmur

Jugular Venous Pulsations - JVP (see Figure 2) height of column of blood filling internal jugular vein, related to RA and RV filling and dynamics, measured as X cm above sternal angle (ASA) (which lies 5cm above the RA; normal JVP is 2-4 cm ASA) distinguishing features of the JVP vs carotid impulse location - between heads of the sternocleidomastoid muscle, coursing towards angle of jaw multiple waveforms in normal patient non-palpable obliterated with pressure at base of neck soft, undulating quality changes with degree of incline and inspiration (normally drops on inspiration) transient increase with abdominal pressure/Valsalva maneuver descents are clinically more prominent than waves at the bedside normal waveforms a wave = atrial contraction - precedes carotid pulse x descent = atrial relaxation c wave = bulging up of TV during RV systole (may reflect carotid pulse in neck) x prime descent = descent of base of heart during ventricular systole v wave = passive atrial filling against closed AV valve y descent = early rapid atrial emptying following opening of AV valve - occurs after carotid pulse felt

MCCQE 2006 Review Notes

Cardiology C5

BASIC CLINICAL CARDIAC EXAMCONT. ...

pathological waveforms loss of "a" wave A fib, atrial standstill absent venous pulse RHF/CHF, SVC obstruction, cardiac tamponade giant "a" waves contraction of atrium against increased resistance (RVH, PS, TS, pulmonary HTN) with every beat cannon a waves contraction of atrium against closed TV as in AV dissociation (AV dissociation, PVC); not with every beat systolic venous pulsation (c-v waves) regurgitation of blood into venous system with ventricular contraction as in TR (rapid y) sharp "y" descent increased venous pressure as in constrictive pericarditis (y>x phenomenon) Hepatojugular reflux (HJR) positive response correlates better increased pulmonary capillary wedge pressure (PCWP) (L-sided failure) than R-sided failure sustained > 4 cm rise in JVP with firm abdominal compression postivie response seen in TR, RV failure, pulmonary HTN, CHF, increased PCWP Kussmauls sign a paradoxical rise in the JVP on inspiration differential diagnosis: constrictive pericarditis, right ventricular MI high venous pressure a x c x1 y v

Figure 2. Jugular Venous Pulsations

CARDIAC DIAGNOSTIC TESTS

ECG INTERPRETATION-THE BASICS
Key Features rate rhythm axis waves and segments hypertrophy and chamber enlargement ischemia/infarction miscellaneous Rate each small box is 0.04 sec; each large box is 0.2 sec. if rhythm is regular, rate is obtained by dividing 300 by number of large squares between two R waves with irregular rhythms note the average ventricular rate over 10 seconds normal adult rate = 60-100 bpm bradycardia < 60 bpm tachycardia > 100 bpm Rhythm ask four questions Are there P waves present? Are the QRS complexes wide or narrow? What is the relationship between the P waves and QRS complexes? Is the rhythm regular or irregular? definition of normal sinus rhythm has a P wave preceding each QRS complex, and a QRS after each P P wave axis is normal (negative in aVR and positive in II) PR interval is normal and constant P wave morphology is constant C6 Cardiology MCCQE 2006 Review Notes

CARDIAC DIAGNOSTIC TESTS . CONT. ..

Axis (see Figure 3) deviation - limb leads: normal = positive QRS in I and aVF axis is perpendicular to lead in which QRS is isoelectric QRS axis points toward ventricular hypertrophy and away from infarction see Ventricular Hypertrophy and Hemiblocks sections rotation - precordial leads: normally isoelectric QRS in V 3 , V 4 clockwise = isoelectric QRS in V5 , V 6 counterclockwise = isoelectric QRS in V 1 , V2 (i.e. tall R wave in V , see below) 1
90 aVR 180 Left Axis Deviation (LAD) 30, aVL I NORMAL AXI S III Right Axis Deviation (RAD) 90 aVF II

Figure 3. Axes of Electrocardiographic Limb Leads Waves and Segments P wave - atrial depolarization, smooth contour, entirely positive or negative PR interval - rate dependent; reflects slowing of impulse through the AV node which is governed by parasympathetic and sympathetic discharge QRS complex - ventricular depolarization; any Q wave in V1-3 is abnormal; R wave increases in amplitude and duration through V 1 -V5 ; S wave is largest in V2 and gets progressively smaller ST segment - above or below the baseline; point the QRS meets the ST segment is called the J point QT interval - should be < 1/2 of the RR interval interval is rate related (increased HR > decreased QT) T wave - ventricular repolarization normal = negative in aVR, flat or minimally negative in limb leads; otherwise positive
R Q P P
DURATION

T U

(seconds)

0.12 0.12-.20

< 0.12 1/2 RR

Figure 4. ECG Waveforms and Normal Values

Illustration by Marc Dryer

HYPERTROPHY AND CHAMBER ENLARGEMENT

Right Ventricular Hypertrophy (RVH) QRS < 0.12 seconds, R/S ratio > 1 in V , R/S ratio < 1 in V and V6 , R > 7 mm in V 1 5 1 right axis deviation (RAD) (> 90) Asymmetric ST segment depression and T wave inversion in V 1 and V2 (RV strain pattern) Left Ventricular Hypertrophy (LVH) S in V1 or V2 + R in V or V6 > 35 mm 5 S in V1 or V2 or R in V or V > 25 mm 5 6 R in aVL > 11 mm R in I + S in III > 25 mm left axis deviation (LAD) (> 30) with slightly widened QRS asymmetric ST segment depression and T wave inversion (LV strain) leads I, aVL, V4-6 left atrial enlargement (LAE) MCCQE 2006 Review Notes Cardiology C7

CARDIAC DIAGNOSTIC TESTS. . CONT. .

Right Atrial Enlargement(RAE) (P Pulmonale) P wave > 2.5 mm (in height) in leads II, III or aVF Left Atrial Enlargement (LAE) (P Mitrale) P wave duration > 0.11s best seen in leads I, II, aVL, V4-V6 large, biphasic P wave in V1 with deep terminal component that is at least one square wide (0.04 sec) and one square deep (1 mm) notched P with interpeak interval > 0.04 seconds in I, II or aVL Clinical Pearl 1 DDx of tall R wave in V RVH, Posterior MI, WPW, HCM (septal hypertrophy), Duchenne muscular dystrophy, and dextrocardia.

ISCHEMIA / INFARCTION(see Figure 5)

During an ischemic event/acute MI, the ECG changes with time may include: ischemia: T waves invert at site of injury injury: ST segment elevation +/ tall peaked T waves, hyperacute" T waves at area of injury, with reciprocal ST segment depression acute MI = ST elevation in 2 or more contiguous leads in an arterial territory necrosis: Q waves develop: signifies completed transmural infarct significant if > 1 mm wide (> 0.04 seconds) or if > 1/3 the amplitude of QRS NOTE: Q waves are normally present in lead V1 and non-significant Qs often present in lead III DDx for ST Segment Changes elevation early repolarization (normal variant) acute MI post MI Prinzmetal's angina (coronary vasospasm) acute pericarditis ventricular aneurysm LBBB depression angina (ischemia) subendocardial infarction (non Q-wave MI) acute posterior wall MI (V 1 and V2 ) LVH or RVH with strain digitalis effect (scooping or hockey stick) hypokalemia, hypomagnesemia
LBBB, RBBB, WPW

T Wave

Acute days (avg. 3-5) ST segment elevation

Illustration by Victoria Rowsell

Recent weeks-months (avg. 2-6 months) T wave inversion

Just significant Qs

Old months-years (avg. > 6 months)

Figure 5. ECG changes with Ischemia/Infarction

C8 Cardiology

MCCQE 2006 Review Notes

CARDIAC DIAGNOSTIC TESTS . CONT. ..

Table 4. Areas of Infarction
Infarct Area anteroseptal anterior anterolateral extensive anterior inferior lateral* posterior right ventricle Usual Involved Vessel left anterior descending (LAD) Q waves
2 V1 , V 4 V3 , V 3 I, aVL, V-V6 1 I, aVL, V - V6

right coronary artery (RCA) circumflex RCA (accompanies inf. MI) circumflex (isolated post. MI) RCA (most often)

II, III, aVF

5 I, aVL, V, V6 1 V6 , mirror image V and V2 5 V4 R (V R and V6 R) (right sided chest leads)

*often no ECG changes because small infarcts and lateral wall is late in the depolarization (QRS complex)

Variations in Cardiac Vascular Anatomy Table 4 describes anatomy of "right-dominant" circulation (80%) compare with left-dominant circulation (15%) posteroinferior LV supplied by LCA balanced circulation (5%) dual supply of posteroinferior LV by RCA and LCA
left main coronary artery (LCA) right coronary artery (RCA) acute marginal circumflex left anterior descending (LAD) septal perforator obtuse marginal diagonal

posterior interventricular

Figure 6. Anatomy of the Coronary Arteries (right anterior oblique projection)

MISCELLANEOUS ECG CHANGES

Electrolyte Disturbances hyperkalemia peaked T waves, flat P, wide QRS, long PR interval, elevated ST segment

Illustrations by Pascale Tranchemontagne

hypokalemia flattened T waves, U waves, ST depression, prolonged Q-T interval

Illustrations by Pascale Tranchemontagne

hypocalcemia prolonged Q-T interval hypercalcemia shortened Q-T interval MCCQE 2006 Review Notes Cardiology C9

CARDIAC DIAGNOSTIC TESTS. . CONT. .

Hypothermia prolonged intervals, sinus bradycardia, slow A fib beware of muscle tremor artifact Osborne or J wave deflection Early Pericarditis early - diffuse ST segment elevation +/ "PR segment depression" early upright T waves later - isoelectric ST segment and T waves flat or inverted tachycardia Low Voltages definition - total QRS height in precordial leads < 10 mm, limb leads < 5 mm DDx inappropriate voltage standardization pericardial effusion (e.g. tamponade) barrel chest (COPD), obesity hypothyroidism dilated cardiomyopathy, myocardial disease, myocarditis amyloidosis/infiltrative cardiomyopathy Drugs Digoxin therapeutic levels may be associated with Dig effect T wave depression or inversion ST downsloping or scooping QT shortening +/ U waves Illustration by Seline McNamee slowing of ventricular rate in A Fib toxic levels associated with tachyarrhythmias (especially paroxysmal atrial tachycardia (PAT)) with conduction blocks PVCs, bigeminy classic regularization of ventricular rate in A fib due to complete AV dissociation Quinidine, phenothiazines, tricyclic antidepressants (TCAs) prolonged QT interval, U waves Other Cardiac Conditions hypertrophic cadiomyopathy (HCM) ventricular hypertrophy, LAD, septal Q waves Myocarditis conduction blocks, low voltage Pulmonary Disorders chronic obstructive pulmonary disease (COPD) low voltage, RAD, poor R wave progression chronic cor pulmonale can produce RAE and RVH with strain multifocal atrial tachycardia (MAT) Massive pulmonary embolus (PE) sinus tachycardia and A fib are the most common arrhythmias T I RVH with strain, RBBB, S, QIII , TIII (inverted T) (S1 Q3 3 )

AMBULATORY ECG (HOLTER MONITOR)

24-48 hr ECG recording with patient diary of symptoms to determine correlation between symptoms and abnormalities indications 1. detect intermittent arrhythmias 2. relate symptoms to dysrhythmias 3. detect myocardial ischemia Two-dimensional (2-D) ECHO: anatomy - ultrasound (U/S) reflecting from tissue interfaces determines LV systolic ejection fraction (LVEF) chamber sizes wall thickness valve morphology pericardial effusion wall motion abnormalities complications of acute MI Doppler: blood flow U/S reflecting from intracardiac RBCs determines blood flow velocities to estimate valve areas and determine intracardiac gradients Colour flow imaging determines: valvular regurgitation valvular stenosis shunts MCCQE 2006 Review Notes

ECHOCARDIOGRAPHY

C10 Cardiology

CARDIAC DIAGNOSTIC TESTS . CONT. ..

Transesophageal Echo (TEE) high quality images but invasive more sensitive for prosthetic heart valves to identify cardiac sources of systemic emboli, intracardiac thrombi, tumours, debris within the aorta, valvular vegetations, and infective endocarditis aortic dissection (see CORONARY ANGIOGRAPHY Cardiac and Vascular Surgery Chapter) technique: injection of radiopaque dye into coronary arteries via percutaneous femoral catheter information obtained: coronary anatomy, LVEF with ventriculography, hemodynamic indices Indications: Diagnosis: gold standard for detecting and quantifying CAD Prognosis: post-MI Guiding Therapy: e.g. CABG vs. PTCA vs. medical therapy complications (%): death (0.1), stroke (0.07), MI (0.07), other major (1.0-2.0), minor (10)

CARDIAC STRESS TESTS AND NUCLEAR CARDIOLOGY

indications assessment of chest pain (detection of CAD) risk stratification post-MI preoperative screening and risk assessment assessment of response to therapy assessment of myocardial viability stressors physical stressors: treadmill or bicycle pharmacological stressors increased coronary flow: dipyridamole (Persantine), adenosine increased myocardial O 2 demand: dobutamine (1-selective agonist) ischemia detectors ECG: observe for ischemic changes during stress ECHO: visualize myocardial effects of ischemia SPECT myocardial nuclear perfusion studies tracers infused during stress + thallium-201 (201Tl, a K analogue) technetium-99 (99Tc)-labelled tracer (sestamibi = Cardiolyte) SPECT images of the heart obtained during stress and at rest 4h later fixed defect = impaired perfusion at rest and during stress (infarcted) reversible defect = impaired perfusion only during stress (ischemic) Other imaging techniques: PET, MRI, ultrafast CT, TEE (uncommonly used) ventricular function assessment (LVEF, RVEF, ventricular size and volume, wall motion anomalies, etc.) Radionuclide angiography (MUGA): 99Tc- radiolabelled RBCs ECHO Ventriculography

Table 5. Attributes and Limitations of Various Stress Tests

Factor Sensitivity Specificity Localizing ischemia Additional info compared with GXT Treadmill Test (GXT) 65-70% 65-70% poor N/A Stress Echo 90% 90% good rest & exercise LVEF, plus all other echo parameters COPD, obesity Nuclear Perfusion 80-85% 90% good rest LVEF, lung uptake, infarct size, LV size good rest & exercise LVEF, regional wall motion, Radionuclide Angiography 80-85%

LV volumes, RV function

Clinical or technical limitations

abnormal resting ECG, pretest probability very important $

obesity, attenuation artifacts

arrhythmias

Relative cost

$$

$$$$

$$$

Modified from : Anon. Mayo Clinic Proceedings . 1996; 71:43-52.

MCCQE 2006 Review Notes

Cardiology C11

CARDIAC DIAGNOSTIC TESTS. . CONT. .

Indication

Diagnostic and prognostic purposes?

Localization of ischemia?

Direct measurement of Vo 2 max., timing of cardiac transplanation, or selected patients with unexplained dyspnea?

Able to exercise?

Able to exercise?

Able to exercise?

Yes

No

Yes

Yes

Pharmacologic stress imaging

Cardiopulmonary exercise test

Normal findings on resting ECG Patient not taking digoxin?

No

Exercise imaging study Local expertise with the technique Primary question to be answered Patient characteristics Cost

Yes

Standard treadmill exercise test

Figure 7. Algorithm for test selection for an individual patient.

From: Anon. Mayo Clinic Proceedings 1996; 71;43-52

ARRHYTHMIAS
MECHANISMS OF ARRHYTHMIAS 1. ALTERED IMPULSE FORMATION
divided into two potentially arrhythmogenic processes: AUTOMATICITY = the ability of a cell to depolarize itself to threshold and, therefore, generate an action potential cells with this ability are known as pacemaker cells SA node, purkinje cells throughout atria bundle of His, bundle branches purkinje cells in fascicles and peripheral ventricular conduction system automaticity is influenced by neurohormonal factors: sympathetic and parasympathetic drugs: e.g. Digoxin has vagal effect on SA and AV nodes but sympathetic effect on other pacemaker sites local ischemia/infarction or other pathology blockage of proximal pacemaker (SA node) impulses which allows more distal focus to control the ventricular rhythm TRIGGERED ACTIVITY = abnormal depolarization occurring during or after repolarization oscillations of the membrane potential after normal depolarization lead to recurrent depolarization prolonged QT interval predisposes (e.g. electrolyte disturbances, antiarrhythmic drugs) postulated mechanism of Torsades de Pointes

C12 Cardiology

MCCQE 2006 Review Notes

ARRHYTHMIAS. . . CONT.
2. ALTERED IMPULSE CONDUCTION
re-entry phenomenon which requires parallel electrical circuit in which two limbs have different refractory periods, e.g. AVNRT conduction blocks - partial or total ventricular pre-excitation congenital abnormality in which ventricular myocardium is electrically activated earlier than by the normal AV nodal impulse e.g. bypass tract in WPW syndrome increased LA size > increased risk of A fib bradycardia predisposes via temporal dispersion in refractory periods; e.g. tachy-brady syndrome hypoxia/acidosis lowers the threshold for V fib electrolyte disturbances, e.g.: hypokalemia, imbalances of Ca +2 , Mg+2 infection, e.g.: myocarditis or infective endocarditis (causing abscess and complete heart block) cardiomyopathies, degenerative disease, infiltration (e.g. sarcoid) ischemia, increased sympathetic tone

OTHER ETIOLOGIC FACTORS

CLINICAL APPROACH TO ARRHYTHMIAS

ARRHYTHMIA BRADYARRYTHMIA (< 60 BPM)

CONDUCTION DELAY

TACHYARRHYTHMIA (> 100 BPM)

sinus bradycardia sinus arrest escape rhythms junctional ventricular

AV nodal conduction blocks 1, 2, 3 fascicular block bundle branch block

IRREGULAR A Fib MAT Atrial flutter (variable block) frequent APBs, VPBs REGULAR WIDE COMPLEX SVT with aberrancy (or BBB) ventricular tachycardia

NARROW COMPLEX

SVT Atrial flutter AVNRT WPW (retrograde conduction through bypass tract)

Figure 8. Clinical Approach to Arrhythmias

BRADYARRHYTHMIAS
Presentation often asymptomatic symptoms can include dizziness, fatigue, dyspnea and presyncope or syncope effects of bradycardia depend on rate, and patient's co-morbid conditions (e.g. heart failure) DDx Sinus Bradycardia sinus rhythm at regular heart rate less than 60 bpm caused by excessive vagal tone: spontaneous (vasovagal syncope), acute MI (inferior), drugs, vomiting, hypothyroidism, increased intracranial pressure (ICP) treatment: if symptomatic, atropine +/ electrical pacing (chronic) Sinus Arrhythmia irregular rhythm with normal P wave and constant, normal PR interval normal variant - inspiration accelerates the HR; expiration slows it down pathological - uncommon, variation not related to respiration Sinus Arrest or Exit Block sinus node stops firing (arrest) or depolarization fails to exit the sinus node (exit block) depending on duration of inactivity, escape beats or rhythm may occur - next available pacemaker will take over, in the following order atrial escape (rate 60-80): originates outside the sinus node within the atria (normal P morphology is lost) junctional escape (rate 40-60): originates near the AV node; a normal P wave is not seen may occasionally see a retrograde P wave representing atrial depolarization moving backward from the AV node into the atria ventricular escape (rate 20-40): originates in ventricular conduction system no P wave; wide, abnormal QRS (ECG tracing) treatment: stop meds which suppress the sinus node ( blockers, CCB, Digoxin); may need pacing MCCQE 2006 Review Notes Cardiology C13

ARRHYTHMIAS. . . CONT.
Sick Sinus Syndrome (SSS) includes above sinus node disturbances, when pathologic causes: structural SA node disease, autonomic abnormalities, or both bradycardia may be punctuated by episodes of SVT, especially A fib or atrial flutter (tachy-brady syndrome) treatment: pacing for bradycardia; meds for tachycardia

CONDUCTION DELAYS
AV Node Conduction Blocks look at the relationship of the P waves to the QRS complexes 1st degree - constant prolonged PR interval (> 0.2 seconds) all beats are conducted through to the ventricles no treatment required if asymptomatic 2nd degree (Mobitz) - not all P waves followed by QRS; distinguish Type I from Type II Mobitz Type I (Wenckebach) - due to AV node blockage progressive prolongation of the PR interval until a QRS is dropped treatment: none unless symptomatic; atropine

Mobitz Type II - due to His-Purkinje blockage all-or-none conduction; QRS complexes are dropped at regular intervals (e.g. 2:1, 3:1, etc.) with stable PR interval (normal or prolonged) risk of developing syncope or complete heart block treatment: pacemaker (ventricular or dual chamber) 3rd degree or complete heart block - no P wave produces a QRS response complete AV dissociation (atria and verntricles contracting independently; may see P waves "marching through" QRSs) can have narrow junctional QRS or wide ventricular QRS (junctional vs ventricular escape rhythm) rate usually 30-60 bpm may cause Stokes-Adams attacks: syncope associated with brief cardiac arrest treatment: pacemaker (ventricular or dual chamber)

Bundle Branch and fascicular Blocks RBBB, left anterior fascicle and left posterior fascicle should each be considered individually, and combination (i.e. bifascicular) block S should also be noted Bundle Branch Blocks (BBB) QRS complex > 0.12 seconds
RBBB

LBBB

RSR' in V1 and V2 (rabbit ears), with ST segment depression and T wave inversion presence of wide (or deep) S wave in I, V 6 widely split S 2 on auscultation RBBB

note

broad or notched monophasic R wave with prolonged upstroke and absence of initial Q wave in leads V 6 , I and aVL, with ST segment depression and T wave inversion large S or QS in V 1 paradoxically split S 2 on auscultation with BBB the criteria for ventricular hypertrophy become unreliable with LBBB, infarction is difficult to determine

V1

V6

ARRHYTHMIAS. . . CONT. Hemiblock

block of anterior or posterior fascicle of LBB anterior hemiblock normal QRS duration; no ST segment or T wave changes left axis deviation (> 45), with no other cause present small Q in I and aVL, small R in II, III and aVF posterior hemiblock normal QRS duration; no ST segment or T wave changes right axis deviation (> 110 degrees), with no other cause present small R in I and aVL, small Q in II, III and aVF

LBBB MCCQE 2006 Review Notes

C14 Cardiology

ARRHYTHMIAS. . . CONT.
TACHYARRHYTHMIAS
Presentation symptoms, when present, include palpitations, dizziness, dyspnea, chest discomfort, presyncope or syncope may precipitate CHF, hypotension, or ischemia in patients with underlying disease incessant untreated tachycardias can cause cardiomyopathy (rare) includes supraventricular and ventricular rhythms DDx

1. SUPRAVENTRICULAR TACHYARRHYTHMIAS

narrow (i.e., normal) QRS complex or wide QRS if aberrant ventricular conduction or pre-existing BBB aberrancy = intraventricular conduction delay associated with a change in cycle length (i.e., with tachycardia); not normal pattern for the individual

Sinus Tachycardia sinus rhythm at a rate greater than 100 bpm Etiology: fever, hypotension, thyrotoxicosis, anemia, anxiety, hypovolemia, PE, CHF, MI, shock, drugs (EtOH, caffeine, atropine, catecholamines) treatment: treat underlying disease; consider propranolol if symptomatic Premature Beats Atrial Premature Beat (APB) single ectopic supraventricular beat originating in the atria P wave contour of the APB differs from that of a normal sinus beat Junctional Premature Beat a single ectopic supraventricular beat that originates in the vicinity of the AV node there is no P wave preceding the premature QRS complex, but a retrograde P wave may follow the QRS if AV nodal conduction is intact treatment: none unless symptomatic; blockers or CCB Atrial Flutter regular; atrial rate 250-350 bpm, usually 300 etiology: IHD, thyrotoxicosis, MV disease, cardiac surgery, COPD, PE, pericarditis ventricular conduction is variable e.g. 2:1, 3:1, 4:1 block, etc. ECG: sawtooth inferior leads; narrow QRS (unless aberrancy) carotid massage (check first for bruits), Valsalva or adenosine: increases the block (i.e. slows pulse), brings out flutter waves treatment rate control: blocker, verapamil, Digoxin medical cardioversion: procainamide, sotalol, amiodarone, quinidine electrical cardioversion: DC shock (@ low synchronized energy levels: start at 50 J)

Clinical Pearl Narrow complex tachycardia at a rate of 150 is atrial flutter with 2:1 block until proven otherwise. Multifocal Atrial Tachycardia (MAT) irregular rhythm; atrial rate 100-200 bpm; at least 3 distinct P wave morphologies and 3 different P-P intervals present on ECG probably results from increased automaticity of several different atrial foci hence varying P-P, P-R, and R-R intervals, varying degrees of AV block common in COPD, hypoxemia, hypokalemia, hypomagnesemia, sepsis, theophylline or Digoxin toxicity if rate < 100 bpm, then termed a Wandering Atrial Pacemaker carotid massage has no effect in MAT treatment: treat the underlying cause; if necessary try metoprolol (if no contraindications)

MCCQE 2006 Review Notes

Cardiology C15

ARRHYTHMIAS. . . CONT.
Atrial Fibrillation (A fib) seen in 10% of population over 75 years old the majority of cardiogenic strokes and peripheral thromboembolic events occur in association with A fib Etiology: CAD, valvular disease, pericarditis, cardiomyopathy, PE, HTN, COPD, thyrotoxicosis, tachy-brady syndrome, EtOH (holiday heart) irregularly irregular ventricular rate; narrow QRS unless aberrancy, undulating baseline; no P waves atrial rate 400-600 bpm, ventricular rate variable depending on AV node, around 140-180 bpm wide QRS complexes due to aberrancy may occur following a long short R-R cycle sequence (Ashman phenomenon") lose atrial contribution to ventricular filling (no a waves seen in JVP) carotid massage: may slow ventricular rate A fib resistant to cardioversion - significant LA enlargement, longer duration of A fib major issues to be addressed with A fib: Rate control (ventricular) beta blocker, verapamil, digoxin Anti-coagulation (prevention of thromboembolic phenomenon) warfarin for paroxysmal or chronic A fib balance risk of bleeding 1%/year vs. risk of clot (warfarin reduces thromboembolic event rate by 67% in nonrheumatic A fib) Cardioversion OK without anticoagulation within 48 hours of onset (by history) of A fib if > 48 hours after onset MUST anticoagulate at least 3 weeks prior to cardioversion and 4 weeks after cardioversion alternate option is TEE prior to eraly electrical cardioversion to rule out clot (controversial) medical - sotalol, amiodarone, Class I agent if normal LV function (e.g. IV procainamide, propafenone) electrical - synchronized DC cardioversion (Diltiazem) treat any etiology that can be identified Note drug - refractory symptomatic A fib may be referred for AV node ablation followed by permanent pacemaker insertion

Paroxysmal Supraventricular Tachycardia (PSVT) sudden onset regular rhythm; rate 150-250 bpm usually initiated by a supraventricular or ventricular premature beat common mechanisms are AV nodal reentry and accessory tract reentry
atrioventricular nodal tachycardia (AVNRT) accounts for 60-70% of all SVTs

retrograde P waves may be seen but are usually lost in the QRS complex treatment acute: Valsalva or carotid massage (check first for bruits), adenosine especially if associated with WPW (adenosine is 1st choice if unresponsive to vagal maneuvers); if no response, try metoprolol, digoxin, verapamil; DC shock if signs of cardiogenic shock, angina, or CHF chronic: blocker, verapamil, Digoxin, anti-arrhythmic drugs, EPS catheter ablation

2. VENTRICULAR TACHYARRHYTHMIAS
Premature Ventricular Contraction (PVC) or Ventricular Premature Beats (VPB) QRS width greater than 0.12 seconds, no preceding P wave, bizarre QRS morphology premature in the cardiac cycle, may be followed by a prolonged pause (compensatory) origin: LBBB pattern = RV site; RBBB pattern = LV site rules of malignancies with PVCs frequent, (> 10/hour), consecutive ( 3 = VT) or multiform (varied origin) PVCs falling on the T wave of the previous beat ("R on T phenomenon"): vulnerable time in cycle with risk of VT or V fib ) PVCs in isolation not treated, as risks not altered, no effect on mortality treatment: since no evidence to suggest that treatment decreased mortality, PVCs are not usually treated consider blockers if symptomatic palpitations C16 Cardiology MCCQE 2006 Review Notes

ARRHYTHMIAS. . . CONT.
Accelerated Idioventricular Rhythm benign rhythm - originates in terminal Purkinje system or ventricular myocardium represents a ventricular escape focus that has accelerated sufficiently to drive the heart Etiology: sometimes seen during acute MI (especially during reperfusion) or Digoxin toxicity regular rhythm, rate 50-100 bpm rarely requires treatment treatment: if symptomatic, lidocaine, atropine Ventricular Tachycardia (VT) a run of three or more consecutive PVCs rate > 100 minute is called VT etiology note: only with memomorphic VT CAD with MI is most common underlying cause sustained VT (longer than 30 seconds) is an emergency, prestaging cardiac arrest and requiring immediate treatment rate 120-300 bpm broad QRS, AV dissociation, fusion beats, capture beats, left axis deviation, monophasic or biphasic QRS in V1 with RBBB, concordance V-V6 1

fusion beat occurs when an atrial impulse manages to slip through the AV node at the same time that an impulse of ventricular origin is spreading across the ventricular myocardium the two impulses jointly depolarize the ventricles producing a hybrid QRS complex that is morphologically part supraventricular and part ventricular capture beat occurs when an atrial impulse manages to capture the ventricle and get a normal QRS treatment (for acute sustained VT) hemodynamic compromise DC cardioversion no hemodynamic compromise - DC shock, lidocaine, amiodarone, type Ia agents (procainamide, guinidine) Ventricular Fibrillation (V fib) medical emergency; pre-terminal event unless promptly cardioverted most frequently encountered arrhythmia in adults who experience sudden death mechanism: simultaneous presence of multiple activation wavefronts within the ventricle no true QRS complexes - chaotic wide tachyarrhythmia without consistent identifiable QRS complex no cardiac output during V fib refer to ACLS algorithm for complete therapeutic guidelines

Torsades de Pointes polymorphic VT - means "twisting of the points" looks like VT except that QRS complexes rotate around the baseline changing their axis and amplitude ventricular rate greater than 100, usually 150-300 etiology: seen in patients with prolonged QT intervals congenital long QT syndromes drugs - e.g. Class IA (quinidine), Class III (sotalol), phenothiazines (TCAs), erythromycin electrolyte disturbances - hypokalemia, hypomagnesemia other - nutritional deficiencies treatment: IV magnesium, temporary pacing, isoproterenol and correct underlying cause of prolonged QT, DC cardioversion if hemodynamic compromise present

MCCQE 2006 Review Notes

Cardiology C17

ARRHYTHMIAS. . . CONT.
Table 6. Differentiation of VT vs. SVT with Aberrant Conduction*
VT Clinical Clues carotid massage cannon a waves neck pounding ECG Clues AV dissociation fusion beats initial QRS deflection axis no response may be present may be present may be seen may be seen may differ from normal QRS complex extreme axis deviation SVT may terminate not seen not seen not seen not seen same as normal QRS complex normal or mild deviation

* if patient > 65, presence of previous MI or structural heart disease then chance of VT > 95%

PREEXCITATION SYNDROMES
Wolff-Parkinson-White (WPW) Syndrome bypass pathway called the Bundle of Kent connects the atria and ventricles congenital defect, present in 3:1.000 criteria (delta wave) PR interval is less than 0.12 seconds wide QRS complex due to premature activation repolarization abnormalities delta wave seen in leads with tall R waves slurred initial upstroke of QRS complex the two tachyarrhythmias most often seen in WPW are PSVT and A fib carotid massage, vagal maneuvers, and adenosine can enhance the degree of pre-excitation by slowing AV nodal conduction note: if wide complex A fib, concern is that anterograde conduction is occurring down a bypass tract; therefore do not use agents that slow AV conduction (e.g. Digoxin) as may increased conduction through the bypass tract and precipitate V fib. In WPW and A fib use IV procainamide Lown-Ganong-Levine Syndrome the PR interval is shortened to less than 0.12 seconds the QRS complex is narrow and there is no delta wave

PACEMAKER INDICATIONS

SA node dysfunction symptomatic bradycardia AV nodal - infranodal block Mobitz II complete heart block symptomatic carotid sinus hypersensitivity

PACING TECHNIQUES

temporary: transvenous (jugular, subclavian, femoral) or external pacing permanent: transvenous into RA, apex of RV or both; power source implanted under clavicle can sense and pace atrium, ventricle or both new generation = rate responsive, able to respond to physiologic demand nomenclature e.g. VVIR V - chamber paced : ventricle : ventricle V - chamber sensed I - action : inhibit R - rate responsive

C18 Cardiology

MCCQE 2006 Review Notes

ISCHEMIC HEART DISEASE (IHD)

BACKGROUND
Epidemiology commonest cause of cardiovascular morbidity and mortality male: female ratio = 2:1 with all age groups included (Framingham study) = 8:1 < age 40 = 1:1 > age 70 disparity due to protective effect of estrogen peak incidence of symptomatic IHD is from ages 50 to 60 in men and ages 60 to 70 in women spectrum of IHD/CAD ranges anywhere from asymptomatic to sudden death Atherosclerosis and IHD atherosclerosis and thrombosis are by far the most important pathogenetic mechanisms in IHD Major Risk Factors For Atherosclerotic Heart Disease smoking risk can be halved by cessation of smoking diabetes mellitus (DM) micro and macrovascular complications hypertension (HTN) depends on degree and duration family history (FHx) first degree male relative < 55 or first degree female relative < 60 hyperlipidemia Other Minor Risk Factors obesity > 30% above ideal weight sedentary lifestyle hyperhomocysteinemia Preventative Measures smoking cessation tight glycemic control in diabetics BP control major reason for the recent decrease in IHD lipid-modifying therapy dietary measures e.g. mild alcohol consumption weight loss exercise improves weight, HTN, cholesterol and glycemic control family screening (high risk groups)

ANGINA PECTORIS
Definition symptom complex resulting from an imbalance between oxygen supply and demand in the myocardium Pathophysiology of Myocardial Ischemia O2 Demand Heart Rate Contractility Wall Tension Figure 9. Physiological Principles Etiology decreased myocardial oxygen supply atherosclerotic heart disease (vast majority) coronary vasospasm (variant angina= Prinzmetals Angina) severe aortic stenosis or insufficiency thromboembolism severe anemia arteritis (e.g. Takayasus syndrome, syphilis, etc.) aortic dissection congenital anomalies MCCQE 2006 Review Notes Cardiology C19 O2 Supply Length of Diastole Coronary Diameter Hemoglobin SaO2

ISCHEMIC HEART DISEASE (IHD) . . CONT. .

increased myocardial oxygen demand myocardial hypertrophy severe tachycardia severe hyperthyroidism severe anemia DDx musculoskeletal (MSK) disease rib fracture intercostal muscle tenderness costochondritis (Tietzes syndrome) nerve root disease (cervical radiculitis) gastrointestinal (GI) disease peptic ulcer disease (PUD) reflux esophagitis esophageal spasm and motility disorder (may be improved by NTG) pulmonary disease pulmonary embolism (PE) pneumothorax pneumonia cardiovascular (CV) disease aortic dissection (asymmetrical BP and pulses, new AR murmur) pericarditis Other intercostal neuritis (shingles) anxiety note careful history and physical required consider risk factors for each entity beware cardiac and non-cardiac disease may coexist Diagnosis of Angina Pectoris history classically precordial chest pain, tightness or discomfort radiating to left shoulder/arm/jaw dyspnea or fatigue may present as "chest pain equivalents," especially in females associated with diaphoresis or nausea predictably precipitated by the "3 E's" Exertion, Emotion and Eating brief duration, lasting < 10-15 minutes and typically relieved by rest note: always list the presence or absence of the cardiac risk factors in a separate subsection in the history (e.g., + FHx, + HTN, +DM, + smoking, - hypercholesterolemia) stress testing (see Cardiac Diagnostic Tests section) Variant Angina (Prinzmetals Angina) vasospasm of coronary arteries results in myocardial ischemia may occur in normal or atherosclerotic vessels typically occurs between midnight and 8 am unrelated to exercise; relieved by Nitrates typically ST elevation on ECG (may be confused with acute MI) diagnose by provocative testing with ergot vasoconstrictors (rarely done) Syndrome X patient has typical symptoms of Angina yet has normal angiogram may show definite signs of ischemia during exercise testing pathogenesis thought to be due to inadequate vasodilator reserve of coronary resistance vessels has better prognosis than patient with overt atherosclerotic disease Medical Treatment blockers (first line therapy) decrease overall mortality decrease heart rate, contractility, and to a lesser degree, blood pressure (afterload) increase coronary perfusion avoid agents with intrinsic sympathomimetic activity (ISA) (e.g. Acebutolol) (these increase demand) nitrates used for symptomatic control no clear impact on survival decrease myocardial work and, therefore, oxygen requirements through venous dilatation (decrease preload) and arteriolar dilatation (decrease afterload) dilate coronary arteries maintain daily nitrate-free intervals to try to prevent nitrate tolerance calcium channel blockers (CCB) variably decrease afterload, decrease heart rate and decrease contractility, produce coronary dilatation
ECASA

all patients decrease platelet aggregation lipid lowering C20 Cardiology MCCQE 2006 Review Notes

. ISCHEMIC HEART DISEASE (IHD) . . CONT.

Coronary Artery Disease (CAD) Lipid Therapy

Trial primary prevention secondary prevention WOSCOPS
AFCAPS

Drug pravastatin lovastatin pravastatin simvastatin pravastatin

Dose 40 20-40 40 20-40 40

CHD Event Reduction 31% 24% 23% 34% 24%

LIPID 4S CAR E

2000 Canadian Guidelines for Treatment of Dyslipidemia

Level of Risk (Definition)
(History of cardiovascular disease or 10 yr risk of CAD > 30%)

LDL < 2.5 <3 <4 <5

Target Values

TC:HDL Ratio <4 <5 <6 <7

Tryglycerides <2 <2 <2 <3

Very High

High

(10 yr risk of CAD 20-30%)

Moderate (10 yr risk 10-20%) Low (10 yr risk < 10%)

Risk calculated based on Framingham data: dertermined by gender, age group, total cholesterol level, HDL level, SBP, history of smoking

treatment strategy short acting nitrates on PRN basis to relieve acute attacks and PRN prior to exertion be careful when combining blockers and verapamil/diltiazem both decrease conduction and contractility and may result in sinus bradycardia or AV block use nitrates and CCB for variant angina
low likelihood non-nuclear + medical follow-up nuclear stress testing + cath + nuclear stress testing medical follow-up intermediate likelihood otherwise healthy high likelihood poor surgical candidate with multiple co-morbidities

low risk medical management

high risk
PTCA, CABG

Figure 10. Diagnostic Strategies in the Management of IHD Indications for Angiography strongly positive exercise test significant, reversible defects on thallium scan refractory to medical therapy or patient unable to tolerate medical therapy unstable angina

MCCQE 2006 Review Notes

Cardiology C21

ISCHEMIC HEART DISEASE (IHD) . . CONT. .

Percutaneous Transluminal Coronary Angioplasty (PTCA) uses a balloon inflated under high pressure to rupture atheromatous plaques may be used as primary therapy in angina, acute MI, post-MI angina or in patients presenting with bypass graft stenosis optimally used for proximal lesions free of thrombus and distanced from the origins of large vessel branches not in Left Main primary success rate is > 80% use of intracoronary stent is associated with a lower restenosis rate (compared with PTCA alone) complications (overall 3-5%) mortality < 1% MI 3-5% intimal dissection + vessel occlusion requiring urgent CABG Surgical Treatment- Coronary Artery Bypass Grafting (CABG) indications - for survival benefit, or symptomatic relief of angina stable angina (survival benefit for CABG shown) left main coronary disease three-vessel disease with depressed LV function multi-vessel disease with significant proximal LAD stenosis unstable angina (see below) above indications or continuing angina despite aggressive medical therapy complications/failed PTCA
comparison of CABG with PTCA studies: RITA, GABI, BARI, EAST, ERACI, CABRI

highly select patient population - no left main disease and minimal LV dysfunction overall no difference in survival, but PTCA group had more recurrent ischemia and required more interventions BARI, subset analysis - CABG superior in patients with DM and multi-vessel IHD predictors of poor outcome previous cardiac surgery urgent/emergent case, preoperative IABP gender (relative risk for F:M = 1.6:1) advanced age (> 70), DM, co-morbid disease CABG operative mortality elective case < 1% elective case, poor LV function 1-3% urgent case 1-5% overall (1980-1990) 2.2% efficacy: > 90% symptomatic improvement in angina conduits and patency 90% patency at 10 years internal mammary (thoracic) artery saphenous vein graft 50% patency at 10 years radial/gastroepiploic/inferior 85% patency at 5 years epigastric arteries (improving with experience)
poor LV function (EF < 40%), history of CHF, NYHA III or IV

ACUTE CORONARY SYNDROMES (ACS)

Spectrum of ACS A. Unstable Angina B. Acute Myocardial Infarcion C. Sudden Death

A. UNSTABLE ANGINA/NON ST ELEVATION MI (NSTEMI)

Definition accelerating pattern of pain increased frequency longer duration occurring with less exertion less responsive to treatment (eg. require higher doses or more frequent doses) angina at rest new onset angina angina post-MI post-angiography post-CABG note that unstable angina is a heterogeneous group and can be divided into a higher and lower risk groups C22 Cardiology MCCQE 2006 Review Notes

ISCHEMIC HEART DISEASE (IHD) . . CONT. .

Significance thought to represent plaque rupture and acute thrombosis with incomplete vessel occlusion Diagnosis history ECG changes ST depression or elevation T wave inversion no elevation of cardiac enzymes Management oxygen hospitalization/monitoring bed rest anti-anginal medications sublingual or IV nitroglycerine blockers are first line therapy aim for resting heart rate of 50-60 CCB are second line therapy (use if blockers contraindicated, or if patient has refractory symptoms despite aggressive treatment with ECASA, nitrates, and blockers) evidence suggests that they do not prevent MI or decrease mortality be cautious using verapamil/diltiazem with blockers use non-dihydropyridines if cannot use blockers otherwise may use amlodipine or long-acting nifedipine if concomitant blockade
ECASA

160-325 mg/day IV heparin or Plavix (GPIIB/IIIA inhibitor) angiography with view to potential PTCA or CABG used to map areas of ischemia if aggressive medical management is unsuccessful may use intra-aortic balloon pump (IABP) to stabilize before proceeding with revascularization used to increase coronary perfusion during diasole proceed to emergency angiography and PTCA or CABG

B. ACUTE ST ELEVATION MYOCARDIAL INFARCTION (STEMI)

Definition syndrome of acute coronary insufficiency resulting in death of myocardium Infarct Diagnosis Based on 2 of 3 - History, ECG, Cardiac Enzymes history sudden onset of characteristic chest pain for > 30 minutes duration may be accompanied by symptoms of heart failure (e.g. SOB, leg edema, etc.) ECG changes criteria: ST elevation of at least 1 mm in limb leads and 2 mm in precordial leads evolution of ECG changes in Q-wave MI 1st abnormal T waves 2nd ST-T elevations (hours post-infarct) 3rd significant Q waves (hours to days post-infarct) 4th inverted T waves, or may become flat or biphasic (days to weeks) cardiac enzymes follow CK-MB q8h x 3, Troponin q8h x 3 cardiac Troponin I and/or T levels provide useful diagnostic, prognostic information and permit early identification of an increased risk of mortality in patients with acute coronary syndromes Troponin I and T remain elevated for 5 to 7 days beware up to 30% are unrecognized or "silent" due to atypical symptoms DM elderly patients with HTN post heart-transplant (because of denervation) draw serum lipids within 24-48 hours because the serum values are unreliable after 48 hours, but become reliable again 8 weeks post-MI

MCCQE 2006 Review Notes

Cardiology C23

ISCHEMIC HEART DISEASE (IHD) . . CONT. .

Patient Evaluation unstable angina history physical exam ECG enzymes ST elevation presumed acute MI assess for thrombolysis positive enzymes acute MI non ST elevation sample enzymes negative enzymes unstable angina non cardiac chest pain

Figure 11. Diagnostic algorithm in acute IHD Etiology coronary atherosclerosis + superimposed thrombus on ruptured plaque (vast majority) vulnerable "soft" plaques more thrombogenic coronary thromboembolism infective endocarditis rheumatic heart disease intracavity thrombus cholesterol emboli severe coronary vasospasm arteritis coronary dissection consider possible exacerbating factors see Angina Pectoris section

Plasma Enzyme Level x Normal

CK-MB

ISCHEMIC HEART DISEASE

. . . CONT. DAYS POST-MI

Figure 12. Cardiac Enzyme Profile in Acute MI Further Classification of MIs Q wave associated with transmural infarctions, involving full thickness of myocardium non-Q wave usually associated with non-transmural (subendocardial) infarctions, involving 1/3 to 1/2 of myocardial thickness in-hospital mortality from non-Q wave infarction is low (< 5%) but 1 year mortality approaches that of Q wave infarction Management goal is to minimize the amount of infarcted myocardium and prevent complications emergency room measures ECASA 325 mg chewed stat oxygen sublingual nitroglycerine morphine for pain relief, sedation, and venodilation blockers to reduce heart rate if not contraindicated

C24 Cardiology

MCCQE 2006 Review Notes

ISCHEMIC HEART DISEASE (IHD) . . CONT. .

thrombolytic therapy (see Table 7) benefits of thrombolysis shown to be irrespective of age, sex, BP, heart rate, or history of MI or DM indications for thrombolytic therapy A. at least 0.5 hours of ischemic cardiac pain and B. any of the following ECG changes thought to be of acute onset at least 1 mm of ST elevation in at least two limb leads at least 1 mm of ST elevation in at least two adjacent precordial leads or new onset complete BBB C. presentation within 12 hours of symptom onset choice of thrombolytic agents include streptokinase and rt-PA patients having previously received streptokinase must receive alternate agent due to development of immunity heparin
PTCA, CABG

Long-Term Measures antiplatelet/anticoagulation therapy ECASA 325 mg daily nitrates alleviate ischemia but may not improve outcome blockers (first line therapy) start immediately and continue indefinitely if no contraindications decrease mortality CCB NOT recommended as first line treatment - Short Acting Nifedipine is contraindicated! Diltiazam and Verapamil are contraindicated in MI with associated LV dysfunction
ACEI

decrease mortality stabilize endothelium and prevent adverse ventricular remodeling strongly recommended for symptomatic CHF reduced LVEF (< 40%) starting day 3 to 16 post-MI (SAVE trial) anterior MI lipid lowering agent (HMG-C0A reductase inhibitors or niacin) if total cholesterol > 5.5 or LDL > 2.6 coumadin (for 3 months) for large anterior MI, especially if LV thrombus seen on 2D-ECHO see Figure 13 for post critical care unit (CCU) strategy Table 7. Contraindications to Thrombolytic Therapy in AMI
Absolute active bleeding aortic dissection acute pericarditis cerebral hemorrhage (previous or current) Relative GI, GU hemorrhage or stroke within past 6 months major surgery or trauma within past 2-4 weeks severe uncontrolled hypertension bleeding diathesis or intracranial neoplasm puncture of a noncompressible vessel significant chest trauma from CPR

Indications for Post-thrombolysis Heparin tPA used for thrombolysis Anterior MI Ventricular aneurysm Post-thrombolysis angina A fib Previous deep vein thrombosis (DVT), PE, or ischemic stroke Prognosis 20% of patients with acute MI die before reaching hospital 5-15% of hospitalized patients will die risk factors infarct size/severity age co-morbid conditions development of heart failure or hypotension post-discharge mortality rates 6-8% within first year, half of these within first 3 months 4% per year following first year risk factors LV dysfunction residual myocardial ischemia ventricular arrhythmias history of prior MI resting LVEF is most useful prognostic factor MCCQE 2006 Review Notes Cardiology C25

ISCHEMIC HEART DISEASE (IHD) . . CONT. .

Table 8. Complications of Myocardial Infarction
Complication Arrhythmia (a) tachycardia (b) bradycardia Myocardial Rupture (a) LV free wall (b) papillary muscle (MR) (c) ventricular septum (VSD) Shock/CHF Post Infarct Angina Recurrent MI Thromboembolism Pericarditis (Dressler's) transmural infarction inferior infarction anterior infarction septal infarction LV/RV infarction aneurysm persistent coronary stenosis multivessel disease reocclusion mural thrombus in Q wave infarction post-MI autoimmune (Dresslers) 1-7 days 1-7 days 1-7 days within 48 hours anytime anytime 7~10 days, up to 6 months 1-7 days 2-8 weeks pericardiocentesis or surgery surgery surgery fluids, inotropes, IABP
PTCA or CABG sinus, AF, VT, VF

Etiology

Presentation early/late early

Therapy see Arrhythmia section

sinus, AV block

aggressive medical therapy

see above heparin, warfarin NSAIDs NSAIDs, steroids

Acute MI Risk Stratification Cardiogenic Shock (5% - 10%) ST Elevation or LBBB and Presentation 12 hours (25% - 45%) Thrombolysis
? Rescue PTCA, CABS

CCU

Acute

No ST Elevation and Presentation > 12 hours (50% - 70%)

No Reperfusion (19% - 45%)

Reperfusion (55% - 81%)

Non-Acute Risk Stratification In-Hospital

High-Risk (30% - 35%)

prior MI CHF Recurrent Ischemia High-Risk Arrhythmia Cardiac Catheterization

Intermediate/Low-Risk (65% - 70%) Non-invasive Stress Testing

Ischemia or Poor Functional Status Cardiac Catheterization

Normal Results

No further testing at this time

Please note that Echocardiography is done routinely post-MI. It is controversial whether an EF < 40% is by itself an indication for coronary angiography.

Figure 13. Acute MI and Predischarge Risk Stratification

C26 Cardiology

MCCQE 2006 Review Notes

ISCHEMIC HEART DISEASE (IHD) . . CONT. .

C. SUDDEN DEATH
Definition unanticipated, non-traumatic death in a clinically stable patient, within 1 hour of symptom onset immediate cause of death is V fib (most common) ventricular asystole Significance accounts for ~ 50% of CAD mortalities initial clinical presentation in up to 20% of patients with CAD Etiology primary cardiac pathology ischemia/MI LV dysfunction severe ventricular hypertrophy hypertrophic cardiomyopathy (HCM) AS QT prolongation syndrome congenital heart disease high risk patients multi-vessel disease LV dysfunction Management Acute resuscitate with prompt CPR and defibrillation Long Term Survivors identify and treat underlying predisposing factors IHD cardiac catheterization to evaluate cardiac anatomy, LV function and need for revascularization Holter monitoring electrophysiologic studies Treatment antiarrhythmic drug therapy amiodarone, blockers surgery revascularization to treat ischemia map-guided subendocardial resection cryoablation, radiofrequency ablation implantable cardioverter-defibrillator Prognosis 1 year mortality post-resuscitation 20-30% predictors of recurrent cardiac arrest in the "survivor" of sudden cardiac death remote MI CHF LV dysfunction extensive CAD complex ventricular ectopy abnormal signal-averaged ECG

HEART FAILURE
overall, CHF is associated with a 50% mortality rate at five years see Colour Atlas R3 and R4 Definitions and Terminology inability of heart to maintain adequate cardiac output to meet the demands of whole-body metabolism and/or to be able to do so only from an elevated filling pressure(forward heart failure) inability of heart to clear venous return resulting in vascular congestion (backward heart failure) either the left side of the heart (left heart failure) or the right side of the heart (right heart failure) or both (biventricular failure) may be involved there may be components of ineffective ventricular filling (diastolic dysfunction) and/or emptying (systolic dysfunction) most cases associated with poor cardiac function (low-output heart failure) but some are not due to intrinsic cardiac disease (high-output heart failure; this is discussed separately below) CHF is not a disease itself - it is a syndrome involving variable degrees of both forward and backward heart failure MCCQE 2006 Review Notes Cardiology C27

HEART FAILURE. . . CONT.

Pathophysiology two components primary insults initiating the disease process compensatory responses which exacerbate and perpetuate the disease process in chronic heart failure Primary damage myocyte loss overload Necrosis, apoptosis Pump dysfunction Neurohumoral activation DIG ACEI Edema, tachycardia vasoconstriction, congestion Diuretics Figure 14. Pathogenesis of CHF CHF Ventricular remodeling dilatation hypertrophy Stretch

ACEI -blockers

Clinical Pearl What are the five commonest causes of CHF? coronary artery disease (60-70%) idiopathic (20%) often in the form of dilated cardiomyopathy valvular (e.g. AS, AR and MR) HTN alcohol (may cause dilated cardiomyopathy) Etiologies of Primary Insults consider predisposing, precipitating and perpetuating factors the less common causes of CHF toxic e.g. adriamycin, doxorubicin, radiation, uremia, catecholamines infectious e.g. Chagas disease(very common cause worldwide), Coxsackie, HIV endocrine e.g. hyperthyroidism, DM, acromegaly infiltrative e.g. sarcoidosis, amyloidosis, hemochromatosis genetic e.g. hereditary hypertrophic cardiomyopathy, Freidriechs Ataxia metabolic e.g. thiamine deficiency, selenium deficiency peripartum precipitants ( H-E-A-R-T F-A-I-L-E-D) H - HTN (common) E - endocarditis/environment (e.g. heat wave) A - anemia R - rheumatic heart disease and other valvular disease T - thyrotoxicosis F - failure to take meds (very common) A - arrhythmia (common) I - infection/ischemia/infarction (common) L - lung problems (PE, pneumonia, COPD) E - endocrine (pheochromocytoma, hyperaldosteronism) D - dietary indiscretions (common) it is important to differentiate an exacerbation due to a reversible cause from progression of the primary disease for treatment and prognosis cardiac response to myocardial stress pressure overload results in hypertrophy (e.g. HTN) volume overload results in cardiac dilatation (e.g. AR) systemic response to ineffective circulating volume activation of sympathetic nervous and renin-angiotensin systems result in salt and H 2 O retention with intravascular expansion increased increased heart rate and myocardial contractility increased afterload compensated heart failure becomes decompensated as cardiac and systemic responses overshoot treatments are directed at these compensatory overshoots C28 Cardiology MCCQE 2006 Review Notes

COMPENSATORY RESPONSES IN HEART FAILURE

HEART FAILURE. . . CONT.

SYSTOLIC vs. DIASTOLIC DYSFUNCTION
Systolic Dysfunction (impaired ejection of blood from the heart) impaired myocardial contractile function hallmark is impaired stroke volume and/or ejection fraction symptoms predominantly due to decreased cardiac output examples MI myocarditis dilated cardiomyopathy Diastolic Dysfunction (defect in ventricular filling) 1/3 of all patients evaluated for clinical diagnosis of heart failure have normal systolic function (ejection fraction (EF)) ability of LV to accept blood is impaired due decreased compliance transiently by ischemia permanently by severe hypertrophy (HTN, AS), infiltrative disease, MI (due to scarring) or HCM ischemia causes stiffness of LV because relaxation of myocardium is active and requires energy/ATP increased LV filling pressures produce venous congestion upstream (i.e. pulmonic and systemic venous congestion) clues to diagnosis: S 4 , HTN, LVH on ECG/ECHO, normal-size heart on CXR, normal EF apex beat sustained but not displaced treatment: blockers, verapamil, diltiazem or ACEI Table 9. Signs and Symptoms of L vs. R Heart Failure
Left Failure low cardiac output (forward) fatigue syncope systemic hypotension cool extremities slow capillary refill peripheral cyanosis MR Cheyne-Stokes breathing pulsus alternans S3 dyspnea orthopnea PND basal crackles cough hemoptysis Right Failure TR S3 (right-sided)

venous congestion (backward)

peripheral edema hepatomegaly hepatic tenderness pulsatile liver increased JVP positive HJR Kussmauls sign

SLEEP-DISORDERED BREATHING

45-55% of patients with CHF (systolic and diastolic heart failure) have sleep disturbances, which include Cheyne-Stokes breathing, central and obstructive sleep apnea associated with a worse prognosis and greater LV dysfunction nasal continuous positive airway pressure (CPAP) is effective in treating Cheyne-Stokes respiration/sleep apnea with improvement in cardiac function and symptoms a variety of factors may create a situation of relative heart failure by demanding a greater than normal cardiac output for a variety of reasons rarely causes heart failure in itself but often exacerbates existing heart failure or puts a patient with other cardiac pathology "over the edge" DDx: anemia, thiamine deficiency, hyperthyroidism, A-V fistula, Paget's disease of bone

HIGH-OUTPUT HEART FAILURE

Investigations work up involves assessment for precipitating factors and treatable causes of CHF blood work CBC (increased WBC - possible infectious precipitant; decreased Hb - anemia as a precipitant/exaccerbating factor) electrolytes dilutional (hypervolemic) hyponatremia indicates end-stage CHF sign of neurohormonal activation and poorer prognosis hypokalemia secondary to high renin state BUN, Cr may be elevated due to prerenal insult be wary of ATN with diuretic therapy MCCQE 2006 Review Notes

Cardiology C29

HEART FAILURE. . . CONT.

ECG chamber enlargement abnormal rhythms ischemia/infarction chest x-ray signs of pulmonary congestion peribronchiolar cuffing vascular redistribution Kerley B Lines interstitial pattern fluid in lung fissures alveolar filling if gross pulmonary edema also look for cardiomegaly (cardiac/thoracic (C/T) > 0.5) atrial enlargement pericardial effusion pleural effusion echocardiography is the primary diagnostic method to determine

atrial or ventricular dimensions wall motion abnormalities valvular stenosis or regurgitation pericardial effusion radionuclide angiography (MUGA) provides more accurate ejection fraction measurements than echocardiography; however, it provides little information on valvular abnormalities myocardial perfusion scintigraphy (Thallium or Sestamibi SPECT) determines areas of fibrosis/infarct or viability angiogram in selected patients Long-term Management of CHF short term goals of therapy are to relieve symptoms and improve the quality of life long term goal is to prolong life by slowing, halting, or reversing the progressive LV dysfunction treat the cause/aggravating factors symptomatic measures oxygen, bed rest, elevation of head of bed control of sodium and fluid retention sodium restriction (2 gm/d), requires patient education fluid restriction and monitor daily weights diuretics - for symptom control, mortality benefit demonstrated with spironolactone (RALES study) furosemide (40-500 mg/day) for potent diuresis metalozone may be used with furosemide to increase diuresis vasodilators goal is to arteriodilate (decrease afterload) and venodilate (increase preload), thereby improving cardiac output and venous congestion in hospital, monitor response to therapy with daily weights and measurement of fluid balance and follow renal function ACEI: standard of care (improves survival) strongly recommended for all symptomatic patients all asymptomatic patients with LVEF < 35% post-MI setting if symptomatic heart failure asymptomatic LVEF < 40% anterior MI clearly shown to decrease mortality and slow progression in these settings hydralazine and nitrates second line to ACEI decrease in mortality not as great as with ACEI amlodipine may be of benefit in dilated cardiomyopathy angiotensin II receptor blockers e.g. losartan preliminary evidence suggests benefit inotropic support digitalis inhibits Na/K ATPase leading to decreased Na/Ca exchange and increased intracellular [Ca hence increasing myocardial contractility improves symptoms and decrease hospitalizations (DIG trial); patients on digitalis glycosides may worsen if these are withdrawn no impact on survival excellent choice in setting of CHF with atrial fibrillation C30 Cardiology

EF (LV Grade I (EF = 60%), II (40-59%), III (21-39%), IV (= 20%)

2+

],

MCCQE 2006 Review Notes

HEART FAILURE. . . CONT.

other agents blockers - recommended for functional class (FC) II-III patients should be used cautiously, titrate slowly because may initially worsen CHF postulated that these agents interfere with neurohormonal activation carvedilol confers survival benefit in FC II-III CHF metoprolol has been shown to delay time to transplant, decreased hospitalizations in dilated cardiomyopathy and to decrease mortality (MERIT study) CCB (have equivocal effect on survival) antiarrhythmic drugs if required, amiodarone is drug of choice class I anti-arrhythmics associated with increased mortality in CHF

ACUTE CARDIOGENIC PULMONARY EDEMA

Definition left-sided backward heart failure leading to severe pulmonary congestion with extravasation of capillary fluid into the pulmonary interstitium and alveolar space Clinical Manifestations tachycardia, tachypnea, diaphoresis severe left-sided venous congestion Management, use mnemonic "LMNOP" make sure to treat any acute precipitating factors (e.g. ischemia, arrhythmias) sit patient up with legs hanging down if blood pressure is adequate L - Lasix - furosemide 40 mg IV, double dose q1h as necessary M - Morphine 2-4 mg IV q5-10 minutes decreased anxiety vasodilation N - Nitroglycerine topical 2 inches q2h (or IV) O - Oxygen P - Positive airway pressure (CPAP or BiPAP) decreased need for ventilation and decreased preload other vasodilators as necessary in ICU setting nitroprusside (IV) hydralazine (PO) sympathomimetics potent agents used in ICU/CCU settings dopamine agonist at dopamine D1 (high potency), 1-adrenergic (medium potency), and 1-adrenergic receptors (low potency) "low-dose" causes selective renal vasodilation (D1 agonism) "medium-dose" provides inotropic support (1 agonism) "high-dose" increase systemic vascular resistance (SVR), which in most cases is undesirable ( 1 agonism) dobutamine acts at 1 and 1 adrenoceptors selective inotropic agent (1 agonism) also produces arterial vasodilation ( 1 antagonism) phosphodiesterase inhibitors (amrinone, Inocor) effects similar to dobutamine (inhibits PDE > cAMP > inotropic effect and vascular smooth muscle relaxation (decrease SVR) adverse effect on survival when used as long-term oral agent inotropic support (dopamine, dobutamine) if necessary consider PA line to monitor capillary wedge pressure consider mechanical ventilation if needed rarely used but potentially life-saving measures rotating tourniquets phlebotomy

CARDIAC TRANSPLANTATION

indications - end stage cardiac disease (CAD, DCM, etc.) failure of maximal medical/surgical therapy poor 6 month prognosis absence of contraindications ability to comprehend and comply with therapy 1 year survival 85%, 5 year survival 70% complications: rejection, infection, graft vascular disease, malignancy Cardiology C31

MCCQE 2006 Review Notes

CARDIOMYOPATHIES
Definition intrinsic myocardial disease not secondary to CAD, valvular heart disease, congenital heart disease, HTN or pericardial disease The diagnosis of any of the following mandates exclusion of the above conditions: dilated cardiomyopathy (DCM) hypertrophic cardiomyopathy (HCM) restrictive cardiomyopathy (RCM) myocarditis

DILATED CARDIOMYOPATHY
Etiology idiopathic (risk factors: male, black race, family history) alcohol inflammatory (subsequent to myocarditis) collagen vascular disease: SLE, PAN, dermatomyositis, progressive systemic sclerosis infectious: post-viral (Coxsackie), Chagas disease, Lyme disease, Rickettsial diseases, acute rheumatic fever neuromuscular disease: Duchenne muscular dystrophy, myotonic dystrophy, Friedreich ataxia metabolic: uremia, nutritional deficiency (thiamine, selenium, carnitine) endocrine: thyrotoxicosis, DM familial peripartum toxic: cocaine, heroine, glue sniffing, organic solvents radiation induced drugs: chemotherapeutics (adriamycin) Pathophysiology clinical manifestations CHF systemic or pulmonary emboli arrhythmias sudden death (major cause of mortality due to fatal arrhythmia) Investigations 12 lead ECG ST-T wave abnormalities poor R wave progression conduction defects (e.g. BBB) arrhythmias chest x-ray global cardiomegaly (globular heart) signs of CHF echocardiography 4-chamber enlargement depressed ejection fraction MR and TR secondary to cardiac dilatation endomyocardial biopsy: not routine, used to diagnose infiltrative RCM and myocarditis, or to rule out a treatable cause angiography: selected patients Natural History prognosis depends on etiology generally inexorable progression overall once CHF - 50% 5 year survival cause of death usually CHF or sudden death systemic emboli are significant source of morbidity Management treat underlying disease - e.g. abstinence from EtOH treat CHF (see Heart Failure section), blockade (e.g. metoprolol, carvedilol) and ACEI (+/ AII receptor inhibitors) to decrease remodeling anticoagulation to prevent thromboembolism (coumadin) absolute - A fib, history of thromboembolism or documented thrombus clinical practice is to anticoagulate if EF < 20% treat symptomatic or serious arrhythmias immunize against influenza and pneumococcus surgical therapy cardiac transplant - established definitive therapy LVAD volume reduction surgery (role remains unclear) cardiomyoplasty (latissimus dorsi wrap) C32 Cardiology MCCQE 2006 Review Notes

CARDIOMYOPATHIES. . CONT. .
HYPERTROPHIC CARDIOMYOPATHY (HCM)
Pathophysiology defined as unexplained ventricular hypertrophy (not due to systemic HTN or AS). Histopathologic features are myocardial fiber disarray, myocyte hypertrophy, and interstitial fibrosis cause is felt to be a genetic defect involving 1 of the cardiac sarcomeric proteins (> 100 mutations associated with development of autosomal dominant inheritance) clinical manifestations asymptomatic dyspnea angina presyncope/syncope- LV outflow obstruction or arrhythmia CHF arrhythmias sudden death (may be first manifestation) Henodynamic Classification hypertrophic obstructive cardiomyopathy (HOCM): dynamic outflow tract (LVOT) obstruction either resting or provocable LVOT obstruction nonobstructive hypertrophic cardiomyopathy: decreased compliance and diastolic dysfunction (impaired filling) complications: obstruction, arrhythmia, diastolic dysfunction Hallmark Signs of HOCM pulses rapid upstroke pulse bifid pulse precordial palpation PMI: localized, sustained, double impulse, triple ripple (triple apical impulse) precordial auscultation normal or paradoxically split S 2 S4 harsh, systolic, diamond-shaped murmur at LLSB or apex, enhanced by squat to standing or valsalva (murmur secondary to LVOT obstruction and asociated mitral regurgitation) Table 10. Factors Influencing Obstruction in Hypertrophic Cardiomyopathy
Increased Obstruction (decreased murmur) inotropes, vasodilators, diuretics hypovolemia tachycardia squat to standing position Valsalva maneuver Amylnitrite inhalation Decreased Obstruction (decreased murmur)
vasoconstrictors

negative inotropes

volume expansion bradycardia squatting from standing position sustained handgrip (isometrics)

Investigations 12 lead ECG LVH prominent Q waves or tall r wave in V 1 echocardiography LVH - asymmetric septal hypertrophy (most common presentation) systolic anterior motion (SAM) of anterior MV leaflet resting or dynamic ventricular outflow tract obstruction MR (due to SAM and associated with LVOT obstruction) diastolic dysfunction LAE cardiac catheterization increased LV end-diastolic pressure variable systolic gradient across LV outflow tract Natural History variable potential complications: A fib, VT, CHF, sudden death risk factors for sudden death most reliable history of survived cardiac arrest/sustained VT family history of multiple sudden deaths other factors associated with increased risk of sudden cardiac death (SCD) syncope VT on ambulatory monitoring marked ventricular hypertrophy prevention of sudden death in high risk patients = amiodarone or implantable cardioverter defibrillator (ICD) MCCQE 2006 Review Notes Cardiology C33

CARDIOMYOPATHIES. . CONT. .
Management avoid extremes of excertion avoid factors which increase obstruction infective endocarditis prophylaxis for patients with obstructive HCM treatment of obstructive HCM medical agents blockers disopyramide CCB only used in patients with no resting/provocable obstruction patients with drug-refractory symptoms options 1. surgical myectomy 2. septal ethanol ablation 3. dual-chamber pacing treatment of ventricular arrhythmias - AMIO or ICD adult first-degree relatives of patients with HCM should be screened (physical exam, ECG, 2D-ECHO) serially every 5 years

RESTRICTIVE CARDIOMYOPATHY (RCM)

Etiology infiltrative amyloidosis (especially in primary amyloidosis associated with light chain disease), sarcoidosis non-infiltrative scleroderma, idiopathic myocardial fibrosis storage diseases hemochromatosis (especially in DM, cirrhosis), Fabry's disease, glycogen storage diseases endomyocardial endomyocardial fibrosis (Africans), eosinophilic: Loeffler's endocarditis or eosinophilic endomyocardial disease radiation heart disease pseudoxanthoma elasticum carcinoid syndrome (associated TV or PV dysfunction) Pathophysiology infiltration of the myocardium > decreased ventricular compliance > diastolic dysfunction clinical manifestations CHF - diastolic dysfunction predominates arrhythmias Investigations 12 lead ECG low voltage non-specific, diffuse ST-T wave changes (no correspondence with vascular territory) +/ nonischemic Q waves chest x-ray mild cardiac enlargement echocardiography normal pericardium, normal or only slightly decreased systolic function, impaired ventricular filling and diastolic dysfunction cardiac catheterization end-diastolic ventricular pressures endomyocardial biopsy to distinguish etiology (especially for infiltrative RCM) Natural History depends on etiology generally poor prognosis Management exclude constrictive pericarditis treat underlying disease supportive care treat coexisting CHF, arrhythmias anticoagulation consider cardiac transplantation - depending on etiology

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CARDIOMYOPATHIES. . CONT. .
MYOCARDITIS
inflammatory process involving the myocardium (an important cause of dilated cardiomyopathy)

Etiology idiopathic infectious viral: Coxsackie virus B, Echovirus, Poliovirus, HIV, mumps bacterial: S. aureus, C. perfringens, C. diphtheriae , Mycoplasma, Rickettsia fungi spirochetal (Lyme disease Borrelia burgdorferi ) Chagas disease ( Trypanosoma cruzi ), toxoplasmosis acute rheumatic fever (Group A -hemolytic Streptococcus) drug-induced: emetine, doxorubicin collagen vascular disease: systemic lupus erythematosus (SLE), polyarteritis nodosa (PAN), rheumatoid arthritis (RA), dermatomyositis (DMY) sarcoidosis giant cell myocarditis Clinical Manifestations constitutional illness acute CHF chest pain - associated pericarditis or cardiac ischemia arrhythmias (may have associated inflammation of conduction system) systemic or pulmonary emboli sudden death Investigations 12 lead ECG non-specific ST-T changes +/ conduction defects blood work increased CK, Troponin, LDH, and AST with acute myocardial necrosis +/ increased WBC, ESR, ANA, rheumatoid factor, complement levels perform blood culture, viral titers and cold agglutinins for Mycoplasma chest x-ray enlarged cardiac silhouette echocardiography dilated, hypokinetic chambers segmental wall motion abnormalities Natural History usually self-limited and often unrecognized most recover may be fulminant with death in 24-48 hours sudden death in young adults may progress to dilated cardiomyopathy few may have recurrent or chronic myocarditis Management supportive care restrict physical activity treat CHF treat arrhythmias anticoagulation treat underlying cause if possible

MCCQE 2006 Review Notes

Cardiology C35

VALVULAR HEART DISEASE

see Cardiac Surgery Chapter

INFECTIVE ENDOCARDITIS (IE)

Etiology
Strep viridans (commonest, spontaneous Enterococcus (Group D strep, SBE) Staphylococcus epidermidis

bacterial endocarditis (SBE) on abnormal valve prosthetic, MVP, etc.)

Staph aureus (enter through break in skin: IV drug abusers, usually rightsided, catheter-associated sepsis) Strep bovis(underlying GI malignancy)

(prosthetic valve)

others: gram-negative bacteria, Candida, HACEK organisms ( Haemophilus species, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella , and Kingella Pseudomonas (IV drug) ), frequency of valve involvement: MV >> AV > TV > PV risk of IE in various cardiac lesions (JAMA 1997;227:1794) high risk: prosthetic heart valves, previous IE, complex cyanotic congenital heart disease, surgically constructed systemic to pulmonary shunts or conduits moderate risk: most other congenital cardiac malformations, acquired valvular dysfunction, HCM, MVP with MR and/or thickened leaflets Pathogenesis and Symptomatology usually requires source of infection, underlying valve lesion, +/ systemic disease/immunocompromised state portal of entry: oropharynx, skin, GU, drug abuse, nosocomial infection > bacteremia > diseased valve/high flow across valve > turbulence of blood across valve > deposition of bacteria on endocardial surface of valve (vegetation = clump of fibrin, platelets, WBCs and bacteria) > endocarditis > septic embolization symptoms fever, chills, rigors night sweats 'flu-like' illness, malaise, headaches, myalgia, arthralgia dyspnea, chest pain Signs fever, regurgitant murmur (new onset or increased intensity), constitutional symptoms, anemia signs of CHF (secondary to acute MR, AR) peripheral manifestations: petechiae, Osler's nodes ("ouch!" raised, painful, 3-15 mm, soles/palms), Janeway lesions ("pain away!" flat, painless, approx. 1-2 cm, on soles/plantar surfaces of toes/palms/fingers), splinter hemorrhages (especially on proximal nail bed, distally more commonly due to local trauma) CNS: focal neurological signs (CNS emboli), retinal Roth spots clubbing (subacute) splenomegaly (subacute) microscopic hematuria (renal emboli or glomerulonephritis) active sediment weight loss Investigations blood work: anemia, uncreased ESR, positive rheumatoid factor serial blood cultures (definitive diagnosis) echocardiography (transesophageal > sensitivity than transthoracic) vegetations, degree of regurgitation valve leaflet perforation, abscess serial ECHO may help in assessing cardiac function Natural History adverse prognostic factors CHF, Gram () or fungal infection, prosthetic valve infection, abscess in valve ring or myocardium, elderly, renal failure, culture negative IE mortality up to 30% relapses may occur - follow-up is mandatory permanent risk of re-infection after cure due to residual valve scarring Complications CHF (usually due to valvular insufficiency) systemic emboli mycotic aneurysm formation intracardiac abscess formation leading to heart block renal failure: glomerulonephritis due to immune complex deposition; toxicity of antibiotics

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VALVULAR HEART DISEASE. CONT. ..

Management medical antibiotic therapy tailored to cultures (penicillin, gentamicin, vancomycin, cloxacillin) minimum of 4 weeks treatment serial ECGs - increased PR interval prophylaxis (JAMA 1997;227:1794) dental/oral/respiratory/esophageal procedures amoxicillin 2 g 1 hour prior GU/GI (excluding esophageal) procedures high risk: ampicillin + gentamicin moderate risk: amoxicillin, ampicillin, or vancomycin surgical indications: refractory CHF, valve ring abscess, valve perforation, unstable prosthesis, multiple major emboli, antimicrobial failure, mycotic aneurysm

RHEUMATIC FEVER
Epidemiology school-aged children (5-15 yr), young adults (20-30 yr), outbreaks of Group A -hemolytic Streptococcus, upper respiratory tract infection (URTI), social factors (low socioeconomic status (SES), crowding) Etiology 3% of untreated Group A -hemolytic Streptococcus (especially mucoid, highly encapsulated stains, serotypes 5, 6, 18) pharyngitis develop acute rheumatic fever Diagnosis 1. Modified Jones criteria (1992): 2 major, or 1 major + 2 minor major criteria pancarditis polyarthritis Sydenham's chorea erythema marginatum subcutaneous nodules minor criteria previous history of rheumatic fever or rheumatic heart disease polyarthralgia increased ESR or C-reactive protein (CRP) increased PR interval (first degree heart block) fever plus 2. Supported evidence confirming Group A Streptococcus infection: history of scarlet fever, group A streptococcal pharyngitis culture, rapid Ag detection test (useful if positive), anti-streptolysin O Titers (ASOT) Clinical Features Acute Rheumatic Fever: myocarditis (DCM/CHF), conduction system(sinus tachycardia, A fib), valvulitis (acute MR), pericarditis (does not usually lead to constrictive pericarditis) Chronic: Rheumatic Valvular heart disease: fibrous thickening, adhesion, calcification of valve leaflets resulting in stenosis/regurgitation, increased risk of IE +/ thromboembolic phenomenon. Onset of symptoms usually after 10-20 year latency from acute carditis of rheumatic fever. Mitral valve most commonly affected. Management acute treatment of Streptococcal infection (benzathine penicillin G 1.2 MU IM x 1 dose) prophylaxis to prevent colonization of URT (age < 40): benzathine penicillin G 1.2 MU IM q3-4 weeks, within 10 yr of attack management of carditis in rheumatic fever: salicylates (2g qid x4-6 wk for arthritis), corticosteroids (prednisone 30 mg qid x4-6wk for severe carditis with CHF)

AORTIC STENOSIS
Etiology congenital (bicuspid > > unicuspid) > calcified degeneration or congenital AS acquired degenerative calcified AS (most common) - "wear and tear" rheumatic disease Definition AS = narrowed valve orifice (aortic valve area: normal = 3-4 cm2 severe AS = < 1.0 cm2 2 critical AS = < 0.75 cm ) Note: low gradient AS with severely reduced valve area (< 1.0 cm 2 ) and normal gradient in setting of LV dysfunction Pathophysiology pressure overloaded LV: increased LV end-diastolic pressure (EDP), concentric LVH, subendocardial ischemia > forward failure outflow obstruction: fixed cardiac output (CO) LV failure, pulmonary edema, CHF MCCQE 2006 Review Notes Cardiology C37

VALVULAR HEART DISEASE. CONT. ..

Symptomatology ASD (triad of Angina, Syncope, and Dyspnea; prognosis associated with onset) angina (exertional): due to concentric LVH and subendocardial ischemia (decreased subendocardial flow and increased myocardial O 2 demand), may have limitation of normal activity or resting angina in tight AS (associated with < 5 year survival) syncope: due to fixed CO or arrhythmia (< 3 year survival) dyspnea (LV failure): systolic +/ diastolic dysfunction, pulmonary edema, may have orthopnea, if secondary RHF may have ascites, peripheral edema, congestive hepatomegaly (< 2 years) Signs of AS pulses apical-carotid delay pulsus parvus et tardus (decreased amplitude and delayed upstroke) narrow pulse pressure, brachial-radial delay thrill over carotid precordial palpation PMI: sustained (LVH) +/ diffuse (displaced, late, with LV dilation) +/ palpable S 4 systolic thrill in 2nd right intercostal space (RICS) +/ along left lower sternal bender (LLSB) precordial auscultation most sensitive physical finding is SEM radiating to right articular head SEM diamond shaped (crescendo-decrescendo), harsh, high-pitched, peaks progressively later in systole with worsening AS, intensity not related to severity, radiates to neck, musical quality of murmur at apex (Gallavardin phenomenon) +/ diastolic murmur of associated mild AR S 2 soft S2 , absent A 2 component, paradoxical splitting (severe AS) ejection click S 4 early in disease (increased LV compliance) S 3 only in late disease (if LV dilatation present) Investigations 12 lead ECG
LVH and strain +/ LBBB, LAE/A fib

chest x-ray post-stenotic aortic root dilatation, calcified valve, LVH + LAE, CHF (develops later) ECHO test of choice for diagnosis and monitoring valvular area and pressure gradient (assess severity of AS) LVH and LV function shows leaflet abnormalities and "jet" flow across valve cardiac catheterization r/o CAD (i.e. especially before surgery in those with angina) valvular area and pressure gradient (for inconclusive ECHO) LVEDP and CO (normal unless associated LV dysfunction) Natural History asymptomatic patients have excellent survival (near normal) once symptomatic, untreated patients have a high mean mortality 5 years after onset of angina, < 3 years after onset of syncope; and < 2 years after onset of CHF/dyspnea the most common fatal valvular lesion (early mortality/sudden death) ventricular dysrhythmias (likeliest cause of sudden death) sudden onset LV failure other complications: IE, complete heart block Management asymptomatic patients - follow for development of symptoms serial echocardiograms supportive/medical avoid heavy exertion IE prophylaxis avoid nitrates/arterial vasodilators and ACEI in severe AS indications for surgery onset of symptoms: angina, syncope, or CHF progression of LV dysfunction moderate AS if other cardiac surgery (i.e. CABG) required surgical options (see Cardiac and Vascular Surgery Chapter) AV replacement excellent long-term results, procedure of choice open or balloon valvuloplasty children, repair possible if minimal disease adults (rarely done): pregnancy, palliative in patients with comorbidity, or to stabilize patient awaiting AV replacement - 50% recurrence of AS in 6 months after valvuloplasty complications: low CO, bleeding, conduction block, stroke

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VALVULAR HEART DISEASE. CONT. ..

AORTIC REGURGITATION (AR)
Etiology supravalvular (aortic root disease with dilatation of ascending aorta) atherosclerotic dilatation and aneurysm; cystic medial necrosis annuloaortic ectasia (Marfan syndrome); dissecting aortic aneurysm; systemic HTN; (idiopathic Aortic root dilation); syphilis; connective tissue diseases (ankylosing spondylitis, psoriatic arthritis, Reiter syndrome, rheumatoid aortitis) valvular congenital abnormalities (bicuspid AV, large VSD); connective tissue diseases (SLE, rheumatoid arthritis, etc.); rheumatic fever (+/ associated AS); IE; myxomatous degeneration; deterioration of prosthetic valve acute AR IE aortic dissection trauma acute rheumatic fever failed prosthetic valve Pathophysiology and Symptomatology AR = blood flow from aorta back into LV (diastolic run-off) volume overload > LV dilatation > increased SV and more diastolic run-off > high SBP and low DBP (wide pulse pressure) LV dilatation combined with increased SBP > increased wall tension = pressure overload > LVH symptoms dyspnea/orthopnea/PND fatigue and palpitations (arrhythmias or hyperdynamic circulation) decreased DBP > decreased coronary perfusion; LVH > increased myocardial O 2 demand symptoms syncope, angina (only if severe AR) usually symptomatic only after onset of LV failure (late in disease), LAE presents earlier onset of symptoms Signs of chronic AR pulses increased volume, Waterhammer (bounding and rapidly collapsing) Bisferiens pulse - twice beating in systole; occurs inpresence of combined AS and AR de Musset's sign - head bobbing due to increased PP pistol-shot sounds over femoral artery (without compression) Traubes sign: double sound heard with the stethoscope lightly applied over the artery Quincke's sign - pulsatile blushing of nail beds (nonspecific) Corrigan's pulse - visible carotid pulse Hill's test:- femoral-brachial SBP difference > 20 (greater differences correlate with more severe AR) Duroziezs test: light proximal compression of femoral artery produces systolic-diastolic murmur over femoral artery other - pulsating uvula (Mueller), liver (Rosenbach), pupil (Gandolfi), or spleen (Gerhard) precordial palpation heaving apex (hyperdynamic), displaced point of maximal impulse (PMI) (volume overload) precordial auscultation S 1 - soft in severe AR (early closure of MV) S 2 - soft or absent (severe AR), may be loud if calcified S 3 in severe AR (early LV decompensation) early diastolic decrescendo murmur (EDM) - high-pitched, at LLSB (cusp disease) or RLSB (aortic root disease), length correlates with severity, best heard with patient sitting, leaning forward on full expiration systolic ejection murmur (SEM) (physiologic, high flow murmur)- in aortic area Austin Flint murmur - diastolic rumble at apex, secondary to regurgitant jet on anterior MV leaflet acute AR - most of these signs are absent (SV not yet increased) patient usually presents in CHF, tachycardia, soft S 1 , soft or absent S 2 , short early diastolic murmur, preclosure of MV (ECHO) Investigations 12 lead ECG
LVH, LAE

chest x-ray LV enlargement, LAE, aortic root dilatation echocardiography (TTE) gold standard for diagnosis and assessment of severity of AR regurgitant jet from aorta into LV association of aortic leaflet morphology, LV size, LVF, aortic root size fluttering of anterior MV leaflet Doppler most sensitive radionuclide imaging serial resting and exercise EF (normal increased with exercise > 5%) for serial monitoring of patients with asymptomatic severe AR sensitive sign of decreased LV function: failure to increase EF with exercise cardiac catheterization coronary angiography indicated if age > 40 increased LV volume; CO normal or decreased (LV dysfunction); increased LVEDP MCCQE 2006 Review Notes Cardiology C39

VALVULAR HEART DISEASE. CONT. ..

Natural History mild to moderate AR - few symptoms chronic progression to severe AR (may be asymptomatic more than 10 years) once symptomatic, prognosis is much worse mean mortality 4 years after onset of angina, 2 years after CHF severe acute AR - only 10-30% live more than 1 year after diagnosis late complications: arrhythmias, CHF, IE Management asymptomatic follow with serial ECHO - assess LV size and function +/ afterload reduction: nifedipine, ACE inhibitors IE prophylaxis medical restriction of activities treat CHF (non-pharmacological, afterload reduction, Digoxin, and diuretics) acute AR: may stabilize with IV vasodilators before surgery surgical acute AR leading to LV failure - best treated surgically chronic severe AR - indications for surgery (generally operate prior to onset of irreversible LV dysfunction): symptomatic patients with chronic severe AR progression of LV dilatation consider if poor LVEF (< 55%) at rest, or failure to increase EF with exercise (with serial MUGA assessment) surgical options AV replacement mechanical, bioprosthetic, homograft, or sometimes pulmonary autograft (Ross procedure) valve may be used valve repair (rare in AR) subcommissural annuloplasty for annular dilatation

MITRAL STENOSIS
Etiology congenital (rare) acquired RHD (most common) (especially developing nations; F > M): Pathophysiology and Symptomatology 2 2 normal MV area = 4-6 cm , hemodynamically significant MS with MV orifice < 2 cm MS = LV inlet obstruction > LAE > increased LA pressure > increased pulmonary vascular resistance > increased right-sided pressure > right-sided CHF symptoms (2-5 year progression from onset of serious symptoms to death, slower progression seen in the elderly) early: SOB/cough only with exertion or during high output states (fever) late: resting SOB/CP, activity limitation, orthopnea, hemoptysis complications: recurrent PE, pulmonary infections (bronchitis, pneumonia), LA thrombi (systemic emboli: brain, kidney, spleen, arm) dyspnea (exertional, increased HR > decreased diastolic filling time > increased LA pressure and pulmonary congestion) orthopnea/PND (increased venous return > increased LA pressure > pulmonary congestion) cough, hoarseness, hemoptysis palpitations (A fib secondary to LAE) LV inlet obstruction > fixed CO symptoms dyspnea fatigue low exercise tolerance atrial kick crucial - CO may decrease with A fib (loss of atrial kick), pregnancy, or tachycardia (shortened diastolic filling period) Signs of MS general examination mitral facies (mitral flush, pinched and blue facies), hepatic enlargement/pulsation, ascites, peripheral edema (all secondary to TR and RV failure) pulse +/ irregularly irregular (A fib), may be small volume
JVP

giant "a" waves (Pulmonary HTN, TS), "a" waves lost in A fib, elevated plateau (RV failure),
v waves (TR)

precordial palpation apex - inconspicuous LV (tapping apex) palpable S 1 palpable P2 (in severe MS, pulmonary HTN) left parasternal lift (RV tap) palpable diastolic thrill at apex C40 Cardiology MCCQE 2006 Review Notes

VALVULAR HEART DISEASE. CONT. ..

precordial auscultation loud S 1 (when valves are heavily calcified and not pliable > no closure of MV ( no S 1 ) loud P2 (widely split S 2 ) OS (lost if heavily calcified and not pliable), heard best in expiration at apex after P2 mid-diastolic rumble (low pitch, heard with bell) - at apex, best in LLDB position and post-exercise a longer murmur and a shorter A 2 -OS interval (both caused by 8 LAP) correlate with worse MS presystolic accentuation of diastolic murmur due to atrial kick (lost with A fib) if pulmonary HTN present - loud P2, PR (Graham Steel murmur) associated murmurs: soft systolic apical murmur (MR), Pansystolic murmur at LSB (TR) chest examination crackles (pulmonary congestion) Investigations 12 lead ECG normal sinus rhythm/A fib, LAE (P mitrale), RVH (RAD) chest x-ray LA enlargement (LA appendage, double contour, splaying of carina), pulmonary congestion (Kerley B lines), pulmonary hemosiderosis (diffuse nodularity) MV calcification, flattened left heart border echocardiography (TTE) gold standard thickened calcified valve, fusion of leaflets, LAE, PAP, associated TR Doppler can estimate valvular area cardiac catheterization/ coronary angiography concurrent CAD in patients if age > 45 yr (males), > 55 yr (females) Natural History symptoms arise > 15-20 years after initial rheumatic involvement of the valve, followed by severe incapacitation (i.e. class IV NYHA symptoms) about 3 years later complications of A fib: acute respiratory decompensation; systemic and cerebral embolization (often no evidence of residual atrial thrombus) other complications: IE, pulmonary hemorrhage, cardiac cachexia Management avoid factors that increase LA pressure (tachycardia, fever, vigorous exercise, etc.) medical treat A fib (rate control, cardioversion) anticoagulation - if A fib or previous embolus IE prophylaxis diuretics and rate control (beta-blockers) indications for surgery MV area < 1.0 cm 2 with symptoms worsening pulmonary HTN IE systemic embolization unacceptable lifestyle limitations due to symptoms surgical options (see Cardiac and Vascular Surgery Chapter) closed commisurotomy rarely performed in North America balloon valvuloplasty transthoracic echo (TTE) determines suitability for valvuloplasty (based on morphology of leaflets and subchordal apparatus) open commisurotomy best procedure if valve amenable to repair all the above "turn the clock back" - re-stenosis will develop MV replacement if immobile leaflets/heavy calcification, severe subvalvular disease, MR
NYHA class III or IV

MITRAL REGURGITATION
Etiology annulus LV dilatation (CHF, DCM, myocarditis); mitral annular calcification; IE (abscess) leaflets congenital (e.g. clefts); myxomatous degeneration (MVP, Marfans); IE; rheumatic heart disease; collagen vascular disease chordae trauma/tear; myxomatous degeneration; IE; acute MI papillary muscles and LV wall ischemia/infarction; rupture; aneurysm; HCM MCCQE 2006 Review Notes Cardiology C41

VALVULAR HEART DISEASE. CONT. ..

Pathophysiology and Symptomatology chronic MR = gradually increase flow across MV (into LA) during systole > progressive LAE > decreased fraction of SV flows forward > LV dilatation (to decrease SV and maintain CO) > increased LV wall tension > CHF "MR begets MR" - MR causes LV dilatation which in turn leads to annulus dilatation increased MR symptoms few symptoms initially (LAE generally can prevent an increase in PAP and the subsequent pulmonary edema) later: dyspnea, PND/orthopnea, fatigue and lethargy palpitations acute MR = sudden onset of MV incompetence > increased LA pressure > increased PAP > pulmonary edema > RV failure (acute onset CHF) Signs of MR pulse quick and vigorous (unless LV failure) precordial palpation apex - displaced, hyperdynamic, enlarged due to LV dilatation +/ left parasternal lift (LA expands with MR), apical thrill precordial auscultation S 1 normal, soft, or buried in murmur S 3 usually present holosystolic murmur - at apex, usually radiates to axilla, sometimes to base or back (posteriorly directed jet) MR murmur secondary to mitral valve prolapse (MVP) - usually mid-systolic papillary muscle dysfunction - typically a late systolic whoop or honk mid-diastolic rumble - increase flow across valve (often no MS) severity - gauge by LV dilatation, S 3 , diastolic flow rumble A fib, CHF, pulmonary HTN develop late acute MR > CHF, S and S 4 present; usually S 1 and S 2 normal with soft or absent murmur early in systole; 3 often a diastolic flow murmur Investigations 12 lead ECG LAE, left atrial delay (bifid P waves), possible LVH chest x-ray LVH, LAE, pulmonary venous HTN echocardiography etiology - flail leaflets, vegetations, etc. severity - regurgitant volume/fraction/orifice area LV function - increased LV/LA size; EF color flow mapping shows abnormal jet from LV to LA cardiac catheterization assess coronary arteries ventriculography - contrast fills LA to assess flow and chamber contours prominent left atrial "v" wave on Swan-Ganz Management medical asymptomatic - serial echocardiograms to monitor progress IE prophylaxis symptomatic - decreased preload (diuresis) and decreased afterload (ACEI) for severe LV dysfunction and MR in poor surgical candidate surgical acute MR - generally best managed surgically chronic MR - indications for surgery persistent symptoms (NYHA class II) despite optimal medical therapy onset of LV dysfunction or increased LV volume or size, even if asymptomatic surgical options (see Cardiac and Vascular Surgery Chapter) valve repair for MR secondary to myxomatous degeneration preferred (low mortality), often technically difficult MV replacement if unable to repair MV attempt to conserve chordal structures/connections, correction of MR achieved

MITRAL VALVE PROLAPSE (MVP)

Etiology myxomatous degeneration of chordae and leaflets which are thickened, voluminous and redundant (too big for the orifice) leaflets displaced into LA during systole 3-5% of population (F > M) alone, or with connective tissue diseases (e.g. Marfans) may be associated with pectus excavatum, straight back syndrome, and other MSK abnormalities C42 Cardiology MCCQE 2006 Review Notes

VALVULAR HEART DISEASE. CONT. ..

Symptoms click-murmur syndrome atypical chest pain (prolonged, non-exertional, stabbing) dyspnea, hyperventilation, anxiety, panic, palpitations, presyncope, fatigue - no causal relations or mechanisms found +/ symptoms of MR Signs of MVP Clinical diagnosis based on presence of mid-systolic click +/ murmur mid-systolic click (tensing of redundant valve tissue, billowing of posterior leaflet in mid-systole) mid to late systolic murmur(regurgitation after prolapse of MV leaflets) maneuvers to change LV volume (exaggerate the disproportion of the valve with respect to the annulus) squat to stand, or Valsalva > decreased venous return, decreased ventricular filling > earlier click and louder and longer murmur Investigations 12 lead ECG nonspecific ST-T wave changes, PSVT, ventricular ectopy ECHO posterior systolic prolapse of MV leaflets into LA assess severity of MR Natural History excellent prognosis (usually benign) risk of complications is most dependent on degree of MR progressive MR; severe MR (beware of ruptured chordae); IE; arrhythmias; thromboembolism; sudden death Management asymptomatic without MR - excellent prognosis (vast majority) follow-up q 3-5 years blockers - for palpitations, pain, anxiety anticoagulation - if systemic embolism for MR - IE prophylaxis, standard indications for MV repair/replacement

TRICUSPID VALVE DISEASE

Etiology TS: rheumatic, congenital, carcinoid syndrome, fibroelastosis TR: RV dilatation (commonest cause), IE (iv drug users), rheumatic, Ebstein anomaly, AV cushion defects, carcinoid, tricuspid prolapse, trauma Symptoms right heart failure fatigue pedal edema, abdominal pain (liver congestion), ascites dyspnea (may reflect right heart forward failure) Signs carotid pulse: irregular if A fib and low volume
JVP

increased JVP prominent "a" waves in TS large v waves in TR ("cv" waves) positive HJR and Kussmaul's sign (rise in JVP with inspiration) precordial palpation for left parasternal lift (RV) in TR precordial auscultation note: all right sided sounds are louder with inspiration, except a pulmonary ejection click TS: diastolic rumble in 4th left intercostal space (LICS) TR: holosystolic murmur along LLSB (Carvallo's murmur); may behave like an ejection murmur RV S3 along LLSB (with inspiration) abdominal examination hepatomegaly (congestion) with systolic pulsations from TR edema, ascites: 2 to fluid retention Investigations 12 lead ECG TS: RAE

chest x-ray TS: dilatation of RA without pulmonary artery enlargement TR: RA + RV enlargement ECHO diagnostic MCCQE 2006 Review Notes Cardiology C43

TR: RAE, RVH, A fib

VALVULAR HEART DISEASE. CONT. ..

Management supportive diuretics, preload reduction TV surgery usually determined by need for other interventions (e.g. MVR of r associated MS)

PULMONARY VALVE DISEASE

much less commonly involved Etiology pulmonary stenosis (PS): usually congenital; rheumatic uncommon; carcinoid pumonary regurgitation (PR): secondary to dilatation of valve ring pulmonary HTN (MS - most common, COPD, recurrent PE) rheumatic, IE Symptoms chest pain, syncope, dyspnea, leg edema (RV failure and CHF) Signs PS PR systolic murmur - maximum at 2nd LICS pulmonary ejection click; normal/loud/soft P2; right sided S

early diastolic murmur at base Graham Steel (diastolic) murmur at 2nd and 3rd LICS increasing with inspiration; no peripheral stigmata of AR

Investigations 12 lead ECG RVH chest x-ray prominent pulmonary arteries if pulmonary HTN enlarged RV ECHO diagnostic - RVH, RV dilatation; PS or PR by Doppler Management IE prophylaxis PR rarely requires treatment (well tolerated if systemic vascular resistance is normal) valve replacement may be required PS balloon valvuloplasty, depending on severity

PROSTHETIC VALVES

bioprosthetic valves porcine heterograft, bovine pericardial, human homograft low incidence of thromboembolism, anticoagulation often not required (use ASA only), ideal for those with contraindications to anticoagulation (pregnancy) degeneration of valve after 10 years on average higher failure rate in the mitral position contraindicated in children due to rapid calcification mechanical valves better predictability of performance and durability used preferentially if risk of reoperation is high always requires anticoagulation to prevent thromboembolism contraindications: bleeding tendency (e.g. peptic ulcer disease (PUD)), pregnancy (Coumadin is teratogenic) target INR = 2.5-3.5 post-op complications valve failure valve thrombosis (< 1%/year) valve degeneration IE (often < 1 year after surgery, Staph. epidermidis) bleeding problems due to anticoagulation (major: 1%/year) thromboembolism (2-5% per patient-year despite adequate anticoagulation) conduction abnormalities

C44 Cardiology

MCCQE 2006 Review Notes

PERICARDIAL DISEASE
ACUTE PERICARDITIS
Etiology idiopathic is most common: usually presumed to be viral infectious viral: Coxsackie virus A, B (most common) bacterial: Staph, Strep, septicemia TB fungal: histoplasmosis, blastomycosis protozoal post-MI: acute (direct extension of myocardial inflammation, 1-7 days), Dressler's syndrome (autoimmune, 2-8 weeks) post-pericardiotomy (e.g. CABG), other trauma metabolic: uremia (common), hypothyroidism neoplasm: Hodgkins, breast, lung, renal cell carcinoma, melanoma collagen vascular disease: SLE, periarteritis, RA, scleroderma vascular: dissecting aneurysm infiltrative disease (sarcoid), drugs (e.g. hydralazine), radiation Presentation diagnostic triad: chest pain, friction rub, and ECG changes chest pain - alleviated by sitting up and leaning forward, pleuritic, worse with deep breathing and supine position pericardial friction rub - may be uni-, bi- or triphasic +/ fever, malaise Investigations 12 lead ECG initially elevated ST in anterior, lateral and inferior leads +/ depressed PR segment, the elevation in the the ST segment is concave upwards > 2-5 days later ST isoelectric with T wave flattening and inversion chest x-ray normal heart size, pulmonary infiltrates echocardiography assess pericardial effusion Management treat the underlying disease anti-inflammatory agents (NSAIDs, steroids if severe or recurrent); analgesics Complications recurrences, atrial arrhythmias, pericardial effusions, tamponade, residual constrictive pericarditis

PERICARDIAL EFFUSION
Etiology two types of effusions: transudative (serous) CHF, hypoalbuminemia/hypoproteinemia, hypothyroidism exudative (serosanguinous or bloody) causes similar to the causes of acute pericarditis may develop acute effusion secondary to hemopericardium (trauma, post MI myocardial rupture, aortic dessection) physiological consequences depend on type and volume of effusion, rate of effusion development, and underlying cardiac disease Symptoms none or similar to acute pericarditis dyspnea, cough extra-cardiac (esophageal/recurrent laryngeal nerve/tracheo-bronchial/phrenic nerve irritation) Signs JVP: increased with dominant "x" descent arterial pulse: normal to decreased volume, decreased PP auscultation: distant heart sounds +/ rub Investigations 12 lead ECG low voltage, flat T waves chest x-ray cardiomegaly, rounded cardiac contour (water bottle) ECHO (procedure of choice) fluid in pericardial sac pericardiocentesis establishes diagnosis Management mild: frequent observation with serial ECHO, treat the cause, anti-inflammatory agents for inflammation severe: may develop cardiac tamponade MCCQE 2006 Review Notes Cardiology C45

PERICARDIAL DISEASE. . . CONT.

CARDIAC TAMPONADE
major complication of pericardial effusion cardiac tamponade is a clinical diagnosis

Pathophysiology and Symptomatology high intra-pericardial pressure > decreased venous return > decreased diastolic ventricular filling > decreased CO > hypotension + venous congestion symptoms tachypnea, dyspnea, shock Signs x descent only, absent y descent hepatic congestion Clinical Pearl Classic quartet: hypotension, increased JVP, tachycardia, pulsus paradoxus. Becks triad: hypotension, increased JVP, muffled heart sounds. Investigations 12 lead ECG electrical alternans (pathognomonic variation in R wave amplitude), low voltage ECHO pericardial effusion, compression of cardiac chambers (RA and RV) in diastolic cardiac catheterization mean RA, LA, LV and RV diastolic pressures all high and equal Management pericardiocentesis ECHO-, ECG-guided pericardiotomy avoid diuretics and vasodilators (these decrease venous return to already under-filled RV > decrease LV preload > decrease CO) fluid administration may temporarily increase CO treat underlying cause

CONSTRICTIVE PERICARDITIS
Definition chronic pericarditis resulting in fibrosed, thickened, adherent, and/or calcified pericardium Etiology any cause of acute pericarditis may result in chronic pericarditis major causes are tuberculous, radiation-induced, post-cardiotomy, idiopathic Symptoms dyspnea, fatigue, palpitations abdominal pain Signs general examination - mimics CHF (especially right-sided HF) ascites, hepatosplenomegaly, edema increased JVP, Kussmaul's sign (paradoxical increase in JVP with inspiration), Friedrich's sign (prominent y descent > x descent) pressures: BP normal to decreased, +/ pulsus paradoxus precordial examination: +/ pericardial knock (early diastolic sound) Investigations 12 lead ECG low voltage, flat T wave, +/ A fib chest x-ray pericardial calcification, effusions
CT/MRI/TEE

pericardial thickening cardiac catheterization equalization of RV and LV diastolic pressures, RVEDP > 1/3 of RV systolic pressure Management medical: diuretics, salt restriction surgical: pericardiectomy Table 11. Differentiation of Constrictive Pericarditis vs. Cardiac Tamponade
Characteristic JV Kussmauls sign P Pulsus paradoxus Pericardial knock Hypotension Constrictive Pericarditis y > x Present 1/3 of cases Present Mild-moderate Tamponade x > y Absent (JVP too high to see change) Always Absent Severe

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MCCQE 2006 Review Notes

SYNCOPE
Definition sudden, transient disruption of consciousness and loss of postural tone with spontaneous recovery usually caused by generalized cerebral hypoperfusion Etiology cause of 50% of cases of syncope is unknown cardiac electrical tachycardia: VT, Torsades de pointes, SVT, rapid A fib bradycardia: sick sinus syndrome, 2 or 3 (Stokes-Adams attack) AV block pacemaker failure mechanical outflow obstruction: left-sided (AS, HOCM, MS, LA myxoma), right-sided (PS, PE, pulmonary HTN) myocardial: CAD/MI, LV dysfunction other: tamponade extra-cardiac neurally mediated vasomotor vasovagal - the "common faint " (50%) situational/visceral: micturition/defecation syncope, cough syncope, Valsalva, ocular pressure, etc. carotid sinus syncope psychiatric: somatization, panic, anxiety other: exercise, high altitude, drug-induced orthostatic hypotension: drug-induced (e.g. antihypertensives), venous pooling (postural, pregnancy), autonomic neuropathy (primary: Shy-Drager, secondary: DM), hypovolemia (blood loss, diuresis), pheochromocytoma neurological: vertebrobasilar TIA/stroke, subarachnoid hemorrhage, cervical spondylosis, seizure, subclavian steal metabolic: hypoxia, hypoglycemia, hypocapnia Clinical Manifestations history and physical examination are critical - reflect underlying pathology in 40-50% (attention to cardiac and neurological exams) (see Neurology Chapter) Table 12. Differentiation of Seizure vs. Syncope
Characteristic Facial colour (lateral) tongue biting Aura Nausea, diaphoresis Level of concsciousness (LOC) Reoriention Todds paralysis Setting Attacks Age CK Positive EEG Syncope Pale Rare No Common before Brief Within seconds No Rare when recumbent Infrequent Variable Normal No Seizure Cyanotic Common Sometimes Uncommon May be longer Within minutes Sometimes Anytime Repeated Younger (< 45) Increased Sometimes

Investigations directed by results of history and physical examination +2 blood work: CBC, electrolytes, MgV, Ca , BUN, creatinine, glucose, ABG, CK-MB ECG ECHO carotid Doppler Holter monitor, loop Holter tilt-table testing electrophysiological study (EPS)

MCCQE 2006 Review Notes

Cardiology C47

SYNCOPE . . . CONT.
Management treatment of underlying cause
SYNCOPE

Normal history and physical exam

History suggests cardiac

disease; or physical exam abnormal

Physical exam reveals orthostatic hypotension

Consider culprit medications or dehydration

Neurocardiogenic syncope (ie. vasovagal)

Cardiogenic syncope

Normal neurologic exam

Abnormal neurologic exam

Do tilt testing if recurrent

24 h monitoring

Consider post-ganglionic automic insufficiency

Consider peripheral neuropathy, DM, Shy-Drager Syndrome

Figure 15. Approach to the Patient with Syncope

EVIDENCE-BASED CARDIOLOGY
CONGESTIVE HEART FAILURE
(NEJM 1991; 325:303)

VeHEFT-I: Hydralazine/Isorbide Dinitrate decreases mortality in patients with CHF. (NEJM 1986; 314:1547) VeHEFT-II: Enalapril decreases mortality compared to Hydralazine/Isorbide Dintrate in patients with CHF. CONSENSUS: Enalapril decreases mortality compared to placebo in severe CHF. (NEJM 1987; 316:1429) DIG TRIAL: Digoxin decreased rate of hospitalization, improves symptoms and exercise capacity, but has no mortality benefit compared to placebo. (NEJM 1997; 336:525) PRAISE: Amlodipine has no mortality benefit over placebo in CHF, except decreases mortality in patients with non-ischemic dilated CM (NEJM 1996; 335:1107) US-CARVEDILOL STUDY: Carvedilol is superior to placebo for morbidity and mortality in class II and
III heart failure (NEJM 1996;334:1349)

MERIT: Metoprolol is superior to placebo for morbidity and mortality in class II and III heart failure (Lancet 1999; 353:2001) RALES: Aldosterone antagonism with Spironolactone in addition to standard treatment decreases mortality in
patients with FC III-IV heart failure (NEJM 1999;341: 709)

ISCHEMIC HEART DISEASE

non-Q wave MI. (NEJM 1997; 337:447)

GUSTO I: There is increased survival after acute MI in patients treated with rt-Pa and IV Heparin compared to Streptokinase (NEJM 1993; 329:673) ESSENCE: Enoxaparin decreases mortality vs. unfractionated heparin in patients with unstable angina or PURSUIT: Integrelin (IIb/IIIa inhibitor) decreased mortality when given to patients with high risk unstable angina (e.g. resting chest pain for >15 mins within last 24hrs + increases TnI/ECG changes) or non-Q wave MI, and benefit increases if patients go for PTCA or CABG (Circulation 1996; 94:2083) BARI: subset analysis - CABG as an initial strategy has survival benefit over PTCA in diabetic patients with multivessel disease (NEJM 1996;335:217)
HOPE: Ramipril decreases rate of death, MI, and CVA in patients with CAD, Hx of CVD, PVD, or DM +1 other

cardiac risk factor, all who are not known to have any LV dysfunction. (NEJM 2000; 342:145)

ATRIAL FIBRILLAITON

5 RCTs (SPAF-I, AFASAK, SPINAF, CAFA, BAATAF) level demonstrated 67% decrease in thromboembolic rate

in patients treated with coudamin in setting of nonrheumatic AF)

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Table 13. Commonly Used Cardiac

EXAMPL 1 1 , , 1 1 2 and anti sotalol (1, 2, class III anti, ,
1 2

DRUG

MECHANSIM ACTIO

INDIC TION

SIDE

CONTRA-

TION

atenolol )
1

MCCQE 2006 Review Notes

( , Lowers demand HR 2 BP and A stable class II to III nightmares, memory loss, hallucination depression of responses to hypoglycemia in +/ adverse effects on lipid exacerbation of phenomenon and diltiaze see able anorexia, 2nd line agent for IHD (1st 2nd line agent for IHD (1st diastolic sick sinus second or third degree V severe AMI with sick sinus second or third degree V severe AMI pregnancy A Fib with bypass tract anterograde verapam see able nifedipin see able captopr enalapr ramip peripheral vasodilator CHF (including postafterload reduction with little in CO, HR or post-MI also in fluid anterior due to inhibition of aldosterone productio dry cough (5-15% of renal angioedema reversible membranous dizziness (< renal losartan blocks angiotensin II receptor peripherally vasodilates and aldosterone bilateral renal artery

severe bradycardia, high-degree heart caution in asthmatics (contraindicated severe caution in patients with peripheral phenomenon and caution in

CALCIUM BLOCKE (CC

NOTE evidence that short acting nifedipine associated with increased mortality severe poorV unstable angina or threatened MI in absence bilateral renal artery pregnancy documented angioedema 2 to

COMMONLY USED CARDIAC MEDICATIONS

ACE

Cardiology C49

ANGIOTENSI BLOCK

DRUG Furosemid loop acute pulmonary interferes with creation severe hypertonic medullary refractory diuretic effect within 1 hour hypercalcemia (use oral administration, within 30 with saline after IV symptomaltic relief of CHF in dinitrate form (always with hydralazine in postural tolerance develops rapidly continuous use; maintain at least nitrate-free hours per Absolute high degree V active peptic hypochloremic metabolic severe severe hypersensitivity to furosemide or

EXAMPL

MECHANSIM ACTIO

INDIC TION

SIDE

CONTRA-

TION

C50 Cardiology
sublingual/ patch/ produce venous, arteriolar nitroglyceri coronary isosorbide Digox

DIURET

NITRTE

ANI-

COMMONLY USED CARDIAC MEDICATIONS . . . CONT.

TPase inhibitor intracellular Na resulting in 2 of Na+ for 2+ C results in inotropic and cell positive inotrope-increases contractio blocksV (decreased refractory and conduction time) depresses SA

cardiac V blocks (e.g. enkebac atrial tachycardia with tachycardias (eg atrioventricul dissociation, junctional bradyarrhythmias (e.g. bradycardia, sinus sinoatrial regularization of R-R interval in A anorexia, blurred or yellow nausea,vomiting, dyspepsia, peptic tinnitus, vertigo, hearing leukopenia, purpura,

Relativ arrhythmogenic states hypokalemia, acute MI, myocarditis, frequent PVCs, with anterograde conduction bypass tract, acute chronic cor pulmonale , dysfunction in the absense of systolic dysfunction risk of complete V block/ sick sinus incomplete V active peptic

ANTI- TELE

AS

cyclooxygenase interferes platelet by production thromboxane

acute Post Post Post TIA/

MCCQE 2006 Review Notes

impaired renal perfusion leading fluid dermatological or hypersensitivity

COMMONLY USED CARDIAC MEDICATIONS . . . CONT.

Table 14. Beta-Blocker Actions
Clinical Effects -Activity -Activity ISA Bronchoconstriction Orthostatic Hypotension Lipid Adverse Effects CNS Adverse Effects Propranolol non-selective N N +++ ++ +++ Atenolol 1 N N + ++ + Acebutolol 1 N +++ + ++ Labetalol non-selective 1 + ++ +++ + ++

CALCIUM CHANNEL BLOCKERS (CCB)

major subtypes are represented by diltiazem (benzothaizepine), verapamil (phenylalkylamine) and nifedipine (dihydropyridine) diltiazem and verapamil are strong cardiodepressants, whereas the dihydropyridines are strong vasodilators

Table 15. Calcium Channel Blocker Actions

Clinical Effects Coronary Vasodilator Peripheral Vasodilator Contractility Sinus Rate AV Conduction Diltiazem ++ + <> 9 9 Verapamil ++ ++ 9 9 9 Nifedipine +++ +++ <> 8 <>

ANTI-ARRHYTHMIC DRUGS
1
++ slow Ca influx

MEMBRANE

0 Na+ influx threshold 4 Na+ influx TIME

3 K+ efflux

Figure 16. Representative Action Potential

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Cardiology C51

COMMONLY USED CARDIAC MEDICATIONS . . . CONT.

Table 16. Antiarrhythmic drugs (Vaughn-Williams Classification)
Class Agent Ia Quinidine Procainamide Disopyramide Indications SVT, VT Side Effects Torsades de Pointes (all Ia) diarrhea lupus-like syndrome anti-cholinergic effects confusion, stupor, seizures GI upset, tremor Mechanism of Action moderate Na + channel blockade slows phase O upstroke prolongs repolarization and thus slows conduction mild Na + channel blockade shortens phase 3 repolarization marked Na + channel blockade markedly slows phase 0 upstroke blockers decreases phase 4 depolarization blocks K channel prolongs phase 3 repolarization and so prolongs the effective refractory period

Ib

Lidocaine Mexiletine

VT

Ic

Propafenone Flecainide Encainide Propranolol Metoprolol etc. Amiodarone*

1 SVT, VT A Fib2

exacerbation of VT (all Ic) negative inotropy (all Ic) bradycardia and heart block (all Ic) bronchospasm, negative inotrophy, bradycardia, AV block, impotence, fatigue photosensitivity, pulmonary toxicity, hepatotoxicity, hyper/hypothyroidism beta-blocker effects, Torsades de Pointes, hypotension bradycardia, AV block hypotension

II

1 SVT, A Fib

III

SVT, VT A Fib

Sotalol Bretylium (IV) I V Verapamil Diltiazem

SVT, VT , A Fib VT SVT A Fib

CCB slow phase 4 spontaneous depolarization and so slows conduction in areas such as AV node

Amiodcrone hcs class I, II, III, IV, properties

All anti-arrhythmics have potential to be pro-arrhythmic In the landmark CAST trial, two class Ic agents (encainide, flecainide) prevented VPBs post MI but significantly increased mortality

REFERENCES
Ischemic Heart Disease Lindahl, B., et al. Markers of Myocardial Damage and Inflammation in Relation to Long-Term Mortality in Unstable Coronary Artery Disease. New England Journal of Medicine. 2000; 343:1139-1147. Rauch, U., et al. Thrombus Formation on the Atherosclerotic Plaques: Pathogenesis and Clinical Consequences. Annals of Internal Medicine. 2001; 134: 224-238. The Arterial Revascularization Therapies Study Group. Comparison of Coronary-Artery Bypass Surgery and Stenting for the Treatment of Multivessel Disease. New England Journal of Medicine. 2001; 344:1117-1124.
Turpie, A. G. G. and Antman, E. M. Low-Molecular-Weight Heparins in the Treatment of Acute Coronary Syndromes. Archives of

Internal Medicine. 2001; 161: 1484-1490.

Yeghiazarians, Y., Braunstein, J. B., Askari, A., and Stone, P. H. Review Article: Unstable Angina Pectoris. New England Journal of

Medicine. 2000; 342:101-114.

Nuclear Cardiology Lee TH and Boucher CA. Noninvasive tests in patients with stable coronary artery disease (Review). N Engl J Med 2000; 344:1840-5. Cardiomyopathies Feldman AM and McNamara D. Myocarditis (Review). N Engl J Med 2000; 343:1388-98.

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