Cardiology Procedures 2017 - Hendel

Cardiology Procedures
ERRNVPHGLFRVRUJ
Robert C. Hendel • Carey Kimmelstiel
Editors
Cardiology Procedures
A Clinical Primer
ERRNVPHGLFRVRUJ
Editors
Robert C. Hendel, MD Carey Kimmelstiel, MD
Cardiovascular Division Division of Cardiology
Professor of Medicine and Radiology Tufts Medical Center
University of Miami Miller School of Associate Professor of Medicine
Medicine Tufts University School of Medicine
Miami, FL Boston, MA
USA USA
ISBN 978-1-4471-7288-8 ISBN 978-1-4471-7290-1 (eBook)

DOI 10.1007/978-1-4471-7290-1
Library of Congress Control Number: 2016955806
© Springer-Verlag London 2017

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For our trainees – past, present, and future....
Through training and life-long learning, we
impact on those who entrust their care to us
…. And for our colleagues who make our
cloudy days sunny.
R. Hendel and C. Kimmelstiel
To my mentors and family who have guided my
professional career and attempted to instill not only
knowledge but wisdom, and with special gratitude
to my father, Stanley Hendel, whose century
of experience continues to inspire all of those
around him
R. Hendel
To Laurie, Dana and Matt who have always been there
to support me in good and difficult times and to my
parents who every day asked me: “What did you learn
in school today?”
C. Kimmelstiel
Foreword
The last 50 years have witnessed remarkable growth in our understanding of cardio-
vascular disease. Furthermore, the ability of physicians to diagnose and treat patients
with cardiovascular disorders has expanded in step with the enlarging knowledge con-
cerning the pathophysiology of heart and vascular diseases. Effective therapy for
patients with these disorders can only occur when an accurate diagnosis has been
made. For example, starting in the early 1950s, invasive cardiac diagnostic ability and
effective cardiac surgical intervention advanced together. The latter half of the twen-
tieth century and the early years of the twenty-first century have seen explosive growth
in our ability to perform accurate and economically appropriate invasive and noninva-
sive diagnostic evaluations followed by appropriate therapeutic interventions.
In this regard, Drs. Hendel and Kimmelstiel have assembled in this text an
impressive array of experts who have clearly and concisely reviewed the essential
features of the totality of cardiologic diagnostic and therapeutic procedures. Each
chapter concisely describes the indications for the various procedures followed by
explicit instructions for preparing patients for the test or intervention described.
Subsequent material then succinctly describes the most effective and safe method
for carrying out the specific test or intervention. Didactic material is elegantly sup-
plemented by informative case presentations.
This text will be of great value to cardiology trainees and experienced cardiolo-
gists who desire a concise and well-illustrated source of information covering car-
diac diagnostic and therapeutic procedures. Drs. Hendel and Kimmelstiel are to be
congratulated on assembling an outstanding group of experts in the field and for
bringing so much useful information together in such a visually and didactically
outstanding fashion. I am particularly happy with this outstanding text since I helped
train both of the editors during my time at the University of Massachusetts Medical
School in Worcester, Massachusetts.
Joseph S. Alpert, MD
Professor of Medicine
University of Arizona College of Medicine
Tucson, Arizona
Editor-in-Chief, The American Journal of Medicine
vii
Contents
Part I Noninvasive Cardiology
1 Transthoracic Echocardiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
Eddy Karnabi
2 Transesophageal Echocardiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17
Eddy Karnabi
3 Contrast Echocardiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27
Cesia Gallegos, Eddy Karnabi, and Robert C. Hendel
4 Exercise Stress Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35
Eddy Karnabi
5 Cardiopulmonary Exercise Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45
Alexis P. Rodriguez
6 Pharmacologic Stress Testing. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53
Eddy Karnabi and Robert C. Hendel
7 Stress Echocardiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63
8 Single Photon Emission Computed Tomography. . . . . . . . . . . . . . . . . . 71
Eddy Karnabi
9 Positron Emission Tomography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81
Eddy Karnabi
10 Radionuclide Angiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91
Cesia Gallegos
11 Cardiac Computed Tomography (CT) . . . . . . . . . . . . . . . . . . . . . . . . . . 97
Arieh Fox
ix
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x Contents
12 Cardiac Magnetic Resonance. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105

Cesia Gallegos
Part II Critical Care
13 Central Venous Cannulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115

Saleh Alshalash and Carey Kimmelstiel
14 Right Heart Catheterization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 123
Christopher Madias and Carey Kimmelstiel
15 Pericardiocentesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133
16 Procedural Sedation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141
Grace M. Wu
17 Endotracheal Intubation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147
Aaron E. Brice
Part III Electrophysiology
18 The Electrocardiogram. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 157

Alexis P. Rodriguez
19 Ambulatory Electrocardiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163
Douglas W. Laidlaw and N.A. Mark Estes III
20 Tilt Table Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 173
Alexis P. Rodriguez
21 Electrophysiologic Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 179
Jonathan Weinstock and Christopher Clyne
22 Temporary Transvenous Pacing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 187
Alawi A. Alsheikh-Ali and Mark S. Link
23 Cardiac Pacemakers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 195
Constancia F.C. Macatangay
24 Biventricular Pacing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 205
Chris Healy and Juan F. Viles-Gonzalez
25 Implantable Cardioverter Defibrillators (ICD) . . . . . . . . . . . . . . . . . . 211
Camilo A. Gomez
26 Pacemaker Interrogation and Programming . . . . . . . . . . . . . . . . . . . . 219
D. Michael Farmer and Munther Homoud
27 Cardioversion and Defibrillation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 229
Aaron E. Brice
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Contents xi
Part IV Interventional Cardiology
28 Coronary Angiography. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237

Nima Aghili, Edouard Daher, and Carey Kimmelstiel
29 Coronary Blood Flow Measurements . . . . . . . . . . . . . . . . . . . . . . . . . . 249
Morton J. Kern
30 Percutaneous Coronary Intervention . . . . . . . . . . . . . . . . . . . . . . . . . . 263
Yousef Bader, Manny C. Katsetos, and Carey Kimmelstiel
31 Alcohol Septal Ablation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 275
Carey Kimmelstiel
32 Transcatheter Closure of Atrial Septal Defects
and Patent Foramen Ovale. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 283
Francisco Garay, Qi-Ling Cao, and Ziyad M. Hijazi
33 Balloon Valvuloplasty . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 295
Ted Feldman
34 Transcatheter Aortic Valve Replacement . . . . . . . . . . . . . . . . . . . . . . . 307
Jason B. Coker, James N. Hadstate, Andrew R. Weintraub,
and Daniel H. Steinberg
35 Endomyocardial Biopsy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 317
Johny Kuttab and Carey Kimmelstiel
36 Circulatory Support Devices . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 325
Navin K. Kapur and Michele Esposito
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 337
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Part I
Noninvasive Cardiology
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Chapter 1
Transthoracic Echocardiography
Eddy Karnabi
Echocardiography has become the most widely used imaging procedure in patients
with cardiovascular disease. The basis of echocardiography relies on the transmis-
sion and reflection of ultrasound waves from a transducer and interaction with dif-
ferent tissue interfaces to generate a digital image. The images obtained include
M-Mode, 2D, 3D and Doppler (CW: continuous wave, PW: pulse wave, color and
tissue Doppler) to define both normal and abnormal structures and pathologies. The
uses include evaluation of the structures of the cardiac chamber walls, the systolic
and diastolic performances of the ventricles, the structure and function of the native
or prosthetic cardiac valves, evidence of pericardial effusion and constriction, the
appearance of the proximal great vessels and inferior vena cava, and the presence of
abnormal intracardiac shunting.
Indications
The American College of Cardiology (ACC) and American Heart Association (AHA)
published guidelines for the clinical application of echocardiography in 1997 (with an
update in 2003) for various cardiovascular conditions [1]. In 2011, the ACCF/ASE/
AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR Appropriate Use Criteria for
Echocardiography were published with the level of appropriateness to guide physicians
[2]. These of indications are extensive and generally includes usefulness in the acute
setting and in patients with cardiac signs and symptoms, patients with valvular heart
disease, hypertension, heart failure and cardiomyopathies, cardiac masses and pericar-
dial diseases, suspected cardiovascular sources of emboli, and aortic diseases (Table 1.1).
E. Karnabi, MD, PhD, FASE

Cardiology Division, Northeast Cardiology Associates (NECA), Eastern Maine Medical
Center (EMMC), One Northeast Drive, Bangor, ME 04401, USA
e-mail: [email protected]
© Springer-Verlag London 2017 3

R.C. Hendel, C. Kimmelstiel (eds.), Cardiology Procedures,
DOI 10.1007/978-1-4471-7290-1_1
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4 E. Karnabi
Table 1.1 Appropriate indications for transthoracic echocardiography

1. Symptoms or conditions potentially related to suspected cardiac etiology including but not
limited to chest pain, shortness of breath, palpitations, TIA, stroke, or peripheral embolic
event
2. Prior testing that is concerning for heart disease or structural abnormality including but
not limited to chest X-ray, baseline scout images for stress echocardiogram, ECG, or
cardiac biomarkers
3. Frequent VPCs or exercise-induced VPCs, Sustained or non-sustained atrial fibrillation,
SVT, or VT
4. Clinical symptoms or signs consistent with a cardiac diagnosis known to cause
lightheadedness/presyncope/syncope (including but not limited to aortic stenosis,
hypertrophic cardiomyopathy, or HF), Syncope when there are no other symptoms or
signs of cardiovascular disease
5. Evaluation of suspected pulmonary hypertension including evaluation of right ventricular
function and estimated pulmonary artery pressure, Routine surveillance (>1 year) of
known pulmonary hypertension without change in clinical status or cardiac exam,
Re-evaluation of known pulmonary hypertension if change in clinical status or cardiac
exam or to guide therapy
6. Hypotension or hemodynamic instability of uncertain or suspected cardiac etiology
7. Acute chest pain with suspected MI and non-diagnostic ECG when a resting
echocardiogram can be performed during pain, Evaluation of a patient without chest pain
but with other features of an ischemic equivalent or laboratory markers indicative of
ongoing MI
8. Suspected complication of myocardial ischemia/infarction, including but not limited to
acute mitral regurgitation, ventricular septal defect, free-wall rupture/tamponade, shock,
right ventricular involvement, HF, or thrombus
9. Initial evaluation of ventricular function following ACS, Re-evaluation of ventricular
function following ACS during recovery phase when results will guide therapy
10. Respiratory failure or hypoxemia of uncertain etiology
11. Known acute pulmonary embolism to guide therapy (e.g., thrombectomy and
thrombolytics), Re-evaluation of known pulmonary embolism after thrombolysis or
thrombectomy for assessment of change in right ventricular function and/or pulmonary
artery pressure
12. Severe deceleration injury or chest trauma when valve injury, pericardial effusion, or
cardiac injuries are possible or suspected
13. Re-evaluation of known valvular heart disease with a change in clinical status or cardiac
exam or to guide therapy
14. Routine surveillance (>3 years) of mild valvular stenosis without a change in clinical
status or cardiac exam, Routine surveillance (>1 year) of moderate or severe valvular
stenosis without a change in clinical status or cardiac exam
15. Routine surveillance (>1 year) of moderate or severe valvular regurgitation without a
change in clinical status or cardiac exam
16. Initial postoperative evaluation of prosthetic valve for establishment of baseline, Routine
surveillance (>3 years after valve implantation) of prosthetic valve if no known or
suspected valve dysfunction, Evaluation of prosthetic valve with suspected dysfunction or
a change in clinical status or cardiac Exam, Re-evaluation of known prosthetic valve
dysfunction when it would change management or guide therapy
(continued)
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1 Transthoracic Echocardiography 5
Table 1.1 (continued)

17. Initial evaluation of suspected infective endocarditis with positive blood cultures or a new
murmur, Re-evaluation of infective endocarditis at high risk for progression or
complication or with a change in clinical status or cardiac exam
18. Suspected cardiac mass
19. Suspected cardiovascular source of embolus
20. Suspected pericardial conditions, re-evaluation of known pericardial effusion to guide
management or therapy
21. Guidance of percutaneous noncoronary cardiac procedures including but not limited to
pericardiocentesis, septal ablation, or right ventricular biopsy
22. Evaluation of the ascending aorta in the setting of a known or suspected connective tissue
disease or genetic condition that predisposes to aortic aneurysm or dissection (e.g., Marfan
syndrome), Re-evaluation of known ascending aortic dilation or history of aortic
dissection to establish a baseline rate of expansion or when the rate of expansion is
excessive, Re-evaluation of known ascending aortic dilation or history of aortic dissection
with a change in clinical status or cardiac exam or when findings may alter management
or therapy
23. Initial evaluation of suspected hypertensive heart disease
24. Initial evaluation of known or suspected HF (systolic or diastolic) based on symptoms,
signs, or abnormal test results, Re-evaluation of known HF (systolic or diastolic) with a
change in clinical status or cardiac exam without a clear precipitating change in
medication or diet, Re-evaluation of known HF (systolic or diastolic) to guide therapy
25. Initial evaluation or re-evaluation after revascularization and/or optimal medical therapy to
determine candidacy for device therapy and/or to determine optimal choice of device
26. Known implanted pacing device with symptoms possibly due to device complication or
suboptimal pacing device settings
27. To determine candidacy for ventricular assist device, Optimization of ventricular assist
device settings, Re-evaluation for signs/symptoms suggestive of ventricular assist
device-related complications
28. Monitoring for rejection in a cardiac transplant recipient
29. Cardiac structure and function evaluation in a potential heart donor
30. Re-evaluation of known cardiomyopathy with a change in clinical status or cardiac exam
or to guide therapy
31. Screening evaluation for structure and function in first-degree relatives of a patient with an
inherited cardiomyopathy
32. Baseline and serial re-evaluations in a patient undergoing therapy with cardiotoxic agents
33. Initial evaluation of known or suspected adult congenital heart disease, Known adult
congenital heart disease with a change in clinical status or cardiac exam, Re-evaluation to
guide therapy in known adult congenital heart disease
Contraindications
Transthoracic echocardiography has no contraindications, as the use of ultrasound

has no adverse effects when used for cardiac imaging. However, ultrasound waves
have the potential to cause thermal bioeffects depending on the intensity and length
of exposure that are determined by the frequency, focus, power output, depth, perfu-
sion, tissue density; these bioeffects are considered minimal.
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6 E. Karnabi
Contrast agents, when used, include the following contraindications:

1. Clinical instability with hypotension in such cases as acute myocardial infarc-
tion, worsening or clinically unstable heart failure, life threatening ventricular
arrhythmias, respiratory failure, severe emphysema, pulmonary embolism;
2. Right-left, bidirectional, or transient right-to-left cardiac shunts;
3. Hypersensitivity to contrast agents.
For additional details about contrast agents, please see Chap. 3 (Contrast
echocardiography)
Equipment
The necessary equipment for performing an echocardiographic exam includes the

portable echocardiography unit, a suitable ultrasound transducer (typically
2–4 Mhz) and an experienced sonographer or physician. The ultrasound transducer
uses a piezoelectric crystal (such as quartz or titanate ceramic) to generate and
receive ultrasound waves. The received waves are converted to electrical signals and
displayed on the echocardiographic machine. The equipment is portable and allows
examination in multiple locations aside from the echocardiography laboratories.
Technique
The echocardiographic examination starts by connecting the ECG electrodes and

positioning the patient comfortably in the left lateral decubitus position to obtain
optimal images (Obtaining images in supine position are possible if patients are
unable to lie on their side). The ultrasound transducer is applied (using a water sol-
uble gel) to the parasternal, apical, subcostal and in some cases suprasternal notch
to obtain the usual images of an echocardiographic protocol. Parasternal long axis
(PLAX), parasternal short axis (PSAX), apical 4 (A4C), 2 (A2C), and 3-chamber
(A3C or long axis), subcostal, and suprasternal notch images are obtained. Doppler
echocardiography (color flow, continuous and pulsed wave) is used to determine
regurgitant and stenotic flow across valves and measure the velocity, pressure gradi-
ents, and volumetric flow. Tissue Doppler (mitral annulus) is used in determining
diastolic function.
1. The parasternal long axis view (PLAX) (Fig. 1.1) with the transducer slightly
left of the sternum is initiated with the 2D evaluation of a sagittal view of the left
ventricle (LV) (long axis view). This view allows evaluation of the structure and
systolic function of the LV including LV outflow tract, left atrium (LA), the
structure and motion of the aortic valve (AV) right and non-coronary cusps, the
proximal aortic size and wall characteristics, and a portion of the right ventricular
outflow. The posterior pericardium can also be evaluated for thickening or
ERRNVPHGLFRVRUJ
Fig. 1.1 Parasternal long axis (PLAX) views: (a) shows PLAX with the LA, LV, MV-mitral valve
with anterior and posterior leaflets, AV-aortic valve with RCC-right coronary cusp and NCC-non-
coronary cusp. The RV lies anteriorly and posteriorly the pericardium and descending aorta are
seen. In the PLAX, the anteroseptal and inferolateral walls of the LV are evaluated for any wall
motion abnormalities. Panel (b) shows an RV inflow view with the RV, RA, the TV-tricuspid valve
as well as the ostia of the IVC-inferior vena cava and the CS-coronary sinus
presence of pericardial effusion and more posteriorly pleural effusion. The sep-
tum is visualized and information can be obtained on the presence of a ventricu-
lar septal defect (VSD).
2. A parasternal right ventricular (RV) inflow (Fig. 1.1) view can be obtained by
medial angulation of the transducer from the parasternal long axis position. This
allows visualization of the tricuspid valve (TV), right atrium (RA), coronary
sinus (CS), and RV inflow tract. Tricuspid regurgitation can be evaluated and
using continuous flow (CW) Doppler, right ventricular systolic pressure (RSVP)
can be calculated.
3. Parasternal short axis view (PSAX) (Fig. 1.2) is orthogonal to the long axis view.
It is obtained by rotating the transducer 90°. Cross sectional evaluation of the LV,
mitral valve (MV), AV, and LA are obtained, as well as views of the interatrial
septum, RA, TV, RV outflow tract, PV, proximal PA and main PA branches.
Doppler studies allow assessment of aortic regurgitation, tricuspid regurgitation,
PA velocity, and the presence of pulmonic stenosis or regurgitation. Shunts that
can be assessed in this view include membranous and supracristal VSD, patent
ductus arteriosus (PDA), atrial septal defects (ASD) and patent foramen ovale
(PFO)
4. Apical four chamber (A4C) view (Fig. 1.3): The transducer is placed on the left
side of the chest as far inferiorly and laterally as possible to obtain views of the
four chambers, including the mitral and tricuspid valves. This view allows
assessment of the LV apex, inferoseptal and anterolateral walls and the lateral
RV wall. The view is useful for evaluation of global LV systolic performance and
the presence of LV apical aneurysm and thrombus. Diastolic performance can be
determined by Doppler assessment of mitral inflow, pulmonary vein, and mitral
annular (tissue Doppler) motion. This is the best view for assessing the presence
and degree of mitral and tricuspid stenosis and regurgitation and is useful for
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8 E. Karnabi
Fig. 1.2 Parasternal short axis (PSAX) views: (a, b) At the aortic level in diastole (AV closed) and
systole (AV open). Note the three cusps: RCC, LCC, and NCC (located at the IAS-interatrial sep-
tum). Also seen are the LA, RA, IAS with slight dropout, RV outflow, PV-pulmonary vein and
MPA-main pulmonary artery. Panel (c) shows short axis of the LV at the mitral valve level showing
the anterior and posterior leaflets. Panel (d) shows a short axis of the LV at the papillary muscle
level with the AL-anterolateral and PM-posteromedial papillary muscles from [1]
assessing the extent of pericardial effusion, and respirophasic characteristics of

mitral and tricuspid characteristics that may include pericardial tamponade. RV
and RA invagination or compression also suggesting tamponade can be seen in
these views. Doppler interrogation for muscular VSD is best accomplished in
this view. Saline intravenous injections for R-L shunts are best determined in this
view.
5. Apical 2 chamber (A2C) view (Fig. 1.3): Rotation of the transducer 60° counter-
clockwise provides visualization of the LV, MV, and LA. This view allows evalu-
ation of the LV inferior and anterior walls, further evaluation for mitral
regurgitation, and may be the best view for demonstration of LV pseudoaneu-
rysm, which usually involves the inferior wall.
6. Apical 3 chamber (A3C) view (Fig. 1.3): Rotating the transducer 60° clockwise
and tilting is slightly anteriorly allows visualization of the LV, MV, LA, LV
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Fig. 1.3 Apical views. (a) Apical 4 chamber (A4C) view showing the LA, RA, RV, LV (anterolat-
eral and inferoseptal walls), and the MV/TV. (b) Apical 5 chamber (A5C) with slight anterior
angulation of the transducer, the aorta is opened and the aortic valve can be seen and interrogated
with CW to evaluate for AS, and PW of the LVOT to measure the SV-stroke volume. (c) Apical 2
chamber (A2C) showing the LA, MV and LV (Anterior and inferior walls). (d) Long axis (A3C)
showing the LA, LV, MV, and AV. Similar to the PLAX, the anteroseptal and inferolateral walls of
the LV are seen from [5]
outflow tract, AV and proximal aorta. It is the best view for Doppler interrogation
for aortic stenosis, subaortic stenosis and aortic regurgitation.
7. Subcostal view (Fig. 1.4): The transducer is placed in the epigastrium just below
the subxiphoid process. It is the best view for evaluating RA and RV free wall
motion, and presence of PFO or ASD. The inferior vena cava is best viewed in
this location. The diameter of which is measured and used to estimate RA pres-
sure. The abdominal aorta can be seen several centimeters below the diaphragm,
which allows the evaluation of aneurysms or dissection at this level.
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10 E. Karnabi
Fig. 1.4 Subcostal and suprasternal TTE views: (a) A subcostal view with the four chambers LA,
LV, RA, and RV are seen. This is the best view to evaluate for the presence of IAS-interatrial septal
defects such as ASDs or PFOs using color flow Doppler. (b) Suprasternal notch view showing the
aortic arch, RPA-right pulmonary artery and LA. This view is used to evaluate for the presence of
aortic coarctation and diastolic flow reversal to determine the severity of aortic regurgitation
8. Suprasternal view (Fig. 1.4): This view allows Doppler assessment of the ascend-
ing aortic velocities in aortic stenosis an can provide 2D imaging of the trans-
verse and proximal descending thoracic aorta. Doppler assessment of the
descending aorta in this view may be useful for the diagnosis of PDA and
coarctation.
In general, standard images can be obtained in most patients with limitations
in those with extremes of weight, with severe lung hyperinflation (i.e. severe
COPD), or in patients in which access to the chest wall is precluded in setting of
thoracic bone malformations, open-heart surgery or other thoracic surgeries. In
difficult to image patients, ultrasound contrast agents are used to improve image
quality.
Data Interpretation
Physicians with specialized training should perform data interpretation as estab-

lished by competency guidelines from the ACC/AHA/ASE to generate a formal
report. It is important to use a consistent systemic approach with special attention
directed to the clinical question.
A systemic approach includes the following:
Left Ventricle: Chamber dimension, wall thickness, fractional shortening (FS), ejec-
tion fraction, regional wall motion abnormalities, stroke volume, diastolic char-
acteristics and presence of VSD [3].
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Right Ventricle: Chamber dimension, wall thickness and global function.

Left atrium: size, presence of masses or cor triatriatum.
Right atrium: Size, abnormal motion suggesting pericardial tamponade.
Proximal aorta: size, evidence of dissection and fibrocalcific changes.
Proximal PA: size, presence of PDA.
Valves: Stenosis, regurgitation, vegetations, calcification, prolapse, bicuspid and
other AV abnormalities.
Congenital anomalies: PFO, ASD, VSD, cor triatriatum, Ebstein anomaly, transpo-
sition of ventricles and other congenital abnormalities.
Pericardium: Pericardial effusion, tamponade, constriction.
Hemodynamic: Hemodynamics play an important role in echocardiography and is
helpful in evaluating the degree of right to left or left to right shunting, degree of
mitral and aortic stenosis, regurgitant flow, PA systolic pressure.
Flows can be calculated using the formula Flow Rate = Area (πr2) × Vmax. πr2
represents the area across a circle assuming the left ventricular outflow tract (LVOT)
is circular in shape. The volume is calculated as Volume = Area (πr2) × VTI (Velocity
time integral: measured by tracing the CW or PW signal). The stroke volume (SV)
can be calculated using multiple methods, with the use of the LVOT being the most
accurate: SV = Area (LVOT) × VTI (PW LVOT). The SV can also be calculated by
SV = EDV − ESV by tracing the LV in end diastole and end systole and using the
biplane summation method to calculate volumes.
The pressure gradients across valves can be calculated using the Bernoulli equa-
tion Δp = 4 V2. Another method to evaluate aortic stenosis is by measuring the mean
pressure gradient (PG) by tracing the CW AV signal or approximating it by calculat-
ing 2/3 or 0.7 of max PG. The aortic valve area (AVA) is calculated using Newton’s
2nd law of conservation of energy (Flow in = flow out), therefore, AVA × VTI = CSA
(LVOT) × VTI (PW at LVOT). CSA of LVOT = πr2. R = radius of the LVOT,
CSA = Cross sectional area, VTI = Velocity time integral. Lastly, a dimensionless
index defined as DVI = VTI (LVOT) divided by VTI (AV) is used to estimate sever-
ity with a value less than 0.25 signifying severe. This method avoids the error of
measuring the LVOT diameter because LVOT squared- results in squaring any error
obtained.
Table 1.2 shows the classification of the severity of aortic stenosis.
Mitral stenosis can be evaluated with several methods including the determina-
tion of the mean pressure gradient by tracing the CW signal across the mitral valve
Table 1.2 Recommendations for classification of AS severity [4]

Aortic sclerosis Mild Moderate Severe
Aortic jet velocity (m/s) <2.5 2.6–2.9 3.0–4.0 >4.0
Mean PG (mm Hg) – <20 20–40 >40
AVA (cm2) – >1.5 1.0–1.5 <1.0
Indexed AVA (cm2/m2) – >0.85 0.60–0.85 <0.6
Velocity ratio – >0.50 0.25–0.50 <0.25
PG pressure gradient, AVA aortic valve area
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12 E. Karnabi
Table 1.3 Recommendations for classification of MS severity [4]

Mild Moderate Severe
Valve area MVA >1.5 1.0–1.5 <1.0
Mean PG (mm Hg) <5 5–10 >10
PA pressure (mm Hg) <30 30–50 >50
The above recommendations are based on the ASE guidelines, however, the AHA/ACC most
recent guidelines; define an area >1.5 as progressive, <1.5 as severe, and an area <1.0 as very
severe
MVA mitral valve area, PG pressure gradient, PA pulmonary artery
or by calculating the mitral valve area (MVA) by planimetry using the parasternal
short axis at the mitral valve level. Additionally, MVA may also be determined by
pressure half time (PHT), which is defined as the time for the LA to LV pressure
gradient to fall to half its peak. A deceleration time (DT) can be calculated from the
slope and PHT = 0.29 × DT and MVA = 220/PHT (Table 1.3).
Quantification of valvular regurgitation can be achieved using volumetric methods
or PISA. The volumetric methods, uses the principle of “What goes in, must come
out”. Therefore, the regurgitant volume (RV) across the MV RV (MR) = SV (MV) –
SV (LVOT) and RV (AI) = SV (LVOT) – SV (MR). The ERO (Effective regurgitant
orifice) can be calculated by dividing the regurgitant volume (RV) by the VTI of the
regurgitant valve (MR or AI). The regurgitant fraction is calculate by dividing the RV
by the SV at the valve i.e., if MR then SV of MV and if AI then SV LVOT. Using the
PISA method, by adjusting the aliasing velocity and creating a hemisphere of isove-
locity, calculations can be made to quantify regurgitation with the ERO measuring
lesion severity and RV measuring volume overload from the regurgitation. ERO = 2πr2
× Va (Aliasing velocity)/Vmax of MR, RV = ERO × MR VTI, and RF = RV/SV of
mitral valve. Similar calculations are made for aortic regurgitation. Tables 1.4 and 1.5
demonstrate the ASE criteria for classification of mitral and aortic regurgitation.
The RVSP and PASP can be estimated. The right atrial pressure (RAP) is esti-
mated using the size or diameter of the IVC. If the IVC diameter is <2.1 cm, the
RAP is given a value of 3 mmHg. If the IVC diameter is >2.1 cm and collapses with
a sniff or <2.1 cm and is non-collapsed, then a value of 8 mmHg is given. If the IVC
is >2.1 cm and is non-collapsed, then a value of 15 mmHg is given. The RVSP can
be calculated using the TR velocity by applying the Bernoulli equation with
RVSP = 4 V2 (TR) + RAP. The pulmonary artery systolic pressure (PASP) is esti-
mated to be equal to the RVSP unless pulmonary stenosis is present.
Finally, shunts such as ASD and VSD can be estimated using the Qp/Qs ratio.
The formula to calculate the shunt is Qp/Qs = RVOT CSA × RVOT VTI/LVOT CSA
× LVOT VTI.
The assessment of diastolic dysfunction is an integral part of a routine echocar-
diographic examination especially in heart failure patients [6]. Assessment of dia-
stolic dysfunction usually includes measurement of mitral inflow and peak early
filling (E-wave) and late diastolic filling (A-wave) velocities, E/A ratio, decelera-
tion time (DT) of early filling velocity and the IVRT (isovolemic relaxation time).
Pulmonary venous flow is performed with a PW Doppler at the right upper pulmo-
nary vein. Measurements include peak systolic (S) velocity, peak antegrade
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Table 1.4 Qualitative and quantitative parameters in grading mitral regurgitation severity [5]
LA and LV size Normal Normal or Usually dilated
dilated
Color flow jet area Small, central jet Variable Large jet (>10 cm2 or >40 % of
LA)
Mitral inflow-PW A wave dominant Variable E wave dominant
Jet density-CW Faint Dense Dense
Jet contour-CW Parabolic Usually Early peaking-triangular
parabolic
Pulmonary vein Systolic Systolic blunting Systolic flow reversal
flow dominance
VC width (cm) <0.3 0.3–0.69 >0.7
RV (ml) <30 30–59 >60
RF (%) <30 30–49 >50
EROA (cm2) <0.2 0.2–0.39 >0.4
LA left atrium, LV left ventricle, PW pulse wave, CW continuous wave, VC vena contracta, RV
regurgitant volume, RF regurgitant fraction, EROA effective regurgitant orifice area
Table 1.5 Qualitative and quantitative parameters in grading aortic regurgitation severity [5]
LA and LV size Normal Normal or dilated Usually dilated
Jet width in LVOT-color Small, central jet Intermediate Large jet
flow
Jet density-CW Faint Dense Dense
Jet deceleration rate-CW >500 500–200 <200
(PHT, ms)
Diastolic flow reversal in Brief early Intermediate Prominent holodiastolic
descending aorta-PW diastolic reversal reversal
VC width (cm) <0.3 0.3–0.6 >0.6
Jet width/LVOT width, % <25 25–64 >65
Jet CSA/LVOT CSA, % <5 5–59 >60
RV (ml) <30 30–59 >60
RF (%) <30 30–49 >50
EROA (cm2) <0.1 0.1–0.29 >0.3
LA left atrium, LV left ventricle, LVOT left ventricular outflow tract, PHT pressure half time, PW
pulse wave, CW continuous wave, VC vena contracta, RV regurgitant volume, RF regurgitant frac-
tion, EROA effective regurgitant orifice area
diastolic (D) velocity, S/D ratio, and the peak A reversal in late diastole. The time
difference between it and the mitral A wave duration (Ar-A) is used in assessing
diastolic dysfunction. PW tissue Doppler of the septal and lateral mitral annulus is
performed in the A4C. The early diastolic annular velocity e′ is integral in the
assessment of diastolic function. Normal diastolic function is defined by a septal e′
>8 and lateral e′ >10. If the values are <8 and <10 respectively, multiple parameters
are evaluated (E/A, DT, Ar-A, Valsalva ΔE/A) to determine the grade of diastolic
dysfunction I, II, or III.
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14 E. Karnabi
Complications
As mentioned, echocardiography is generally very safe with no complications. The

key procedural complications are usually related to contrast administration or inac-
curacy of data.
Clinical Vignettes
Case 1
Sixty-five-year-old male with history of hypertension, hyperlipidemia and heavy

alcohol and tobacco use was admitted with 2 weeks of worsening dyspnea on exer-
tion, orthopnea and cough with clear sputum production. His vitals include a blood
pressure (BP) of 80/44, heart rate (HR) 126 and respiratory rate (RR) of 22.
Physical exam is significant for distant heart sounds, few crackles and lower extrem-
ity edema. ECG is remarkable for low voltage and electrical alternans. 2D trans-
thoracic images are shown in (Fig. 1.5).
Fig. 1.5 Case #1. (a) Parasternal long axis; (b, c) Short axis, (d). Four chamber view (see text for
details)
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The TTE images clearly show a large circumferential pericardial effusion that is
causing hemodynamic compromise and tamponade. Pericardial effusions are classi-
fied as small (less than 1 cm), moderate (1–2 cm), and large (>2 cm). In this case,
the effusion is 3–4 cm with diastolic collapse or invagination of the right-sided
chambers. The treatment of choice is emergent pericardiocentesis.
Case 2
Eighty-five year old male with hypertension, hyperlipidemia, prostate cancer s/p
radiation and surgery presented with worsening clinical status over the last year
with episodes of chest pain, dyspnea and an episode of syncope that prompt the
admission. His Vitals are stable. Physical examination is notable for a grade 3/6
systolic murmur at the right upper sternal border with radiation to the carotids, S2
is diminished, lungs bibasilar crackles. ECG unremarkable. Transthoracic echo-
cardiographic images are shown in (Fig. 1.6).
The TTE images show severe calcifications of the aortic valve with a slit like
opening during systole indicating the presence of severe aortic stenosis (As shown
in the upper panels). The lower panels show a continuous wave through the aortic
valve, a pulse wave at the LVOT level, and a CW of the aortic regurgitation
Δp = 4(4 m/s)2 is 64 mmHg. The mean PG is calculated by tracing the CW across
the aortic valve or 2/3 of the Peak PG. AVA is calculated at 0.9 cm2 indicative of
severe AS per guidelines (AVA < 1 cm2) and in symptomatic patients should be
referred for aortic valve replacement.
Fig. 1.6 (a) Parasternal long axis (severe calcification of the aortic valve) (b) zoom on aortic valve
(c) Parasternal short axis (d) Continuous wave Doppler through the aortic valve to measure the
peak and mean aortic stenosis gradients. (e) Pulse wave Doppler at the LVOT to calculate the aortic
stroke volume. (f) Continuous wave Doppler through the aortic valve to quantify the pressure half
time of aortic regurgitation
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16 E. Karnabi
References
1. Cheitlin MD, et al. ACC/AHA guidelines for the clinical application of echocardiography:
executive summary. A report of the American College of Cardiology/American Heart
Association Task Force on practice guidelines (Committee on clinical application of echocar-
diography). Developed in collaboration with the American Society of Echocardiography. J Am
Coll Cardiol. 1997;29(4):862–79.
2. American College of Cardiology Foundation Appropriate Use Criteria Task, F, et al. ACCF/
ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011 appropriate use criteria for
echocardiography. A report of the American College of Cardiology Foundation Appropriate
Use Criteria Task Force, American Society of Echocardiography, American Heart Association,
American Society of Nuclear Cardiology, Heart Failure Society of America, Heart Rhythm
Society, Society for Cardiovascular Angiography and Interventions, Society of Critical Care
Medicine, Society of Cardiovascular Computed Tomography, and Society for Cardiovascular
Magnetic Resonance Endorsed by the American College of Chest Physicians. J Am Coll
Cardiol. 2011;57(9):1126–66.
3. Lang RM, et al. Recommendations for cardiac chamber quantification by echocardiography in
adults: an update from the American Society of Echocardiography and the European
Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 2015;28(1):1–39 e14.
4. Baumgartner H, et al. Echocardiographic assessment of valve stenosis: EAE/ASE recommen-
dations for clinical practice. J Am Soc Echocardiogr. 2009;22(1):1–23; quiz 101–2.
5. Zoghbi WA, et al. Recommendations for evaluation of the severity of native valvular regurgita-
tion with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr.
2003;16(7):777–802.
6. Nagueh SF, et al. Recommendations for the evaluation of left ventricular diastolic function by
echocardiography. J Am Soc Echocardiogr. 2009;22(2):107–33.
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Chapter 2
Transesophageal Echocardiography
Eddy Karnabi
Transesophageal echocardiography (TEE), in comparison to transthoracic echocar-

diography (TTE), provides superior image resolution/quality and has become the
test of choice in many circumstances. Improved image quality is due to the decreased
distance and the absence of bone or lung between the transducer and the heart.
However, it is an invasive procedure and hence, should be reserved for indications
where TTE provides inadequate diagnostic information.
Indications
The most common indications for TEE are as follows: detection of a cardiac source
of embolism as in atrial fibrillation or stroke; evaluating the left atrial appendage
(LAA) for a thrombus; endocarditis (vegetations) and its complications; valvular
disorders especially the mitral and prosthetic valves, diagnosing atrial septal defects
(ASD) and patent foramen ovale (PFO); evaluating the thoracic aorta (dissection)
and intracardiac masses/tumors. Table 2.1 shows a list of the appropriate indications
of TEE based on the ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/
SCMR Appropriate Use Criteria [1]:

Cardiology Division, Northeast Cardiology Associates (NECA),
Eastern Maine Medical Center (EMMC), One Northeast Drive, Bangor, ME 04401, USA

DOI 10.1007/978-1-4471-7290-1_2
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18 E. Karnabi
Table 2.1 Indications for transesophageal echocardiography [2, 3]

1. Use of TEE when there is a high likelihood of a nondiagnostic TTE due to patient
characteristics or inadequate visualization of relevant structures
2. Evaluation for cardiovascular source of embolus with no identified noncardiac source
3. To diagnose infective endocarditis with a moderate or high pretest probability (e.g., staph
bacteremia, fungemia, prosthetic heart valve, or intracardiac device)
4. Evaluation of valvular structure and function to assess suitability for, and assist in planning
of, an intervention
5. Guidance during percutaneous noncoronary cardiac interventions including but not limited
to closure device placement, radiofrequency ablation, and percutaneous valve procedures
6. Suspected acute aortic pathology including but not limited to dissection/transsection
7. Re-evaluation of prior TEE finding for interval change (e.g., resolution of thrombus after
anticoagulation, resolution of vegetation after antibiotic therapy) when a change in therapy
is anticipated
8. Evaluation to facilitate clinical decision making with regards to anticoagulation,
cardioversion, and/or radiofrequency ablation
Contraindications
Absolute contraindications Relative contraindications

Perforated viscous Restricted cervical mobility such as
atlantoaxial joint disease
Esophageal pathology (stricture, tumor, Recent upper GI bleeding
diverticulum, scleroderma, Mallory-Weiss tear)
Active upper GI bleeding History of GI surgery
Recent upper GI surgery Esophagitis, peptic ulcer disease
Esophagectomy Barrett’s esophagitis
History of dysphagia
Prior radiation to the chest
Coagulopathy, thrombocytopenia
Thoracoabdominal aneurysm
Symptomatic hiatal hernia
Equipment
Similar to a TTE, the necessary equipment’s are the portable echocardiography

unit; an ultrasound probe with multiplane imaging capabilities and trained person-
nel in sedation and transesophageal echocardiography based on the ACC/AHA
competency guidelines. The TEE probe is a modified gastroesophageal probe with
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2 Transesophageal Echocardiography 19
a 3–7 Mhz ultrasound transducer at its tip. The diameter of an adult transducer is
9–14 mm and can be maneuvered in a left-right direction and retroflexion/ante-
flexion using a rotating knob/wheel at the proximal operator end. The transducer
tip is equipped with a multiplane that can be rotated from 0° to 180°.
The TEE room should be equipped with vitals monitor to record BP, HR, pulse
oximeter, oxygen supply, oral suction, bite guard, pillow wedge to position the
patient, and a cardiopulmonary resuscitation crash cart.
In addition to the physician, at least two additional personnel are required: a
sonographer to operate the echocardiographic machine, optimize and acquire
the images, and a nurse that will be monitoring the patient vitals (BP, HR, RR,
oxygen saturation), administering sedatives/analgesics, and suctioning the
oropharynx.
Technique
The procedure starts with patient and room preparation. The room should be
equipped with all the supplies/medications required as indicated above. TEE is con-
sidered a semi-invasive procedure and a thorough conversation should be performed
with the patient explaining the indications, alternatives and possible complications;
informed consent should then be obtained. To avoid or reduce the risk of aspiration,
the patient should be NPO for at least 6 h. Prior to the start of the procedure, a
review of the patients’ history, medications, allergies and laboratory data should be
performed. A physical exam should also be performed with attention made to the
respiratory, cardiovascular system and the Mallampati score (Class I–IV) (Also see
Chap. 17). The physical status classification according to the American Society of
Anesthesiologists (ASA) should be performed, Classes I–VI, with a level of III and
above requiring anesthesiology support. A recent coagulation profile should be
reviewed and if patients are on anticoagulation, those agents should be held hours
or days prior depending on the type of agent.
The patient is positioned in left lateral decubitus position at a 30–45° inclination
to reduce the risk of aspiration. Local anesthesia spray is then performed using
tongue depressors to anesthesize the oropharynx. A bite guard is placed to protect
the TEE probe from inadvertent biting. Two techniques have been described for the
esophageal intubation: hands-in or hands-out techniques. Using the hands-in tech-
nique, two fingers are placed inside the oropharynx and are used to depress the
tongue and guide the probe (transducer ultrasound facing towards the tongue)
towards the posterior pharynx. If patient is under conscious sedation, he/she can be
asked to swallow which assists the probe to easily intubate the esophagus. If resis-
tance is encountered at any point, the probe should not be forced further. The probe
has markings to help with localization (distance from incisors to mid esophagus
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20 E. Karnabi
Fig. 2.1 ME (Mid esophageal) TEE images: (a) 4 chamber view (0–10°) showing the LA, LV, RA,
RV with the mitral and tricuspid valve. Note that the mitral valve is divided into anterior (A1–3)
and posterior scallops (P1–3). In this view, A2 and P2 are seen. (b) 2 chamber view (50–70°) show-
ing the LA and LV with the mitral valves and P1, A2, and P3 scallops. (c) 3 chamber view or long
axis (120–140°) showing the LA, LV, mitral valve (A2, P2 scallops) and the aorta with the aortic
valve
approx. 30–35 cm and distance to the stomach 40–45 cm). Throughout the proce-
dure, the vital signs should be monitored and the oropharynx suctioned as
necessary.
A comprehensive TEE examination is then performed to answer the indication of
the study as described below in data interpretation. A key to performing a TEE
examination is understanding the terminology of probe manipulation: advancing or
withdrawing the probe, flex to the right or left, and anteflexing anteriorly or retro-
flexing posteriorly. Once the procedure is done, the probe is removed and sent for
proper cleaning and the patient monitored for at least 2 h NPO until the gag reflex
has returned and the patient recovered from the sedation. If the procedure is elec-
tive/outpatient study, he/she is suitable for discharge under the care of a responsible
adult with avoidance of driving for at least 12 h.
Data Interpretation
According to the American Society of Echocardiography (ASE), a comprehensive

TEE examination includes 28 views. The three primary positions used are upper
esophageal (UE), midesophageal (ME), and transgastric (TG). At the ME level, a 5
chamber (5C) at transducer angle 0–10°, 4C at angle 0–10° slight retroflexion, 2C
angle 50–70°, and 3C or long axis views at an angle of 120–140° are obtained
(Fig. 2.1). At the UE level, a transducer angle of 25–45° will show the aortic valve
in short axis, 50–70° shows the pulmonic valve, 90–110° shows the bicaval view
and the interatrial septum (Fig. 2.2). The left atrial appendage (LAA) is usually seen
at an angle of 60° with slight counterclockwise rotation (Fig. 2.2). In the TG views,
a transducer angle of 0–20° will show the LV in short axis at the mitral valve and
papillary levels, an angle of 90° shows the LV, mitral valve, and papillary muscles
in long axis (Fig. 2.3). Clockwise rotation of the probe will reveal the right side
including the RV and the tricuspid valve (Fig. 2.3). In cases of aortic stenosis, the
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Fig. 2.2 UE (Upper Esophageal) TEE images: (a) Short axis of the aortic valve 25–45° showing
a tricuspid aortic valve with non-coronary cusp-NCC (at the interatrial septum-IAS), LCC-left
coronary cusp, and RCC-right coronary cusp. Note the LA is most posterior and closer to the
probe. IAS-inter atrial septum is seen separating the LA and RA. TV-tricuspid valve and the RV
outflow tract. (b) The PV-pulmonary valve and MPA-main pulmonary arteries are seen with slight
increase in the multiplane to 50–70°. (c) The probe is withdrawn slightly to above the aortic valve
level where the LAA-left atrial appendage can be seen with pectinate muscles at its apex. (d) A
bicaval view is shown at 90–110° with clockwise rotation with the IAS-interatrial septum, foramen
ovale, and RAA-right atrial appendage. Note the location of SVC-superior vena cava and IVC-
inferior vena cava
aortic valve velocity can be obtained in the TG either at 0° deep TG or at 120° TG

(Fig. 2.4). Finally, the aortic views are obtained by rotating the probe 180° degrees
either clockwise or counterclockwise so that the probe is facing posteriorly to image
the descending aorta and distal aortic arch (Fig. 2.5). An example in which TEE is
extremely useful is in evaluation of mitral valve prolapse as shown in (Fig. 2.6).
Complications
Rates of major TEE complications range from 0.2 to 0.5 % and the rate of TEE
associated mortality is estimated to be less than 0.01 %. The risk with the use of
local anesthetics to anesthesize the oropharynx using benzocaines include
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22 E. Karnabi
Fig. 2.3 TG (Transgastric) TEE images: (a) Short axis view (0°) of the LV showing the
Al-anterolateral and PM-posteromedial papillary muscles. (b) X-plane through the short axis or
multiplane at 90° shows the LV in long axis with mitral valve posterior and anterior leaflets. (c, d)
Right sided views from the TG level are obtained by clockwise rotation of the probe. Panel (c)
shows the TV-tricuspid valve in short axis and (d) in long axis
methemoglobinemia that presents as central cyanosis, oxygen desaturation, and

brownish color to a blood sample. The risks associated with esophageal intubation
include trauma to the oropharynx such as dental trauma, laryngeal/pharyngeal lac-
erations, bleeding, sore throat and hoarseness, laryngospasm/bronchospasm, and
inadvertent tracheal intubation. Similarly, esophageal or gastric trauma, laceration,
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Fig. 2.4 TG TEE view of

the aortic valve at 0° deep
TG. Alternatively, the
aortic valve velocity can be
evaluated at 120°
TG. These are the two
views that are used in cases
of aortic valve stenosis that
produces the most parallel
angle to the transducer for
continuous wave flow
interrogation
Fig. 2.5 Aortic TEE images: (a) Descending aorta in short axis (0°) and long axis (90°) showing
absence of atherosclerosis. In comparison, panel (b) shows a severely diseased descending aorta
with ulcerated atherosclerotic plaques
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24 E. Karnabi
Fig. 2.6 Mitral valve prolapse images: (a, b) show severe prolapse of the posterior mitral valve
leaflet (shown in arrow). Panel (c) shows severe eccentric mitral regurgitation with an anteriorly
directed jet
bleeding, perforation and rupture can occur. The risk associated with sedation
whether conscious sedation, MAC (Monitored anesthesia care), or general sedation
include hypotension, respiratory depression, aspiration, arrhythmias, and even
death. The risks of complications can be reduced dramatically by appropriate patient
selection, careful manipulation of the probe during insertion and study, and experi-
ence in conscious sedation and the assistance of anesthesiology. Reversal agents
should be available bedside in cases such as methemoglobinemia or respiratory
depression. The reversal agents are methylene blue (1–2 mg/kg IV ×1) for methe-
moglobinemia, flumazenil (0.2 mg IV qmin) for benzodiazepines and naloxone
(0.4–2 mg IV q2–3 min) for opioid overdose/reversal.
Clinical Vignettes
Case 1
Sixty-four-year-old female with a history of ovarian cancer, hyperlipidemia has been

experiencing occasional palpitations over the last 3 months associated with occa-
sional lightheadedness. Two weeks ago, the palpitations became more frequent and
were associated with a few pre-syncopal episodes. In the ER, she was noted to be in
atrial fibrillation with rapid ventricular response. TEE images are shown in (Fig. 2.7).
The TEE images show UE-upper esophageal views of the LAA-left atrial
appendage that clearly shows a small thrombus (arrow). Therefore, cardioversion
and catheter ablation are contraindicated. Thrombolytics have no role in treatment
of LAA thrombi. The patient should receive at least 4 weeks of anticoagulation,
followed up by re-evaluation and possible cardioversion.
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Case 2
Fourty-two-year-old male with a history of polysubstance abuse and intravenous

drug use (IVDU) presented to the ER with fever, shills, shortness of breath, with
unstable vitals: hypotension (BP 70/35) and tachycardic (HR 135). A 2D echo was
performed, followed by a TEE (Fig. 2.8).
The patient is presenting with hemodynamically unstable septic shock due to
mitral valve endocarditis with a large vegetation (arrow) on the posterior mitral
leaflet causing severe eccentric mitral regurgitation. The source is most likely due to
IV drug use. The patient should be treated for antibiotics, however, considering the
size of the vegetation, the severity of associated mitral regurgitation, he should be
evaluated by cardiothoracic surgery.
Fig. 2.7 (a–c) TEE views of the left atrial appendage in multi-plane angulations showing the pres-
ence of a thrombus
Fig. 2.8 (a), (b) Two chamber views showing the presence of a large vegetation on the mitral
valve (c). Using color Doppler, severe eccentric mitral regurgitation can be visualized as a conse-
quence of the vegetation
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26 E. Karnabi
References
1. American College of Cardiology Foundation Appropriate Use Criteria Task, F, et al. ACCF/
ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011 appropriate use criteria for
echocardiography. A report of the American College of Cardiology Foundation Appropriate
Cardiol. 2011;57(9):1126–66.
2. Hahn RT, et al. Guidelines for performing a comprehensive transesophageal echocardiographic
examination: recommendations from the American Society of Echocardiography and the
Society of Cardiovascular Anesthesiologists. J Am Soc Echocardiogr. 2013;26(9):921–64.
3. Hilberath JN, et al. Safety of transesophageal echocardiography. J Am Soc Echocardiogr.
2010;23(11):1115–27; quiz 1220–1.
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Chapter 3
Contrast Echocardiography
Despite the development of improved imaging techniques, contrast echocardiogra-

phy (CE) may be indispensable in cases where optimal ventricular delineation is
essential, as it enhances endocardial border delineation and offers assessment about
intracardiac blood flow [1, 2].
The mechanism of the use of contrast with echocardiography lies in the principle
of acoustic impedance, where the change in density from one medium to another
causes reflection of sound waves, reason for the use of microbubble contrast agents
since gas is less dense than blood.
Indications
Agitated saline provides contrast in the right heart and enables detection of shunts,
the first clinical use of CE, as the microbubbles remain in the right heart and then
diffuse into the lungs, unable to access the left heart unless a right-to-left heart shunt
exists.
C. Gallegos, MD
Section of Cardiovascular Medicine, Yale University School of Medicine, 333 Cedar Street,
New Haven, CT 06520-8017, USA
R.C. Hendel, MD, MASNC, FACC, FAHA (*)
Cardiovascular Division, University of Miami, Miller School of Medicine,
1400 NW 12th Avenue, Suite 2022, Miami, FL 33133, USA

DOI 10.1007/978-1-4471-7290-1_3
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28 C. Gallegos et al.
The indications for CE with agitated saline use include:

1. Cardiac and extracardiac shunts: atrial septal defects (ASD) and ventriculoseptal
defects (VSD)
2. Patient foramen ovale (PFO)
3. Structure identification, particularly the right heart
4. Evaluation of Tricuspid Regurgitation
5. Evaluation of Congenital heart disease
The assessment of left ventricular (LV) function is the most common indication
for contrast use particularly for left ventricular opacification (LVO) in patients with
suboptimal images, which happen in about 5–10 % of cases. The endpoint is to
enhance the endocardial border definition (EBD), as well as assessment of dimen-
sions, volume, and wall motion.
Indications for the use of contrast agents include [1–3]:
1. Assessment of LV function, especially when two or more segments are not
seen on non-contrast images mainly due to respiration, and increased heart
rate,
2. To delineate LV structure and measure volumes and ejection fraction
3. For definite diagnosis when the following are suspected: apical hypertrophic car-
diomyopathy, ventricular non-compaction, apical thrombus, and complications
of myocardial infarction such as LV aneurysm, pseudoaneurysm, and myocar-
dial rupture.
4. For use with stress echocardiography when two or more segments of the LV are
not well identified during stress, for the assessment of wall motion abnormali-
ties, to increase accuracy, and increase the reader’s confidence.
5. To assist in the detection and identification of intracardiac masses including
tumors and thrombi.
6. To enhance Doppler signals when spectral profiles cannot be obtained with stan-
dard examination and are not visible.
7. Although not yet FDA approved, contrast injection can be used in myocardial
perfusion imaging.
Contraindications
Although generally safe and effective, contrast agents have some

contraindications:
• Hypersensitivity to an agent
• For perflutren protein-type a microspheres (Optison) or perflutren lipid micro-
spheres (Definity)_ known hypersensitivity to blood, blood products, or
albumin
• Fixed right to left, bidirectional or transient right to left cardiac shunts.
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3 Contrast Echocardiography 29
Equipment
For the detection of shunts, agitated saline is the method of choice. The saline contrast
should be composed of bacteriostatic normal saline cannula agitated with 0.5 ml of
room air, between two 10 ml syringes. For this, a three-way stopcock should be used,
as well as a >20 gauge IV line, preferably in the right arm. The aim is to inject 5 ml of
saline and 0.2 ml of air from one syringe to the other prior to immediate injection [1, 4].
There are three FDA approved contrast agents: Optison (GE Healthcare,
Princeton, NJ), Lumason (Bracco Diagnostics Inc., Monroe Township, NJ; also
known as SonoVue), Definity (Lantheus Medical Imaging, North Billerica, MA).
Optison is perfluropropane gas on human albumin coating, whereas Definity uses
the same gas but has a phospholipid shell. Other agents have been approved in
Canada, Europe, some Latin American and Asian countries. These contrast agents
are stable and small in size (2–6 um) allowing the passage through the pulmonary
capillary bed and causing the opacification of the left sided chambers. Because
small lumen catheters increase bubble destruction, for administration of contrast, a
20-gauge or greater needle is usually recommended. A flush is required for the use
of contrast, hence is generally better to use a three-way stopcock.
Technique
Harmonic imaging the current standard technique for echocardiography, and its
original use was to enhance the detection of contrast. Contrast microbubbles inter-
act with the ultrasound waves in a nonlinear fashion and generates a second har-
monic frequency that enhances the detection of the microbubbles. For its optimal
use, the transmit power must be reduced from >1.0 to approximately 0.4–0.6.
However this gives the possibility of contrast destruction with subsequent equivocal
results in assessment of the myocardium [4]. Hence, there are contrast-specific
imaging modalities, namely low-power, or low Mechanical Index (MI), which
delivers best left ventricular opacification and endocardial border definition. MI in
these cases is usually between 0.15 and 0.3. With the use of these techniques, less
contrast is necessary, minimizing the risk for any adverse effects.
As mentioned above, an infusion pump can be used, as well as an IV bolus, or
a diluted bolus, which must be set up prior to starting the procedure. During a rest
study, the rate of IV bolus is usually 0.5–1.0 mL/s, with subsequent slow saline flush
administration that is to be stopped when contrast is seen in the right ventricle. Repeat
doses as necessary may be required. During stress, the contrast should be injected
about 30 s prior to exercise termination. For the infusion method, the contrast should
be diluted in a 10 ml syringe, or in a 50 ml bag of normal saline, after which the
infusion rate must be adjusted. If using the 10 ml syringe, it is usually recommended
to slowly push 0.5–1 ml every few minutes, whereas if the saline bag is utilized the
rate will determined by the appearance of a contrast image, usually at 150–200 ml/h.
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Data Interpretation
For conventional CE with agitated saline, the presence of contrast/bubbles in the left
heart indicates the possibility of an intracardiac shunt. The bubbles created do not
appear in the left chambers (as the size precludes its passage through the pulmonary
capillaries) unless there is a communication between the right and left cardiac
chambers in cases of right to left shunts. However, in case of a left to right shunt,
negative contrast effect is visualized. For instance, a PFO is diagnosed when more
than three bubbles pass from right to left within 34 cardiac cycles (Fig. 3.1). Based
on the number of bubbles, the PFO is then defined as being small (3–10), medium
(10–20), or large (>20 bubbles). If the bubbles are seen >5 cardiac cycles, a pulmo-
nary arteriovenous malformation is suggested. With transthoracic echocardiogra-
phy, the apical four-chamber view is used. Injection of agitated saline from the left
arm, in comparison to the usual injection from the right arm, may help detect the
presence of a persistent left superior vena cava (Fig. 3.2) draining into the coronary
sinus. Agitated saline bubbles strengthen the Doppler signals from the right heart
chamber and augments the tricuspid regurgitation (TR) signal to record the TR gra-
dient used to calculate the right ventricular systolic pressure (RVSP).
In particular cases, for example, in the evaluation of LV masses or thrombi, con-
trast agents have been shown to improve its diagnosis. A thrombus for instance, is
usually seen as a non-opacified structure. Contrast is also useful for the diagnosis of
non-compaction, in which the addition of an agent allows for the myocardial layers
to be clearly displayed and the ratio to be calculated (2:1 non compacted to com-
pacted myocardium is the usual finding). Contrast can be used in the identification
Fig. 3.1 Bubble study

with Saline injection
showing the presence of a
PFO with saline bubbles
opacifying the right-sided
chambers and multiple
bubbles passing into the
left cardiac chambers
(arrow)
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of complications of myocardial infarction such as LV aneurysm, pseudoaneurysm,

and myocardial rupture.
CE for stress testing also yields important information, given that images tend
to be worse during stress. Thus, addition of contrast provides a marked improve-
ment in images, and increases the percentage of wall motion abnormalities
visualized.
Complications
As mentioned earlier, CE is generally safe, however side effects have been noted, but
tend to be mild and transient, although severe hypersensitivity reactions have been
reported. In clinical trials, the most common side effects per contrast agents were [4]:
• SonoVue: Headache (2.1 %), Nausea and chest pain (1.3 %)
• Optison: Headache (5.4 %), Nausea and/or vomiting (4.3 %) warm sensation or
flushing (3.6 %), dizziness (2.5 %)
• Definity (Luminity): Headache (2.0 %), flushing (1.0 %) Back pain (0.9 %) rash,
urticarial, anaphylaxis.
Fig. 3.2 Use of contrast in delineating unknown structures (a) Four chamber view showing the
presence of a persistent left SVC (PLSVC). (b) A bubble study with the use of saline injection
from a left arm vein confirms the presence of the persistent left SVC (arrow) draining into the
coronary sinus (enlarged). PLSVC is a common variation of the thoracic venous system. In isola-
tion, this entity is benign but it is frequently associated with other cardiac abnormalities
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In summary, contrast agents are safe, effective, and recommended for use
with echocardiography, improving the results of echocardiographic imaging
studies [4, 5].
Clinical Vignettes
Case 1
78 year-old male with history or prior anterior wall myocardial infarction, hyper-
tension, hyperlipidemia presented to the hospital with left sided weakness for 3 days
duration. In ER, as part of his evaluation, a 2D echocardiogram was performed. For
better assessment of LV apex, contrast was injected. Images are shown in (Fig. 3.3).
This case shows the presence of apical infarction with akinetic segment and
the presence of a moderate size apical aneurysm with a thrombus on a stalk
(arrow), that is clearly detected with contrast but can sometimes be missed dur-
ing a standard echocardiographic examination. In such cases, anticoagulation is
recommended.
Fig. 3.3 Use of contrast in delineating area of infarction and thrombus. Panel (a) and (b) demon-
strates apical aneurysm with a thrombus on a stalk (arrow). See Case #1 text for details
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Fig. 3.4 Use of contrast in echocardiography to identify and delineate post-MI aneurysm (arrow).
(a) Four-chamber view without contrast. (b) Anterolateral aneurysm noted with contrast.
See Case #2 text for details
Case 2
85 year-old female with no significant cardiac history presented to the hospital with
2 weeks of chest pain and shortness of breath. While in the ER, she was noted to be
in cardiogenic shock requiring inotropic and pressor support. A STAT echo per-
formed is shown in (Fig. 3.4).
The images shown represent a complication of myocardial infarction with A.
without contrast and B. with contrast. The use of contrast clearly helps in establish-
ing the diagnosis of an anterolateral aneurysm as a complication of MI.
References
1. Stewart MJ. Contrast echocardiography. Heart. 2003;89:342–8.

2. Mulvagh SL, DeMaria AN, Feinstein SB, Burns PN, Kaul S, Miller JG, et al. Contrast echocar-
diography: current and future applications. J Am Soc Echocardiogr. 2000;13(4):331–42.
3. Mulvagh SL, Rakowski H, Vannan MA, Abdelmoneim SS, Becher H, Bierig SM, et al.
American Society of Echocardiography consensus statement on the clinical applications of
ultrasonic contrast agents in echocardiography. J Am Soc Echocardiography Off Pub Am Soc
Echocardiography. 2008;21(11):1179–201; quiz 281.
4. Senior R, Becher H, Monaghan M, Agati L, Zamorano J, Vanoverschelde JL, et al. Contrast
echocardiography: evidence-based recommendations by European Association of
Echocardiography. Eur J Echocardiography J Working Group Echocardiography Eur Soc
Cardiol. 2009;10(2):194–212.
5. Boolani H, Main ML. Update on contrast echocardiography: safety and utility. Curr
Cardiovascular Imaging Reports. 2012;5(6):410–9.
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Chapter 4
Exercise Stress Testing
Eddy Karnabi
Exercise testing (ET) is a well-validated procedure for the diagnosis of coronary

artery disease (CAD) and assessing functional capacity and prognosis. Exercise
stress tests may detect myocardial ischemia along the ischemic cascade (Fig. 4.1) as
a result of a mismatch between myocardial oxygen delivery (from coronary blood
flow impairment) and myocardial oxygen demand. It is simple and easy to perform
the test, with minimal equipment required.
There is two types of exercise stress tests that can be performed: bicycle and
treadmill with the latter being the most widely used in the US. The advantages that
bicycle ergometry have over treadmill is the ability to be performed in patients with
weight bearing problems, patients with gait/balance and orthopedic abnormalities,
a cleaner (less noise) ECG for interpretation, and the ability to take direct measure-
ments of workload in watts which has a linear relationship with myocardial oxygen
consumption (MVO2).
Indications
The most common indications according to the 2002 ACC/AHA guidelines for
exercise testing and the 2014 guidelines for stable ischemic heart disease [1–3] are
(Table 4.1).
Most commonly, ET is used in the diagnosis of ischemic heart disease in patients
with intermediate pretest probability of CAD and/or risk stratification of patients
with intermediate or high pretest probability of CAD based on age, gender, and
symptoms (Table 4.2).
E. Karnabi, MD, PhD FASE


DOI 10.1007/978-1-4471-7290-1_4
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36 E. Karnabi
Ischemic cascade
Magnitude of ischemia Stress Angina

echo
ECG changes
Nuclear Systolic dysfunction/WMA

imaging
Diastolic dysfunction
Perfusion abnormalities
Duration of ischemia
Fig. 4.1 The ischemic cascade: represent the magnitude of ischemia in relation to the increasing
duration of ischemia. The initial changes seen are perfusion abnormalities detected with nuclear
myocardial perfusion imaging. With increasing ischemia, diastolic dysfunction followed by sys-
tolic dysfunction occurs. At this stage, wall motion abnormalities (WMA) are detected by stress
echocardiography. It is only at the late stages, that ECG changes and angina develops
Table 4.1 Indications for 1. Symptoms suggestive of CAD

exercise ECG stress testing
2. Acute chest pain after ACS is ruled out
3. Recent ACS not treated with coronary angioplasty
4. Known CAD and change in clinical status
5. Prior incomplete revascularization
6. Valvular heart disease
7. Newly diagnosed cardiomyopathy
8. Certain cardiac arrhythmias
9. Pre-op cardiac assessment prior to non-cardiac surgery
Table 4.2 Pretest probability of CAD

Age Typical/definite Atypical/probable Non-anginal
(year) Gender angina angina chest pain Asymptomatic
30–39 Men Intermediate Intermediate Low Very low
Women Intermediate Very low Very low Very low
40–49 Men High Intermediate Intermediate Low
Women Intermediate Low Very low Very low
Women Intermediate Intermediate Low Very low
Women High Intermediate Intermediate Low
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4 Exercise Stress Testing 37
There are several conditions in which exercise tests should be combined with an
imaging modality; either myocardial perfusion imaging (MPI-SPECT or PET) or
echocardiography. These conditions include: ventricular paced rhythm, left bundle
branch block (LBBB), pre-excitation (Wolff-Parkinson-White syndrome), >1 mm
ST depression at rest, patients taking digoxin, previous PCI/CABG, left ventricular
hypertrophy (LVH), and right bundle branch block (RBBB) which precludes ST
segment interpretation in leads V1–3.
ET may also be used for patients with valvular heart disease (such as mitral ste-
nosis, aortic stenosis, and aortic regurgitation) to assess for symptoms; this is usu-
ally performed in conjunction with echocardiography.
Contraindications (Table 4.3)
Table 4.3 Contraindications to exercise stress testing [1]

Absolute contraindications to exercise stress testing
Acute myocardial infarction (within 2 days)
High risk unstable angina
Uncontrolled cardiac arrhythmias
Symptomatic severe aortic stenosis
Uncontrolled symptomatic heart failure
Acute pulmonary embolus or pulmonary infarction
Acute myocarditis or pericarditis
Acute aortic dissection
Relative contraindications to exercise stress testing
Left main coronary stenosis or it’s equivalent
Moderate stenotic valvular heart disease
Electrolyte abnormalities
Severe arterial hypertension
Tachyarrhythmias or bradyarrhythmias
Hypertrophic cardiomyopathy and other forms of outflow tract obstruction
Mental or physical impairment leading to inability to exercise adequately
High degree atrioventricular block
Equipment
The equipment for a treadmill ECG stress test includes the treadmill, ECG elec-
trodes, BP cuff, and the recording computer system that controls the stress test-
ing protocol being used. In addition, a physician or physician assistant/nurse
practitioner should supervise the test (with a physician on site). The exercise
protocols in practice are the Bruce protocol, Modified Bruce protocol, Naughton,
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38 E. Karnabi
Table 4.4 Bruce protocol

Stage Minutes % Grade MPH METS
1. 3 10 1.7 5
2. 6 12 2.5 7
3. 9 14 3.4 10
4. 12 16 4.2 13
5. 15 18 5.0 15
6. 18 20 5.5 18
7. 21 22 6.0 20
Blake, and Cornell protocols. Each varies according to the speed and grade
parameters. The Bruce protocol is the most widely used and validated; the pro-
tocol is divided into 3-min stages that increase in speed and inclination
(Table 4.4).
The disadvantages of the Bruce protocol is the large variations in workload
between stages and therefore, lowering the diagnostic sensitivity and reducing the
value in evaluating functional capacity. The modified Bruce protocol provides a
lower workload for patients with poor cardiovascular fitness and in less fit/sedentary
and older individuals with stages of 0 and ½ being included at 0 and 5 % grades
respectively at 1.7 MPH. The Naughton protocol is well suited for older debilitated
patients (less intense); with the Blake protocol for younger and fit patients; In addi-
tion, the ramp protocol is especially useful in heart failure patients in conjunction
with cardiopulmonary metabolic testing.
Technique
The tests starts with patient preparation: NPO for at least 4–6 h and instructed
to bring comfortable clothing and shoes for the procedure. A thorough review
of the patients’ history, medications and physical exam should be performed. A
proper indication as listed in Table 4.1 should be reviewed. The patient should
sign an informed consent after explaining the indication, possible complications
and risks of the procedure, which include a risk of 1:10,000 of a serious adverse
event (MI or death), and alternative testing. If the test is being done for the
diagnosis of CAD, then certain cardiovascular drugs should be withheld if pos-
sible, such as beta-blockers, non-dihydropyridine calcium channel blockers
(diltiazem and verapamil), and digoxin, certain antiarrhythmics (e.g.
Amiodarone and sotalol), or anti-anginal medications (nitrates); this ideally
should be done after discussion and under the supervision of their supervising
physician. If the test is for functional purpose or to assess symptoms or isch-
emia, on optimal medical treatment, then cardiovascular medications should be
continued.
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The next step is to choose the optimal stress test to achieve a satisfactory
workload. The choice is usually between a Bruce and Modified Bruce protocol
depending on the patients’ ability to exercise appropriately to reach the target
heart rate response, which is 85 % of his/her age, predicted maximal heart rate
(APMHR) (220-Age.) A patient’s capacity is also predicted based on the
reported activity level and direct observation prior to the test. The preferred
approach is a symptom-limited exercise testing and not simply achieving 85 %
of the APMHR.
A baseline ECG should be performed to exclude significant abnormalities that
can render the ECG non-diagnostic such as: pre-excitation (Wolff-Parkinson-White
syndrome), ventricular-paced rhythm, left bundle branch block (LBBB), more than
1 mm ST depressions at rest, digoxin use with associated ST abnormalities, and left
ventricular hypertrophy (LVH) with ST-T wave abnormalities. Next the patient is
instructed on the body position during the treadmill exercise by walking erect, near
the front of belt with the hands resting on the handrail.
Data are obtained during each stage of the protocol and in recovery with
attention paid to any ST depressions or elevations and arrhythmias. Blood pres-
sure measurements should be performed prior to exercise and during the last
minute of each stage, as well as during recovery. A normal hemodynamic
response to exercise is an increase in systolic and decrease in diastolic pres-
sures. The patient should be visually monitored for any signs of distress and
asked frequently about the development of symptoms such as exercise limiting
or non-limiting angina. As mentioned, most exercise stress tests should be
symptom limited maximal stress tests. Achievement of 85 % of APMHR is not
an indication for termination of the test. The testing endpoints can be patient
related or physician related. In general, if a patient is requesting to stop, it is
usually an indication to terminate the test especially if it is associated with
symptoms (such as chest pain, dyspnea, dizziness, claudications and fatigue) or
arrhythmia. The clinician on the other hand, can decide to terminate the test if
there are marked ST depressions or elevations, a new bundle branch block that
cannot be distinguished from ventricular tachycardia (VT), new high grade AV
block, sustained VT or ventricular fibrillation, increasing frequency of ven-
tricular ectopy, and onset of supraventricular tachyarrhythmias, as well as
hypotensive BP response to exercise.
Table 4.5 lists the absolute and relative indications for terminating exercise
testing:
If the test is performed in conjunction with myocardial perfusion imaging, the
radiopharmaceutical is injected as close to the peak exercise and the patient encour-
aged to exercise for at least 1 min after the injection.
Post-exercise recovery period should follow the termination of the test; the
patient should be continued to be monitored until the HR < 100–110 and SBP < 160
or at the baseline level. It is common and not pathologic for the BP to fall in the
immediate post-exercise period.
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40 E. Karnabi
Table 4.5 Indications for terminating exercise testing

Absolute indications
Drop in systolic blood pressure of >10 mmHg from baseline BP despite an increase in workload,
when accompanied by other evidence of ischemia
Moderate to severe angina
Increasing nervous system symptoms (e.g., ataxia, dizziness, or near-syncope)
Signs of poor perfusion (cyanosis or pallor)
Technical difficulties in monitoring ECG or systolic BP
Subject’s desire to stop
Sustained ventricular tachycardia
ST elevation (≥1.0 mm) in leads without diagnostic Q-waves (other than V1 or aVR)
Relative indications
Drop in systolic BP of ≥10 mmHg from baseline BP despite an increase in workload, in the
absence of other evidence of ischemia
ST or QRS changes such as excessive ST depression (>2 mm of horizontal or downsloping
ST-segment depression) or marked axis shift
Arrhythmias other than sustained ventricular tachycardia, including multifocal PVCs, triplets of
PVCs, supraventricular tachycardia, heart block, or bradyarrhythmias
Fatigue, shortness of breath, wheezing, leg cramps, or claudication
Development of bundle-branch block or IVCD that cannot be distinguished from ventricular
tachycardia
Increasing chest pain
Hypertensive response (systolic BP of >250 mmHg and/or a diastolic BP > 115 mmHg)
Data Interpretation
Interpretation should be performed by an experienced physician. The test can be

positive, negative, or non-diagnostic. A test is non-diagnostic if the patient does not
achieve the target heart rate of 85 % (APMHR = 220-age), or if the baseline ECG is
abnormal making the ST changes un-interpretable during exercise. In such cases,
the ET is combined with an imaging modality.
The data are analyzed for ECG abnormalities, arrhythmias, symptoms, and func-
tional capacity.
ECG abnormalities ST-segment changes deviating from the isoelectric line
(determined by the PR segment) are measured 80 milliseconds (ms) beyond the
J-point. A normal response to exercise is <1 mm ST horizontal or downsloping
depressions, or <15 mm when upsloping ST depression is noted (Fig. 4.2). A few
diagnostic principles for interpreting ET are: (1) The more leads with ST changes
present, the higher probability of ischemia; (2) ST depressions do not localize
ischemia to an area of the myocardium; (3) horizontal or downsloping ST depres-
sion >1 mm and upsloping depression of >2 mm is abnormal; (4) ischemic ST
depression usually occur in the lateral leads (I, V4–6); (5) isolated inferior
changes are usually false positive findings secondary to diaphragmatic motion
and/or atrial repolarization; (6) changes in R wave amplitude or T wave inversion
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80 ms 80 ms 80 ms
J-point J-point J-point

J-point
Baseline ECG Classic upsloping >1mm horizontal >1mm downsloping >1mm ST elevation
response to exercise ST depression ST depression
Fig. 4.2 ST segment changes at baseline and during exercise. Classic normal upsloping is seen in
normal individuals if the ST segment returns to the isoelectric line by 80 ms after the J-point.
Abnormal responses are >1 mm horizontal, downsloping and upsloping ST depressions 80 ms past
the J-point
are not specific markers of ischemia; (7) ST elevation in the setting of Q-waves,
represent a prior MI and is the result of abnormal wall motion such as in dyski-
netic segment or aneurysm; (8) ST segment elevation represents ischemia and
may localize the area of ischemic myocardium; (9) U wave inversion may be
associated with ischemia.
Arrhythmias Sustained VT and VF although rare, are abnormal findings that should
prompt further evaluation.
Time to recovery of both ST changes and heart rate are two additional parameters
to analyze. If rapid recovery (<1 min) of ST changes occurs, the less likelihood
ischemia is present. Heart rate recovery is another important prognostic indicator. It
is considered abnormal if the difference between maximum HR at peak stress and
at 1 min into recovery is 12 beats or less.
Blood pressure monitoring is another important aspect of exercise testing for safety
and diagnostic reasons. A normal hemodynamic response is an increase in systolic
BP and a decrease in diastolic BP. The test can be terminated if there is a drop of
systolic BP with increasing workload especially to below the resting BP or exces-
sive systolic BP elevation (SBP > 260). The patient’s symptoms should be recorded
throughout the procedure and reported.
Prognosis The Duke Treadmill Score (DTS) calculated as: exercise minutes –
(5 × maximal ST changes) – (4 × angina score) is an important predicator of mortal-
ity. The angina score is defined as no angina = 0, non-limiting angina = 1, and
limiting angina = 2. A low DTS score is >5, intermediate risk DTS −10 to <5, and
high risk DTS < −10. The functional capacity is calculated based on the exercise
time with an exercise period of 6 min yielding 7 METS; this is associated with a
lower mortality rate independent of any ST changes.
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42 E. Karnabi
Diagnostic accuracy The sensitivity of exercise stress tests is approximately 68 %

and specificity of 70 %, which can be improved with careful patient selection.
Myocardial perfusion imaging with exercise stress testing enhances the diagnostic
sensitivity and specificity especially in patients with patients with resting ECG
abnormalities as mentioned above.
Complications
Complications of exercise testing are rare especially in the healthy low risk patients
and increases in the CAD and arrhythmia patients. Arrhythmic events are common
in those with a history of prior arrhythmia and can occur in up to 10 %; on the con-
trary, in healthy subjects the overall incidence is approximately 0.1 %. The most
common arrhythmia is atrial fibrillation. VT and VF are rare and occur in 6 per
10,000 tests and <1 per 10,000 test respectively. Death is extremely rare but may
occur in 1 per 25,000 tests. Other cardiovascular complications include ischemia
with angina and infarction, brady-arrhythmias such as bundle branch blocks and AV
blocks, congestive heart failure, hypertension, hypotension and aneurysm rupture.
Non-cardiovascular complications include pulmonary (asthma, bronchospasm,
exacerbation of underlying pulmonary disease), gastrointestinal (nausea, vomiting),
neurological (dizziness, syncope, stroke), and musculoskeletal (muscle cramps,
joint pain, exacerbation of musculoskeletal disease, back pain) which are more
common.
Clinical Vignettes
Case 1
Fifty year old male with hypertension and hyperlipidemia who has been experi-
encing episodic chest discomfort during lifting and with heavy exertion. The
pain is described as a sharp pain in the mid chest without any radiation. His
baseline ECG was normal. His primary care physician sent him for an exercise
ECG stress testing. He was able to exercise for 5:29 min at which point the test
was terminated after he started experiencing non-limiting chest pain and the
ECG findings as noted in (Fig. 4.3). His blood pressure at peak stress was
152/68.
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Fig. 4.3 Case #1 (see text for details)
The case presents a patient in the intermediate risk group with atypical chest
pain. According to Bayes theorem and the appropriateness criteria, he should
undergo an exercise stress test especially with a normal baseline ECG. During max-
imal exercise, the patient experienced chest pain with >2 mm ST depressions in
inferior leads and >3 mm ST depressions in lateral leads (V4–6). This is considered
a positive response. The patient had a cardiac catheterization that showed 95 % ste-
notic left circumflex artery.
Case 2
Sixty-eight-year-old female with history of left breast cancer s/p mastectomy and
radiation, hypertension, tobacco use is being evaluated for pre-op testing and risk
stratification prior to contralateral mastectomy. A stress test was ordered. She was
able to reach stage 3 when suddenly she started feeling palpitations and lighthead-
edness. The tracings are shown in (Fig. 4.4).
The tracings show the patient converting from sinus tachycardia to a sustained
ventricular tachycardia, which is an abnormal response indicative of ischemia or
infarction and is associated with a worse outcome and increased mortality. Further
evaluation is warranted.
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44 E. Karnabi
References
1. Gibbons RJ, et al. ACC/AHA 2002 guideline update for exercise testing: summary article. A
report of the American College of Cardiology/American Heart Association Task Force on
Practice Guidelines (Committee to update the 1997 exercise testing guidelines). J Am Coll
Cardiol. 2002;40(8):1531–40.
2. Wolk MJ, et al. ACCF/AHA/ASE/ASNC/HFSA/HRS/SCAI/SCCT/SCMR/STS 2013 multi-
modality appropriate use criteria for the detection and risk assessment of stable ischemic heart
disease: a report of the American College of Cardiology Foundation Appropriate Use Criteria
Task Force, American Heart Association, American Society of Echocardiography, American
Society of Nuclear Cardiology, Heart Failure Society of America, Heart Rhythm Society,
Society for Cardiovascular Angiography and Interventions, Society of Cardiovascular
Computed Tomography, Society for Cardiovascular Magnetic Resonance, and Society of
Thoracic Surgeons. J Am Coll Cardiol. 2014;63(4):380–406.
3. Fihn SD, et al. 2014 ACC/AHA/AATS/PCNA/SCAI/STS focused update of the guideline for
the diagnosis and management of patients with stable ischemic heart disease: a report of the
American College of Cardiology/American Heart Association Task Force on Practice
Guidelines, and the American Association for Thoracic Surgery, Preventive Cardiovascular
Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of
Thoracic Surgeons. J Am Coll Cardiol. 2014;64(18):1929–49.
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Chapter 5
Cardiopulmonary Exercise Testing
Alexis P. Rodriguez
Introduction
The concomitant gas exchange measurement furthers the modality of exercise test-
ing by estimating oxygen consumption at different exercise intensities. Oxygen con-
sumption, in turn, can be approximated to the measurable metabolic equivalent
(MET). Cardiopulmonary exercise testing (CPET) remains the sole method for the
direct MET measurement. During this test, many variables are recorded including
the expiratory ventilation, pulmonary gas exchange (oxygen uptake and carbon diox-
ide output), along with electrocardiogram (ECG) and blood pressure recordings [1].
Indications
Assessment of a patient with CPET allows for the evaluation of unexplained dys-
pnea, exercise intolerance, and cardiopulmonary disease extent including the evalu-
ation of patients with heart failure. Additionally, there are new emerging applications
of this diagnostic tool including the evaluation of congenital heart disease in adults,
pulmonary hypertension, arrhythmia-induced heart failure, rate-response and biven-
tricular pacemaker evaluation, disability-fitness assessment, and even prior to pul-
monary resection. As more clinicians familiarize with this test, and data continue to
emerge, CPET applications will continue to broaden including in the distinction and
evaluation of pulmonary versus cardiac pathologies [1].
A.P. Rodriguez, MD
University of Miami, Miller School of Medicine, Miami, FL, USA

DOI 10.1007/978-1-4471-7290-1_5
ERRNVPHGLFRVRUJ
46 A.P. Rodriguez
Contraindications
Absolute contraindications include acute myocardial infarction, unstable angina and

arrhythmias, acute myopericarditis, severe symptomatic aortic insufficiency, acute pul-
monary embolism, uncontrolled asthma, and cognitive impairment limiting subject’s
cooperation. The ordering clinician should also be aware of relative contraindications.
These include, left main (or three-vessel) coronary disease, severe uncontrolled (pulmo-
nary) hypertension, high degree AV block, hypertrophic cardiomyopathy, moderate val-
vular stenosis, pregnancy, and orthopedic impairment. Furthermore, the test should be
terminated early at the patient’s request, severe ischemia on ECG, extreme blood pres-
sure responses, hypoxia, among others. On the other hand, some patients report discom-
fort with the facemask, mouthpiece, or nose clip. Thus, all these should be addressed
before starting the test. While all these appear commonsense, they serve to prove the need
for comprehensive initial patient assessment, and close monitoring during the exam.
Equipment
The CPET aim is to progressively increase subject’s workload as tolerated. This can
be attained by exercising the individual on either a treadmill or cycle ergometer. The
former is generally considered more appropriate for active subjects while also
allowing for higher oxygen consumption. On the other hand, the latter is preferred
in those at risk of falls, requires less training, and allows for blood pressure record-
ing more expeditiously. Besides the treadmill or cycle ergometer, the patient is out-
fitted with either a mask or mouthpiece for the gas sampling. Blood pressure is also
reordered serially throughout the test. A metabolic cart is used to measure the expire
gases. For accurate recordings, this system should be monitored and meticulously
calibrated to produce consistent results [2]. Figure 5.1 shows the air sealed mask
used for gas analysis.
Fig. 5.1 Air-sealed face

mask with tubing
connected to gas analyzer,
used to determine gas flow
and values during
metabolic testing
ERRNVPHGLFRVRUJ
5 Cardiopulmonary Exercise Testing 47
Technique
Different testing protocols have been developed for functional testing. Patient capa-
bilities and diagnostic goals generally determine the choice of CPET and protocol
modality. However, the principle is similar for all these, and requires the incremen-
tal monitored exercise effort until maximal exertion is reached. Some of these
include the Balke and Ware, Naughton, and ramp protocols. Irrespective of the one
used, it should be individualized and tailored to yield fatigue-limited exercise,
which, in ideal circumstances, should occur between 8 and 12 min. Shorter evalua-
tions produce unreliable non-linear relationships between oxygen uptake and work
performed. Contrariwise, more protracted regiments may result in testing termina-
tion due to specific muscle fatigue, as opposed to cardiopulmonary endpoints.
Finally, patients should be discouraged from significant handrail support since it
alters the relationship between oxygen uptake and work, by effectively reducing the
latter for any given measurement of the former.
Data Interpretation
During exercise, oxygen uptake (Vo2) can be estimated by the Fick Equation:
Vo 2 = ( SV ´ HR ) ´ ( Cao 2 - Cvo 2 )
SV represents the stroke volume, HR the heart rate, Cao2 the arterial oxygen
content, and Cvo2 the mixed venous oxygen. At maximal exercise, this equation
would reflect the subject’s ability to take in, exchange, transport, and utilize oxygen
for aerobic metabolism. The Vo2 response to exercise is linear until a maximum is
reached, and then begins to plateau. With higher metabolic workloads, the arterio-
venous oxygen difference increases, which is a physiologic response best noted in
trained athletes. On the other hand, exercise intolerance is evidenced by any changes
in the Fick equation that results in an abnormally low Vo2max, such as suboptimal
maximal heart rate response, decrease stroke volume, decrease in Cao2, or increase
in Cvo2 [3].
Other important estimations include the respiratory exchange ratio (RER) and
the ventilatory anaerobic threshold (VAT). The former is calculated by dividing the
carbon dioxide output by the oxygen uptake. The RER is determined by the main
source of metabolic fuel used; with a ratio of 1 indicative of carbohydrates while <1
represents a mix of carbohydrates and fat, or protein. RER may increase during
exercise due to either buffered lactic acid or hyperventilation. Conversely, VAT, or
anaerobic threshold, is a determinant of exercise capacity. This principle relies in
the fact that at lower workloads metabolism is mostly aerobic whereas there is a
shift to lactate production with increasing exercise intensity. The VAT can be deter-
ERRNVPHGLFRVRUJ
48 A.P. Rodriguez
mined by directly measuring blood lactic acid or bicarbonate content, or less reli-
ably through non-invasive techniques. Figure 5.2 shows a metabolic test graph
report. Normal parameters for CPET and patterns of abnormal results are shown in
Tables 5.1 and 5.2, respectively.
a
VO2 VCO2 VE/VO2 HR
4.0 4.0 60 220
3.6 3.6 54 198
3.2 3.2 48 176
2.8 2.8 42 154
2.4 2.4 36 132
2.0 2.0 30 110
1.6 1.6 24 88
1.2 1.2 18 66
0.8 0.8 12 44
0.4 0.4 6 22
0.0 AT RC 0
0.0 0
0 1 2 3 4 5 6 7 8 9 10
Time (Mid 5 of 7)
Fig. 5.2 Exercise metabolic test of a patient with history of heart failure. Panel a demonstrates the
continuous calculation of metabolic information, with the horizontal axis corresponding to time in
minutes. The green curve represents VE/VO2, heart rate in black, VO2 in red, and VCO2 in blue. The
vertical line labeled AT represents the aerobic threshold whereas RC represents the beginning of
the recovery portion of the test. AT is reached at the point where the VO2 and VCO2 curves cross each
other. From this point, VCO2 continues to be generated linearly whereas VO2 reaches a plateau. Panel
b lists all of the quantitative data. In this patient, the exertion portion started at 3:15 min, AT was
reached at 7:13 min, and maximal VO2 at 9:01 min. RER was 1.14, functional capacity was less
than 75 % of predicted, VO2 at anaerobic threshold was 13.7 ml/kg/min in the range of 40–49 % of
the predicted maximum. The heart rate reserve was high while on beta blocker, over 15 %. The VE/
VO2 was 24.4
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b
Spirometry
– FVC FEV1 1/FVC MVV –
Predicted 5.13 3.95 77 152
Pre
% Predicted
Exercise
Rest AT VO2 Max Pred AT / VO2 Max (%) VO2 Max/pred (%)
Time (min) 3:15 7:13 9:01
Ex time (min) 3.56 5.44
Speed (MPH) 1:1 2.7 2.6 104
Grade (%) 0:0 14:0 20:9 67
Borg PE
---- Oxygen Cons

VO2 (mL/kg/min) 3.0 13.7 15.2 28.7 90 53
VO2 (mL/min) 310 1407 1569 2955 90 53
VCO2 (mL/min) 256 1413 1481 3576 79 50
RER 0.83 1.00 1.14 88
METS 0.9 3.9 4.4 8.2 90 53
---- Ventilation
VE BTPS (L/min) 8.0 37.8 45.8 158.0 83 29
Vt BTPS (L) 0.68 2.04 2.43 84
RR (br/min) 12 19 19 98
BR (%) 94.9 76.1 71.0 107
VE/VO2 26 27 29 37 92 78
VE/VCO2 31 27 26 31 104 83
VE/MVV (%)
---- Cardiac ----

HR (BPM) 60 89 106 167 84 64
VO2/HR (mL/beat) 5 16 15 18 107 84
sysBP (mmHg) 110 128 128 100
diaBP (mmHg) 88 80 80 100
SpO2 (%)
Fig. 5.2 (continued)
CPET Complications
The most widely reported complications are those associated with exercise testing
(Chap. 4). and include fatigue, shortness of breath, cardiac arrhythmia, syncope,
and bronchospasm albeit unusually. The others are more complicated and may
require intervention, which can range from medications to more advanced tech-
niques such as cardioversion for unstable arrhythmias. Intolerance of the mask may
be a complication preventing adequate data collection.
ERRNVPHGLFRVRUJ
50 A.P. Rodriguez
Table 5.1 Predicted normal parameters for CPET

Variable Predicted and normal range values
VO2, max (ml/min) Based on age, gender, and height
Lower limit of normal <80 % predicted
Resting VO2, (ml/min) 150 + (6 × weight in kg)
250–300 in larger obese individuals
Peak Heart Rate (bpm) 220 – age
210 – (age × age)
90 % predicted ± 15 bpm
Oxygen Pulse (mL/beat) (Predicted VO2, max)/(Predicted max HR)
Normal – 80 % predicted (about 15 mL/beat in men, and 10 mL/
beat in women)
Minute ventilation (L/ Peak Exercise: 70–80 % of MVV
min)
Maximum tidal volume 60 % of functional vital capacity
VE/VCO2 Early in exercise 25–35
VE/VO2 Early in exercise 25–35
VD/VT 0.25–0.35 at rest
Should decrease with exercise
PETCO2 (mmHg) 38–42
Declines after ventilator support
PETO2 (mmHg) 95–100
Rises after ventilator support
A-a O2 gradient Rest: 10–20
Peak exercise: 15–30
SaO2 (%) >95 % and should remain constant throughout
Respiratory exchange Rest: 0.6–1.0
ratio Peak exercise: 1.1–1.3
Clinical Vignettes
Case 1
A 54 year-old gentleman with a history of heart failure with reduced ejection

fraction (HFrEF) of non-ischemic etiology is referred by his heart failure physician.
His EF has been less than 30 % for the last 2 years. He is compliant with his goal-
directed optimized medical regiment, and over the last year he received a bi-
ventricular pacemaker, upgraded from his prior AICD. He has not been admitted
for symptom exacerbation over the last 6 months, but complaints of shortness of
breath with minimal exertion. He has otherwise, no significant medical comorbid
conditions, and has a reliable social and family support. The patient undergoes
CPET and his oxygen uptake (Vo2) is calculated at 9 ml/kg/min, and his respiratory
exchange ratio (RER) is estimated at 1.20.
ERRNVPHGLFRVRUJ
Table 5.2 Cardiopulmonary exercise testing patterns in normal and individuals with various
pathologies
Cardiopulmonary exercise testing
Cardiov. Pulm. Vasc. Neurom.
Variable Normal disease COPD disease disease
VO2, max Normal Decreased Decreased Decreased Decreased
Heart rate Absent to Absent to Large Small Large
reserve small reserve small reserve (>30 bpm) (20– (>30 bpm)
(<20 bpm) (<20 bpm) 30 bpm)
VE, max/MVV <0.8 <0.8 >0.8 <0.8 <0.8
(Ventilatory
reserve)
Ventilatory Present Present Absent Present Usually
threshold present
Dead space Decreased Decreased Decreased Stable or Decreased
(VD/VT) increased
O2 Sat Within Within Decreased Decreased Within normal
normal limits normal limits limits
End tidal CO2 Decreased Decreased Increased or Decreased Increased or
stable stable
Reason for Lower Lower Dyspnea Dyspnea, Fatigue
early extremity extremity lower
termination fatigue fatigue extremity
fatigue
This heart failure patient is referred for risk-stratification purposes. He still com-
plaints of shortness of breath with minimal exertion, despite optimized medical
therapy, as well as BiV-AICD. CPET has been used, and published trials have been
reported, for the stratification of heart failure patients, and in the prediction of their
mortality. His oxygen uptake is low while his respiratory exchange ratio is high.
This combination is rather worrisome despite no late admissions for acutely decom-
pensated heart failure symptomatology. This particular cohort of patients is classi-
fied as “very high risk.” Patients with Vo2 below 10 ml/kg/min, especially with
RER > 1.15, are at the highest risk for adverse cardiovascular events and their
mortality rate is higher than any other heart failure group. Indeed, these results war-
rant further evaluation for more advanced heart failure therapies, i.e. ionotropes,
ventricular devices, or cardiac transplantation.
In contrast, patients with Vo2 values ranging between 10 and 18 ml/kg/min should
have their minute ventilation (VE) and carbon dioxide output (Vco2) measured for
further stratification. The slope, or rate of change, of the curve between VE and Vco2
is then estimated. If the slope is greater, or equal to 35 then the patient is considered to
have a mortality similar to those with Vo2 below 10 ml/kg/min, which would warrant
re-stratification by RER determination. In turn, those with lower slope values, less than
35, are at moderate risk. Finally, if the Vo2 is higher than 18 ml/kg/min, these patients
are deemed low risk and regular follow up with their cardiologist is indicated.
ERRNVPHGLFRVRUJ
52 A.P. Rodriguez
Case 2
A 45 year old lady with history of pulmonary arterial hypertension (PAH) diag-
nosed by echocardiography and right sided catheterization (RHC) is referred for
CPET evaluation prior to starting bosentan and revatio. Her right ventricular sys-
tolic pressure by 2D echo and RHC was estimated at 75 and 85 mmHg respectively.
She undergoes successful initial evaluation by lower extremity ergometer, and her
VO2 is 9 mL/kg/min. The VE/Vco2 slope was estimated at 61.
This patient presents with an established PAH diagnosis. She is being referred prior
to starting therapy for her condition. From the values obtained by echocardiography
and RHC, the severity of her disease can be estimated. This is further corroborated by
her low VO2 and high VE/Vco2 slope, both of which are consistent with severe PAH. In
fact, they are indicative of a high-risk patient, who requires aggressive expeditious
intervention. There is extensive published data on the role of CPET in PAH. Serial
testing is indicated after starting therapy for conditioning monitoring, and possible
improvement. In patients whose CPET values trend towards normalization, so do the
RHC hemodynamics, 2D echocardiography, NT-proBNP, and symptoms. While
CPET has no role in the screening of this pathology as of yet, it has been suggested for
high-risk patients, especially those with genetic predisposition. Neither is CPET
meant to be the unique monitoring method in this patient population; however, it
should be employed as another non-invasive tool, which has been extensively
validated.
References
1. Albouaini K, Egred M, Alahmar A, Wright DJ. Cardiopulmonary exercise testing and its appli-
cation. Postgrad Med J. 2007;83(985):675–82.
2. American Thoracic Society; American College of Chest Physicians. ATS/ACCP statement on
cardiopulmonary exercise testing. Am J Respir Crit Care Med. 2003;167(2):211–77.
3. Brooks GA. Anaerobic threshold: review of the concept and directions for future research. Med
Sci Sports Exerc. 1985;17(1):22–34.
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Chapter 6
Pharmacologic Stress Testing
Eddy Karnabi and Robert C. Hendel
Exercise stress testing is usually the preferred stress testing modality unless the
patient is unable to exercise or achieve the target heart rate response or possess con-
traindications to exercise. Additionally, in the presence of LBBB or ventricular
paced rhythm, pharmacological stress testing is the modality of choice. Because the
sensitivity of pharmacological stress ECG alone is low, a cardiac imaging modality
is needed. Pharmacological stress testing is divided into vasodilator stress with the
three available agents: adenosine, dipyridamole, or regadenoson or with a catechol-
amine, dobutamine.
Vasodilator stress is usually in combination with myocardial perfusion imaging
(SPECT-single photon emission computed tomography or PET-positron emission
tomography), and less frequently with coronary artery CT and cardiac magnetic
resonance. Vasodilators agents exert their effects by acting on the adenosine recep-
tors by increasing coronary blood flow and causing a hyperemic response. The
rationale behind using vasodilators is due to the significant coronary artery vasodi-
lation that results in three to fourfold increase in blood flow (Fig. 6.1). A normal
coronary artery will exhibit a normal hyperemic response. In a stenotic coronary
segment, relative flow heterogeneity is induced which is visualized with myocardial
perfusion imaging, with a relative decrease tracer activity within the potentially
ischemia zone of myocardium (Fig. 6.2).
The very short half-life of adenosine mandates that the infusion continue during
the radiopharmaceutical delivery and uptake (1–2 min). However, the offset of
hyperemia is also very rapid. In contrast, dipyridamole and regadenoson have a
E. Karnabi, MD, PhD FASE (*)

R.C. Hendel, MD, MASNC, FACC, FAHA
Cardiovascular Division, University of Miami, Miller School of Medicine,

DOI 10.1007/978-1-4471-7290-1_6
ERRNVPHGLFRVRUJ
54 E. Karnabi and R.C. Hendel
Auto-regulation flow = pressure/resistance
Rest 1 ml/gm/min
4 Hyperemia 2–4 ml/gm/min
Coronary Flow Rate

(ml/gm/min)
3 Hyperemia
1
Rest
20 40 60 80 100
Percent stenosis by diameter
Fig. 6.1 Auto-regulation of flow in normal and hyperemic states (Adapted from Gould et al. [3]).
At rest, coronary flow rate is approximately 1 ml/g/min. As coronary stenosis worsens to ~90 %,
symptoms develop. During vasodilator pharmacological stress testing, coronary flow rates increase
two to fourfold and coronary stenosis can be detected at 60–70 % stenosis
Fig. 6.2 Coronary flow in normal and stenotic a

arteries during rest and vasodilator stress
testing. In normal state (a), flow distal to
stenosis is compensated by vasodilation distal
to the obstruction. During vasodilator stress
testing (b), non-obstructed coronary arteries
induce hyperemic response with increased
flow. However, in stenotic arteries, the area Rest
distal to stenosis is already maximally dilated
at rest and cannot further dilate during stress.
This creates a relative hypoperfusion on MPI
compared to the normally perfused
myocardium
b
Stress
longer duration of action and may require reversal with aminophylline should side
effect develop. Regadenoson is a selective A2A agonist, which limits the stimula-
tion of non-vasodilatory receptors and reduces adverse effects. Additionally, this
agent is not depend on weight based dosing.
Dobutamine is most commonly used with echocardiography but may also be
used in conjunction with nuclear cardiology methods and CMR. Similar to exercise
testing, dobutamine induces a positive inotropic and chronotropic response with
ERRNVPHGLFRVRUJ
6 Pharmacologic Stress Testing 55
increase in heart rate and systolic pressure, thereby, increasing myocardial oxygen
consumption and induces ischemia and wall motion abnormalities or perfusion
defects in the myocardium supplied by a stenotic coronary artery.
Indications
The indications for pharmacological stress testing is similar to exercise stress test-
ing (see Chap. 4) and according to the 2002 ACC/AHA guidelines [1] (Table 6.1).
Contraindications
All pharmacologic testing modalities should be avoided in patients with unstable

clinical conditions such as hypotension, decompensated heart failure, unstable cor-
onary syndromes or recent ACS, uncontrolled arrhythmias, and severe aortic steno-
sis. Absolute contraindication is hypersensitivity to any of the stress agents.
With regards to the use of vasodilator stress, the contraindications are related to
the effects on the other adenosine receptors (Table 6.2).
Table 6.1 Indications for stress testing

1. Symptoms suggestive of CAD
2. Acute chest pain after ACS is ruled out
3. Recent ACS not treated with coronary angioplasty
4. Known CAD and change in clinical status
5. Prior incomplete revascularization
6. Newly diagnosed cardiomyopathy
7. Certain cardiac arrhythmias: atrial fibrillation, PVCs, VT
8. Pre-op cardiac assessment prior to non-cardiac surgery
Table 6.2 Contraindications for vasodilator stress testing [2]

1. Asthma or COPD with active wheezing
2. Second or third degree AV block
3. Profound bradycardia (<40)
4. SBP < 90
5. Use of methylxanthines (aminophylline, caffeine) in last 12 h
6. Recent use of dipyridamole
7. Known hypersensitivity for the stress agent
8. Critical AS
9. Use of regadenoson or adenosine in patients taking dipyridamol
ERRNVPHGLFRVRUJ
Table 6.3 Contraindications to dobutamine stress testing

1. Recent ACS
2. Severe symptomatic AS (Mean PG > 40)
3. LV outflow obstruction
4. Arrhythmias: SVT with rapid response, hx of VT
5. Uncontrolled hypertension
6. Aortic dissection or large aneurysm
In cases of asthma or severe COPD with ongoing wheezing, and high degree AV
block, dobutamine is an acceptable alternative. Dobutamine is a positive inotropic
and chronotropic agent and should be avoided in situations where the hemodynamic
effects may exacerbate existing conditions (Table 6.3).
In cases of severe hypertension and uncontrolled atrial fibrillation, vasodilator
stress is an acceptable alternative. Atropine, when used in conjunction with dobuta-
mine, should be avoided in patients with glaucoma, obstructive uropathy and pros-
tate hypertrophy, and chronic lung disease.
Equipment
The equipment required are similar to those of exercise testing: room with a bed/
stretcher, peripheral IV line, crash cart, ECG and BP recording, and an infusion
pump for dobutamine, adenosine or dipyridamole. The monitor with vital signs and
ECG recording is recorded every minute during the infusion and 3 min during recov-
ery. In addition to the crash cart medications, an access to nitroglycerin, beta-blockers
and aminophylline is required in case side effects and/or complications arise.
Technique
Vasodilator Stress Patient preparation includes NPO status for at least 4–6 h and
avoidance of caffeine and methylxanthines for at least 24 h. A careful review of his-
tory and a physical exam is performed to detect any cardiac abnormalities such as
severe AS or active wheezing. Informed consent is obtained after reviewing for
appropriate indications. A peripheral IV is started and ECG electrodes connected
and baseline BP recorded. ECG is reviewed to detect any contraindications for test-
ing. Depending on the protocol, either an infusion or injection is performed
(Fig. 6.3). Adenosine is given as a continuous infusion at a rate of 140 mcg/kg/min
over 6 min (Fig. 6.3). The radiotracer or contrast agent is injected after 3 min.
Dipyridamole is administered as 0.56 mg/kg IV over 4 min or 142 mcg/kg/min, fol-
lowed by radiotracer injection after 7 min (Fig. 6.3). Regadenoson is given as a
rapid injection of 0.4 mg over 10 s, followed by a saline flush (Fig. 6.3). Monitoring
involves ECG recording every minute and BP every 2–3 min. If patient exhibits an
adverse reaction or becomes symptomatic, either stopping the infusion (adenosine)
ERRNVPHGLFRVRUJ
Fig. 6.3 Pharmacological a

stress infusion protocols
[2]. (a) Adenosine stress Adenosine infusion
infusion protocol, (b) 140 mcg/kg/min
Dipyridamole stress
Radiotracer
infusion protocol, (c)
injection
Regadenoson stress Stop
infusion protocol, (d) infusion MPI imaging
Dobutamine stress infusion
protocol
45–60 min
0 3 6
b
Dipyridamole infusion
142 mcg/kg/min
Stop
infusion Radiotracer
injection
MPI imaging
45–60 min
0 4 7
c
Rapid Regadenoson
infusion 0.4 mg
Flush Radiotracer
injection
MPI imaging
45–60 min
0 0.5
Radiotracer
d injection
MPI imaging
Dobutamine infusion 40
30
20
10
Atropine
5
1-2 mg
3 6 9 12
ERRNVPHGLFRVRUJ
Table 6.4 Indications for stopping a vasodilator

1. Hypotension with SBP < 80 or 20 mmHg fall that is accurate
2. ST depressions >3 mm without angina or >2 mm with angina
3. Persistent 2nd or 3rd° AV block
4. Severe angina, dyspnea, dizziness, headache, syncope
5. Arrhythmias
6. Active wheezing
or giving a reversal agent (dipyridamole, regadenoson), aminophylline 125 mg IV

over 1 min should be done. Of note, aminophylline, if possible, should be delayed
for at least 1-min post tracer/contrast administration to allow uptake, which will
reflect the hyperemic state (Table 6.4).
Dobutamine Stress Patient preparation includes NPO status for at least 4–6 h and
avoidance of beta-blockers for 24 h. A careful review of history and a physical exam
is performed to detect any cardiac abnormalities such as severe AS. Informed con-
sent is obtained after reviewing for appropriate indications. A peripheral IV is
started and ECG electrodes connected and baseline BP recorded. ECG is reviewed
to detect any contraindications for testing. Dobutamine is infused at gradual increas-
ing doses from 5, 10, 20, 30, and 40 mcg/kg with the option of giving 1–2 mg atro-
pine after 30 mcg/kg dose to achieve 85 % APMHR (Fig. 6.3). The infusion should
be terminated immediately with the development of unwanted effects and reversal
with IV beta blockers is advised for continued ischemia.
Data Interpretation
Similar to the exercise testing, pharmacological stress testing may be reported as

positive, negative or non-diagnostic ECG response depending on the ECG changes
observed (see Chap. 4). Isolated pharmacological ECG testing has low sensitivity and
is always combined with other forms of imaging especially with vasodilator stress.
Complications
Death and serious complications from pharmacological stress testing are very rare
(<1/10,000) in the properly selected patients. Adverse effects, although common
(50–75 % incidence), are usually mild and bothersome but without major safety
concerns. They are either self-limited and dissipate with the cessation if infusion or
if intolerable, a reversal agent can be given (Table 6.5).
Combining low-level exercise and vasodilator stress reduces the side effects and
enhances image quality and increases detection of myocardial ischemia. The
ERRNVPHGLFRVRUJ
Table 6.5 Common adverse effects of Vasodilators

pharmacological stress agents
Flushing
Chest pain
Dizziness
Dyspnea
GI discomfort
Nausea
Headache
ST changes
AV block
Hypotension
Dobutamine
Chest pain
Headache
Palpitations
GI discomfort
Nausea
Dyspnea
ST changes
Arrhythmias
Hypertension
exceptions are left bundle branch block and ventricular paced rhythm where the
increased heart rate results in artifacts.
Clinical Vignettes
Case 1
Seventy-four year old female with multiple risk factors for coronary artery disease
including a strong family history, active tobacco use, diabetes mellitus, hyperlipid-
emia with occasional chest discomfort is sent for vasodilator pharmacological
stress testing. She denied any history of COPD or cardiac conduction abnormali-
ties. Physical exam is normal with no active wheezing. ECG at baseline was normal
without ST or T wave abnormalities. Adenosine stress testing was performed. Two
minutes post infusion the patient started complaining of lightheadedness; the ECG
obtained is shown in (Fig. 6.4).
The patient had an adverse adenosine A1 receptor effect with complete AV
block. The first step in urgent management should be immediately stopping the
adenosine infusion and injecting 125 mg IV aminophylline, if the heart block per-
ERRNVPHGLFRVRUJ
sists. With regadenoson and dipyridamole, this adverse effect usually occurs after
the stress agent administration. Thus, aminiophylline and additional patient moni-
toring is necessary.
Case 2
Fifty-four-year-old male with long standing history of smoking and cocaine use was
admitted to the hospital with chest pain. He was ruled out for ACS and sent for
stress testing. An exercise stress testing could not be performed due to lower extrem-
ity amputation. During the physical examination, he was actively wheezing, there-
fore, dobutamine stress test was performed. During the infusion, the patient
complained of angina. An ECG is shown in (Fig. 6.5).
The ECG shows development of ST elevations during dobutamine infusion;
myocardial infarction during testing is a rare side effect that should be promptly
recognized and treated urgently with cardiac catheterization. The dobutamine infu-
sion should be terminated immediately and NTG administered. Also, a beta-blocker
should be given, so as to reduce the increased myocardial oxygen demand provoked
by dobutamine.
ERRNVPHGLFRVRUJ
Case 3
Sixty-four year-old female with multiple cardiovascular risk factors admitted to the
hospital with atypical chest pain. After ACS was ruled out with negative cardiac
biomarkers, she underwent a pharmacological stress test with regadenoson.
Following the 0.4 mg IV infusion she developed flushing, dizziness and intractable
headache. What is the next best step in management?
This case presents a common side effect of regadenoson which may include
flushing, chest pain, dizziness, dyspnea, GI discomfort, nausea, headache, hypoten-
sion, ST changes and AV block. Ideally, for optimal tracer uptake, reversal agent’s
administration, such as aminophylline, should be delayed for 1 min to allow uptake
by the myocardium. In this particular case, if the headache is intractable, amino-
phylline should be given, otherwise, mild symptoms can be treated with caffeine
consumption.
References
1. Gibbons RJ, et al. ACC/AHA 2002 guideline update for exercise testing: summary article. A
report of the American College of Cardiology/American Heart Association Task Force on
Practice Guidelines (Committee to update the 1997 exercise testing guidelines). J Am Coll
Cardiol. 2002;40(8):1531–40.
2. Henzlova MJ, et al. ASNC imaging guidelines for SPECT nuclear cardiology procedures:
stress, protocols, and tracers. J Nucl Cardiol. 2016. doi:10.1007/s12350-015-0387-x.
3. Gould KL, Lipscomb K, Hamilton GW. Physiologic basis for assessing critical coronary steno-
sis. Instantaneous flow response and regional distribution during coronary hyperemia as mea-
sures of coronary flow reserve. Am J Cardiol. 1974;33(1):87–94.
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Chapter 7
Stress Echocardiography
For more than 40 years ago, the decrease in contractile function of the heart during
acute ischemia/infarction has been demonstrated with two-dimensional echocar-
diography and it was around the 1980s that the impact of its use with pharmacologi-
cal stress became clinically obvious. Stress echocardiography (SE), is an inexpensive,
relatively simple procedure with high diagnostic accuracy, that may be performed
either with exercise (treadmill or bicycle) or with pharmacological stress, predomi-
nantly dobutamine.
Indications
Currently, there are about 50 indications for (SE) which can be classified into the
following groups:
• Localization of coronary ischemia and diagnosis of CAD
• Prognosis and risk stratification in patients with established diagnosis
• Preoperative risk assessment
C. Gallegos, MD
Section of Cardiovascular Medicine, Yale University School of Medicine,
333 Cedar Street, New Haven, 208017, USA
R.C. Hendel, MD (*)
Cardiovascular Division, Miller School of Medicine, University of Miami,

DOI 10.1007/978-1-4471-7290-1_7
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Table 7.1 Common indications for stress echocardiography and their appropriateness [1]
Indication Appropriate use
Evaluation of ischemic equivalent/symptoms in patient with intermediate Appropriate
pretest probability
Acute Chest pain with low TIMI score and negative troponins Appropriate
Acute Chest pain with definite ACS Inappropriate
Detection of CAD in an asymptomatic patient with low CAD risk Inappropriate
Detection of CAD in patient with new-onset heart failure or left Appropriate
ventricular systolic dysfunction
Evaluation of arrhythmia without ischemic equivalent and no prior cardiac Appropriate
evaluation: Sustained VT, Ventricular fibrillation, frequent PVCs
Perioperative risk assessment for low-risk surgery Inappropriate
Perioperative risk assessment for intermediate risk surgery in patient with Inappropriate
moderate to good functional capacity
Stress echo for risk assessment in patient within 3 months of an ACS with Inappropriate
no recurrent symptoms and after complete revascularization
Stress echo for risk assessment in patient within 3 months of an ACS to Appropriate
evaluate for inducible ischemia
• Evaluation after revascularization, both surgical and percutaneous coronary

intervention
• Special subsets comprise estimation of severity of valvular disease especially in
aortic stenosis, hypertrophic cardiomyopathy, pulmonary hypertension, dyspnea
of suspected cardiac origin, and in patients with history of CAD scheduled for
elective high-risk surgical procedures
SE is often used when the electrocardiogram (ECG) exercise stress test is
non-diagnostic, and with patient who have an uninterpretable baseline ECG
Table 7.1 lists some of the indications based on the 2011 Appropriate Use
Criteria for Echocardiography and the 2014 Multimodality Appropriateness
Criteria.
Contraindications
Contraindications for stress echocardiography are those that are present for
either exercise testing (Chap. 4) or pharmacologic stress testing (Chap. 6).
Absolute contraindications for cardiac stress testing include: hemodynamic
instability, decompensated heart failure, acute myocardial infarction, including
the presence of a new left bundle branch block, patient with acute chest pain and
high pre-test probability of CAD, acute aortic dissection, high-risk unstable
angina, and severe aortic stenosis symptomatic or with severe left ventricle (LV)
enlargement or systolic dysfunction. Absolute indications to terminate stress
testing include moderate to severe angina, sustained ventricular tachycardia,
near syncope, drop in systolic pressure > than 10 mmHg from baseline in addi-
tion to other sings of ischemia [2, 3].
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7 Stress Echocardiography 65
Relative contraindications rely on the technique and comorbidities. In about 5 %

of cases, a poor acoustic window will severely limit the value stress echocardiogra-
phy. A difficult resting echocardiogram serves as a cue that no interpretable results
would be obtained during this test. Contrast administration should be considered for
improved opacification of the LV cavity (Chap. 3). Additionally, some conditions
may reduce the diagnostic accuracy of the test, including preexisting wall motion
abnormalities that tether adjacent segments. Hypertrophic cardiomyopathy and
other cardiomyopathies may also be problematic. Uncontrolled hypertension may
also prevent attaining an adequate level of stress.
Equipment
The stress portion of this procedure may be performed with exercise or with phar-
macological stressors-all required equipment should therefore be present, as out-
lined in previous chapters.
Ultrasound contrast agents may be needed for either with exercise or pharmaco-
logical studies and should be administered when two or more segments are not well
visualized to improve accuracy by opacifying the LV and enhancing the endocardial
border, and reducing the frequency of equivocal findings (Chap. 3).
A blood pressure cuff is required for registering blood pressure at rest and during
every stage of the test. A 12-lead ECG should be performed at rest with monitoring
throughout the examination. For the echocardiographic images, an ultrasound sys-
tem that permits one to one registration of images both during rest and stress to
enable concomitant comparison is necessary. A workstation is then necessary for
posttest analysis and interpretation, equipped with software that allows for split and
quad-screen displays for concurrent comparisons of the images at the various stages
of stress. This is essential to be able to elicit subtle wall motion changes. The
advances in digital imaging also allow assessing multiple cardiac cycles during
stress, hence improving interpretation analysis. Image backup is should be per-
formed. Most importantly, highly qualified professionals that are skillful in the
imaging technique should perform and interpret the study.
Technique
All methods of stress testing should include standardize protocols and monitoring
of vital signs at rest and during stress, rest/stress ECG. A baseline echocardiogram
is performed to assess for ventricular function, chamber sizes and pressures, wall-
motion thickness, aortic root, and valves morphology and functionality and to
screen for contraindications for the test, significant pathology, and to ensure ade-
quate image quality [2, 3]. If endocardial resolution is not optimal in two or more
segments, then intravenous contrast enhancement should be performed as described
in Chap. 3. Subsequently, left ventricle images are obtained from two parasternal
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views: long and short, and apical-long axis, apical four-and two-chamber view both
at rest and then at stress. Comparison of rest and stress images is performed to
assess LV function and regional wall motion abnormalities.
Doppler imaging can also be performed for the measurement of pressure and
flow gradients when assessing for valvular diseases and estimation of pulmonary
artery systolic pressures, both at rest and peak stress.
The test is completed either by exercise-limiting symptoms or completion of the
protocol, as with all forms of stress testing, but should also be terminated with the
development new or worsening wall motion abnormalities (i.e., akinesis of more
than two LV segments) in addition to the usual indications.
Exercise
When the choice is treadmill, imaging is usually not feasible during exercise and is
actually performed immediately afterwards, aiming to complete image acquisition
within 1 min from cessation of exercise. This assumes that the ischemia will persist
for at least that time; hence if it recovers rapidly, false-negatives occur. The patient
must be rapidly transferred from the treadmill to the appropriate supine position.
This requires patient cooperation and a well-coordinated approach by staff. If a
stationary bike is used, workload is increased every 2–3 min and images in this case
are obtained at peak stress. Although true stress images may also be obtained with
treadmill exercise, this method is challenging and infrequently performed.
Pharmacologic Stress Testing
Dobutamine is the preferred pharmacologic stress agent for stress echocardiography

(Chap. 6). It is performed on a continuous infusion beginning at 5 μg/kg/min, with
increasing dosages to a maximum of 50 μg/kg/min; if target heart rate not is
achieved, atropine may be used in doses ranging from 0.25 to 0.5 mg to a total of
2.0 mg [1, 2, 4]. Image acquisition should occur at baseline and for each level of
dobutamine stress. Ideally, the peak stress images should be obtained after the target
heart rate is achieved.
Data Interpretation
Grading of each of the 16 segments is performed at rest and with stress both at
low and intermediate stages and described as normal, hyperdynamic, hypokinetic,
akinetic, dyskinetic, or aneurysmal. Timing of wall motion is also considered.
Table 7.2 shows the interpretation of regional wall motion abnormalities based on
findings at rest and during stress.
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Table 7.2 Interpretation of regional wall motion abnormalities [5]

Rest Stress Interpretation
Normal wall motion & Hyperdynamic Normal
Contractility
Normal wall motion New wall motion abnormality or lack Ischemia
of hyperdynamic wall motion
Wall motion: Worsening hypokinesis akinesis or Ischemia
Hypokinesis dyskinesis
Wall motion: Unchanged Infarction
Hypokinesis
Akinetic Improved to hypokinesis or to normal Viable (Hibernating)
wall motion (Biphasic response) Myocardium
Adapted from Oh et al. [5]
The final report must include all the protocol information, vital signs, heart rate
achieved and blood pressure response, level of stress tolerated and its adequacy,
doses of the medications that were used, changes in ECG, presence or absence of
symptoms, systolic function and wall motion description.
Complications
Life threatening complications including asystole, acute myocardial infarction, sus-

tained ventricular tachycardia, pulmonary edema or sudden cardiac death do occur
be in less than 1/1000 [2]. However, “bothersome” side effects do occur, as noted in
Chaps. 4 and 6.
Clinical Vignettes
Case 1
A 62 year-old woman was brought to the Emergency Department with a 8-h his-
tory of atypical chest pain that began when she was notified that her husband was
in a car accident and in critical condition. The chest pain had resolved spontane-
ously. She had history of dyslipidemia, hypertension, and diet-controlled diabetes
mellitus. Initial ECG demonstrated very mild ST- elevation in V1-V3 and tropo-
nins were negative. As part of her initial work-up, she underwent e
echocardiography.
Figure 7.1 demonstrates a positive stress echo study showing images at rest (a)
and stress (b). During stress, there is marked akinesis and ballooning of the apex,
apical anterior/lateral/septum and inferior. The patient underwent a cardiac
catheterization that showed normal coronaries consistent with apical ballooning/
Takotsubo’s cardiomyopathy.
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Rest Stress Rest Stress

a c
b d
Case 2
A 55 year-old male with presented with history of atypical chest pain that had
resolved upon arrival to the Emergency Department. He had a past medical history
of well-controlled HTN and dyslipidemia and no previous cardiac history. ECG
demonstrated LVH but no acute ST-T wave abnormalities. Troponins were negative.
Given intermediate pretest probability for CAD and uninterpretable ECG, he under-
went exercise echocardiography (Fig. 7.2). He completed 12 min of a Bruce proto-
col, achieving a heart rate of 92 % of the maximum predicted heart rate. There was
an additional 2 mm horizontal ST depression with exercise, but the patient did not
develop chest pain.
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The stress echo was normal. Panels A-D show Parasternal long axis (PLAX),
Parasternal short axis (PSAX), Apical 4 chamber (AP4) and Apical 2 chamber
(AP2) acquired at end systole during rest and peak exercise. Note the normal sys-
tolic excursion/wall motion and thickening during peak exercise. The ST segment
response to exercise was a false-positive result, likely related to the baseline ECG
abnormalities.
References
1. American College of Cardiology Foundation Appropriate Use Criteria Task Force; American
Society of Echocardiography; American Heart Association; American Society of Nuclear
Cardiology; Heart Failure Society of America; Heart Rhythm Society, et al. ACCF/ASE/AHA/
ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011 Appropriate Use Criteria for
Echocardiography. A Report of the American College of Cardiology Foundation Appropriate
Cardiol. 2011;57(9):1126–66.
2. Sicari R, Nihoyannopoulos P, Evangelista A, Kasprzak J, Lancellotti P, Poldermans D, et al.
Stress echocardiography expert consensus statement: European Association of
Echocardiography (EAE) (a registered branch of the ESC). Eur J Echocardiogr J Working
Group Echocardiogr Eur Soc Cardiol. 2008;9(4):415–37.
3. Marwick TH. Stress echocardiography. Heart. 2003;89:113–8.
4. Pellikka PA, Nagueh SF, Elhendy AA, Kuehl CA, Sawada SG, American Society of
Echocardiography. American Society of Echocardiography recommendations for performance,
interpretation, and application of stress echocardiography. J Am Soc Echocardiogr Off Publ
Am Soc Echocardiogr. 2007;20(9):1021–41.
5. Oh JK, Seward JB, Tajik AJ. The echo manual. 3rd ed. Philadelphia: Lippincott Williams &
Wilkins; 2006.
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Chapter 8
Single Photon Emission Computed
Tomography
Eddy Karnabi
Single-Photon Emission Computed Tomography (SPECT) is the most widely used

nuclear imaging technique in cardiology, playing an important role in the detection
of coronary artery disease (CAD), viability assessment, and risk stratification.
Myocardial perfusion imaging (MPI) improves the sensitivity and specificity over
standard exercise stress testing and provides information regarding systolic function
and wall motion abnormalities with gated SPECT.
Indications
According to the appropriate use criteria [1] (Table 8.1).
Contraindications
The contraindications to the use of exercise and pharmacological (adenosine, dipyr-

idamole, regadenoson, dobutamine) stress testing are presented in previous chap-
ters. The contraindications specifically for nuclear cardiology include patients who
received iodine I-131 therapy within 12 h or technetium-99 studies within 48 h. In
addition, due to the radiation exposure, SPECT is contraindicated in pregnancy and
breast-feeding. Finally, uncooperative patients who are unable to lie supine for at
least 30 min are not encouraged to undergo the procedure. In rare instances, it is
contraindicated if there is an allergic potential to the radiopharmaceutics.

Cardiology Division, Northeast Cardiology Associates (NECA), Eastern Maine
Medical Center (EMMC), One Northeast Drive, Bangor, ME 04401, USA

DOI 10.1007/978-1-4471-7290-1_8
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72 E. Karnabi
Table 8.1 Appropriateness use criteria for SPECT

1 Acute chest pain (or ischemic equivalent) after definite ACS is ruled out
2 In chronic stable chest pain, patients with intermediate to high pretest probability or low
pre-test probability in which the ECG is un-interpretable and unable to exercise
3 In asymptomatic patients, patients with high CHD (defined by >20 % 10 year risk)
4 In asymptomatic patients with new cardiomyopathy and a depressed systolic function with
no prior CAD evaluation
5 Patients with arrhythmias such as VT or new onset atrial fibrillation
6 Patients with elevated cardiac enzymes without evidence of ACS
7 Patients have an abnormal prior stress testing and present with new or worsening
symptoms
8 Pre-operative evaluation in intermediate risk population or if undergoing vascular surgery
if functional capacity can not be assessed or is poor and if there is one or more risk factors
for CAD.
9 In post-revascularization patients who are symptomatic or were incompletely
re-vascularized
10 Asymptomatic or symptomatic CABG patients if performed >5 years prior, (Uncertain
indication in asymptomatic patients >2 years post PCI)
11 Myocardial Viability study using Thalium-201 or technetium 99m radiotracer in
combination with SPECT as an alternative to other imaging modalities to asses viability
Equipment
The essential tool for performing a SPECT study is the gamma or scintillation cam-
era that detects the gamma rays (photons) produced from the injected radiopharma-
ceutical agents [2].
A gamma camera consists of a single crystal, usually sodium iodide crystal
(NaI), a collimator, and photomultiplier tubes (PMT). The NaI crystal is able to
scintillate when subjected to ionizing radiation in form of photons. The collimator
is designed to limit by attenuation, the detection of gamma rays to those traveling in
certain directions. The photomultiplier tubes convert photon energy and scintilla-
tion within the crystal into electrical energy that is processed by the pulse height
analyzer. The energy spectrum obtained consists of a photopeak and multiple
Compton scatters. Only signals in the specific energy range of the radiotracer (the
photopeak) are processed and the counts analyzed.
The basic components of the gamma camera have not changed much over the
years except for upgrading from scintillation detectors to semi-conductor detectors
such as Cadmium Zinc Telluride (CZT) detectors with improved count detection
and thus images.
The radiopharmaceutical tracers [3] used are thallium-201 and technetium-99m
based agents, Tc-99m sestamibi and Tc-99m tetrofosmin, Due to the energy spec-
trum, effective half life and more favorable dosimetry, the technetium agents are
preferred for gated SPECT imaging. These agents emit photons with a single pho-
topeak of 140 keV and have a half-life of 6 h. After injection, 40–60 % is extracted
by the myocardium and myocardial washout/redistribution is minimal requiring two
injections at rest and peak exercise.
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8 Single Photon Emission Computed Tomography 73
Technique
After performing an exercise or a pharmacological stress test and the injection of

the pharmaceutical radiotracer, images are obtained. The images obtained by
gamma cameras are 2 dimensional (2D) images of a 3 dimensional (3D) object.
Multiple 2D planar projections are acquired from multiple angles to reconstruct a
3D image using a reconstruction algorithm.
Imaging times post injection for technetium-based agents, scanning can start
15–20 min after exercise and 45–60 min after rest or pharmacological stress testing.
The routine position to acquire images is supine with arms above the head. In cases
of significant inferior wall attenuation, the addition of prone images helps eliminate
the inferior wall attenuation, creates more uniform breast attenuation, less motion
artifact, but may cause an artifactual anteroseptal defect. The gamma camera is
placed as close to the patient as possible for improved resolution with either one of
the orbital types: circular or non circular (elliptical or body contour). In a double
headed camera, planar images are obtained in a 180° arc that extends from 45° right
anterior oblique (RAO) to 45° left posterior oblique (LPO). The acquisition type
could be a “step and shoot”, continuous, or continuous “step and shoot”. For a dual
head camera, low dose studies usually takes 25–30 s/step and for high dose studies
20–25 s per step which translates to approximately 12–16 min total time for the
study. Using a single head camera will yield double the time to acquire the images.
Hybrid SPECT-CT systems are in use and play an essential role in attenuation
correction.
Radiopharmaceutical protocols [3]:
1. One day dual isotope (discouraged and less widely used due to the high radiation
exposure)
2. Two day technetium based tracer
3. One day single isotope (Rest-stress or stress-rest)
4. Stress only imaging with ECG gated SPECT and validated attenuation
correction
5. One day stress-delay thallium imaging for viability
Single isotope usually technetium based one day protocol is the most widely
used. A rest injection is performed with low dose 8–9 mCi followed by SPECT
imaging 45–60 min afterwards. After a 3-h delay, stress testing is performed and
high dose 25–30 mCi is injected followed by SPECT imaging 15–30 min for exer-
cise and 45–60 min for pharmacological stress testing (Fig. 8.1). The advantages
of a single day protocol is good validation, fast tract protocol, easier image inter-
pretation, able to determine transient ischemic dilation (TID), and validated atten-
uation correction. The 2-day protocols advantage is high quality rest and stress
images as a result of using high dose injections with rest and stress. This is benefi-
cial in an obese patient but requires 2 days to complete the study. More recently,
stress only images are being performed; if SPECT images are normal, the rest
images are not required.
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74 E. Karnabi
Inject stress dose

Inject rest dose
25–30 mCi
8–9 mCi
Stress Exercise or
Rest SPECT Pharmacological Stress SPECT
30–60 min 45–60 min

0 Delay ~ 3 h
Fig. 8.1 Typical 1-day rest-stress technetium protocol. Rest dose of 8–9 mCi is injected followed
by rest SPECT images 30–60 min. After a delay of approximately 3 h, the stress portion is per-
formed followed by stress tracer injection of 25–30 mCi. After 15 min for exercise or 45–60 min
for pharmacological stress testing, the stress SPECT images are obtained
For SPECT viability studies, thallium-201 2.5–3.5 mCi is injected followed by

rest images at 15 min post injection. Redistribution images are delayed 4 h to detect
viable myocardium. Further delayed or late redistribution mages can be obtained
24 h post injection as well.
Data Interpretation
The radiotracer is distributed throughout the myocardium, however, more predomi-

nantly in the left ventricle. The standard SPECT views include the short axis from
apex to base, vertical long axis, and horizontal long axis (Fig. 8.2). Data interpreta-
tion involve following a review sequence as outlined by the ASNC guidelines [4]
and involves: examining the unprocessed images for image quality, artifacts such as
motion artifacts (vertical or horizontal), breast or subdiaphragmatic artifacts, extra-
cardiac uptake, and increased lung uptake, followed by examining for perfusion
abnormalities fixed or reversible between rest and stress images, examining the
polar map or bulls eye, and examining the gated SPECT images for wall motion
abnormalities and ejection fraction.
As coronary flow decreased due to coronary obstruction, less radiotracer uptake
occur which translates to lower count on the perfusion images. Defects can be
reversible or fixed. Fixed defects are areas with absent tracer uptake on both rest and
stress images. Fixed defects represent a scarred or infarcted myocardium or a viable
hibernating myocardium. Differentiating a scarred myocardium from a viable myo-
cardium requires either thallium-201 SPECT redistribution viability study or PET
based study. Reversible defects are defined as normal perfusion images at rest but
with decreased uptake on stress images; this pattern is consistent with ischemia.
The ischemic myocardium can usually be traced to a coronary distribution Left
anterior descending (LAD), Circumflex (Cx), or Right coronary artery (RCA)
(Fig. 8.3) unless multiple territories are involved. Quantitative analysis is performed
by comparing count densities from the stress using the short axis images with a
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Fig. 8.2 A normal myocardial perfusion imaging showing the short axis from apex to base (usual
presentation is stress images on top and rest images on bottom), horizontal long axis showing
septum and lateral walls, and vertical long axis showing the anterior and inferior myocardium
Fig. 8.3 A polar plot or bulls eye with semiquantification using the 17-segment model. The LAD
(left anterior descending) territory is between 9 and 1 O’clock, Cx (Circumflex) territory between
5 and 8 O’clock, and RCA (right coronary artery) territory between 2 and 5 O’clock. On the left,
gated SPECT images are shown during diastole (bottom) and systole (top)
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76 E. Karnabi
a b
SPECT myocardial perfusion imaging
Vertical
1. Basal anterior Short axis long axis
2. Basal anteroseptal
3. Basal inferoseptal 1 Apical Mid Basal Mid
4. Basal inferior 1
5. Basal inferolateral 7 7
13
6. Basal anterolateral 2 8 12 2 6
7. Mid anterior 8 13 6
12 14 16
17
8. Mid anteroseptal 9 11
9. Mid inferoseptal 14 17 16 15 3 5
10
10. Mid inferior
9 11 4
11. Mid inferolateral 3 15 5
12. Mid anterolateral
13. Apical anterior 10 LAD RCA LCX
14. Apical septal
15. Apical inferior 4
16. Apical lateral
17. Apex
Fig. 8.4 SPECT myocardial perfusion imaging showing the 17-segment model and Coronary
distribution (Adapted from the Cerqueira et al. [5]). LAD left anterior descending artery, RCA right
coronary artery, LCX left circumflex artery. (a) indicates terminology of each of the 17 segments
and there location on a polar map. (b) depicts the location of the segments on short axis and verti-
cal long axis views and the empirically allocated vascular territory
Table 8.2 The five point Normal perfusion 0

model
Mild decreased counts 1
Moderate decreased counts 2
Severe decreased counts 3
Absent uptake 4
Table 8.3 Semiquantitative Number of segments Percent of LV

defect analysis
Small 1–2 5–10
Moderate 3–4 15–20
Large >5 >20
normal count profile from a cohort of normal patients. A bulls eye or a polar map is
displayed (Fig. 8.3), however, this method should only be used in conjunction with
visual analysis. Using the 17-segment model (Adapted from Cerqueira et al. [5])
(Fig. 8.4), a score may be given to each segment (Table 8.2).
Three scores are obtained: SRS summed rest score; SSS summed stress score
and SDS summed difference score (SDS = SSS−SRS). The SRS shows the extent
and severity of infarction, SDS extent and severity of ischemia, and SSS extent and
severity of both ischemia and infarction (Table 8.3).
Similarly, the percent LV myocardium involved can be calculated by number of
segments affected divided by 68 (4 points per each segment multiplied by 17
segments) × 100.
An important part in interpretation is the detection of transient ischemic dilation
(TID). TID is most likely due to diffuse subendocardial ischemia. It is calculated by
dividing Stress EDV (End-diastolic volume)/Rest EDV. Cutoff value of >1.22 for
dual isotope and >1.12 for single isotope studies is considered significant. However,
the threshold is higher for pharmacological stress testing >1.36 since the physiology
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in vasodilator stress is to redirect perfusion away from the endocardium. TID in

combination with an abnormal perfusion images signifies extensive CAD either
multi-vessel disease or proximal LAD disease and correlates with worse prognosis.
However, TID in combination with normal perfusion images has low specificity for
multi-vessel disease and is not associated with adverse prognosis. This is usually
encountered in patients with significant left ventricular hypertrophy (LVH) espe-
cially with a hypertensive response that results in subendocardial ischemia from the
thick ventricular walls.
Gated SPECT imaging improves the specificity of MPI by differentiating a
fixed defect from an infarction/scar and an artifact. Wall motion abnormalities
can be detected as well as an estimation of systolic function and an ejection
fraction (EF).
Artifact recognition is an important part of SPECT imaging and include
instrumentation-related artifacts (center-of–rotation, non-uniformity etc.) and
patient-related artifacts (patient motion, attenuation, etc.).
Finally, the report should not only describe the clinical indication, the technical
features of the examination, and the imaging results but also include the impression
whether the study is normal or abnormal and addressing the perfusion abnormalities
by noting the size, severity and location of each abnormality. Recognition of arti-
facts if present, addressing regional or global wall motion abnormalities with esti-
mation of EF, inclusion of ECG findings, and integration with the clinical information
to address the indication of the study.
Complications
The complications to myocardial perfusion imaging are related to the radiation

exposure both to the patients and to the staff. Ionizing radiation has been linked to
solid cancers and leukemia. Hence, the principle of ALARA (As low as reasonably
achievable) applies.
Clinical Vignettes
Case 1
Sixty year old male with multiple risk factors for CAD including hypertension,
hyperlipidemia, and extensive tobacco history with limited functional status due to
claudication for over the past year and significant vascular disease involving the
femoral artery is referred for a pharmacological stress test myocardial perfusion
imaging prior to vascular surgery. The MPI images are shown in Fig. 8.5.
This case shows a normal myocardial perfusion imaging during rest and stress
with a normal bulls eye or polar plot. His annual event rate is less than 1 % and he
should be able to proceed with the planned vascular bypass surgery.
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78 E. Karnabi
Case 2
Seventy-eight-year-old male with hypertension, CAD with prior myocardial infarc-

tion was admitted to the hospital with chest pain. A myocardial perfusion stress
testing was performed with images shown in Fig. 8.6.
This case presents a patient with a prior MI in the LAD and RCA territories and
evidence of a small amount of peri-infarct ischemia in the anterior wall.
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References
1. Hendel RC, et al. CCF/ASNC/ACR/AHA/ASE/SCCT/SCMR/SNM 2009 appropriate use cri-

teria for cardiac radionuclide imaging: a report of the American College of Cardiology
Foundation Appropriate Use Criteria Task Force, the American Society of Nuclear Cardiology,
the American College of Radiology, the American Heart Association, the American Society of
Echocardiography, the Society of Cardiovascular Computed Tomography, the Society for
Cardiovascular Magnetic Resonance, and the Society of Nuclear Medicine. Circulation.
2009;119(22):e561–87.
2. Holly TA, et al. Single photon-emission computed tomography. J Nucl Cardiol. 2010;17(5):
941–73.
3. Henzlova MJ, et al. ASNC imaging guidelines for SPECT nuclear cardiology procedures:
stress, protocols, and tracers. J Nucl Cardiol. 2016;23(3):606–39.
4. Douglas PS, et al. ACCF/ACR/AHA/ASE/ASNC/HRS/NASCI/RSNA/SAIP/SCAI/SCCT/
SCMR 2008 health policy statement on structured reporting in cardiovascular imaging. J Am
Coll Cardiol. 2009;53(1):76–90.
5. Cerqueira MD, et al. Standardized myocardial segmentation and nomenclature for tomographic
imaging of the heart. A statement for healthcare professionals from the Cardiac Imaging
Committee of the Council on Clinical Cardiology of the American Heart Association.
Circulation. 2002;105(4):539–42.
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Chapter 9
Positron Emission Tomography
Eddy Karnabi
Positron emission tomography (PET) imaging has increased substantially in recent

years. PET allows noninvasive evaluation of myocardial blood flow, function,
and metabolism. The advantages of cardiac PET imaging over SPECT are [1]:
improved image quality (especially in obese patients) with high both temporal and
spatial resolution, relatively short imaging protocols, routine attenuation correction
(depth independent), providing peak stress ejection fraction (EF)-no time delay
between hyperemic response and imaging and true quantification of myocardial
blood flow and myocardial metabolism. In addition, PET provides equal sensitiv-
ity with higher specificity and diagnostic accuracy compared to SPECT. However,
cardiac PET still faces the challenges of being less available, with a greater cost,
less expertise, challenges of performing exercise stress due to the short half-life
of the currently available radiotracers making pharmacological stress testing the
only current option (until the availability of new radiopharmaceutical agents), and
reimbursement issues.
Indications
The indications for cardiac PET [2, 3] are similar to those for cardiac SPECT in
term of myocardial perfusion imaging for the diagnosis and risk stratification of
CAD. However, its role is extended to patients with an equivocal SPECT. In addi-
tion, cardiac PET is used as a viability study in patients with ischemic cardiomyopa-
thy. Recently, there has been an increased use in heart failure and in the identification
of cardiac sarcoidosis (Table 9.1).


DOI 10.1007/978-1-4471-7290-1_9
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82 E. Karnabi
Table 9.1 Indications for positron emission tomography

1 Intermediate likelihood of CAD and/or risk stratification in patients with intermediate
and high likelihood of CAD when
Equivocal SPECT
Unable to exercise
Able to exercise but ECG with LBBB or ventricular paced rhythm
2 Evaluation of myocardial viability
3 Evaluation of heart failure (Cardiac Sarcoidosis)
4 Quantification of myocardial blood flow
Contraindications
The contraindications to cardiac PET are similar to SPECT (Chap. 8), which
include the standard contraindications to pharmacological stress testing when PET
perfusion imaging is being done. Inability to lie flat or lie still for the period of
acquisition, claustrophobia and extreme weight (>350–400 lbs.) are usually pre-
ferred not to undergo PET imaging. Finally, women who are pregnant or breast-
feeding are contraindication.
Equipment
The equipment required for a standard cardiac PET examination includes the radio-
nuclides and the PET camera, mostly as a hybrid (with CT) unit. The radionuclides
used for PET imaging have a considerably shorter half-life as compared to SPECT
tracers. PET radionuclides are produced either from a cyclotron such as fluoro-2-
deoxyglucose F-18 FDG and N-13 ammonia or a generator such as rubidium Rb-82.
As the name implies, PET imaging involves a positron that collides with an electron
to produce two 511 keV gamma rays/photons emitted collinear to each other at 180°
angle. The PET detectors are configured to only register the photon pairs if they
strike opposite detectors at approximately the same time that has been termed the
coincidence detection. The summations of multiple coincidence events are used to
reconstruct the PET image to be used for analysis.
The CT scanner provides addition information such as coronary artery calcium
scoring and/or noninvasive coronary angiography, but more importantly for PET
imaging is in registration and attenuation correction.
The PET camera, similar to SPECT, is made of multiple small detector crystals
arranged in a 360° ring and photomultiplier tubes to convert the scintillation events to
electrical signal and digitalization to provide the counts that are used in quantification and
image processing. Three types of detector crystals are available: (1) Bismuth germanate
(BGO) (2) Lutetium oxyorthosilicate (LSO) (3) Gagolinium oxyorthosilicate (GSO).
The clinically available PET tracers for myocardial perfusion studies are
Rb-82, and N-13 ammonia. Figure 9.1 shows the radiotracers myocardial uptake
ERRNVPHGLFRVRUJ
9 Positron Emission Tomography 83
O-15 H2O
5
er
ac
Myocardial tracer uptake
4 tr
al
Ide
N-13 Ammonia
3
Thallium-201
2 Rubidium-82
Tc-99m Sestamibi
Tc-99m Tetrofosmin
1 Plateau-”Roll-Off”
0 1 2 3 4
Flow (mg/min/g)
Fig. 9.1 Relationship of the myocardial uptake of the radiopharmaceutical to blood

flow. O-15 water is the ideal tracer
Table 9.2 PET radiotracers Myocardial

perfusion Myocardial metabolism
Rubidium-82 F-18 = Glucose metabolism
Ammonia N-13 C-11 acetate = Oxidative metabolism
Water O-15 C-11 palmitate = fatty acid metabolism
F-18 agent
in relation to coronary blood flow with O-15 being the ideal tracer and the roll-off
phenomenon seen with other tracers at higher coronary blood flows. N-13 ammo-
nia, due to the short half-life (10 min), requires an on-site (nearby) cyclotron. It
has excellent myocardial uptake/retention with established flow quantification
and applications in exercise and pharmacological stress testing. Rubidium-82 is
produced on-site from a Strontium-82 generator (replaced every 4 weeks) with a
half-life of 76 s. Due to the short half-life, it can only be used in pharmacological
stress testing. It has with high extraction at high flows (enhances the detection of
moderate-severe CAD). Rb-82 is extracted by myocardial cells via the Na/K
ATPase pump. The radiation dosimetry from Rb-82 varies from 1.75 to 7.5 mSv
total effective dose. Depending on the left ventricular ejection fraction, typically
imaging can commence 70–90 s after the injection if LVEF >50 % and delayed
slightly longer (~110 s) if LVEF <50 %.
For metabolism imaging, the F-18 FDG tracer (the only FDA approved agent),
an analog to glucose, is used. F-18 is produced in a cyclotron and decays with a
half-life of 110 min, which allows sufficient time to be produced and distributed in
a radius of several hours from the production site. FDG is transported into the cells
similar to glucose and is then phosphorylated by hexokinase to FDG-6-phosphate,
which is then trapped in the myocardium for PET imaging. The whole body dosim-
etry from 10 mCi dose is 7 mSv (Tables 9.2 and 9.3).
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84 E. Karnabi
Table 9.3 Properties of PET radiotracers

Positron
Uptake/ range FDA
Tracer Production Half-life Compound metabolism (mm) approval
Perfusion O-15 Cyclotron 2.1 min H2O Freely 0.36 ×
diffusible
N-13 Cyclotron 10 min NH3 Extraction 0.28 √
Na/K ATPase
Rb-82 Generator 76 s RbCl Extraction K 1.6 √
channels
Metabolism C-11 Cyclotron 20.4 min Acetate, Active 0.22 √
Palmitate extraction
F-18 Cyclotron 110 min Deoxyglucose Glucose 0.18 √
transporter
a
Perfusion
Radiotracer Radiotracer
injection injection
Tomogram/ Transmission Calcium Emission Stress Emission

scout scan scan score scan scan test scan
Rest PET MPI Stress PET MPI
b
Metabolism
F-18 FDG
Radiotracer
injection
injection
(10–15 mCi)
Tomogram/ Transmission Emission Glucose FDG uptake by Emission

scout scan scan scan manipulation myocytes scan
Rest PET MPI Rest F-18 FDG PET MPI
Fig. 9.2 Sample PET protocols for myocardial perfusion (a) and metabolism/Viability (b)
Technique
Patient preparation for pharmacological stress testing and myocardial perfusion

imaging is similar to what was previously described in the previous Chap. 6
(Pharmacologic Stress) and 8 (SPECT). For myocardial perfusion imaging (Fig. 9.2),
an overnight fast of at least 6 h is required. Following the stress portion, Rb-82 or
N-13 is injected at peak hyperemia through a peripheral IV line and emission scans
are performed.
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Viability studies require a specified protocol for glucose manipulation. In order

to allow the myocardium to utilize glucose, an overnight fast of at least 6–12 h
(Step1) is required as patient metabolic preparation is key to successful F-18 FDG
imaging to assess viability. The most common metabolic preparation for viability
imaging is the use of an oral load of glucose 25–100 g (Step 2) followed by supple-
mental IV insulin (Step 3) as needed.
The imaging parameters include patient positioning supine with the arms raised
above the shoulder level. To localize the heart within the field of view (FOV), a
tomogram or scout CT is performed followed by a transmission scan for attenuation
correction. Rest or stress emission scans are then performed. For the FDA approved
radiotracers, the dose used are: for Rb-82 is 40–60 mCi, N-13 ammonia 10–20 mCi,
and for F-18 FDG 5–10 mCi. The scan duration for Rb-82 is 3–7 min, N13 ammo-
nia 10–15 min, and for F-18 FDG 10–30 min.
Of note, rest-stress MPI and viability PET protocols (Fig. 9.2) may be combined
to provide information on both ischemia and viability.
Data Interpretation
As outlined by the ASNC guidelines on radionuclide imaging [4], the sequence

involves analyzing the raw images, followed by assessment of perfusion abnormali-
ties, evaluation of gated images for left ventricular function, quantification of myo-
cardial blood flow. In addition, with hybrid PET/CT scans, coronary artery calcium
and/or coronary CT angiography may be included in the report. Non-cardiac find-
ings should be reviewed and mentioned such as pleural or pericardial effusions,
aortic disease and calcifications, mediastinal or lung masses or nodules. The rest
and stress perfusion images and metabolism images should be analyzed for the
extent and severity of abnormalities. Extra-cardiac findings should be carefully
examined for uptake in organs other than the myocardium particularly the lungs and
the mediastinum. Similar to SPECT imaging, PET images are presented in short
axis from apex to base, horizontal long axis with septal and lateral walls, and verti-
cal long axis showing the anterior and inferior walls. Interpretation of PET perfu-
sion data (similar to what is described in Chap. 8) should be performed visually/
qualitatively first with identification of location and defect severity and extent. The
extent can be qualitatively described as small (5–10 % of the LV), medium (10–
20 % of the LV), or large (>20 %) of the LV. Defect severity is expressed as mild,
moderate, or severe. Myocardium with stress induced perfusion abnormalities,
which have normal stress imaging represent ischemia. Perfusion abnormalities
present both at rest and stress i.e. fixed defects represents an area of scan or infarc-
tion. The 17-segment model with the 5-point scale (Fig. 8.4) is used for the semi-
quantitative analysis as outlined in the SPECT chapter.
Absolute quantification of myocardial blood flow is an important aspect of PET
imaging that helps in assessing the physiological significance of a known coronary
artery stenosis especially if it is in the intermediate range. Both relative and absolute
ERRNVPHGLFRVRUJ
86 E. Karnabi
quantification is possible. Quantitative assessment of blood flow is in ml of blood

per min per gram of myocardium and is validated for N-13 and Ru-82.
ECG Gated PET images at rest and peak stress provides information on LV func-
tion and volumes. Unlike post-stress SPECT, PET images are obtained at peak hyper-
emia and stress. Regional and global wall motion abnormalities can be identified.
Assessment of myocardial viability plays a central role in PET imaging. Viability
studies are able to differentiate a scarred or infarcted myocardium from a hibernat-
ing myocardium, which upon revascularization might restore LV function. Rest per-
fusion imaging is compared to metabolism imaging using FDG uptake (Fig. 9.3). A
myocardial perfusion abnormality in combination with no FDG uptake signifies an
infarcted and scarred myocardium. An increase in FDG uptake relative to a perfu-
sion abnormality i.e. a mismatch signifies a viable myocardium (Table 9.4).
Myocardial perfusion Myocardial metabolism

(Rb-82) (FDG)
1. Transmural scar
(Perfusion-metabolism match)
2. Hibernating myocardium
(Perfusion-metabolism mismatch)
3. Non-transmural scar
4. Myocardial stunning
(Reverse mismatch)
Fig. 9.3 Myocardial perfusion and metabolism patterns
Table 9.4 Myocardial perfusion and metabolism patterns

Myocardial blood Myocardial FDG glucose
flow loaded Regional function
Normal Normal Normal Normal

Hibernating
Transmural scar
Non-Transmural scar Partially Partially /Normal

Stunning Normal /
NICMP Normal Normal

NICMP non ischemic cardiomyopathy, FDG fluorodeoxyglucose, / increase/decrease
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The standard reporting algorithm of myocardial perfusion and metabolism

PET studies includes: patient information, indication for the study, history and
key clinical findings, type of the study, summary of stress data with stress ECG
interpretation, image description and interpretation for perfusion and metabolism,
and final impression whether the study is normal or abnormal.
Complications
The complications to pharmacological stress perfusion imaging are presented

elsewhere. The risk of PET imaging include radiation exposure and risk of solid
cancers and leukemia due to stochastic effects of ionizing radiation. For instance,
the total body effective dose of radiation exposure from a myocardial perfusion
using Rubidium RB-82 is approximately 4.1 mSv and from F-18 fluorodeoxyglu-
cose myocardial viability scan is approximately 7.0 mSv. In order to prevent or
limit the effects of ionizing radiation, the principle of ALARA (As low as reason-
ably achievable) should be followed. Hence, appropriate indications for testing
should be followed per the ACC/AHA and ASNC appropriate use criteria. Once a
proper indication is confirmed, it is important to limit the amount of radiation and
to use the lowest possible dose of radioisotopes to obtain accurate images for
interpretation.
Clinical Vignettes
Case 1
Seventy-two year old man presents with mild stroke and chest pain. History
includes smoking (50 pack year), elevated cholesterol, diabetes. During hospital-
ization, the resting ECG demonstrated mild inverted t-waves and TnI elevation,
also mild. The patient was obese, BMI 35. The patient underwent a rest/stress
dipyridamole PET study with mild chest pain but no ECG changes. Images are
shown in Fig. 9.4.
There was TID and two separate perfusion abnormalities. There was a medium
moderate/severe completely reversible antero/lateral and inferolateral defect as well
as medium moderate/severe reversible anteroseptal, apical and inferoseptal defect
confined to the apical regions. These findings were consistent with 2 vessel isch-
emia, circumflex and left anterior descending arteries. The patient underwent coro-
nary catheterization which showed LAD which was occluded in the mid region, a
ramus with 60–70 % stenosis and circumflex proximal 90 % stenosis. This case
demonstrates the ability of rest/stress PET to identify not only CAD, but the sever-
ity. The accuracy of PET to predict multivessel CAD is significantly better than
SPECT (Courtesy of Gary V Heller, MD, PhD).
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88 E. Karnabi
Stress-Rb82
Rest-Rb82
Short Axis
Stress-Rb82
Rest-Rb82
Vertical-Long Axis
Stress-Rb82
Rest-Rb82
Horizontal-Long Axis
Case 2
Sixty-eight year old female patient presents with congestive heart failure and chest
pain. The patient’s history includes hypertension, and prior MI several years previous.
The patient had no history of diabetes. She had been stable until recent chest pain.
The patient underwent cardiac catheterization which demonstrated a 60 % ste-
nosis of the left anterior descending (LAD) artery and occluded obtuse marginal
artery as well as an occluded right coronary artery with collateralization from the
LAD. The patient under went a rest/stress dipyridamole PET protocol to evaluate
for stress-induced ischemia and myocardial viability, in view of the diseased LAD
and occluded vessels. The patient had no symptoms or ECG changes during the
pharmacologic stress Fig. 9.5.
Illustrates the rest/stress Rb-82 results, with an FDG viability assessment. There
was normal perfusion in the anterior region with severe fixed defects in the lateral
and inferior regions. Gated PET imaging revealed akinesis of portions of the lateral
wall as well as inferior, with LVEF at both rest and stress of 34 %. The conclusion
was that there was no stress-induced-ischemia and non-viability of the inferior and
lateral regions consistent with the occluded vessels. Because the ischemia work-up
did not demonstrate myocardial viability in areas of concern, a cardiac PET FDG
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Stress
Short Axis
Rest
Short Axis
FDG Short
Axis
Stress
Rest
FDG
Stress
Rest
FDG
study was performed, which demonstrated marked FDG activity in both the inferior
and lateral walls as well as the anterior wall (“mismatch”) consistent with myocar-
dial metabolic viability in both the circumflex and right coronary arteries.
The patient underwent successful by-pass surgery with revascularization of all
three major arteries. Six months later the patient was asymptomatic and an echocar-
diogram revealed mild/moderate hypokinesis of the lateral/inferior walls, with a
global ejection fraction of 46 % (Courtesy of Gary V Heller, MD, PhD).
References
1. Dilsizian V, Bacharach SL, Beanlands RS, et al. PET myocardial perfusion and metabolism
clinical imaging. Am Soc Nucl Cardiol. 2009. doi:10.1007/s12350-009-9094-9.
2. Hendel RC, et al. CCF/ASNC/ACR/AHA/ASE/SCCT/SCMR/SNM 2009 Appropriate Use
Criteria for Cardiac Radionuclide Imaging: a Report of the American College of Cardiology
Foundation Appropriate Use Criteria Task Force, the American Society of Nuclear Cardiology,
the American College of Radiology, the American Heart Association, the American Society of
Echocardiography, the Society of Cardiovascular Computed Tomography, the Society for
Cardiovascular Magnetic Resonance, and the Society of Nuclear Medicine. J Am Coll Cardiol.
2009;53(23):2201–29.
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90 E. Karnabi
3. Klocke FJ, et al. ACC/AHA/ASNC guidelines for the clinical use of cardiac radionuclide imag-
ing – executive summary: a report of the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines (ACC/AHA/ASNC Committee to Revise the
1995 guidelines for the clinical use of cardiac radionuclide imaging). J Am Coll Cardiol.
2003;42(7):1318–33.
4. Douglas PS, et al. ACCF/ACR/AHA/ASE/ASNC/HRS/NASCI/RSNA/SAIP/SCAI/SCCT/
SCMR 2008 health policy statement on structured reporting in cardiovascular imaging.
Endorsed by the Society of Nuclear Medicine [added]. Circulation. 2009;119(1):187–200.
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Chapter 10
Radionuclide Angiography
Cesia Gallegos
Left ventricular function is a key measure for the assessment and management of
cardiac conditions, especially in patients with heart failure and/or valvular disease.
Noninvasive techniques can provide this information, as well as the assessment of
regional wall motion abnormalities.
Radionuclide angiography (RNA) was first used in the 1970s, and is also known
as radionuclide ventriculography (RVG), radionuclide cine angiography (RNCA),
multiple gated cardiac blood pool imaging (MUGA) scan, and equilibrium radionu-
clide angiography (ERNA) [1, 2]. This radioactive count-based technique provides
an accurate and highly reproducible method that is independent of ventricular geom-
etry and is well suited for the serial assessment of global left ventricular (LV) func-
tion. This method may also be used in conjunction with bicycle exercise, although
this is now infrequently performed. Parameters obtained from RNA include the fol-
lowing: global ventricular systolic function, regional wall motion, ventricular vol-
umes, systolic and diastolic function indices, and stroke volume/cardiac output [2].
Indications
1. Evaluation of cardiac function in patients receiving chemotherapy: Perhaps the

common indication, especially in evaluating for chemotherapy-induced cardio-
toxicity, such as with doxorubicin, which may cause a dose-dependent impair-
ment of the LV function, producing a severe and irreversible ventricular
dysfunction before the onset of symptoms of heart failure. In this setting, RNA
is a tool that provides quantitative measures of LV dysfunction in patients who
C. Gallegos, MD
Section of Cardiovascular Medicine, Yale University School of Medicine, 333 Cedar Street,
208017, New Haven CT 06520-8017, FL, USA

DOI 10.1007/978-1-4471-7290-1_10
ERRNVPHGLFRVRUJ
92 C. Gallegos
are or have received therapy with doxorubicin. It can be used for risk stratification
or prognosis, providing information on patients with preexisting cardiac condi-
tions who are at greater risk of developing heart failure. Furthermore, serial
evaluation of the LVEF (left ventricular ejection fraction) at rest can be per-
formed on patient during follow-up while on these therapies, providing essential
details to decide when doxorubicin will be stopped.
2. Known or suspected myocardial infarction
3. Known or suspected coronary artery disease (CAD)
4. Patient with heart valve disease
5. Evaluation of heart failure
6. Other applications: RV dysplasia, cardiomyopathies, aortic regurgitation, candi-
dates for cardiac resynchronization therapy (CRT), candidates for lung trans-
plantation, and candidates/monitoring of heart transplantation.
Contraindications
1. Pregnancy
2. Breast-feeding, depending on the technique used for labeling red blood cells
(RBCs). For instance, for in vivo labeling, it is recommended to stop breastfeed-
ing for at least 12–24 h after the injection.
3. Patients with cardiac arrhythmias, as interpretation may be limited by an irregu-
lar heartbeat. Although with “list mode acquisition” the RR variability can be
corrected, the results may still be unreliable.
Equipment
RNA is performed by labeling a patient’s red blood cells with a radionuclide, technetium-
99m-pertechnate (Tc99m) or human serum albumin (HSA). Therefore, standard IV
supplies are required. The labeling of RBCs with Tc-99m is performed through the use
of FDA approved kits for the in vitro preparation of the Tc-99m labeling. Its content is
not administered to the patient. Each kit consists of three separate nonradioactive com-
ponents: A 10 ml reaction vial with stannous chloride, dextrose and sodium citrate, a
syringe with sodium hypochlorite that must be protected from light to prevent degrada-
tion of the solution and a second syringe with citric acid, sodium citrate, and dextrose.
RBCs are prepared with the solutions in the kit and then the Tc-99m is added and once
labeled, the RBC should be injected to the patient within 30 min.
Image acquisition requires a standard gamma camera equipped with appropriate
collimation. For first-pass RNA however, a dedicated gamma camera with a high
counting efficiency is used for best results. Images will require a workstation for
post-processing. In addition, EKG leads will be placed for monitoring and for gated
image acquisition. Basic life support and resuscitative drugs must be available [2].
ERRNVPHGLFRVRUJ
10 Radionuclide Angiography 93
Technique
As is true for any diagnostic procedure, a complete history and physical examina-
tion must be performed, focusing on indications for testing, current medications,
and allergies/side-effects, cardiac risk factors and current symptoms, as well as
prior cardiac procedures, physical limitations and special precautions. An EKG
must be obtained prior to the study to identify any heart rate variability as it may
limit the ability to interpret the test. Additionally, Occupational Safety and Health
Administration (OSHA) guidelines for handling of blood products and radioactive
material must be followed [2].
For RBC labeling, it can be performed in vivo, modified in vivo, or in vitro, with
the in vitro method being used most often [4]. The in vitro method is performed by
drawing blood from the patient and then the stannous ions are injected to the blood
with the subsequent addition of the Tc-99m to the mixture [4]. While in the in vivo
method, two consecutive injections are required: the ions are injected directly to the
patient’s bloodstream, followed by the injection of the Tc-99m perctechnetate about
20–30 min later. The newly developed in vivo labeling technique, called modified in
vivo, isolates the pretinned RBCs and Tc-99m from other body compartments during
labeling. Tc-99m radiolabeled human albumin is an alternative, however the result-
ing images are of lower quality. The usual administered activity is 555–1110 MBq.
RNA can be performed as “first-pass” or as “equilibrium” [4]. The first-pass
approach observes a bolus of Tc-99m perctechnetate or Tc-99m diethylenetriamine-
pentaacetic acid (DTPA) pass through the right side of the heart to the left and it can
sample multiple cardiac cycles, determining the changes of radioactivity over time.
This allows for the generation of time-activity curves to provide ejection fraction
(EF) measurement of both the right and left ventricles, as well as accurate quantita-
tion of regurgitant lesions. For the RV phase, two to five cycles are summed, and
five to seven cycles are summed for the LV phase, from which LVEF and RVEF can
be performed. This approach is also well suited for shunt detection and evaluation
of RV function, but requires specialized cameras with high count rate capability and
is infrequently performed.
With equilibrium RNA, Tc-99m pertechnate bound to RBCs is the most used [4].
The acquisition time range is 5–10 min per view, involving hundreds to thousands of
heartbeats, which are synchronized with the QRS complex. Every cardiac cycle is
divided into frames, and all the frames within a given RR interval. Equilibrium stud-
ies can be performed during rest or stress, and can be acquired by both planar and
SPECT (single photon computer tomography) methods [3]. Equilibrium RNA uses
the best septal left anterior oblique (LAO) projection, whereby the intraventricular
septum is as vertical as possible. Lateral and anterior views are then obtained, each
approximately 45° from the LAO projection (Fig. 10.1). For LVEF measurement, the
LAO provides the best measurement since this projection separates the RV and LV
and identifies anterolateral, posterolateral, and septal LV motion. Regional wall
motion may also be assessed (Fig. 10.2). Quantification of volumes as well as sys-
tolic and diastolic function is derived from the ventricular time-activity curve [4].
ERRNVPHGLFRVRUJ
94 C. Gallegos
Fig. 10.1 Screen shot obtained at end-diastole demonstrating LAO (upper left), anterior (upper
right) and lateral (lower left) planar projections. Regional wall motion is also displayed in the LAO
image
Data Interpretation
The findings obtained from an RNA scan should be interpreted and reported in a
systematic way. The essential components are: [2]
(a) Cardiac Morphology: Size, orientation, and morphology of various cardiac
chambers, ventricular wall thickness, as well as the pericardial silhouette, which
may all, be evaluated subjectively and reported. When measured, absolute vol-
umes may be included.
(b) Systolic Ventricular function: All LV segments should be assessed qualita-
tively and global LV function should be compared to calculated
ERRNVPHGLFRVRUJ
10 Radionuclide Angiography 95
Fig. 10.2 Case 1 (see text for details)
EF. Reprocessing may be necessary, if there are discrepancies with measure-

ments. Abnormalities should be reported as mild, moderate or severe, hypoki-
nesia, dyskinesia, or akinesia. It is optional to report diastolic filling indices
or systolic emptying indices.
(c) Stress images: These should be displayed side-by-side to the rest images in
cinematic mode. Baseline, peak and recovery LVEF should be reported as
well as any alteration in regional wall motion, RV and LV function and vol-
umes. Cardiac morphology should be reported in a similar way as in a rest
study.
(d) Comparison to other studies: Prior studies should be reviewed and compared
Additionally, diastolic function may also be assessed, especially with an acquisi-
tion greater than 16 frames per cardiac cycle, although this is infrequently per-
formed at the current time. Indices such as peak filling rates and time to peak filling
may be quantitatively determined.
Complications
RNA is a safe noninvasive procedure, however there are a few scenarios that require
special caution.
1. Arrhythmias, in particular during or after stress/exercise as heart rate response
during these is unpredictable
2. Incorrect handling of RBCs during in vitro, which may results in administration
of the labeled cells to the wrong patient.
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96 C. Gallegos
Clinical Vignettes
Case 1
A 43-year-old woman was recently diagnosed with breast cancer, treated with
lumpectomy and radiation therapy. She is now scheduled to begin chemotherapy
with a variety of agents, including doxorubicin. An RNA is performed to obtain a
quantitative assessment of LV function.
Figure 10.2 demonstrates on a single static screen capture most of the key infor-
mation needed to assess cardiac function and subsequently begin chemotherapy.
This depicts a study with a 16 frame per cardiac cycle acquisition. The time activity
curve at the bottom depicts LV filling during the cardiac cycle and even demon-
strates the atrial contribution near the end of diastole. The ED and ES frames dem-
onstrate the area of the LV during end-systole and end-diastole, with the adjacent
region used for background counts. Our patient’s quantitative LVEF was 73 %.
References
1. Strauss HW, Zaret BL, Hurley PJ, Natarajan TK, Pitt B. A scintiphotographic method for mea-
suring left ventricular ejection fraction in man without cardiac catheterization. Am J Cardiol.
1971;28(5):575–80. PubMed PMID: 5116974. Epub 1971/11/01. eng
2. Scheiner JS, Sinusas A, Wittry, M, Royal, H. Society of Nuclear Medicine. Procedure guide-
line for gated equilibrium radionuclide ventriculography. Soc Nucl Med Proc Guidel Manual.
2002:1–7. http://www.snmmi.org/ClinicalPractice/content.aspx?ItemNumber=6414#Cardio
3. Ritchie JL, Bateman TM, Bonow RO, Crawford MH, Gibbons RJ, Hall RJ, O’Rourke RA,
Parisi AF, Verani MS. Guidelines for clinical use of cardiac radionuclide imaging. Report of
the American College of Cardiology/American Heart Association Task Force on Assessment
of Diagnostic and Therapeutic Cardiovascular Procedures (Committee on Radionuclide
Imaging), developed in collaboration with the American Society of Nuclear Cardiology. J Am
Coll Cardiol. 1995;25:521–47.
4. Hesse B, Lindhardt TB, Acampa W, et al. EANM/ESC guidelines for radionuclide imaging of
cardiac function. Eur J Nucl Med Mol Imaging. 2008;35(4):851–85. PubMed PMID: 18224320
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Chapter 11
Cardiac Computed Tomography (CT)
Arieh Fox
Cardiac CT has undergone dramatic advances in technology with applications that

include the assessment of coronary artery disease (CAD), using coronary computed
tomography angiography (CCTA) evaluation of congenital abnormalities and struc-
tural function, and characterization of anatomy prior to valve and electrophysiology
procedures [1, 2]. CT now permits the rapid acquisition of high quality data in the
majority of patients using prospective (radiation-sparing) or retrospective ECG gating,
with outstanding resolution of the coronary arteries as well as other cardiac structures.
Indications
In 2010, the ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR Appropriate

Use Criteria for cardiac Computed Tomography was published with the level of
appropriateness to guide physicians. The list is extensive and generally includes
usefulness in the acute and chronic setting as well as in the symptomatic and asymp-
tomatic patient. The main appropriate indications are listed below (Table 11.1).
Contraindications
Patients must be able to meet the weight requirements of the scanner, have the abil-
ity to lay supine and motionless with arms raised above their shoulders, and follow
simple breathing instructions.
A. Fox, MD
3400 Civic Center Blvd. South Tower, 11th Floor,
Philadelphia, Pennsylvania 19104, USA

DOI 10.1007/978-1-4471-7290-1_11
ERRNVPHGLFRVRUJ
98 A. Fox
Table 11.1 Appropriate indications for cardiac computed tomography [1, 2]

1 Detection of CAD in intermediate risk symptomatic patients without known heart disease
2 Detection of CAD in low risk symptomatic patients without known heart disease who are
unable to exercise or ECG is uninterpretable
3 Detection of CAD in low & intermediate risk acutely symptomatic patients without known
heart disease
4 Detection of CAD/risk assessment in asymptomatic low risk patients with significant
family history or intermediate risk patients with coronary calcium score in individuals
without known CAD
5 New-onset or newly diagnosed Heart Failure (HF) and no prior CAD in low &
intermediate risk patients
6 Preoperative coronary assessment prior to non-coronary cardiac surgery in intermediate
risk patients
7 Normal ECG exercise test & continued symptoms or Duke Treadmill Score-intermediate
risk findings
8 Discordant ECG exercise and imaging results or equivocal stress imaging results
9 Evaluation of new or worsening symptoms in the setting of normal past stress imaging
study
10 Evaluation of graft patency after CABG in a symptomatic patient
11 Assessment of anomalies of coronary arterial and other thoracic arteriovenous vessels or
complex adult congenital heart disease
12 Evaluation of left ventricular function in acute Myocardial Infarction (MI) or HF when
images from other noninvasive methods are inadequate
13 Quantitative evaluation of right ventricular function
14 Assessment of right ventricular morphology in suspected Arrhythmogenic Right
Ventricular Dysplasia
15 Characterization of native and prosthetic cardiac valves with suspected significant valvular
dysfunction and inadequate images from other noninvasive methods
16 Evaluation of cardiac mass (suspected tumor or thrombus) with inadequate images from
other noninvasive methods
17 Evaluation of pericardial anatomy
18 Evaluation of pulmonary vein anatomy, coronary vein mapping or localization of coronary
bypass grafts prior to intervention
Chronic Kidney disease (GFR <60) is a relative contraindication given the

potential for contrast-induced nephropathy (CIN); the risk of CIN must be
weighed against the potential benefits of the study. However, severe kidney dis-
ease (GFR <30, not on dialysis) is an absolute contraindication and an alternative
testing strategy should be pursued. Previous anaphylaxis to iodinated contrast or
an allergic reaction to iodinated contrast after premedication is an absolute
contraindication.
Atrial fibrillation and frequent ectopy are relative contraindications to CCTA and
mandate retrospective gating (acquisition of the entire cardiac cycle) if performed at
all. Additionally, heart rates in excess of 70 BPM are usually associated with exces-
sive cardiac motion and efforts to modulate pulse rate must be undertaken. In this
regard, an inability to tolerate beta-blockers may be a relative contraindication.
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11 Cardiac Computed Tomography (CT) 99
In younger individuals, the risk of potential long-term radiation exposure must

be weighed against the potential benefits of the study. Additionally, dense coronary
calcification may limit the interpretation and utility of the study, however a spe-
cific coronary calcium (Agaston) score that excludes the use of CCTA has not been
recommended in the Society of Cardiovascular Computed Tomography (SCCT)
guidelines.
Equipment
Cardiac CT imaging equipment must meet the minimal technical capabilities

required for the scan indication and the patient’s underlying characteristics.
According to the ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR
Appropriate Use Criteria, cardiac CT generally requires a minimum of 64
multi-detector rows, gantry rotation time no greater than 420 ms, sub millimeter
spatial resolution and cardiac imaging software capable of three-dimensional
post processing with reconstructed axial data, multi-planar reconstructions, and
maximum intensity projections. Additionally, tube potential adjustment must
be available for radiation reduction techniques, such as reducing the voltage
to 100 mV for non-obese patients. Ideally, prospectively triggered ECG scan-
ning and iterative reconstruction should also be available for further radiation
reduction.
Technique
Heart rate control is crucial for obtaining optimal images without significant artifact
and therefore the patient should be given oral beta-blockers the night prior and the
morning of the procedure. If the patient’s heart rate is still elevated (>65 BPM), the
patient should be given an additional dose of IV beta-blocker or calcium channel
blocker as needed. Patients should abstain from caffeine or nicotine for at least
12 hours prior to procedure for purposes of heart rate control.
Nephrotoxic drugs should be discontinued and the patient should be screened for
contrast induced nephropathy risk factors (diabetes mellitus, chronic kidney dis-
ease, congestive heart failure, age >75…) with an accurate history and a serum
creatinine obtained prior to the procedure. Pre-procedural oral and possibly IV
hydration may be necessary based on the patient’s baseline serum creatinine.
Patients with a history of an Iodine allergy or an allergic contrast reaction require
premedication with corticosteroids and histamine antagonists.
Breath holds are performed during image acquisition and theoretically reduce
cardiac motion as well as decrease intrathoracic pressure leading to maximum supe-
rior vena cava flow and contrast enhancement.
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100 A. Fox
A coronary scan (CCTA) should begin at the level of the carina or mid-pulmonary
artery and end 2 cm below the diaphragm unless the patient has bypass grafts, which
would require starting above the arch. A calcium score is often obtained prior to
coronary CT for prognosis and estimate of plaque burden, as well as to optimize
CCTA image acquisition.
Nitroglycerin 0.4–0.8 mg sublingual should be administered prior to image
acquisition to improve image quality by arterial vasodilatation. However, this should
be avoided in patients with systolic blood pressures less than 100 mmHg, significant
aortic stenosis or hypertrophic cardiomyopathy and patients who are using phos-
phodiesterase inhibitors.
The appropriate gating technique should be selected based on the study indica-
tion and the patient’s characteristics. Prospective gating limits the data acquisition
period during the cardiac cycle to the points of least coronary movement and is the
preferred method for coronary artery assessment given its ability to obtain the nec-
essary data while substantially limiting radiation exposure. Retrospective gating
acquires data during the entire cardiac cycle and requires a significantly higher
radiation exposure. This may be useful for patients with arrhythmia, rapid heart
rates or high calcium scores, where artifacts may be a limiting factor and the addi-
tional data acquired throughout the cardiac cycle may be beneficial. ECG pulsed
tube current modification is another gating technique used to limit radiation when
coronary anatomy and evaluation of left ventricular function is required. Tube volt-
age and current should also be adjusted according to the patient’s size to minimize
radiation dose.
Contrast used in cardiac CT is nonionic with high iodine concentration typically
dosed according to patient BMI and given through a vein suitable for administration
at a flow rate of 4–6 mL/s (usually antecubital). Decreased and increased cardiac
output increase and decrease the amount of contrast required.
Data Interpretation
The Society of Cardiovascular Computed Tomography (SCCT) released updated

guidelines in 2014 on the interpretation of coronary CT angiography that are listed
in the table below (Table 11.2).
Individual lesions should be graded on a qualitative and quantitative basis with
the recommended SCCT scale listed below and plaque morphology should also be
described as calcified, non-calcified or mixed (Table 11.3 and 11.4).
Additionally, myocardial chamber cavities and walls should be examined for
dilation, hypertrophy, thinning, hypodense enhancement, shunting, masses and con-
genital anomalies. Reporting of left ventricular and regional function as well as
valvular pathology may be appropriate depending on the clinical indication.
Reports should include a procedure section with complete details of image
acquisition and image reconstruction and a clinical findings section with coronary
findings, non-coronary cardiac findings, and non-cardiac findings.
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Table 11.2 SCCT interpretation guidelines [3]

Non-contrast coronary calcium CT
1. Agatston score should be calculated for the total study (sum of 4 vessels)
2. Presence of calcium in aortic wall, aortic valve, mitral annulus/valve, pericardium, and
myocardium should be documented
3. Noncardiac structures (pleural effusions, pulmonary nodules, mediastinal abnormalities,
and so forth) should be documented
Coronary CT
1. Interpretation should be made on 3-dimensional cardiac-specific interpretation software
2. Recommended image reconstructions should be viewed
3. Interpreters should be prepared to customize image reconstructions if necessary
4. The data set should be previewed for artifacts
5. Noncontrast studies should be reviewed before contrast studies
6. The coronary tree should be examined systematically
7. Lesions should be reviewed in multiple planes and conceptualized in 3 dimensions
8. Lesions should be assessed for stenosis severity, quality, and morphology of plaque
9. Extracoronary cardiac and thoracic anatomy should be examined within the cardiac field of
view
Table 11.3 SCCT 0 Normal Absence of plaque and no luminal stenosis

recommended qualitative
1 Minimal Plaque with negligible impact on lumen
stenosis grading [3]
2 Mild Plaque with no flow-limiting stenosis
3 Moderate Plaque with possible flow-limiting disease
4 Severe Plaque with probable flow-limiting disease
5 Occluded
Table 11.4 SCCT 0 Normal Absence of plaque and no luminal stenosis

recommended quantitative
1 Minimal Plaque with <25 % stenosis
stenosis grading [3]
2 Mild 25–49 % stenosis
3 Moderate 50–69 % stenosis
4 Severe 70–99 % stenosis
5 Occluded
Complications
Potential complications from cardiac CT include iodinated contrast extravasation,

which can rarely lead to ulceration or compartment syndrome, allergic reactions to
iodinated contrast, contrast induced nephropathy and radiation exposure. CIN is
generally defined as a change in serum creatinine of >0.5 mg/dL or a >25 % increase
in serum creatinine from baseline within 2–3 days of contrast exposure. Risk factors
for CIN include hypotension, congestive heart failure, chronic kidney disease, dia-
betes, age older than 75, anemia, and volume of contrast. Radiation exposure should
always be limited to as low as reasonably achievable while still obtaining the neces-
sary results for an appropriate study.
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102 A. Fox
Clinical Vignettes
Case 1
Forty-five-year-old police officer, who is active at baseline and has no significant

past medical history presents to the emergency department (ED) after experiencing
an episode of sharp chest pain earlier in the day. In the ED, the patient was noted
to have an ECG without significant abnormalities and an elevated blood pressure of
160/105 mmHg. CCTA was obtained for detection of CAD in this low risk acutely
symptomatic patient (Fig. 11.1).
This case shows a CCTA with no significant atherosclerotic lesions of the coro-
nary arteries. Included below are the curved multiplanar reformation images of the
Left Anterior Descending (LAD) artery (Fig. 11.1b), Left Circumflex (LCx) artery
(Fig. 11.1c) and the Right Coronary (RCA) artery (Fig. 11.1d) without evidence of
significant atherosclerotic disease.
Case 2
Sixty-four-year-old man with a past medical history significant for hyperlipidemia

presents requesting a preventive cardiovascular evaluation. Previously, the patient
underwent an asymptomatic treadmill stress test with 3 mm ST depressions in the
inferolateral leads followed by a nuclear stress test with abnormal ECG findings but
normal scintigraphic images without evidence of ischemia. Given discordant ECG
exercise and imaging results, a CCTA was obtained for further evaluation.
This case shows a CCTA with severe coronary calcification and significant CAD
in two vessels. There is extensive calcification in the proximal portion of the LAD
with an elongated non-calcified severely stenotic plaque of approximately 70–99 %
(Fig. 11.2b). There is also calcification noted in the LCx but without significant
obstruction (Fig. 11.2a). The proximal portion of the right coronary artery contains
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extensive calcification and an area of low density with markedly reduced contrast,
which suggests a severe stenosis of 70–99 % (Fig. 11.2c).
References
1. Taylor AJ, Cerqueira M, Hodgson JM, Mark D, Min J, O’Gara P, Rubin GD, American College
of Cardiology Foundation Appropriate Use Criteria Task Force; Society of Cardiovascular
Computed Tomography; American College of Radiology; American Heart Association;
American Society of Echocardiography; American Society of Nuclear Cardiology; North
American Society for Cardiovascular Imaging; Society for Cardiovascular Angiography and
Interventions; Society for Cardiovascular Magnetic Resonance. ACCF/SCCT/ACR/AHA/
ASE/ASNC/NASCI/SCAI/SCMR 2010 appropriate use criteria for cardiac computed tomog-
raphy. A report of the American College of Cardiology Foundation Appropriate Use Criteria
Task Force, the Society of Cardiovascular Computed Tomography, the American College of
Radiology,the American Heart Association, the American Society of Echocardiography, the
American Society of Nuclear Cardiology, the North American Society for Cardiovascular
Imaging, the Society for Cardiovascular Angiography and Interventions, and the Society for
Cardiovascular Magnetic Resonance. J Cardiovasc Comput Tomogr. 2010;4(6):407.e1–33.
2. Mark DB, Berman DS, Budoff MJ, Carr JJ, Gerber TC, Hecht HS, Hlatky MA, Hodgson JM,
Lauer MS, Miller JM, Morin RL, Mukherjee D, Poon M, Rubin GD, Schwartz RS, American
College of Cardiology Foundation Task Force on Expert Consensus Documents. ACCF/ACR/
AHA/NASCI/SAIP/SCAI/SCCT 2010 expert consensus document on coronary computed
tomographic angiography: a report of the American College of Cardiology Foundation Task
Force on Expert Consensus Documents. Catheter Cardiovasc Interv. 2010;76(2):E1–42.
3. Leipsic J, Abbara S, Achenbach S, Cury R, Earls JP, Mancini GJ, Nieman K, Pontone G, Raff
GL. SCCT guidelines for the interpretation and reporting of coronary CT angiography: a report
of the Society of Cardiovascular Computed Tomography Guidelines Committee. J Cardiovasc
Comput Tomogr. 2014;8(5):342–58.
4. Raff GL, Chinnaiyan KM, Cury RC, Garcia MT, Hecht HS, Hollander JE, O’Neil B, Taylor
AJ, Hoffmann U, Society of Cardiovascular Computed Tomography Guidelines Committee.
SCCT guidelines on the use of coronary computed tomographic angiography for patients
presenting with acute chest pain to the emergency department: a report of the Society of
Cardiovascular Computed Tomography Guidelines Committee. J Cardiovasc Comput Tomogr.
2014;8(4):254–71.
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Chapter 12
Cardiac Magnetic Resonance
Cesia Gallegos
Cardiac magnetic resonance (CMR) is an imaging modality used for the assessment
of heart, providing both anatomic and physiologic information. Its use has increased
over the last decade given the improvement on imaging acquisition and quality with
growing evidence from clinical trials supporting its value. The high natural contrast
between intracardiac or intravascular blood pool, lack of ionizing radiation, and
three-dimensional nature of this method provide substantial advantages over other
methods, but it is the ability of CMR to characterize tissues that offers unique value
of this technique.
Indications (Table 12.1)
Cardiac anatomy and ventricular function CMR is considered the most reproduc-
ible and accurate in the study of left ventricular (LV) function. Some of the param-
eters routinely reported in functional CMR may include: LV end-diastolic volume
(LVEDV) and LVEDV index, LV stroke volume, LV ejection fraction (LVEF), LV
mass index, and LV end-diastolic and end-systolic diameter. CMR may also be used
for qualitative and quantitative assessment of global and regional wall motion of the
right ventricle (RV). It is usually the first-line diagnostic test for assessing RV func-
tion and it is indicated in the evaluation of patients for suspected arrythmogenic RV
cardiomyopathy or dysplasia, as well as pulmonary arterial hypertension.
Congenital heart disease CMR may be used for the assessment of congenital
shunts, specifically to quantify and follow right and left ventricle volumes and func-
C. Gallegos, MD
Yale University School of Medicine, Section of Cardiovascular Medicine,
333 Cedar Street, PO Box 208017, New Haven, CT 06520-8017, USA

DOI 10.1007/978-1-4471-7290-1_12
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106 C. Gallegos
Table 12.1 Class I and II Indication Class

indications for CMR [1–4]
Arrythmogenic right ventricular dysplasia I
Siderotic cardiomyopathy (in particular thalassemia) I
Dilated cardiomyopathy I
Hypertrophic cardiomyopathy (apical) I
Non compaction cardiomyopathy II
Ventricular thrombus II
Constrictive pericarditis II
Restrictive cardiomyopathy II
tion. CMR is also useful in some forms of atrial (ASD) or ventriculoseptal (VSD)
defects that are challenging for other imaging modalities to identify. The use of
CMR along with angiography and flow measurement is also valuable for the assess-
ment of complex congenital anomalies and the determination of chamber size, func-
tion, and atrial-ventricular relationships. Other congenital conditions in which CMR
has proven to be helpful include pericardial anomalies, as well as valve disease and
coronary artery anomalies.
Assessment of the great vessels It can frequently demonstrate a lesion directly (ste-
nosis) or indirectly, by showing a signal loss resulting from phase incoherence
(abnormal communication). CMR angiography is also used to depict the extent,
size, and shape of aortic aneurysms dissections, thrombus, vascular wall, and adja-
cent soft tissues. Its lack of ionizing radiation provides a tool for serial imaging.
Acquired myocardial and pericardial disease One of the most valuable uses of
CMR is the assessment of adult cardiomyopathies, myocardial fibrosis and infarc-
tion, as well as pericardial disease, including collections, masses, and effusions.
Through the use of phase contrast techniques, CMR can also evaluate for valvular
stenosis or insufficiency. It also characterizes specific tissue configurations of
tumors and masses and their relationship to chambers and valves, making it the
ideal imaging modality as it allows for the assessment of mediastinal, pericardial
and myocardial involvement in one single study.
Coronary artery disease CMR is also useful in the evaluation of chronic ischemic
heart disease, especially with the delineation of myocardial viability through the use
of gadolinium. Vasodilator stress perfusion imaging and dobutamine wall motion
assessment are CMR techniques for the detection and quantitation of inducible
ischemia.
Contraindications
CMR is safe and lacks ionizing radiation, but special caution should still apply.
In all cases, a risk/benefit consideration should be performed prior to each test
and must be informed to each patient. This involves a physician with thorough
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12 Cardiac Magnetic Resonance 107
knowledge of patient safety, possible neurological effects, tissue heat deposition,

the use of contrast as well as other contraindications or special considerations,
which include [3]:
Implantable Devices Common implants, which may present a hazard when under-
going CMR, include pacemakers, ICD’s, cochlear implants, neurostimulators,
hydrocephalus shunts, metal-containing ocular implants, pacing wires, and metallic
cerebral clips [5]. A full list is available in www.mrisafety.com. The clinician must
be aware if the patient has an implantable device and whether or not it is magnetic
resonance (MR) safe, conditional or not safe. If decision is made to perform CMR
to a patient with a device, knowledge of device programming is necessary. Some of
the risks of performing CMR in patients with pacemaker or cardioverter-defibrillators
include burns from generation of an electrical current from the metallic hardware
and the “antenna effect”, device movement, inappropriate discharging and sensing.
Appropriate emergency equipment and medications to treat possible adverse reac-
tions must be readily available.
Contrast media Although more frequent with the use of iodinated contrast,
some patients may require pretreatment prior to injection of contrast media
even if gadolinium is used for prevention of anaphylactic reaction and/or acute
kidney injury. Special caution must be performed in patients with decreased
renal function, especially with a GFR <30 mL/min due to the risk for nephro-
genic systemic fibrosis, a potentially catastrophic complication of gadolinium
exposure.
Pharmacological stress testing in unstable patients similar to any other stress test
modality.
Equipment
The magnetic resonance imaging (MRI) equipment must meet all state and federal
requirements and must be accredited by the Academic College of Radiology
(ACR) [2].
MRI scanners for CMR must have the following specifications:
1. Field strength ≥1.0 T. Most common is 1.5 T
2. Slew rate of at least 70 mT/m/s.
3. MRI scanners should be equipped with ECG gating and multi-channel radiofre-
quency surface coil.
4. MRI-compatible power injector for myocardial perfusion CMR
5. Capability of fast 3D gradient echo imaging, phase-contrast flow quantification,
and fast multislice myocardial perfusion imaging as well as delayed contrast-
enhanced myocardial imaging.
6. FDA-approved software for processing data
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108 C. Gallegos
Technique
MRI is based on imaging of protons within the hydrogen atoms in the human body
that act as tiny magnets. A patient is then placed inside a scanner with a magnetic
field, which the resultant vectors are fine-tuned by computer-controlled adjustments
of small coils placed within the magnet [5].
Unless impeded by body habitus, a phased array surface coil should be used, as
the heart is small and the visual field should be reduced to maintain adequate spatial
resolution. CMR imaging techniques may vary depending on the indication.
Nonetheless, most examinations include short and long-axis cine images from the
heart obtained for ventricular function [3]. For assessment of cardiac morphology,
T1-weighted and/or T2 weighted images of the heart may be beneficial and they
should be gated to the R wave of the ECG.
For evaluation of mass, tumors, or cysts, pericardial disease, and myocardial
inflammation, or perfusion, IV gadolinium is administered. Additionally, in the
particular case of myocardial perfusion assessment, gadolinium must be rapidly
bolused.
For flow quantification, phase contrast imaging may be used. CMR angiography
can be used in addition to other MRI methods as it may provide important informa-
tion about the great vessels.
CMR tagging is another technique in which bands are applied to the heart in end-
diastole, and subsequently cine images are obtained to observe the movement of the
bands, which may provide information about wall motion abnormalities.
Data Interpretation
The CMR imaging planes are oblique to one another and are called “double-
obliques” planes as they are at arbitrary angles with respect to the scanner. There are
three main planes in which the images will be reported: short axis, horizontal long
axis or 4-chamber view, and vertical long axis or 2-chamber view.
Cardiac function is evaluated using cine gradient echo sequences called “bright
blood sequences” used in conjunction with segmented k-space acquisition. For eval-
uation of cardiac morphology “black blood “sequences are also used, for which
there are multiple options: half-Fourier, single-shot, fast spin echo (SS-FSE) being
the most common. Ventricular function can then by quantitatively assessed by
reviewing the dynamic images. For example, chronic transmural ischemia will be
demonstrated by a decrease in the myocardial thickness to less than 6 mm and will
also exhibit a lack of wall thickening during systole. Additionally, myocardial tag-
ging is used to track segmental motion and helps to distinguish compromised myo-
cardium from myocardium that may move irregularly because of its proximity to an
affected area. However, a more reliable indicator of acute myocardial infarction is
delayed contrast enhancement after the administration of IV gadolinium, which
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demonstrates a good correlation between healthy and infarcted myocardium. In

infarcted cells, the gadolinium is retained after a period of washout of other regions
(about 5–10 min), resulting in delayed hyperenhancement. This is particular useful
as a greater extent of transmural infarction can predict areas that are unlikely to
improve after revascularization.
Complications
1. Ferromagnetic items can possibly be dangerous projectiles in the scanner room

and can injury patients and staff
2. Heating of wires of pacemakers and defibrillators, which could result in serious
burns.
3. Nephrogenic sclerosing fibrosis in patients administered gadolinium that have a
reduced GFR.
4. Claustrophobia
Clinical Vignette
Case 1
Sixty-seven year-old male with history of hypertension, diabetes type 2, and chronic
obstructive pulmonary disease presented to the hospital with exertional chest pain,
cough, hypoxemia and elevated troponins. As part of his evaluation, underwent
cardiac catheterization which was non-revealing, and a 2D echocardiogram dem-
onstrated a normal EF without wall motion abnormalities. Given nondiagnostic
work-up, CMR was performed, shown in Fig. 12.1.
Fig. 12.1 Case #1 (see

text for details)
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110 C. Gallegos
The image shown demonstrates an end-diastolic myocardium measuring

18.5 mm at the septum, which was not previously seen on echocardiography. Patient
was found to have COPD exacerbation and elevation of troponins was likely sec-
ondary to demand ischemia in the setting of hypertrophic cardiomyopathy, as they
normalized once the infection was controlled. In this case, CMR allowed for the
identification of LV hypertrophy in segments not visualized well with other diag-
nostic modalities.
Case 2
Fifty-three year old man presented following a 45 min episode of chest pain. His
ECG revealed deep T wave inversions in the anterior leads but he was pain free.
Echocardiography revealed anterior akinesis and an LVEF of 27 %. He was referred
for CMR with LGE to assess myocardial viability.
Figure 12.2 demonstrates a large area of LGE in the anterior wall but it is suben-
docardial, not transmural. Base on this study, with the impression that substantial
viability was present, he was referred for cardiac catheterization and underwent PCI
of a proximal LAD lesion (90 %). Subsequently, an echocardiogram revealed
marked improvement in anterior wall motion and an LVEF of 45 %.
Case 3
A 31 year old woman presented to her physician’s office with severe shortness of
breath. She had had an upper respiratory infection approximately 10 days ago, with
rhinorrhea and cough, but her symptoms had almost completely resolved until 1 day
Fig. 12.2 Case #2 (see

text for details)
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Fig. 12.3 Use of Cardiac Magnetic Resonance in the diagnosis of acute myocarditis. (a) Midseptal
wall edema on T2 weighted images (arrow) (b) Prominent late gadolinium enhancement in the mid
wall of the intraventricular septum
before presentation. She has no pre-existing medical conditions. A chest x-ray was
compatible with pulmonary edema and an echocardiogram revealed severe left ven-
tricular dysfunction. CMR was performed (Fig. 12.3).
These images depict midseptal wall edema on the T2 weighted images (Panel A)
and prominent late gadolinium enhancement in the mid wall of the intraventricular
septum (Panel B). These findings are consistent with acute myocarditis. After an
initially labile hospital course, the patient demonstrated marked clinical improve-
ment over the next week but did have some residual LV dysfunction on discharge.
References
1. Pennell DJ, Sechtem UP, Higgins CB, et al. Clinical indications for cardiovascular magnetic
resonance (CMR): Consensus Panel report. European heart journal. 2004;25(21):1940–65.
PubMed PMID: 15522474.
2. American College of Radiology. ACR–NASCI–SPR practice parameter for the performance
and interpretation of cardiac magnetic resonance imaging (MRI). Diagnostic radiology mag-
netic resonance imaging (MRI) practice parameters and technical standards by the American
College of Radiology. 2014:1–20. http://www.acr.org/~/media/ACR/Documents/PGTS/
guidelines/MRI_Cardiac.pdf
3. Woodard PK, Bluemke DA, Cascade PN, et al. ACR practice guideline for the performance and
interpretation of cardiac magnetic resonance imaging (MRI). J Am Coll Radiol JACR.
2006;3:665–76.
4. Pennell DJ. Cardiovascular magnetic resonance. Circulation. 2010;121:692–705. http://dx.doi.
org/10.1161/CIRCULATIONAHA.108.811547
5. Kwong RY. Cardiovascular magnetic resonance imaging. In: Mann D, editor Braunwald’s heart
disease. 10th ed. Elsevier. Saunders. Philadelphia, PA; 2015. p. 320–37.
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Part II
Critical Care
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Chapter 13
Central Venous Cannulation
Introduction
Central venous cannulation is an essential skill for all cardiovascular specialists and
provides a safe and secure route for the administration of parenteral agents. Often
performed in an emergent fashion, when intravenous access is required for delivery
of potentially life saving medications, this technique may also be used when limited
peripheral options are available.
Indications
Central venous cannulation is required in a variety of clinical scenarios. Current

critical care units utilize central venous lines for inotropic and vasopressor medica-
tions that require infusion via a central venous catheter. In addition, central access
allows for insertion of multi-lumen catheters that can accommodate the infusion of
non-compatible medications using a single access point. While peripheral intrave-
nous lines remain the preferred method for large volume resuscitation, central lines
are commonly used for this purpose. Hyperalimentation, temporary pacemaker
implantation, right heart catheterization for invasive hemodynamic monitoring and
right ventricular (RV) biopsy also require central venous access (Table 13.1).
S. Alshalash, MD (*)
Cardiac Catheterization Laboratory, Tufts Medical Center, 750 Washington Street, Boston,
MA 2111, USA
C. Kimmelstiel, MD
Associate Professor of Medicine, Division of Cardiology, Tufts Medical Center,
Tufts University School of Medicine, 750 Washington Street, Boston, MA 2111, USA

DOI 10.1007/978-1-4471-7290-1_13
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116 S. Alshalash and C. Kimmelstiel
Table 13.1 Indications for central venous cannulation

Indications
Infusion of vasoactive medications Inadequate peripheral access
Right heart catheterization Administration of medication known to cause
phlebitis
Placement of pacing leads Plasmapheresis
Monitoring of central venous pressure Hemodialysis
Right ventricular biopsy
Relative contraindications
Bleeding diathesis Active infection at the access site
Deep vein thrombosis Known distorted anatomy (due to radiation or
prior surgery)
Contralateral pneumothorax (for IJ and SC High pressure ventilation
central lines)
Contraindications
Bleeding is a relative contraindication and benefits should be weighed against risks.

Active infection and deep venous thrombosis (DVT) at the site of cannulation are
contraindications and if present, a different site should be used. For internal jugular
(IJ) and subclavian (SC) venous access, contralateral pneumothorax or high pressure
ventilator settings should prompt consideration of an alternative site (Table 13.1).
Equipment
Central venous cannulation requires a sterile field. Methodological full-body drap-

ing reduces the incidence of central venous line infections. Local anesthetic, an
ultrasound machine with a sterile cover, central line access kit (which includes an
18-gauge needle, syringes, guide wire, scalpel, dilator, and central line -single or
multi-lumen), sterile saline flushes, suture, and a dressing are needed to complete
the procedure. The usual length of central venous catheters is 12–20 cm.
Technique
The site of access should be chosen carefully. The IJ, SC, and femoral veins are
among the most widely accessed sites. Peripherally inserted central catheters
(PICC) are also an option, particularly when the catheter is needed for a longer
period of time (>1 week). Inspection of the site and using ultrasound to identify the
target vessel prior to setting up a sterile field increases the odds of a successful pro-
cedure and obviates the need to change the site because of anatomical anomalies or
DVT. Once the site is identified, meticulous antiseptic technique must be followed
while preparing a sterile field and the access site. The use of ultrasound has become
the standard of care in accessing the IJ vein as it has been shown to reduce the
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13 Central Venous Cannulation 117
incidence of carotid puncture, neck hematoma, hemothorax, pneumothorax, num-

ber of attempts, access time, and catheter related blood stream infection [1]. The
vein is identified using ultrasound; it is compressible and has continuous flow com-
pared to the pulsatile and not-easily compressible artery (Fig. 13.1).
Solely using anatomic landmarks to achieve IJ access, is discouraged as it is associ-
ated with a higher rate of complications [2]. The patient is placed in a supine or
Trendelenburg position, the apex of the triangle formed by the two heads of the sterno-
cleidomastoid and the clavicle is infiltrated with local anesthetic with the needle directed
towards the ipsilateral nipple (Fig. 13.2). The use of a 22-gauge “finder” needle to can-
nulate the vein is sometimes performed to “map the way” for the 18-gauge needle.
Fig. 13.1 The carotid artery (A) and the right internal jugular vein (V) are seen (left image) and
after compression, the vein is no longer visible (right image)
Fig. 13.2 Surface anatomy

and landmarks for right IJ
access. The apex of the
triangle formed by the two
heads of the SCM and the
clavicle is accessed with the
needle pointing towards the
ipsilateral nipple (SCM
sternocleidomastoid muscle)
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For SC vein access, the needle is inserted at the point where the medial third of
the clavicle meets the middle third (just medial to the midclavicular line) and the
needle is inserted using a shallow angle underneath the clavicle with the needle
pointing towards the suprasternal notch. The vein is cannulated underneath the clav-
icle. It is important to position the patient in a Trendelenburg position to distend the
SC vein and increase the odds of venous cannulation. Some operators prefer placing
a pillow or rolled-up towel under the patient, between their shoulder blades. In
patients with coagulopathy the SC vein should, in general, not be used as it is non-
compressible. Aspiration of bright red pulsatile blood indicates arterial puncture
and the needle should be withdrawn and pressure is applied. Aspiration of air bub-
bles may indicate a pneumothorax. The SC vein is associated with less risk of
catheter related systemic infection compared to femoral and IJ routes, but a higher
risk of pneumothorax [3].
The femoral vein is accessed 1 cm below the inguinal ligament approximately
1 cm medial to the femoral artery. Central venous cannulation using the femoral
vein can be done rapidly in unstable patients or during CPR, however, it may be
associated with higher rates of catheter-related blood stream infections.
Once the vein being utilized is accessed with the 18-gauge needle, the guide wire
is inserted and the dilator is passed over the wire to expand the puncture site to
accommodate the catheter. The catheter is inserted over the wire, then aspirated,
flushed, and sutured into place. When the IJ or SC veins are used, the tip of the
catheter should be in the superior vena cava which is confirmed by a subsequent
chest x-ray.
Data Interpretation
The size of the IJ vein when visualized with ultrasound and the respirophasic
variation reflects the volume status of the patient as it is commonly a reflection of
central venous pressure, except in situations where there is an obstruction caused
by DVT, stenosis, or in the presence of moderate to severe tricuspid regurgitation.
Once the vein is cannulated and the sheath is introduced, the central venous pres-
sure can be directly measured using a standard fluid-filled transducer. If the opera-
tor is uncertain as to whether the vein or artery was cannulated, verification should
be made prior to introducing a dilator into the vessel. There are many ways to
verify that the vein was cannulated. A widely used method is observing the blood
return, which is dark and has continuous flow in the central veins compared to
bright red and pulsatile flow in the artery. When uncertainty exists, an oxygen satu-
ration can be performed with a point of care device to assess whether the needle
resides within the venous or arterial system. If an oxygen saturation is not imme-
diately available, fluoroscopy can be utilized, following the course of the guide-
wire, with skilled operators able to discern the typical course of venous or arterial
anatomy. An alternative method involves the infusion of a small amount of con-
trast which can discriminate between the pulsatile artery from the non-pulsatile
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Fig. 13.3 Chest x-ray

showing a pulmonary
artery catheter (PAC) after
insertion from the right IJ
(RIJ) into the right
pulmonary artery
vein. In the absence of fluoroscopy, the wire can be visualized in the long and short
axes using ultrasound. If the operator is still uncertain that the needle is in a central
vein, injection of small amount of agitated saline visualizing the trajectory of the
fluid flow will help to confirm the position of the needle. Alternatively, a phased
array probe can be used to visualize the agitated saline within the right sided car-
diac chambers.
After central venous catheter placement, in the IJ or SC vein, an upright chest
x-ray should be obtained to confirm the position of the central line and to exclude
the presence of pneumothorax or hemothorax. Figure 13.3 depicts the course and
position of a pulmonary artery (PA) catheter. Venous anomalies, such as persistent
left superior vena cava (PLSVC) that drains into the coronary sinus, may present a
confusing radiographic image when left sided venous access is used (Fig. 13.4) [4].
For central lines the chest x-ray is also helpful in confirming the distal tip of the
catheter which should be above the cavoatrial junction to avoid precipitating atrial
arrhythmias and possible trauma to the right atrium (RA) (Fig. 13.5). The correct
position of the tip of the catheter should be in the superior vena cava (SVC) just
proximal to the right atrium RA-SVC junction (Figs. 13.5 and 13.6).
Complications
Arterial cannulation, venous dissection, hematoma, catheter associated DVT or

infection, pneumothorax, hemothorax, and atrial or ventricular arrhythmias espe-
cially during wire insertion are among the most common complications. Constant
visualization of the needle tip, confirmation of the needle position after vessel
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showing a left sided
pacemaker that was
implanted in a child with
persistent left superior
vena cava (PLSVC)
draining into the coronary
sinus (CS). The course of
the venous drainage is
delineated by the
pacemaker lead (left SC
vein which joins left IJ
vein and become left SVC
that drains into the
coronary sinus which
drains into the RA)

showing a central venous
catheter (CVC) inserted
into the right IJ passing
through the superior vena
cava (SVC) into the right
atrium (RA). The tip of the
CVC is seen approximately
1 cm below the RA-SVC
junction
Fig. 13.6 Upright chest x-ray

showing the desired position where
the tip of the central line can be
positioned (rectangle). Lower
positions risk the possibility of
atrial arrhythmias
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cannulation, and meticulous sterile technique will aid in minimizing complications.

Operators should be mindful of the distance between the skin and the anterior wall
of the vein and expect blood return after the needle traverses that distance. If blood
return is not seen, the operator should pause and identify the needle tip as it is not
uncommon for the needle to compress the vein and travel through the posterior wall
without blood return. In this instance, slow withdrawal of the needle should result
in venous cannulation. Of note, access of left IJ or left SC vein carries a risk of
chylothorax.
Clinical Vignettes
Case 1
A 50-year old male with history of DVT and pulmonary embolism, moderate tricus-
pid regurgitation, pulmonary hypertension, diabetes, hypertension and ischemic
cardiomyopathy, presented with dyspnea, a productive cough, leukocytosis, and
bilateral infiltrates on chest x-ray. Physical examination reveals heart rate of 115
beats per minute, regular pulse and a blood pressure of 85/50 mmHg. Auscultation
of the chest reveals bilateral rhonchi, soft S1, normal S2, and an S4. Extremities are
cool and bilateral lower limb swelling is noted. Right heart catheterization is
planned to assess filling pressures, calculate cardiac output, and provide central
venous access to infuse vasoactive medications.
In situations where the filling pressures are likely to help clinicians resuscitate
patients with sepsis and heart failure, the insertion of a pulmonary artery (PA) cath-
eter may be of value. The right IJ provides a direct access point for PA catheter
insertion. This can be achieved with a 5–7 French sheath that can accommodate the
PA catheter. Once the PA catheter is positioned correctly, vasoactive medications
can be given via the lumens of the catheter.
Case 2
A 30-year old male with acute myeloid leukemia presented with fever and fatigue.
Physical examination documented a heart rate of 125 beats per minute, BP
90/60 mmHg, with labs revealing pancytopenia with a profound reduction in the
absolute neutrophil and platelet counts and an INR of 1.8. A central line was
required for infusion of antibiotics and vasoactive medications and for measure-
ment of CVP.
The risk of bleeding is considerable, therefore, the SC vein should be avoided.
Correction of coagulopathy with platelet transfusion prior to the procedure, if fea-
sible, may reduce the risk of bleeding.
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References
1. Bodenham AR. Can you justify not using ultrasound guidance for central venous access? Crit
Care. 2006;10:175. doi:10.1186/cc5079.
2. Karakitsos D, Labropoulos N, De Groot E, Patrianakos AP, Kouraklis G, Poularas J, Samonis
G, Tsoutsos DA, Konstadoulakis MM, Karabinis A. Real-time ultrasound-guided catheterisa-
tion of the internal jugular vein: a prospective comparison with the landmark technique in criti-
cal care patients. Crit Care. 2006;10:R162. doi:10.1186/cc5101.
3. Braner D, Lai S, Eman S, Tegtmeyer K. Central venous catheterization – subclavian vein. N
Engl J Med. 2007;357:e26.
4. Dalili M, Alizadeh A, Haghjoo M. Successful implantation of transvenous pacing system via
persistent left superior vena cava and coronary sinus in small children. Indian Pacing
Electrophysiol J. 2010;10(12):551–5.
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Chapter 14
Right Heart Catheterization
Christopher Madias and Carey Kimmelstiel
Introduction
In the catheterization laboratory and the intensive care unit, right heart catheteriza-
tion (RHC) can provide vital physiologic information. Although clinical trials have
never demonstrated improved outcomes with RHC, when used appropriately, it is
viewed as an invaluable tool for the hemodynamic monitoring and management of
critically ill patients with cardiovascular disease.
Indications
Situations in which RHC may be beneficial include evaluating the etiology of

impaired oxygenation that remains uncertain (i.e., cardiogenic versus non-
cardiogenic). Acute respiratory distress syndrome may be suggested as a cause of
pulmonary edema in the presence of a normal or mildly elevated pulmonary cap-
illary wedge pressure (PCWP). RHC can help guide treatment in patients with
severe left ventricular dysfunction who show clinical deterioration despite
application of standard therapies (e.g., concomitant pulmonary congestion with
hypotension or signs of hypoperfusion). Titration of inotropic or vasodilatory
therapy based on RHC hemodynamic information is commonly referred to as
C. Madias (*)
New England Cardiac Arrhythmia Center, Tufts Medical Center,
750 Washington Street, Boston, MA 02111, USA
C. Kimmelstiel, MD

DOI 10.1007/978-1-4471-7290-1_14
ERRNVPHGLFRVRUJ
124 C. Madias and C. Kimmelstiel
“hemodynamic tailored therapy.” Such tailored therapy is often performed in

patients following cardiac surgery and is often beneficial in managing high-risk
cardiac patients (e.g., critical aortic stenosis) who are undergoing non-cardiac
procedures or operations. RHC may also be beneficial in differentiating the cause
of profound hypotensive states, especially when accurate assessment of volume
status is limited by coexisting conditions, such as morbid obesity. A low cardiac
output (CO) with elevated PCWP and high systemic vascular resistance (SVR)
can indicate cardiogenic shock. A high cardiac output with normal or low PCWP
and decreased SVR can indicate septic shock. A low or normal cardiac output
with low PCWP and normal or high SVR can indicate hypovolemic shock.
Hypotension with equalization of intra-cardiac diastolic pressures can indicate
cardiac tamponade. Distinctive hemodynamic findings of constrictive and restric-
tive physiology can also be revealed by RHC. Finally, RHC can also be useful in
establishing the diagnosis of pulmonary hypertension and assessing the response
to vasodilator therapy. Assessment of pulmonary hypertension with RHC is an
important step in the evaluation of the heart transplant candidate. Patients under-
going evaluation for heart transplantation, who have substantial pulmonary
hypertension that is not reversible with vasodilator therapy, are considered poor
candidates for transplant as right ventricular failure can develop in the trans-
planted heart [1].
A consensus statement containing specific recommendations on the use of RHC
in various cardiovascular disease states was published by the American College of
Cardiology in 1998. Table 14.1 summarizes some of the commonly accepted indi-
cations [2].
Table 14.1 Indications for right heart catheterization

Differentiation of profound hypotensive states (e.g., cardiogenic shock vs. septic shock vs.
hypovolemic shock)
Guidance of therapy in severe left ventricular dysfunction—“hemodynamic tailored therapy”
Assessment of constrictive and restrictive physiology
Cardiac tamponade
Assessment of impaired oxygenation — cardiogenic vs. non-cardiogenic pulmonary edema
Evaluation of pulmonary hypertension
Management of high-risk cardiac patients undergoing non-cardiac procedure or surgery
Assessment of intra-cardiac shunts
Management of complicated myocardial infarction (e.g., cardiogenic shock, mechanical
complications)
Management of patients following cardiac surgery
Heart failure with reduced or preserved ejection fraction (diagnosis and management)
Assessment of candidacy for heart transplantation
Left ventricular assist device dysfunction
Acute pulmonary embolism
Assessment of volume status in renal or hepatic failure
Post operative monitoring after cardiac surgery
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14 Right Heart Catheterization 125
Contraindications
A mechanical prosthetic tricuspid or pulmonic valve are generally considered abso-

lute contraindication for right hear catheterization. Relative contraindications for
RHC include coagulopathy or thrombocytopenia (INR >1.7 or platelet count
<50,000). The ability to temporary pace the patient with left bundle branch block
should be available during RHC as flotation of the pulmonary artery (PA) catheter
through the right ventricle can induce complete heart block in up to 3 % of these
patients [3]. Patients with intra-cardiac devices, such as pacemakers or implantable
cardiac defibrillators, should have RHC performed under fluoroscopy to avoid the
catheter tip getting caught in or dislodging a device lead. The presence of severe
tricuspid regurgitation, right ventricular dilatation, and pulmonary hypertension
might also necessitate the use of fluoroscopic guidance.
Equipment
The Swan Ganz PA catheter is the most widely used catheter for RHC. The balloon
tip allows the catheter to follow the flow of venous blood through the right side of
the heart to the PA. The catheter has multiple lumens that are accessed by various
ports, including a proximal port, a distal port, and a balloon inflation port. These
ports allow for the measurement of pressures as well as the sampling of blood oxy-
gen saturation along the right side of the heart and the PA (Fig. 14.1). A thermistor
mounted to the distal tip of the catheter allows for temperature measurements [1].
Technique
RHC can be performed via the superior vena cava with percutaneous entry through
the internal jugular or subclavian veins, or via the inferior vena cava with percutane-
ous entry through the femoral veins. Internal jugular or subclavian approaches are
less susceptible to infection and are less restraining to the patient and thus are pre-
ferred for bedside management. The right internal jugular approach is preferred
over left as it provides a direct route to the right atrium (RA). The subclavian
approach is preferred via the left side, again due to ease of catheter flotation [1].
Central venous access is obtained as described in the previous chapter. Prior to
flotation, the system should be appropriately leveled and zeroed. Usually attached
to a manifold, the transducer is placed at the level of the mid-axillary line in the
fourth intercostal space (the approximate level of the right atrium) and zeroed by
opening the system to room air. Each port of the PA catheter is then carefully
flushed and full inflation of the balloon is confirmed. An air leak should be excluded
by dipping the balloon in a sterile bowl of saline. If the PA catheter is to be left in
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Fig. 14.1 (a) The pulmonary artery catheter. (b) A schematic showing the proper orientation of
the pulmonary artery catheter when inserted through the left subclavian vein
ERRNVPHGLFRVRUJ
mmHg RV PA
30
20
PCWP
RA
10
Fig. 14.2 Normal right heart pressure tracings. RA right atrium, RV right ventricle, PA pulmonary
artery, PCWP pulmonary artery wedge pressure
place, it should first be inserted through a protective sterile sleeve. The PA catheter
is then inserted through the central venous sheath to approximately 15 cm or until
the RA waveforms are observed. The balloon is inflated and advanced gently.
Fluoroscopy is used in the catheterization lab to direct placement; however, at the
bedside, guidance is provided via the pressure waveforms (Fig. 14.2). Flotation of
the PA catheter from the femoral vein is more difficult and usually requires fluoro-
scopic guidance [3, 4].
To minimize ventricular ectopy, the catheter should be passed rapidly through the
right ventricle (RV) into the PA. From the PA the catheter is then advanced slowly to
wedge position. In general, the PCWP tracing should be reached within 50–55 cm if
the catheter is placed via the internal jugular or subclavian approaches. If the femoral
approach is used, it should be reached at 65–70 cm. In cases of marked respiratory
variation, the PCWP should be measured at end expiration. Once PCWP is recorded
the balloon should be deflated and it should be verified that a clear PA tracing is
obtained. The volume of air required to inflate the balloon for obtaining wedge should
also be checked. If the volume is less than 1.5 cc, the catheter should be pulled back
to avoid “over-wedging.” In the catheterization lab, to evaluate for the presence of
intra-cardiac shunts, screening blood samples are usually drawn for oximetric analysis
from the RA and the PA. Oximetric analysis can also be performed to confirm accu-
rate wedge position by obtaining a blood sample with a saturation of ≥95 % [3, 4].
The PA catheter can determine CO by two techniques – the thermodilution tech-
nique and using the Fick principle to measure oxygen consumption. In performing the
thermodilution technique, a syringe with 10 cc saline is attached to the proximal port,
whose tip is located in the RA when the thermistor on the distal tip is in the PA. The
entire volume of saline is rapidly injected within 4 s in a single, smooth effort. The
change in temperature as recorded by the distal thermistor is plotted over time and the
area under the curve is planimetered to calculate CO (in liters/min). At least three
serial thermodilution measurements should be performed and averaged (more if there
is substantial variability). Factors that interfere with normal flow of saline past the
sensing thermistor, such as low CO, tricuspid regurgitation, and intra-cardiac shunts
(i.e., atrial septal defect) can affect the accuracy of CO determination [4, 5].
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The Fick principle states that the total uptake or release of a substance by an
organ is the product of blood flow to the organ and the arteriovenous (AVO2) con-
centration difference of the substance [4]. Pulmonary blood flow (which is equal to
systemic blood flow in the absence of a significant shunt) is determined by dividing
oxygen consumption (the uptake of oxygen from room air by the lungs) by the arte-
riovenous oxygen difference across the lungs. Oxygen consumption can be mea-
sured by the use of a metabolic hood, but is routinely calculated based on body
surface area. The AVO2 concentration difference is calculated from the difference in
arterial oxygen content (1.36 × hemoglobin × AO2 saturation × 10) minus the mixed
venous (PA) oxygen content (1.36 × hemoglobin × VO2 saturation × 10). Thus CO
can then be calculated:
CO = O 2 consumption ( ml / min ) / AVO 2 difference ( ml / L )

Dividing the cardiac output by body surface area (m2) allows the calculation of car-
diac index (CI).
After the measurement of pressures and determination of CO have been com-
pleted, the pulmonary and systemic vascular resistance can be calculated using the
following formulas:
PVR = ( MPAP - PCWP ) / CO ( wood units ) ´ 80 ( dynes - sec - cm -5

)

(
SVR = ( MAP - RAP ) / CO ( wood units ) ´ 80 dynes - sec - cm
-5
)
Where MPAP = mean pulmonary artery pressure (mmHg), PCWP = Pulmonary
capillary wedge pressure (mmHg), CO = cardiac output (L/min), MAP = mean arte-
rial pressure (mmHg), and RAP = right atrial pressure (mm Hg).
Data Interpretation
RA pressure The normal RA pressure ranges between 1 and 5 mmHg and under
normal conditions decreases with inspiration. The a wave reflects atrial contraction
and occurs just after the P wave on the surface ECG. Elevations of the a wave indi-
cate resistance to RV filling, as can be seen in RV failure/infarction, pulmonic ste-
nosis, or significant pulmonary hypertension. In atrial fibrillation the a wave is
absent due to the lack of organized atrial contraction. The x descent follows and is
due to RA relaxation and caudal recoil of the tricuspid valve during RV contraction.
The c wave, which interrupts the x descent, results from bulging of the closed tri-
cuspid valve into the RA during early systole. The v wave results from venous
inflow into the RA during RV systole. It is prominent in tricuspid regurgitation and
in increased flow, such as seen with atrial septal defect. The v wave is followed by
the y descent that reflects the opening of the tricuspid valve. Prominent y descent
can be seen in constrictive and restrictive states as a result of rapid atrial emptying
into the RV [5].
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Table 14.2 Normal SVO2 0.6–0.75

hemodynamic values
CO 4–8 L/min
CI 2.5–4.0 L/min/M2
RA 1–6 mmHg
RV 25/6 mmHg
PAP 25/10 mmHg
PCWP 8–12 mmHg
SVR 900–1300 dynes-sec-cm−5
PVR 40–150 dynes-sec-cm−5
MAP 70–110 mmHg
RV pressure The normal RV systolic pressure ranges between 15 and 30 mmHg

and the RV end-diastolic pressure between 4 and 8 mmHg. The RV systolic pressure
can be elevated by pulmonic valve disease or pulmonary hypertension. Abrupt ele-
vation and plateau of the RV pressure in early diastole can indicate the presence of
restrictive or constrictive physiology [3, 5].
PA pressure The normal PA systolic pressure is 15–30 mmHg and the PA end-diastolic

pressure is 4–12 mmHg. Elevations in PA pressures are seen in pulmonary hypertension,
left-sided heart failure, mitral valve disease, significant left to right shunt, and pulmonary
disease (e.g., pulmonary embolism, chronic obstructive pulmonary disease) [5].
PCWP The normal mean PCWP is between 4 and 12 mmHg. The PCWP is an
accurate measure of the left atrial (LA) pressure in the absence of pulmonary vascu-
lar disease. It approximates left ventricular filling pressures except in mitral stenosis
and left atrial myxoma, where the LA pressure might be greater than left ventricular
end-diastolic pressure (LVEDP). In acute aortic regurgitation, the LVEDP can be
higher than the LA pressure. Elevation in mean PCWP is seen in left-sided heart
failure, and mitral stenosis or regurgitation. Similar to the RA pressure, the PCWP
has a and v waves, x and y descents. A prominent v wave suggests the presence of
mitral regurgitation [5].
Normal hemodynamic values are summarized in Table 14.2.
Complications
Complications of RHC are rare, but can include pneumothorax/hemothorax, arterial

puncture, bleeding, infection (including cellulitis at the insertion site, bacteremia,
endocarditis and sepsis), venous thrombosis, arrhythmias (including ventricular
arrhythmias and heart block/right bundle branch block), pulmonary artery rupture,
cardiac perforation, air embolism, pulmonary infarction (if the balloon is left in
wedge position too long), and knotting of the catheter. The duration of RHC should
be minimized in order to avoid complications [3, 4].
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Clinical Vignettes
Case 1
A 69 year old woman with history of dilated cardiomyopathy is admitted with pul-
monary vascular congestion. She is treated with lasix and nitrates. However, further
diuresis results in a creatinine rise despite signs of persistent volume overload.
RHC is performed with a BP 88/42 (57) mmHg, RA 14 mmHg, RV 52/7 mmHg,
PA 54/25 (39) mmHg, PCWP 26 mmHg CO 2.7 L/min, CI 1.9 L/min/M2, and SVR
1275 dynes-sec-Cm-5. The phosphodiesterase inhibitor milrinone is initiated along
with further diuresis for treatment of decompensated heart failure.
Case 2
A 54 year old man with history of ischemic cardiomyopathy and NYHA class III-IV
heart failure is transferred to a tertiary care center for cardiac transplant evalua-
tion. Echocardiography from the referring hospital showed diffuse global hypoken-
esis with an LVEF 15 % and was suggestive of pulmonary hypertension with a PA
systolic pressure estimated at ≥70 mmHg.
RHC reveals RA 15 mmHg, RV 76/16 mmHg, PA 75/27 (45) mmHg, PCWP 21,
CO 3.4 L/min, CI 1.8 L/min/M2, and PVR 456 dynes-sec-cm−5 (5.7 wood units). To
assess reversibility of pulmonary hypertension and appropriateness of cardiac trans-
plantation, an infusion of nitroprusside is initiated in the cath lab and titrated gradu-
ally to 3.0 mcg/kg/min. Hemodynamic assessment is repeated with RA 12 mmHg,
RV 62/12 mmHg, PA 60/19 (34) mmHg, PCWP 18 mmHg, CO 5.2 L/min, CI 2.9 L/
min/M2, and PVR 176 dynes-sec-cm−5 (2.2 wood units). Nitroprusside infusion
demonstrates reversible pulmonary hypertension in this patient. Irreversible pulmo-
nary hypertension (>4 wood units) remains an exclusion criteria for cardiac trans-
plant as a normal donor RV will fail in the setting of high recipient PVR.
Case 3
A 75 year old woman with history of diabetes and hypertension presents to the
emergency department more than 10 hours after onset of substernal chest pain.
ECG reveals ST elevation and q waves in leads II, III, aVF suggestive of an evolving
inferior myocardial infarction. Physical exam reveals a harsh holosystolic murmur
along the left sternal border. During cardiac catheterization the patient became
hypotensive requiring multiple pressors and insertion of an intra-aortic balloon
pump. Cardiac catheterization reveals 100 % proximal right coronary artery occlu-
sion. Successful percutaneous angioplasty and stent placement of the right coro-
nary artery is performed.
ERRNVPHGLFRVRUJ
After stent placement, RHC reveals RA 20 mmHg RV 43/21 mmHg PA 45/28

(37) mmHg PCWP 28 mmHg. Oximetric analysis revealed a large step-up in oxy-
gen saturation from RA (47 %) to RV (81 %) suggestive of ventricular septal rup-
ture. Transesophageal echocardiogram in the cath lab confirms rupture of the basal
portion of the inferoposterior ventricular septum with left to right shunt flow. The
patient is referred to cardiothoracic surgery.
Case 4
A 73 year old man with history of hypertension, chronic obstructive pulmonary

disease, and atrial fibrillation is admitted for worsening shortness of breath and
lower extremity edema. This is his third admission in 6 months for heart failure.
Physical exam reveals elevated jugular venous pressure to the mandible, positive
Kussmaul’s sign (elevation of the jugular venous pressure with inspiration), and 2+
pitting lower extremity edema to the knees. Echocardiogram reveals left ventricular
hypertrophy with mild aortic stenosis, normal left ventricular function and a small
circumferential pericardial effusion.
RHC is performed with the following hemodynamic findings: RA 18 mmHg, RV
39/5 (18) mmHg, PA 37/18 mmHg, PCWP 18 mmHg, and LVEDP 18 mmHg.
Simultaneous recording of right and left heart pressures show elevation and equal-
ization of diastolic pressures and the RV and LV pressure tracings reveal a dip and
plateau contour suggestive of constrictive physiology (Fig. 14.3). Subsequent CT of
the chest demonstrates a thickened pericardium.
LV
I
RV
II
25
III
mm Hg
a v
v
RA
Fig. 14.3 Simultaneous right and left heart pressure tracing in a patient with constrictive pericar-
dial physiology. Note the right atrial, right ventricular, and left ventricular diastolic pressures are
elevated and equal (arrow). Right and left ventricular tracings show an early diastolic dip followed
by a plateau as the non-compliant pericardium hinders ventricular filling in early to mid diastole—
the “dip and plateau” sign. RA right atrium, RV right ventricle, LV left ventricle
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References
1. Zipes DP, Libby P, Bonow RO, Braunwald E, editors. Braunwald’s heart disease, a textbook of
cardiovascular medicine. 7th ed. Philadelphia: Elsevier Inc; 2005.
2. Mueller HS, Chatterjee K, Davis KB, et al. ACC expert consensus document. Present use of
bedside right heart catheterization in patients with cardiac disease American College of
Cardiology. J Am Coll Cardiol. 1998;32:840.
3. Griffin BP, Topol EJ, editors. Manual of cardiovascular medicine. 2nd ed. Philadelphia:
Lippincott Williams and Wilkins; 2004.
4. Baim DS, Grossman W, editors. Cardiac catheterization, angiography and intervention.
Philadelphia Lippincott Williams and Wilkins 6th ed. 2000.
5. Kern MJ, editor, The cardiac catheterization handbook. 4th ed. Philadelphia: Mosby Inc.; 2003.
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Chapter 15
Pericardiocentesis
Introduction
Evacuation of pericardial fluid from the pericardial space to treat cardiac tamponade
was initially described in 1653 through surgical incision of the sternum [1].
Advancements in the technique were made with percutaneous needle aspiration in
the nineteenth century and, currently, the procedure is done in a similar manner using
small gauge needles and multi-modality imaging (echocardiography, fluoroscopy, or
both). Cardiac tamponade is a clinical diagnosis and the size of the pericardial effu-
sion required to cause tamponade depends on the rate of fluid accumulation.
Indications
1. Treatment of cardiac tamponade or prevention of impending cardiac tamponade

in patients with moderate to large pericardial effusions and compromised
hemodynamics.
2. Diagnostic aspiration to investigate the etiology of a pericardial effusion.
3. Invasive procedures in the pericardial space (epicardial ventricular tachycardia
[VT] ablation or left atrial appendage [LAA] closure using the Lariat device)
S. Alshalash, MD (*)
Cardiac Catheterization Laboratory, Tufts Medical Center,
750 Washington Street, Boston, MA 2111, USA
C. Kimmelstiel, MD

DOI 10.1007/978-1-4471-7290-1_15
ERRNVPHGLFRVRUJ
Contraindications
In a hemodynamically unstable patient there exist no absolute contraindications to

pericardiocentesis. Uncorrected bleeding conditions is a relative contraindication to
pericardiocentesis. Recurrent pericardial effusion may need surgical treatment with
the creation of a pericardial window (communication between the pericardial and
pleural spaces).
Equipment
Required equipment includes anti-septic solution, sterile drapes, gown and gloves,
local anesthetic, a long small-caliber needle, syringes, alligator clip, guide wire,
scalpel, stopcock, pigtail catheter, collection bag, ECG machine, and imaging
modality of choice (echocardiography and/or fluoroscopy). Commercially available
kits often include all of the needed equipment (Fig. 15.1).
Fig. 15.1 Essential equipment for pericardiocentesis
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15 Pericardiocentesis 135
Technique
There are three established methods to perform pericardiocentesis (Table 15.1). The
most widely used is via a subxiphoid approach; other approaches include the apical
and left parasternal approaches. The echocardiographic window helps in deciding
which approach is most expeditious. Careful examination of the echocardiogram to
“map the way” and choose which angle is needed prior to proceeding with pericar-
diocentesis, is an essential step.
To perform a pericardiocentesis from the subxiphoid approach, the patient is
placed in a supine position usually lying on a wedge which elevates the torso to an
angle of 30–45° which aids in accumulating the pericardial fluid anteriorly
(Fig. 15.2). A sterile field is established. The skin and subcutaneous tissues are infil-
trated generously with a local anesthetic. The needle is inserted at a shallow angle
Table 15.1 Summary of different approaches to pericardiocentesis

Approach Advantages Disadvantages
Subxiphoid Can be done blindly without imaging in cases Possible injury to abdominal
of emergency. Provides access to the anterior structures. Requires the presence
pericardial space. Furthest from pleural space of an anterior collection of fluid.
Difficult in morbidly obese
patients or patients with ascites
Apical Provides access to the apical/posterior Possible access to the pleural
collection. LV wall is thicker than RV, space, causing pneumothorax or
therefore, injury may not result in perforation injury to the LV apex (or LAD)
Left Shortest distance from skin to pericardial Possible injury to the internal
parasternal space, access to the anterior pericardial space, mammary artery and entry into
avoids injury to abdominal structures the pleural space
Fig. 15.2 A wedge is positioned underneath the patient to allow the free-flowing fluid to accumu-
late anteriorly
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Fig. 15.3 Surface anatomy

and landmarks to perform
pericardiocentesis. Via the
subxiphoid approach
just to the left of the xiphoid process immediately inferior to the costal margin
(Fig. 15.3). The needle is advanced underneath the ribs, bevel up, while consciously
making light contact with the overlying periosteum of the rib. This is done in an
effort to avoid contact with the lung. The needle is directed towards the left shoul-
der. A “pop” can usually be felt when the pericardium is entered. At this time the
trochar is removed and, if in the correct location, pericardial fluid will flow under
pressure through the central lumen of the syringe. If no fluid is obtained, the syringe
is removed and the process is repeated, usually with a slightly different angulation.
Currently, pericardiocentesis is rarely done with live echocardiographic guid-
ance. However, some operators employ electrocardiographic (ECG) guidance in an
effort to avoid ventricular perforation. An alligator clip is connected to an ECG lead.
While slowly advancing the needle, the ECG is monitored, watching for ST seg-
ment elevation (a current of injury) which is indicative of contact with the thin-
walled right ventricle. If seen, obviously the needle is withdrawn, the trochar
removed and examination for pericardial fluid flow from the needle lumen is per-
formed. If the operator is using fluoroscopy, then a guidewire is advanced through
the needle, into the pericardial space and is visualized into the pericardium. If the
operator is not sure that the wire is in the pericardial space, injection of a small
amount of contrast may help in defining the position of the needle tip [2]. Using
echocardiography to confirm placement involves injecting agitated saline into the
pericardial space once the needle enters the pericardium and before the guidewire is
inserted into the pericardial space. The agitated saline can be visualized in the peri-
cardial space confirming the position of the tip of the needle (Fig. 15.4). If agitated
saline is seen in a cardiac chamber the needle should be withdrawn. After passing
the guidewire into the pericardial space, a dilator is advanced over the wire to create
a tunnel through the subcutaneous tissues for passage of a pigtail catheter over the
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Fig. 15.4 (a) Modified apical view showing the pericardial effusion. (b) Agitated saline is seen
entering into the pericardial space (arrow) confirming the correct position of the needle tip

showing cardiomegaly.
The anterior ribs are
labeled on the CXR. Left
parasternal access is in
between the 4th-5th or
5th-6th ribs at ≥2 cm away
from the edge of the
sternum
guidewire. The guidewire is then removed from the pigtail catheter and a three-way
stopcock is attached to the proximal end of the pigtail catheter.
Once the pigtail catheter has been placed, the opening pericardial pressure is
recorded, fluid is then aspirated with usually 100 cc sent for laboratory analysis for
cellular analysis and chemistries, usually for the determination of a transudate ver-
sus an exudate. Aspiration is performed until the operator is no longer able to with-
draw any further fluid. At this time the total volume removed is recorded as is the
closing pericardial pressure.
The left parasternal approach involves directing the needle almost perpendicu-
larly to the chest (70–80°) often between the 5th and 6th ribs at least 2–3 cm lateral
to the edge of the sternum to avoid injury to the internal mammary artery which runs
1–1.5 cm from the edge of the sternum (Fig. 15.5). Care must be taken to go over
the rib to avoid injury to the neurovascular bundle which runs in the inferior aspect
ERRNVPHGLFRVRUJ
of the ribs. Echocardiography is used to assess the depth of pockets and to estimate
the angle and depth of tissue to enter into the pericardial space.
For the apical approach, the mid-clavicular line is identified in the fifth intercos-
tal space then echocardiographic images are obtained and the point that has the best
echocardiographic window is marked. The operator should make note of the angle
of the probe as the needle should follow the same angle. The best access point
should be the deepest pocket of fluid as well as that closest to the chest wall.
Data Interpretation
Pericardial fluid is sent to the laboratory for fluid analysis; tests are dependent on
clinical presentation. The most widely used tests include total protein, glucose,
LDH, and culture and sensitivity. Etiology of the effusion can be aided by the deter-
mination of whether the aspirated fluid represents a transudate or exudate. Other
tests include cytology when there is clinical suspicion of a malignant process and
antibody testing (ANA) when the clinical presentation is in keeping with a rheuma-
tological/autoimmune process.
Complications
Possible complications include myocardial injury and puncture or laceration, coro-

nary artery perforation, pneumothorax, laceration of the left lobe of the liver, injury
to the phrenic nerve, and inability to access the pericardium requiring a surgical
window. The damage resulting from inadvertently injuring structures can be mini-
mized using multi-modality imaging, choosing the access site that has the easiest
access to the largest collection of fluid. For example, a posteriorly located pericar-
dial effusion might not be accessible percutaneously even though it is large enough
to cause hemodynamic effects. Some have advocated that another way to minimize
complications is to utilize a small caliber needle such as a micropuncture needle
which is 21-gauge needle as compared to the standard 18-gauge needle. Using the
21-gauge micropuncture needle allows insertion of a 0.018-in. wire that is exchanged
for a 4–5 Fr sheath that can accommodate the standard 0.035–0.038 in. guidewire.
Clinical Vignettes
Case 1
A 45-year old female with stage IV breast cancer presented with progressive short-
ness of breath. Her physical examination was remarkable for a heart rate of 110, a
blood pressure of 90/60 mmHg, oxygen saturation 99 % on room air and a respira-
tory rate of 22/min. Her heart sounds were muffled and jugular venous distension
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Fig. 15.6 Large

circumferential pericardial
effusion is seen in this
apical four-chamber view.
LA left atrium, RA right
atrium, LV left ventricle,
RV right ventricle
was present. Lung auscultation was not remarkable. Chest x-ray revealed cardio-
megaly and normal lung parenchyma. Echocardiography documented a large peri-
cardial effusion that was circumferential measuring 2.1 cm posteriorly in the
parasternal long axis view, 1.8 cm at the apex in the four-chamber window, and
1.9 cm anteriorly using a subcostal window. Figure 15.6 depicts the apical five-
chamber view showing the large pericardial effusion.
This pericardial effusion is most likely to be related to metastatic breast cancer
and is accessible percutaneously via apical, left parasternal, or subxiphoid approach.
Pericardiocentesis was performed, draining 725 cc of bloody fluid resulting in
symptomatic improvement.
Case 2
A 29-year old female with untreated SLE presented with positional chest pain and
shortness of breath. Physical examination showed a heart rate of 115 BPM, blood
pressure 100/75 mmHg, oxygen saturation 98 % on room air; Jugular venous dis-
tention was present. A 16 mmHg pulsus parodoxus was present. ECG showed sinus
tachycardia, diffuse ST-segment elevation, and PR depression. Echocardiography
documented a moderate-sized circumferential pericardial effusion with right atrial
diastolic collapse. Right heart catheterization was performed and revealed the
following pressures (mmHg): right atrium: 14, right ventricle: 50/14; pulmonary
artery 45/14: pulmonary capillary wedge 14 mmHg; cardiac output 3.4 L/min;
cardiac index 2.1 L/min × m2.
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The presence of tachycardia, low pulse pressure, echocardiographic evidence of

diastolic chamber collapse, and low cardiac index demonstrate the hemodynamic
sequelae of cardiac tamponade. Figure 15.4 shows the pericardial effusion with
agitated saline injected into the pericardial space to confirm the position of the
needle tip.
References
1. Loukas M, Walters A, Boon JM, Welch TP, Meiring JH, Abrahams PH. Pericardiocentesis: a
clinical anatomy review. Clin Anat. 2012;25:872–81. doi:10.1002/ca.22032. Wiley Periodicals,
Inc.
2. Ainsworth C, Salehian O. Echo-guided pericardiocentesis, let the bubbles show the way.
Circulation. 2011;123:e210–21.
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Chapter 16
Procedural Sedation
Grace M. Wu
The American College of Emergency Physicians (ACEP) defines procedural seda-

tion as “a technique of administering sedatives or dissociative agents with or with-
out analgesics to induce a state that allows the patient to tolerate unpleasant
procedures while maintaining cardiorespiratory function. Procedural sedation and
analgesia (PSA) is intended to result in a depressed level of consciousness that
allows the patient to maintain oxygenation and airway control independently.”
The Joint Commission on Accreditation of Healthcare Organizations in the United
States (JCAHO) has defined sedation as a continuum of consciousness: analgesia, mini-
mal sedation, moderate sedation and analgesia (formerly termed conscious sedation),
deep sedation and analgesia, general anesthesia, and dissociative sedation (Table 16.1).
Table 16.1 Continuum of depth of sedation: definition of general anesthesia and levels of
sedation/analgesia
Moderate sedation/
Minimal analgesia (conscious Deep sedation/ General
sedation sedation) analgesia anesthesia
Responsiveness Normal response Purposeful response Purposeful response Unarousable,
to verbal to verbal or tactile after repeated or even with
stimulation stimulation painful stimulation painful stimulus
Airway Unaffected No intervention Intervention may be Intervention
required required often required
Spontaneous Unaffected Adequate May be inadequate Frequently
ventilation inadequate
Cardiovascular Unaffected Usually maintained Usually maintained May be
function impaired
Developed by the American society of Anesthesiologists; approved by the ASA House of Delegates
October 13, 1999 [1]
G.M. Wu, MD
University of Miami Miller School of Medicine,
1611 NW 12th Ave, Central Building Suite 600-D, Miami, FL 33136, USA
DOI 10.1007/978-1-4471-7290-1_16
ERRNVPHGLFRVRUJ
142 G.M. Wu
Indications
PSA may be used for any procedure in which a patient’s pain or anxiety may be
excessive and may impede successful completion of the procedure. Common car-
diology procedures include electrical cardioversion, transesophageal echocardio-
gram, diagnostic and ablation procedures for cardiac arrhythmias, coronary
angiography, transcutaneous valve replacements and repair, and insertion of
implantable electronic device [2].
Contraindications
There are no absolute contraindications to PSA. Relative contraindications may

include older age, significant medical comorbidities and signs of a difficult airway. In
older patients, sedating agents should be given at a lower starting dose, using slower
rates of administration and repeated dosing of medications at less frequent intervals.
Patients with major comorbid medical conditions are at increased risk for adverse
events however there is no evidence that alternative approaches (monitored anesthesia
care or general anesthesia) are safer. PSA is relatively contraindicated in patients who
are likely to be difficult to ventilate or oxygenate. Patients who have eaten recently are
not contraindicated to PSA, however if a procedure is not emergent, the American
Society of Anesthesiologists (ASA) recommends that the patient fast for 2 h after
drinking clear liquids and 6 h after ingesting solid foods or cow’s milk [1].
Equipment
Intravenous access should be established. Patients should have constant cardiac and
respiratory monitoring, with careful monitoring of blood pressure, heart rate, respi-
ratory rate, oxygen saturation, end-tidal carbon dioxide level and cardiac rhythm.
Supplemental oxygen is often recommended to maintain oxygen levels during
hypoventilation. In the event of respiratory compromise, equipment for performing
endotracheal intubation and managing the airway should be readily available.
Resuscitation medications, including medications for advanced life support and
reversal agents should be available at bedside [1].
Technique
Ideal pharmacologic agents for PSA will have rapid onset and short duration of
action, maintain hemodynamic stability and lack major side effects (Table 16.2).
Some shorter procedures may be performed with the patient awake or only lightly
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16 Procedural Sedation 143
Table 16.2 Intravenous procedural sedation medications for adults

Repeat dose (as
Medication Initial dose Onset Duration necessary)
Midazolam 0.02–0.03 mg/kg over 2 min; 1–2.5 min 10–40 min May repeat after
maximum 2.5 mg (1.5 mg 2–5 min
maximum if elderly)
Fentanyl 0.5–1 mcg/kg 2–3 min 30–60 min 0.5 mcg/kg every
2 min
Propofol 0.5–1 mg/kg 0.5 min 5 min 0.5 mg/kg every
3–5 min
Etomidate 0.1–0.15 mg/kg 5–15 s 5–15 min 0.05 mg/kg every
3–5 min
Ketamine 1–2 mg/kg over 1–2 min 0.5 min 5–20 min 0.25–0.5 mg/kg every
5–10 min
Elderly patients are at increased risk of adverse events with these agents and dosing should be
adjusted accordingly [3, 4]. See text for details
sedated with concomitant local anesthesia. Agents that depress cardiac function
may be problematic during ablation of ventricular tachycardia. Pre-oxygenation
should usually accompany sedative administration [1].
Benzodiazepines are commonly employed for their ability to produce anxiolysis
and amnesia, however they have no analgesic properties. Midazolam is used most
often due to its ability to penetrate the blood–brain barrier quickly. It can be used
alone or in combination with short acting opioids (e.g., fentanyl). With repeat doses,
midazolam can accumulate in adipose tissue and can prolong sedation. Care must
be taken when using midazolam in the elderly, obese, and patients with renal or
hepatic disease [2, 3].
Opioids are often administered alone or in combination with sedatives in proce-
dures requiring PSA. Short acting agents such as fentanyl, alfentanil and remifent-
anil are used. Fentanyl rarely causes hypotension, however its primary side effect is
respiratory depression, which is potentiated by the coadministration of sedatives.
Coadministration of midazolam and fentanyl is useful when ultrashort-acting
agents (e.g., propofol) are unavailable. The combination of midazolam and fentanyl
may cause hypoxia and apnea, and increase the need for airway intervention and
medication reversal. It is suggested to administer midazolam first and fentanyl
titrated carefully thereafter [2].
Propofol is an ultrashort-acting phenol derivative with highly lipophilic proper-
ties allowing it to cross the blood–brain barrier rapidly and therefore must be dosed
carefully. It is an effective sedative and amnestic but provides no analgesia.
Injecting propofol with lidocaine pretreatment or coadministration can prevent
pain when injecting through intravenous catheter. Additional intraprocedural anal-
gesia can be achieved by pretreatment with short acting opioids (e.g., fentanyl).
Pharmacokinetics of propofol are unchanged in patients with impaired kidney or
liver function. In older patients, the dose should be reduced by 20 % and be given
slowly over 3–5 min. Propofol is contraindicated in patients with allergy to egg
lecithin and soybean oil. Side effects include hypotension and respiratory depres-
ERRNVPHGLFRVRUJ
144 G.M. Wu
sion in patients with severe medical problems (such as sepsis, cardiac dysfunction)
or hypovolemia [3, 5].
Etomidate is an imidazole derivative that is commonly used for rapid sequence
intubation but can be used for PSA as well. Lower doses should be used in patients
with renal or hepatic impairment and in elderly individuals. Etomidate also has no
analgesic properties and similar strategies to reduce pain can be used as with propo-
fol. Myoclonus is the most frequently reported side effect (reported in up to 80 % of
patients). In the event of severe myoclonus, immediate airway support and treat-
ment with benzodiazepine (midazolam 1–2 mg IV, reduced every 60 s) are indi-
cated. Other side effects include respiratory depression, adrenal suppression and
nausea and vomiting [4].
Ketamine is a phencyclidine derivative that acts as a dissociative sedative, pro-
ducing a trance-like state and provides sedation, analgesia and amnesia while pre-
serving the airway. Ketamine is ideal for brief, painful procedures and for patients
who may have a potentially difficult airway or have compromised respiratory func-
tion. Ketamine can cause disorientation, dream-like experiences, or hallucinations
that can be treated with a small dose of midazolam. Other side effects of ketamine
include nausea and vomiting, laryngospasm, tachycardia, hypertension, increased
intracranial and intraocular pressure and hypersalivation. Ketamine has been associ-
ated with longer median times for return to baseline mental status and increased
agitation during recovery [3].
Evaluation
In patients who are at risk of hypotension due to recent illness, dehydration, or car-
diac disease, etomidate or ketamine is preferable to propofol. Patients who have
potentially difficult airways to manage or have compromised respiratory function
can undergo PSA with ketamine. All agents should be given at a lower starting dose
with lower rates of administration and less frequent dosing intervals in elderly
patients [3, 5].
Discharge Criteria
– Additional monitoring for complications inherent to the procedure is

unnecessary
– Vital signs and respiratory and cardiac function should be stable and within
acceptable limits
– Mental status and physical function should return to a point where the patient can
care for himself or herself with minimal to no assistance
– Symptoms such as pain, lightheadedness and nausea should be well-controlled
– The person should be accompanied home by a reliable person who can provide
support and supervision for at least a few hours [1]
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16 Procedural Sedation 145
Complications
PSA is largely considered safe as serious complications occur rarely. Complications

can often be prevented through appropriate selection of patients, proper use of seda-
tive medication and careful monitoring of sedation. The most concerning complica-
tion is dose dependent respiratory compromise causing hypoxia or hypercarbia,
which develops in less than 1 % of cases. Naloxone (0.01–0.1 mg/kg IV or IM, max
2 mg) and flumazenil (0.01 mg/kg IV over 20 s, max 1 mg) may be utilized to
reverse opioids and benzodiazepines, respectively. Significant hypotension and bra-
dycardia may develop in patients with significant cardiac morbidity and patients
receiving beta-blockers. Etomidate may be preferred in these settings. Additional
adverse outcomes may include vomiting and aspiration, and inadequate sedation
preventing completion of the procedure. Combined adverse event rate (adverse
event and failure to perform procedure) occur 15 % of the time. Anesthesiology sup-
port should be readily available in high-risk patients [1].
Clinical Vignettes
Case 1
A 61 year old woman with a past medical history of hypertension, hyperlipidemia is

diagnosed with new onset atrial fibrillation at her PCP’s office. She undergoes DC
cardioversion with midazolam and fentanyl without any complications. In the recov-
ery area, the patient awakens, is oriented to person, place and time, and is commu-
nicative with nurses and staff. She is eating lunch.
While serious adverse events such as hypoxia rarely occur after discharge, it is
common for patients to experience mild symptoms, such as nausea, lightheadedness,
fatigue or unsteadiness for up to 24 h. A reliable person who can provide support and
supervision should be present at the patient’s home for at least a few hours [1].
Case 2
A 42 year old male with no past medical history presents after two episodes of syn-
cope. He also reports episodes of lightheadedness that resolve spontaneously. All
male members of his family died of sudden cardiac death at an early age. EKG
reveals pseudo-right bundle branch block and persistent ST elevation in leads V1 to
V2. Echo is unremarkable. The diagnosis of Brugada syndrome is made and patient
is scheduled for placement of ICD under PSA with propofol. During the procedure,
the patient becomes tachycardic and hypotensive. His SaO2 drops to 82 %.
There are no reports of endotracheal intubation due to propofol induced respira-
tory depression during PSA. Mild hypoxia can usually be managed by interruption
of the propofol and bag-mask ventilation (Fig. 16.1) [5].
ERRNVPHGLFRVRUJ
146 G.M. Wu
Early detection
Stop drugs
Sniffing position
Head-tilt/ chin-lift (if no cervical spine injury)
Jaw thrust maneuver (if concern for C-spine injury)
Cricoid pressure
Reversal agent
Bag-mask ventilation (with oral airway)
LMA ventilation
Intubate
Fig. 16.1 PSA intervention sequence. Proceed down the intervention sequence as patient condi-
tion permits. (a) Head-tilt/chin-lift. (b) Jaw thrust maneuver involves thumbs on the maxilla press-
ing downward and four fingers posterior to the ramus applying upward pressure
References
1. American Society of Anesthesiologists Task Force on Sedation and Analgesia by Non-

Anesthesiologists. Practice guidelines for sedation and analgesia by non-anesthesiologists.
Anesthesiology. 2002;96(4):1004–17.
2. Thomas SP, et al. Sedation for electrophysiological procedures. Pacing Clin Electrophysiol.
2014;37(6):781–90.
3. Gan TJ. Pharmacokinetic and pharmacodynamic characteristics of medications used for mod-
erate sedation. Clin Pharmacokinet. 2006;45(9):855–69.
4. Falk J, Zed PJ. Etomidate for procedural sedation in the emergency department. Ann
Pharmacother. 2004;38(7–8):1272–7.
5. Miner JR, Burton JH. Clinical practice advisory: emergency department procedural sedation
with propofol. Ann Emerg Med. 2007;50(2):182–187.e1.
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Chapter 17
Endotracheal Intubation
Aaron E. Brice
Endotracheal intubation is performed for airway protection or to permit mechanical

ventilation. A flexible plastic tube is inserted through the mouth or nose and passed
through the vocal cords into the trachea where it is secured in place. There are vari-
ous situations where intubation is needed for patient care including both planned
intubation and that done in an urgent or emergent context.
Indications
Specific indications for planned intubation include patients receiving general anes-
thesia, surgery in close proximity to the airway, or surgery in an atypical position.
Indications for unplanned intubation can be broadly divided into several categories
including respiratory failure, acute airway obstruction and loss of protective reflexes
(Table 17.1) [1]. Rapid sequence intubation is the standard technique used in unsta-
ble patients that require prompt securement of the airway using the concurrent
administration of a sedative agent for induction and a neuromuscular blocking agent
for paralysis.
Table 17.1 Emergent indications for endotracheal intubation [1]

Respiratory failure Pulmonary edema, excess secretions, atelectasis, acute respiratory
distress syndrome, hypoventilation, neuromuscular failure
Acute airway obstruction Laryngeal edema, laryngeal spasm, trauma, smoke inhalation,
foreign body, hematoma, tumor, retropharyngeal abscess, epiglottitis
Loss of protective reflexes Drug overdose, stroke, head trauma
A.E. Brice, MD
University of Miami Miller School of Medicine,
1611 NW 12th Ave, Central Building Suite 600-D, Miami, FL 33136, USA

DOI 10.1007/978-1-4471-7290-1_17
ERRNVPHGLFRVRUJ
148 A.E. Brice
Contraindications
Endotracheal intubation may be employed as a life saving measure and in this cir-
cumstance there are few absolute contraindications to its use. However, clinicians
must be mindful of conditions in which intubation may provoke additional prob-
lems. This includes blunt or penetrating trauma to the larynx causing laryngeal frac-
ture or separation of tissue layers. Traction with a laryngoscope, stylet, or
endotracheal tube may cannulate a false lumen or tear the airway. When there is
significant doubt as to the safety of intubation noninvasive oxygenation and ventila-
tion are preferred until a definitive or surgical airway can be created.
Relative contraindications to intubation include patients with a difficult airway.
The mnemonic LEMON (Look, Evaluate, Mallampati Class, Obstruction/Obesity,
Neck mobility) can be used to stratify a difficult airway [2]. Look externally for any
clear visible evidence of potential problems such as micrognathia. Evaluate using
the 3-3-2 rule (Fig. 17.1) to confirm that the mouth can open to fit 3 of the patient’s
fingers between upper and lower incisors, the submandibular space can fit 3 of the
patient’s fingers from chin to angle of the neck, and the space between the superior
aspect of thyroid cartilage and angle of the neck can fit 2 of the patient’s fingers.
Mallampati class (Fig. 17.2) rates the space for oral intubation based on tongue size
and degree of mouth opening from I (most open) to IV (least open). Obstruction and
obesity assess any upper airway impediment caused by tumors, swelling, excess
adipose tissue, or other masses. Neck mobility assesses the patient’s ability to be
placed in the sniffing position in which the head is elevated and neck extended
forward.
Fig. 17.1 3-3-2 rule to

evaluate the difficult
airway. 1 Inter-incisor
distance is three fingers. 2
Hyoid mental distance is
three fingers. 3 Thyroid to
floor of mouth is two
fingers
ERRNVPHGLFRVRUJ
17 Endotracheal Intubation 149
Fig. 17.2 Mallampati class I–IV
Equipment
Assembly of all necessary equipment prior to starting is essential as unforeseen

complications may result in critical delays (Table 17.2).
Laryngoscopes are composed of a handle, blade, and light source. The two most
frequently used blades are the Macintosh which is curved and the Miller which is
straight. The choice of which to use is based on experience and personal preference
[4]. These and other images of essential equipment are displayed in Fig. 17.3.
When there is difficulty visualizing the glottis a bougie or tube introducer is
placed in the trachea and the endotracheal tube is passed over it. Oral and nasal
airways are adjuncts and can be used to prevent the tongue from obstructing the
posterior pharynx.
Endotracheal tubes are measured lengthwise in centimeters and by internal diameter
in millimeters and French. Assemble tubes one size greater and one size smaller than
the estimated tube to be used. Most adults will need at least an 8.0 mm tube but an inap-
propriately small tube will increase the work of breathing and if a bronchoscopy is to
be performed the tube must be sufficiently wide to allow passage of equipment.
Pharmacologic agents for rapid sequence intubation are given IV push and include
both a sedative agent for induction and a neuromuscular blocking agent for paralysis.
Commonly used sedative agents with dosing listed in mg/kg include midazolam
(0.3–0.35), etomidate (0.2–0.6), propofol (2.0–2.5), and ketamine (0.5–2.0). Rapid
paralysis with dosing listed in mg/kg is frequently achieved with succinylcholine
(1.0–1.5), rocuronium (0.6–1.2), atracurium (0.4–0.5), and vecuronium (0.08–0.1).
Table 17.2 Essential equipment [3]

Face mask with bag valve Bougie
100 % oxygen Sedative agent
Oral and nasal airways Neuromuscular blocking agent
Suction device with catheters Local anesthesia
Laryngoscope with handle and blades Syringe to inflate endotracheal cuff
Endotracheal tubes with stylet Tape
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150 A.E. Brice
Fig. 17.3 Essential equipment for endotracheal intubation
Technique
Successful intubation begins with the pre-procedural evaluation but in an emer-

gency some aspects must be omitted. Stepwise technique of rapid sequence intuba-
tion can be remembered with the “Seven P’s” (Preparation, Preoxygenation,
Pretreatment, Paralysis and induction, Protection/Positioning, Placement, and
Postintubation management) [5].
Preparation evaluates the airway, gathers supplies, and ensures the patient is
connected to required lines and monitors. Preoxygenation with 100 % high flow
oxygen with saturation monitoring for 3.5–4 min will replace nitrogen in the
patient’s functional residual capacity with oxygen and increase the time intuba-
tion may be attempted during apnea. Pretreatment with lidocaine or fentanyl may
be used to decrease natural coughing and gagging reflexes during intubation.
Paralysis with induction uses administration of sedative and neuromuscular
blocking agents concurrently by IV push to achieve unconsciousness and muscu-
lar flaccidity. Protection to prevent aspiration consists of applying cricoid pres-
sure with Sellick’s maneuver causing posterior compression of the cricoid
cartilage against the vertebral body to lessen the diameter of the hypopharynx.
Placement of the tube requires the laryngoscope to be held in the left hand and
the gloved right hand opens the mouth by simultaneously pressing the thumb
ERRNVPHGLFRVRUJ
Fig. 17.4 Direct visualization of vocal cords. (a) Blade is under middle of tongue and obscuring
the glottis. (b) Tongue not far enough left and obscuring the glottis. (c) Correct blade placement
with tongue elevated and to the left. (d) Use of curved (Macintosh) blade. (e) Use of straight
(Miller) blade
against lower incisors and index finger against upper incisors in a scissor motion.
The blade is inserted in the right mouth and in a sweeping motion moves the
tongue to the left (Fig. 17.4). The epiglottis is visualized and the blade is
advanced to this point and then elevated forward in a straight line at a 45° angle
to reveal the vocal cords avoiding contact with teeth to prevent trauma. Direct
visualization of the vocal cords is obtained, the tube is passed through them, the
cuff inflated, stylet withdrawn, and correct position of the tube is confirmed.
Postintubation management involves securing the tube, adjusting ventilator set-
tings, and post-procedure monitoring.
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152 A.E. Brice
Data Interpretation
Potentially difficult mask ventilation may be recognized in patients that are body
mass index greater than 26, age 55 or older, edentulous, or with significant facial
hair. If these factors are encountered intubation performed while the patient is
awake with local anesthesia may be preferred.
During preoxygenation when high flow oxygen is used and saturation can-
not be maintained greater than 93 % positive pressure ventilation may be
employed. If saturation is persistently less than 91 % manual ventilation may be
necessary.
Tube placement is measured from lips to distal tube and in average sized adults
is at the 23 cm line for males and 21 cm line for females. Correct tube placement is
determined by visualizing bilateral symmetric expansion of the chest and checking
for breath sounds in both lungs and an absence of sound over the stomach. End-tidal
carbon dioxide measured by calorimetric detection or standard capnography can be
used to confirm tracheal placement. A chest xray shows the degree of tube depth
and the distal tube should rest approximately 3 cm above the carina.
Cuff pressure should be 15–30 mmHg and below the approximate capillary pres-
sure of 32 mmHg. The use of a low pressure, high volume endotracheal tube cuff
will reduce the chance of ischemic injury caused by tissue compression.
Complications
Trauma from the laryngoscope, stylet, or endotracheal tube may damage the air-
way or surrounding soft tissue. Nontraumatic complications including broncho-
spasm, hypoxia, and aspiration of stomach contents can also occur. Significant
cardiovascular events including ventricular tachycardia and ventricular fibrilla-
tion are not common but may warrant antiarrhythmic prophylaxis in patients with
previous arrhythmias or myocardial ischemia. Stimulation of the laryngeal
branches of the vagus nerve may cause bradyarrhythmias that are responsive to
atropine. Mechanical ventilation may cause hypotension from decreased venous
return due to elevated intrathoracic pressure. Initial management consists of bolus
intravenous fluids and evaluation of airway pressures but more serious alternative
causes of hypotension including myocardial ischemia and pneumothorax must
also be considered. When intubation is prolonged patients are predisposed to a
number of potential problems including tracheomalacia, tracheal stenosis, and
tracheal erosion (Table 17.3) [3].
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Table 17.3 Complications from endotracheal intubation [3]

Intraprocedural complications Aspiration
Airway perforation
Laryngospasm
Trauma to dentition or airway
Spinal cord injury
Epistaxis
Ventricular tachycardia
Bradycardia
Endotracheal tube blockage
Tube dislodgement
Bronchus intubation
Postprocedural complications Laryngitis
Laryngeal edema
Hypoglossal nerve compression
Ulceration of airway mucosa
Vocal cord paralysis
Tracheal stenosis
Laryngeal granuloma
Pneumothorax
Clinical Vignettes
Case 1
A 68-year-old man is admitted to the hospital for 1 week of worsening shortness of

breath. He has a medical history of heart failure with an ejection fraction of 30 %
and takes metoprolol, enalapril, and spironolactone at home. On physical exam he
is afebrile, blood pressure is 82/50, heart rate is 108, respiratory rate is 32 and he
is satting 86 % on 70 % oxygen from a nonrebreather mask. He does not know where
he is or the year and attempts multiple times to remove his oxygen mask. His lungs
have bilateral rales and cardiac auscultation elicits an S3 heart sound. Arterial
blood gas reveals pH 7.48, pCO2 32 mmHg, and pO2 58 mmHg. His chest xray
shows cardiomegaly, bilateral pleural effusions, and alveolar edema.
This patient has acute decompensated heart failure with evidence of cardiogenic
shock and requires timely endotracheal intubation and mechanical ventilation. He is
in respiratory distress and must be stabilized. There is no role for noninvasive venti-
lation given his current hemodynamic instability. Other contraindications to noninva-
sive ventilation include altered mental status, increased risk for aspiration, facial
trauma, severe obesity, respiratory arrest, myocardial infarction, and arrhythmias.
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154 A.E. Brice
Case 2
A 42-year-old man is found unresponsive in the street next to an open bag of

unmarked white powder. Paramedics intubate him on the scene and transfer him to
the emergency department. When he arrives he is unresponsive to verbal stimuli but
sternal rub elicits a deep groan. He is afebrile, blood pressure is 98/66, and heart
rate is 115. Oxygen saturation is 84 % on 80 % inspired oxygen. He has reduced
expansion of the left side of his chest with reduced breath sounds on the left. The
endotracheal tube depth is 29 cm. Cardiac exam is unremarkable. Blood glucose is
94 and his cardiac biomarkers are pending. Electrocardiogram shows nonspecific
ST and T wave changes.
This patient has right mainstem bronchus intubation due to excess endotracheal
tube advancement and is likely suffering from drug overdose. His low oxygen satu-
ration can be fixed by withdrawing the tube to a depth of 23 cm in this male patient.
Intubations in the field are more difficult and prone to more frequent complications
given the uncontrolled environment. Correct tube placement must always be
checked by verifying appropriate tube depth, visualizing symmetric chest excur-
sion, auscultating bilateral breath sounds, measuring end-tidal carbon dioxide, and
obtaining a chest xray showing tube depth.
References
1. Ezri T, Warters RD. Indications for tracheal intubation. In: Hagberg CA, editor. Benumof’s
airway management: principles and practice. 2nd ed. Philadelphia: Mosby; 2007.
2. Reed MJ, Dunn MJ, McKeown DW. Can an airway assessment score predict difficulty at intu-
bation in the emergency department? Emerg Med J. 2005;22:99.
3. Irwin RS, Rippe JM, Lisbon A, Heard SO. Airway management and endotracheal intubation.
In: Procedures, techniques and minimally invasive monitoring in intensive care medicine. 4th
ed. Philadelphia: Wolters Kluwer; 2008.
4. Roberts JR, Custalow CB, Thomsen TW, Hedges JR. Tracheal intubation. In: Roberts and
Hedges’ clinical procedures in emergency medicine. 6th ed. Philadelphia: Elsevier Saunders;
2014.
5. Walls RM. Rapid sequence intubation. San Francisco: American College of Emergency
Physicians Scientific Assembly; 1987.
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Part III
Electrophysiology
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Chapter 18
The Electrocardiogram
Alexis P. Rodriguez
Introduction
The invention of the electrocardiogram (ECG or EKG) dates back to the eighteenth
century when Luigi Galvani realized that muscular activity could be induced with
the exposure to an electric field. However, the term itself was not used until the end
of the nineteenth century by Willem Einthoven. Throughout the years, the ECG has
continued to evolve, especially in the tracing recording portion, but has never lost its
great clinical meaning [1].
The physical principle is the recording of physical activity of the heart using skin
electrodes, which detect cardiac myocytes depolarization and repolarization waves.
In general, a positive depolarizing wave that travels towards the electrode creates an
upward deflection in the paper tracing. Conversely, any wave traveling away from
the electrode is recorded as a negative deflection. Finally, the amplitude, duration,
and direction of any deflection depend on that of the electric vector.
Indications
The opinion on ECG indications varies between physicians depending on the patient
and the clinical indications. Nonetheless, it is generally accepted that this test aids
in the diagnosis of overt or suspected cardiovascular disease with follow up record-
ings if there is a change in clinical status. It is also generally accepted for initial
evaluation in high-risk individuals, i.e., older than 40, history of dyslipidemia,
hypertension, or other risk factors. Furthermore, there is a role in the perioperative
A.P. Rodriguez, MD
University of Miami, Miller School of Medicine, Miami, FL, USA

DOI 10.1007/978-1-4471-7290-1_18
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158 A.P. Rodriguez
Superior Posterior
Lead I vector
RA LA
aV Right Left
R
aVL
V6 0°
Le
r
cto
ad
ve
II v
aVF
III V5 30°
ec
ad
tor
Le
V4 60°
V1 V2 V3 75°
LF
Right Inferior Left Anterior
Fig. 18.1 Lead vector for the three standard limb leads, the three augmented limb leads (left), and
the six unipolar precordial leads
setting whether for initial evaluation prior to surgery or afterwards to monitor for
complications. Selected individuals, albeit healthy otherwise, benefit from routine
screening ECGs; these include, athletes, pilots, bus drivers, among others [2].
Equipment and Technique
Cardiac potentials are detected by electrodes placed throughout the torso in specific
arrangements to form the different types of ECG leads (Fig. 18.1). These leads
record the potential difference between two electrodes, the positive and negative.
There are three standard limb leads, three augmented limb leads, and six precordial
leads for a total of twelve leads. Other systems have expanded to other leads to
detect right precordial leads to detect right ventricular abnormalities, or left poste-
rior leads to detect acute posterolateral infarctions.
Technique
The patient is initially asked to lie supine and relax as much as possible. The chest is
exposed so that there is no interaction with lead placement, but recognizing that
patient’s privacy should be maintained at all times. Figure 18.2 reveals the anatomic
landmarks for lead placement. These areas should be identified and cleaned to ensure
appropriate electrode placement and contact with the skin. ECG recorders have spe-
cific manufacturer’s instructions. Nonetheless, beforehand, it is crucial to determine
if there are any possible issues that may interfere with the accurate recording, i.e.,
electrical calibration, signal interference, wandering baseline, among others.
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18 The Electrocardiogram 159
Fig. 18.2 ECG lead

placement
Midclavicular
line
Clavicular line
V1 V
Right 2
nipple V5
V3 V4
Midstrenal
line
Right arm Left arm
Right leg Left leg

(ground)
Data Interpretation
Most ECGs are recorded on standard settings at 25 mm/Section (X Axis) and

10 mm/mV (Y axis). Different settings can be obtained depending on the heart rate,
or voltage. Before attempting to interpret an ECG, the reader should pay close atten-
tion to the standardization. For ease, this can generally be found at either the left or
right sides of the tracing.
The normal ECG is composed of multiple waves and intervals, which represent
the different portions of the cardiac cycle (Fig. 18.3). The P wave, representing
atrial activation is best appreciated in lead II or V1. The PR segment is usually an
isoelectric segment that begins at the end of the P wave and ends with the
QRS. Depression of the P wave is associated with pericardial disease. Ventricular
activation ensues with a number of complex interactions, which are recorded as a
set of deflections that give rise to the QRS. The T wave represents ventricular repo-
larization [3]. The QT interval is measured from the last portion of the QRS to the
end of the T Wave, and represents a measure how fast the ventricles repolarize. A
prolonged QT constitutes a marker for potential ventricular tachyarrhythmias. Since
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160 A.P. Rodriguez
Fig. 18.3 The waves and

intervals in a normal
electrocardiogram
Fig. 18.4 Case 1
the QT measurements vary with heart rates, a standardized measurement, the QTc,
is preferred at times. Different formulas have been derived. The Bazett equation
calculates the QTc by dividing the QT by the square root of the RR interval. The
Firderecia method uses the cube root. Other more complex methods, including
regression analysis exist but are beyond the scope of this book.
Clinical Vignettes
Case 1
50 year-old gentleman with history of hypertension and dyslipidemia presents to the

emergency department referring crushing chest pains for the last 25 min. The ECG
is shown in Fig. 18.4.
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18 The Electrocardiogram 161
Fig. 18.5 Case 2
This ECG is representative of the acute phase of an extensive anterolateral

ST-elevation myocardial infarction (STEMI). There is marked J point and ST-segment
elevation along prominently tall and broad T Waves. STEMIs are generally accom-
panied by ST reciprocal depressions in the opposite leads, in this case these are noted
in III and aVF. A particular case is the inferior STEMI. In this setting, the presence
of right ventricular infarction should be evaluated by the use of, RV leads (VR3,
VR4, VR5, and at times VR6). STEMIs represent a medical emergency that requires
expedited intervention. In this particular patient, the culprit lesion is most likely
located in the right coronary artery. The best benefit is derived from early aggressive
intervention within 90 min of patient’s arrival to the hospital necessitating the need
to obtain the ECG within 10 min of emergency department arrival.
Case 2
24 year old man brought to the Trauma Center after being involved in an unre-
strained motor vehicle head-on collision. Notes severe chest pain at the airbag site
of impact. On arrival to the hospital, he is tachycardic, tachypneic, and diaphoretic.
His initial ECG is shown in Fig. 18.5.
This patient has experienced major trauma to the chest. His symptomatology,
vitals, and ECG are suggestive of a large pericardial effusion with tamponade. The
ECG reveals a sinus tachycardia, with low QRS voltages, which demonstrated elec-
trical alternans, a marker of a large pericardial effusion. This diagnosis should
prompt evaluation with a complete echocardiogram to determine if tamponade
physiology is present.
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162 A.P. Rodriguez
Fig. 18.6 Case 3
Case 3
18 year-old football player that complained during practice of palpitations comes

to the office with the EKG shown in Fig. 18.6
This patient presents with an EKG that reveals preexcitation. These pathways
have a unique ECG pattern with a slurred initial upstroke of the QRS and a short PR
interval. Note the early upright QRS deflections in leads I, II, and aVF, and negative
in aVR and the rS pattern in V1 and V2. The Wolff-Parkinson-White (WPW) syn-
drome, a type of preexcitation, occurs with the presence of such accessory pathways
and tachycardia.
References
1. Fisch C. Evolution of the clinical electrocardiogram. J Am Coll Cardiol. 1989;14(5):

1127–38.
2. Fisch C. Clinical competence in electrocardiography. A statement for physicians from the
ACP/ACC/AHA task force on clinical privileges in cardiology. Circulation. 1995;91(10):
2683–6.
3. Friedberg CK, Zager A. “Nonspecific” ST and T-wave changes. Circulation. 1961;23:655–61.
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Chapter 19
Ambulatory Electrocardiography
Douglas W. Laidlaw and N.A. Mark Estes III
Introduction
Ambulatory electrocardiography (AECG) refers to diagnostic techniques used to

record cardiac rhythm in an outpatient setting. AECG methods provide a recording
of the cardiac rhythm from one or more leads for durations that are variable but can
be up to several years [1–3]. AECG techniques permit evaluation of dynamic car-
diac electrical activity that is frequently intermittent and of short duration. Over the
last several years, new technologies have emerged that allow use of multiple types
of noninvasive and invasive recorders for AECG.
Historically, continuous ambulatory recorders, commonly referred to as Holter
monitors, were developed to record the ECG continuously for a period of 24 h. The
continuous AECG is most commonly performed in patients with symptoms that
occur once daily or more frequently. Contemporary Holter monitoring devices have
time markers and patient-activation indicators. The recorded digital data are ana-
lyzed after completion of the monitoring by computer with technical oversight.
Current Holter monitoring technology does not allow for remote transmission of the
data from the patient for analysis. Typically a Holter monitor report includes infor-
mation about the total number of heart beats, average heart rate, maximum and
minimum heart rate, number of premature atrial and ventricular beats, tachyarrhyth-
mias, ST segment changes, and patient reported symptoms and the associated
recordings of the patient’s rhythm.
D.W. Laidlaw, MD, FHRS (*)

Tufts Medical Center, Boston, MA, USA
N.A.M. Estes III , MD, FACC
New England Cardiac Arrhythmia Center, Tufts Medical Center, Boston, MA, USA

DOI 10.1007/978-1-4471-7290-1_19
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164 D.W. Laidlaw and N.A.M. Estes III
Short-term event monitors are small, pocket-sized, recorders that are carried with the
patient and applied to the skin with electrodes when the patient experiences symptoms.
In addition to the typical hand-held device, wrist-watch units are also available. The
major advantage to event monitors is that they allow the patient to be free from wearing
electrode patches, which are often inconvenient and irritating. However, because the
device is not continuously recording the ECG, any symptom or arrhythmia must last
long enough to permit activation of the recorder. Current short-term event monitors are
capable of transmitting digital data remotely for analysis. However, because these
devices have a low diagnostic yield when compared to other available AECG tech-
niques, they are not commonly used clinically. Typically the short-term event monitors
given information regarding the patient’s rhythm at the time of symptoms
Noninvasive “loop monitors” are capable of recording the patient’s ECG for sev-
eral days, weeks, or months monitors the ECG continuously with hard wiring to
electrode patches. Historically these devices are called loop monitors because these
devices continuously looped their recording tapes. These devices are used for
patients with less frequent symptoms that would not be expected to be captured with
Holter or event monitoring. They are commonly used for 2–4 weeks or longer. This
form of AECG monitoring is typically activated by the patient by triggering the
device to store the cardiac rhythm for up to several minutes. The cardiac rhythm is
stored prior to, during, and after symptoms onset. Recordings can then be transmit-
ted remotely for evaluation. These devices also can be automatically triggered to
record based on pre-specified parameters of heart rate including irregularity. Most
commonly, these devices are programmed to automatically detect bradycardic
arrhythmias, tachyarrhythmias, and atrial fibrillation [4].
Some noninvasive loop monitors have the capacity to record all cardiac rhythms
in a full disclosure fashion continuously for weeks and transmit data remotely.
These real-time continuous cardiac monitoring systems are the newest form of
event monitors and overcome the many limitations of Holter, event monitors and
standard loop monitors. They are worn continuously and automatically record and
transmit arrhythmic event data from an ambulatory patient remotely. This type of
recorder is commonly referred to as mobile outpatient cardiac telemetry [5]. Like
the event recorders transmission can triggered based on parameters of heart rate and
by patient triggered symptoms. These monitors have the capacity similar to event
recorders to transmit remotely. This type of AECG is being use more commonly as
the diagnostic yield is higher than other forms of monitoring.
Occasionally a non-invasive evaluation for symptoms does not provide a diagno-
sis using the above techniques. Under these circumstances long-term implantable
loop recorders (ILR) are currently available [6]. These devices are typically
implanted in the left pectoral region as a simple outpatient procedure. Similar to the
noninvasive loop monitor, the implantable loop monitor can be activated by the
patient at the time of symptoms. ILRs record the patient’s cardiac rhythm prior to,
during, and after a patient triggered event. It also will record the cardiac rhythm
automatically when the heart rate or rhythm falls outside of predetermined param-
eters for low and high heart rates. Recent technology allows reliable detection of
atrial fibrillation, distinguishing it from other rhythms with a high sensitivity and
specificity. Current devices have battery longevity expected to approach 3 years.
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19 Ambulatory Electrocardiography 165
Indications
The most common indication for ambulatory monitoring is assessment of cardiac

arrhythmias or conduction abnormalities as the cause for symptoms such as palpita-
tions, pre-syncope or syncope. Ambulatory monitoring is also indicated for risk
stratification of patients with multiple types of cardiovascular disease. It is also used
for evaluation of therapy and for the detection of silent ischemia. The choice of
recording technique depends on the patient’s symptoms and the indication for the
test (Table 19.1).
Indications for AECG are summarized in the ACC/AHA Guidelines for
Ambulatory Electrocardiography [2]. Common indications for its use include palpi-
tations, unexplained syncope, and ischemia detection in patients with suspected
variant angina (Table 19.2). In addition, AECG may be utilized in special circum-
stances for antiarrhythmic drug monitoring and the assessment of pacemaker and
Implantable Cardioverter-Defibrillator (ICD) function (Table 19.3). Other indica-
tions for ambulatory monitoring include assessment of the average heart rate and
adequacy of rate control in patients with atrial fibrillation. Increasingly, techniques
of ambulatory monitoring are being used to evaluate for otherwise undetected atrial
Table 19.1 Advantages and disadvantages of specific ambulatory ECG recording techniques
Selection of ambulatory ECG recording technique
Recorder Duration
type Advantages Disadvantages of use
Holter 1. Continuous ECG Recording 1. Less useful for 24–48 h
monitor 2. No activation required by patient infrequent symptoms
3. Preferred method for daily 2. Continuous monitoring
symptoms at times uncomfortable/
inconvenient for patients
Noninvasive 1. Intermittent ECG Recording 1. ECG wires must be Weeks –
event 2. Transtelephonic downloading of attached and activated by Months
monitor events for immediate assessment patient with each event
3. Preferred for infrequent 2. Less useful for brief
symptoms (weekly or monthly) symptoms
without causing loss of 3. Less useful for
consciousness arrhythmias that cause loss
of consciousness
Loop 1. Intermittent ECG Recording 1. Continuous wearing Weeks –
monitor 2. Transtelephonic downloading of required Months
events for immediate assessment 2. Recorder must be
3. Preferred for infrequent or brief activated by patient with
symptoms that may cause loss of each event
consciousness
Implantable 1. Continuous monitoring with 1. Must be surgically Up to 3
loop intermittent ECG recording up to inserted years
recorder 40 min 2. Risk of infection
(ILR) 2. Preferred for rare symptoms 3. Higher cost than other
which cause loss of conciousness noninvasive techniques
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Table 19.2 Indications for AECG to assess symptoms possibly related to rhythm disturbances
A. Indications for AECG to assess symptoms possibly related to rhythm disturbances
Class I 1. Unexplained syncope, near syncope, or episodic dizziness in whom the cause is
not obvious
2. Unexplained recurrent palpitations
Class IIb 1. Episodic shortness of breath, chest pain, or fatigue that is not otherwise explained
2. Neurological events when transient atrial fibrillation of flutter is suspected
3. Syncope, near syncope, episodic dizziness, or palpitations in whom a probable
cause other than an arrhythmia has been identified, but in whom symptoms persist
despite treatment
Class III 1. Syncope, near syncope, episodic dizziness, or palpitations in whom other causes
have been identified
2. Cerebrovascular accidents without other evidence of arrhythmia
B. Indications for AECG for ischemia monitoring
Class I None
Class IIa Patients with suspected variant angina
Class IIb 1. Evaluation of patients with chest pain who cannot exercise
2. Preoperative evaluation for vascular surgery of patients who cannot exercise
3. Patients with known coronary artery disease and atypical chest pain syndrome
Class III 1. Initial evaluation of patients with chest pain who are able to exercise
2. Routine screening of asymptomatic patients
Source: Crawford et al. [1]
Table 19.3 Indications for AECG to assess antiarrhythmic drug and device therapy
A. Indications for AECG to assess antiarrhythmic drug therapy
Class I To assess antiarrhythmic drug response in individuals in whom baseline frequency of
arrhythmia has been characterized as reproducible and of sufficient frequency to
permit analysis
Class IIa To detect proarrhythmic responses to antiarrhythmic therapy in patients at high risk
Class IIb 1. To assess rate control during atrial fibrillation
2. To document recurrent or asymptomatic nonsustained arrhythmias during therapy
in the outpatient setting
B. Indications for AECG to assess pacemaker and ICD function
Class I 1. Evaluation of frequent symptoms to exclude myopotential inhibition and
pacemaker-mediated tachycardia and to assist in the programming of advanced
features such as rate responsivity and mode switching
2. Evaluation of suspected component failure or malfunction when device
interrogation is not definitive in establishing a diagnosis
3. To assess the response to adjunctive pharmacological therapy in patients receiving
frequent ICD therapy
Class IIb 1. Evaluation of immediate postoperative pacemaker function after pacemaker or
ICD implantation as an alternative to continuous telemetric monitoring
2. Evaluation of the rate of supraventricular arrhythmias in patients with implantable
defibrillators
Class III 1. Assessment of ICD/pacemaker malfunction when device interrogation or other
available data are sufficient to establish a cause/diagnosis
2. Routine follow-up in asymptomatic patients
Source: Crawford et al. [1]
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fibrillation in patients presenting with cryptogenic stroke. Ambulatory monitoring

techniques can also be used to screen patients for asymptomatic premature ventricu-
lar contractions and nonsustained ventricular tachycardia for purposes of risk strati-
fication. AECG can provide useful information for risk stratification for sudden
cardiac death in selected patients. These include those patients with hypertrophic
cardiomyopathy, long QT syndrome, congenital heart disease, arrhythmogenic right
ventricular dysplasia, ischemic heart disease, and dilated cardiomyopathies
The method of initial ambulatory ECG monitoring for the symptomatic patient
depends largely on the frequency and severity of symptoms. Holter monitoring for
24–48 h is most practical as the initial monitor for patients with daily or near daily
symptoms. Holter monitoring is also a reasonable approach to assess rate control in
patients with atrial fibrillation and for risk stratification for patients with selected
types of cardiovascular disease as noted above. By contrast, noninvasive or invasive
loop monitoring has a higher diagnostic yield in patients with less frequent symp-
toms. Such monitoring is appropriate if symptoms occur weekly or monthly but do
not prevent the patient from activating the device. Currently, there are three distinct
methods for intermittent ECG recording (Table 19.1).
Contraindications
As a simple, non-invasive technique, there are few absolute contraindications for

AECG. However, in patients with previous allergic reactions to the adhesives used in
lead attachment, alternative methods should be used, or the patient should be moni-
tored closely for adverse reactions. As a diagnostic test, the ACC/AHA guidelines [2]
explicitly discourage the use of AECG for patients with syncope or other symptoms if
other causes have been identified. In addition, published guidelines discourage the use
of AECG in patients with strokes who are at low risk without other evidence of
arrhythmia. These guidelines also do not support the use of AECG for the evaluation
of myocardial ischemia, with the exception of suspected variant angina (Table 19.2).
Although not contraindicated, AECG also plays a limited role in the assessment of
pacemaker and ICD function, and should not be used when data available from device
interrogation are sufficient to guide patient management (Table 19.3).
Equipment
The conventional AECG system uses a small, lightweight, battery operated electro-
magnetic tape recorder connected to bipolar electrodes that is capable of recording
in 3 or 12 lead ECG format on a magnetic tape cassette, microcassette, or compact
disk. These devices include patient-activated event markers and encoded time
markers for simplified data retrieval. Recorded data can be converted to a digital
format and analyzed using commercially available software that helps identify
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arrhythmias. Devices that allow trans-telephonic downloading are capable of ECG

transmission via telephone by converting the ECG data into an audio signal. Upon
receipt at a central location, the audio signal is reconstructed into a conventional
ECG recording for printing and analysis.
Newer devices now allow for direct recording of the ECG signal in a digital format.
This technology avoids potential biases introduced by tape recording as well as prob-
lems associated with analog-to-digital conversion before analysis. These recordings
allow for extremely accurate reproductions of the ECG signal for more advanced anal-
ysis by computer algorithms. Digital recording devices are currently limited by higher
costs and smaller storage capacity, although this technology is rapidly advancing.
Techniques of AECG
Correct patient connection to the device is the single most important step in AECG
recording. For standard 24-h Holter monitors, five, seven, or ten electrodes are placed in
standardized lead positions using adhesive gel after the skin sites are shaved and prepped.
From these positions, the operator is able to obtain 3 or 12 lead ECG recordings. The
number and arrangement of lead wires is determined by the operator at the time of the
recording depending on the number of ECG leads that are desired. The operator can
then set the desired duration of time for 3 and 12 lead recording to be obtained by the
device during the recording period. Patients are instructed to wear the recorder for
24–48 h, performing their daily activities as normal. During the recording period,
patients should avoid any activities that could cause the recorder or the electrodes to
become wet. They are also advised to avoid equipment or appliances (such as micro-
wave ovens) that may cause electromagnetic interference. All symptoms, activities, and
medications taken should be recorded by pressing the Event button on the recorder and
entering the event into either the Digital Diary or the paper diary provided.
In comparison to the traditional 24-h Holter monitor, loop monitors utilize two
attached ECG leads that can be worn continuously for several weeks. Patients are
instructed to detach the device for bathing. At the onset of symptoms, the device is
patient-activated for up to 300 s of recording a single ECG lead. In contrast, events
monitors do not require ECG lead attachment at the onset of symptoms. Rather, the
recorder itself contains four ECG electrodes that are held directly to the chest wall
for recording during an episode. Recorded rhythms for both devices then can be
downloaded via telephone to a central location.
Data Interpretation
Following the recording period, the saved ECG can then be analyzed using
commercially available software which displays and prints selected ECG
rhythm strips. In addition, the software provides trend information including
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ST-segments, heart rate (measured R-R interval) and heart rate variability, total
ventricular and supraventricular premature beats, and ventricular tachycardia
and supraventricular tachycardia beat counts. Accuracy of ECG interpretation
varies depending on the amount of background artifact in the recording and
with the software system used for analysis. The system is designed to detect all
important arrhythmia episodes with high sensitivity, but despite advances in
the accuracy of software-based analysis, all recorded rhythms must be over-
read by an experienced clinician. When used in combination with a detailed
diary of patient symptoms, the diagnostic yield of these devices is high. The
ability to temporally correlate ECG abnormalities with patient symptoms is the
unique strength of this technique.
Complications
As a simple, non-invasive test, there are no significant complications resulting from

this technique. However, the risk of misdiagnosis is a potential limitation of ambula-
tory monitoring. In several large studies, correlation between rhythm abnormality
documented using Holter monitoring and symptoms such as syncope was <5 % [3].
If an asymptomatic rhythm abnormality is detected, it may lead to additional unnec-
essary diagnostic testing.
Conclusions
It is evident that the clinician has multiple techniques of AECG monitoring avail-
able as diagnostic tools. The indication for the monitoring as well as the fre-
quency and duration of the symptoms need to be carefully considered in choosing
the best monitoring approach. The likelihood of making a diagnosis for patients
with intermittent, rare symptoms such as syncope, presyncope or palpitations is
increased with extended duration of monitoring. By contrast, when monitoring is
being performed to assess the effects of therapy such as rate controlling drugs in
atrial fibrillation or risk stratification, Holter monitoring for 24–48 h is sufficient.
Holter monitoring is also the appropriate method of AECG monitoring as an
initial step in patients with frequent symptoms occurring daily or more fre-
quently. By contrast, noninvasive loop monitoring is preferred for patients with
less frequent symptoms. In the absence of a diagnosis despite noninvasive loop
monitoring, it is reasonable to move forward with an invasive approach with an
ILR. Clinicians should remember that the ILR are most useful for patients with
extremely infrequent symptoms. However this invasive approach should gener-
ally be reserved for patients in whom noninvasive AECG techniques have failed
to yield a diagnosis.
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Clinical Vignettes
Case 1
A 60 yo male presents with recurrent palpitations. He has a history of anterior myo-

cardial infarction 2 years previously with moderately reduced left ventricular func-
tion (ejection fraction 35 %).
A 24-h Holter monitor is performed which documents an episode of nonsus-
tained monomorphic ventricular tachycardia (VT), corresponding with symptoms
of palpitations (Fig. 19.1). The patient undergoes electrophysiology testing which
reveals inducible sustained VT, and an Implantable Cardioverter Defibrillator (ICD)
is placed.
Case 2
A 65 yo female presents with frequent palpitation, lightheadedness, and two epi-

sodes of syncope. She has a history of paroxysmal atrial fibrillation.
A 24-h Holter monitor is performed which reveals an episode of atrial fibrillation
terminating with a 9.2 s pause and sinus arrest during sleep (Fig. 19.2). She is treated
for sick sinus syndrome with a permanent pacemaker.
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Case 3
A 20 yo male is referred for occasional palpiations. He has no significant past

medical or family history, and does not report dizziness, pre-syncope, or syncope.
A Holter monitor is performed which records an episode of sinus rhythm with
Mobitz II second-degree AV block (Wenckebach) in the early morning hours during
sleep (Fig. 19.3). No other significant arrhythmias were documented despite several
episodes of symptoms. No specific therapy was warranted.
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References
1. Zimetbaum PJ, Josephson ME. The evolving role of ambulatory arrhythmia monitoring in gen-
eral clinical practice. Ann Intern Med. 1999;130:848–56.
2. Crawford MH, Bernstein SJ, Deedwania PC, et al. ACC/AHA guidelines for ambulatory elec-
trocardiography: executive summary and recommendations. A report of the American College
of Cardiology/American Heart Association task force on practice guidelines (committee to
revise the guidelines for ambulatory electrocardiography). Circulation. 1999;100:886–93.
3. Miller JM, Zipes DP. Diagnosis of cardiac arrhythmias. In: Zipes DP, Libby P, Bonow RO,
Braunwald E, editors. Braunwald’s heart disease. A textbook of cardiovascular medicine. 7th
ed. Philadelphia: Elsevier Saunders; 2005. p. 697–712.
4. Afzal MR, Gunda S, Waheed S, et al. Role of outpatient cardiac rhythm monitoring in crypto-
genic stroke: a systematic review and meta-analysis. Pacing Clin Electrophysiol. 2015;38:1236.
5. Joshi AK, Kowey PR, Prystowsky EN, et al. First experience with a Mobile Cardiac Outpatient
Telemetry (MCOT) system for the diagnosis and management of cardiac arrhythmia. Am
J Cardiol. 2005;95:878.
6. Mittal S, Sanders P, Pokushalov E, et al. Safety profile of a miniaturized insertable cardiac
monitor: results from two prospective trials. Pacing Clin Electrophysiol. 2015;38:1464.
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Chapter 20
Tilt Table Testing
Alexis P. Rodriguez
Introduction
Tilt table testing (TTT) was introduced about two decades ago for the evaluation of
patients with unexplained syncope. Initially, it was welcome and spread enthusiasti-
cally through different medical specialties, but its use has decreased due to the rec-
ognition of several limitations when inappropriately employed. Nonetheless, the
generalized consensus still stands that TTT remains an important diagnostic tool in
the correct patient population.
Indications
TTT has been used for the evaluation of postural tachycardia syndrome, inappropri-
ate sinus tachycardia, and vasovagal syncope. It is especially useful in the evalua-
tion of recurrent episodes of syncope in the absence of organic heart disease, or in
patients with prior cardiomyopathy diagnosis in whom other syncope etiologies
have been excluded. Furthermore, TTT is also a practical option to discriminate
between convulsive syncope and epilepsy, to establish a diagnosis of pseudosyn-
cope, and lastly to evaluate patients with hypotension that are less likely to respond
to permanent cardiac pacing. Additionally the diagnosis of delayed orthostatic
hypotension syndrome can be successfully made through TTT after all other diag-
nostic studies are negative. Nonetheless, it should not be used when the vasovagal
syncope diagnosis is certain; or to guide therapy, its response, or lack thereof [1].
A.P. Rodriguez, MD
Cardiovascular Division, University of Miami Miller School of Medicine, Miami, FL, USA

DOI 10.1007/978-1-4471-7290-1_20
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174 A.P. Rodriguez
Fig. 20.1 The patient is secured on a padded table with may be placed in a variety of positions, as
opposed to position
Contraindications
Though a high volume of TTT are performed on a yearly basis, the ordering clini-
cian should be aware of its contraindications. While considered a safe test, compli-
cations still may arise from decreased perfusion to the heart, brain, or other organs.
Some of the most important contraindications include a history of severe tachyar-
rhythimas, electrolyte imbalance, end-stage renal disease, left ventricular outflow
tract obstruction, severe cerebral or coronary artery disease, hypotensive shock,
recent stroke, and lower extremity fracture.
Equipment
The test is performed generally in the electrophysiology laboratory. A tilt table is

required, and should be as comfortable as possible (Fig. 20.1). A blood pressure
monitor, ECG machine, and oxygen saturation monitor are also needed. Since one
of the possible complications is the development of dangerous tachyarrhythmias, a
crash cart with defibrillator should be available. During the testing phase, the room
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20 Tilt Table Testing 175
should remain quiet comfortable by minimizing disruptive noises, or uncomfortable

extreme range of temperatures.
Technique
Multiple protocols have been developed varying the angle tilt, its duration, and the
concomitant use of pharmacologic agents. The patient is placed supine and vital
signs are closely monitored to obtain a personal baseline. It is recommended that if
venous cannulation had been performed prior to the test, the monitoring period
should be longer. Another important consideration is to avoid invasive intra-arterial
blood pressure monitoring during TTT because catheterization may induce in some
individuals a vasovagal reaction. The patient is positioned in a head-up position.
The recommendation is that the tilt angle be between 60° and 70°; however, steeper
angles have been described. Heart rate and blood pressures are recorded every
3–5 min and a symptom diary is maintained. Pharmacologic agents can induce
symptoms in patients that have remained asymptomatic. Isoproterenol, a non-
specific beta agonist, used as an infusion is commonly employed. The infusion is
titrated from 1–3 mcg/min to increase the heart rate up to 25 % above the recorded
baseline, and then the head-up tilt phase of the study begins. Another important
consideration is that isoproterenol is contraindicated in patients with ischemic heart
disease. Nitrates have also been showed to have some use in tilt table testing, intra-
venous infusion or sublingual nitrates. Nitrates work by inducing venodilation, and,
thus, reducing cardiac preload, stroke volume, and output. Yet, it does not hamper
increases in heart rate or arterial constriction. Like isoproterenol, nitrates decrease
the exam duration but are better-tolerated and easier to use [2].
Data Interpretation
Test interpretation depends on the clinical setting for indication in the first place. In
patients without structural heart disease, TTT is determined to be diagnostic for dif-
ferent outcomes. First, for the evaluation of reflex hypotension or bradycardia that
may, or not, be accompanied of spontaneous syncope. Secondly, when the patient
develops progressive orthostatic hypotension even if there are no associated symp-
toms. In selected patients being assessed for POTS, TTT may play a diagnostic role,
but it is still discretionary to the ordering physician. In patients with structural heart
disease, arrhythmias should be excluded before considering a test to be diagnostic.
Reproduction of a syncopal event even in the absence of hypotension or bradycardia
is in turn suggestive of psychogenic pseudosyncope. The rate of false positives and
negatives depends on the patient population; however, these are difficult to estimate
given that there is no gold standard testing for comparison.
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176 A.P. Rodriguez
If the patient has remained asymptomatic during TTT, and there is suspicion for
false negative results, it is recommended that the test be repeated using isoproterenol.
Though relatively safe for most patients, isoproterenol should be avoided in patients
with angina and history of arrhythmia. While most make no discriminations regard-
ing test results when isoproterenol is used, some cardiologists make the distinction
that a test is positive only if there is loss of consciousness or postural tone. Nonetheless,
the most current guidelines do not include separate diagnostic criteria for TTT with
concomitant isoproterenol [2]. Nitrates, like isoproterenol, may increase the rate of
false positives. Trials comparing nitroglycerin to isoproterenol have been conducted,
thus, showing similar results; however, sublingual nitroglyerine was simpler to
administer, much better tolerated, and safer than low-dose isoproterenol [3, 4].
Complications
As previously stated, TTT is rather safe, and severe complications are rare; how-
ever, as with any other medical procedure, there are still some intrinsic risks that
both patient and practitioner should be aware. Potential complications include, pro-
longed hypotension, tachyarrhythmias, syncope, and rarely asystole. Most of these
complications resolve when the table is turned back to the horizontal position.
Nonetheless, precautionary measures should be taken and readily available includ-
ing cardiopulmonary resuscitation equipment.
Clinical Vignettes
Case 1
Mrs. Jones is a 40 year-old lady that comes to the office for evaluation of syncope.
She has a history of hypertension, hypothyroidism, dyslipidemia, and obesity. She
takes synthroid 125 mcg daily, and her primary care physician discontinued hydro-
chlorothiazide over a year ago as her blood pressure seemed better controlled. She
experienced her first syncopal event about 3 months ago while getting up from a
chair, and then another one last week after standing for some time. She recalled that
the same thing used to happen in her “earlier years.” Before both events, she felt her
vision darkened and the room spin for some seconds. Both events were witnessed,
and the loss of consciousness was transitory and resolved by itself. There was no
tongue biting or sphincter incontinence. She had no post-ictal period. However, per
her son, there was some lower extremity jerking movements. She has undergone
extensive diagnostic studies including brain images; thus far, no clear etiology
given. She undergoes TTT with hypotension and reproduction of symptoms.
Mrs. Jones has had two syncopal episodes that have prompted a medical evalua-
tion. After extensive and thorough evaluation, there is no clear etiology. However,
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20 Tilt Table Testing 177
no pertinent positive findings have been noted. While it can be argued, that given the
history, this is very likely consistent with vasovagal syncope, there is the confound-
ing factor of lower extremity jerking, which can also be seen in syncope of cardiac
nature. The TTT is considered to be positive given her vital signs response and
reproduction of symptoms. Mrs. Jones should be advised regarding hydration, pro-
longed standing, or sudden changes in position. The patient should also be educated
on abortive procedures if she experiences an aura.
Case 2
A 28 year old woman is referred for the evaluation of recurrent fainting episodes.
These started about 2 years ago, and have consistently recurred. She has no medi-
cal history, other than generalized anxiety disorder, and takes no medications or
over the counter supplies. The episodes occur without an aura, or clear precipitat-
ing event. These last between 5 and 20 min, and the patient just experiences some
residual weakness and left lower extremity weakness. She has undergone extensive
neurologic evaluation (including MRI and EEG) without a definitive diagnosis.
Furthermore, EKG and echocardiography do not show any abnormalities. At the
primary care physician’s office her blood pressure was borderline low, but other-
wise her vitals were normal. She undergoes TTT, and her vitals remain unchanged
but the patient experiences another episode. A psychiatry consultation is placed,
and the diagnosis is changed to psychogenic seizures and possibly conversion dis-
order. With the patient and her family understanding the diagnosis, psychotherapy
was started and follow up appointments were provided.
This patient comes with complaints of recurrent syncope without a clear explanation.
There is always concern for seizures or syncope of neuro-cardiogenic nature. These
seem to have been ruled out. The possibility of vasovagal syncope has to be considered.
Her blood pressure was marginally low; however, this is a non-specific finding espe-
cially in young healthy individuals. TTTs that reproduce the loss of consciousness with-
out changes in vital signs are suspicious for a psychogenic etiology. The patient and
family should be engaged in the therapy, which should remain empathic and consistent
throughout. It is crucial to recognize that most of these events are involuntary, legitimate,
and disabling to the patient. She should enroll in behavioral and group psychotherapy,
and considered for antidepressant or antipsychotic pharmacotherapy.
References
1. Sheldon RS, Grubb 2nd BP, Olshansky B, Shen WK, Calkins H, Brignole M, et al. 2015 heart
rhythm society expert consensus statement on the diagnosis and treatment of postural tachycar-
dia syndrome, inappropriate sinus tachycardia, and vasovagal syncope. Heart Rhythm.
2015;12(6):e41–63.
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178 A.P. Rodriguez
2. Moya A, Sutton R, Ammirati F, Blanc JJ, Brignole M, Dahm JB, et al. Guidelines for the diag-
nosis and management of syncope (version 2009). Eur Heart J. 2009;30(21):2631–71.
3. Raviele A, Giada F, Brignole M, Menozzi C, Marangoni E, Manzillo GF, et al. Comparison of
diagnostic accuracy of sublingual nitroglycerin test and low-dose isoproterenol test in patients
with unexplained syncope. Am J Cardiol. 2000;85(10):1194–8.
4. Delepine S, Prunier F, Leftheriotis G, Dupuis J, Vielle B, Geslin P, et al. Comparison between
isoproterenol and nitroglycerin sensitized head-upright tilt in patients with unexplained syn-
cope and negative or positive passive head-up tilt response. Am J Cardiol. 2002;90(5):
488–91.
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Chapter 21
Electrophysiologic Testing
Jonathan Weinstock and Christopher Clyne
There are a wide variety of clinical scenarios in which electrophysiology studies

(EPS) may be useful, as a way to diagnose symptoms such as palpitations or syn-
cope, to define mechanisms and possibly treat a documented arrhythmia, or to aid
in determining a patient’s risk for sudden cardiac death from ventricular arrhyth-
mias. Furthermore, EPS may be used to assess known or suspected conduction
abnormalities. Most EPS are performed via electrode catheters in the heart, but
some are performed with non-invasive programmed stimulation (NIPS) that refers
to a limited electrophysiology study performed via an implanted cardiac device,
either a pacemaker or a defibrillator.
Indications
Invasive EPS can be of use in patients with suspected or known sinus node dysfunc-
tion. EPS is helpful in determining a causal relationship between suspected sinus
node dysfunction and symptoms in cases where a non-invasive evaluation has failed
to establish the link. Indications for EPS in patients with known or suspected AV
block, include those in whom His-Purkinje block is suspected as the cause of symp-
toms, but has not been definitively established, including those with pre-existing
conduction abnormalities such as those in whom the surface electrocardiogram
(ECG) documents a bundle branch block.
J. Weinstock, MD (*)
New England Cardiac Arrhythmia Center, Tufts Medical Center,
750 Washington Street, Boston, MA, USA
C. Clyne, MD
Cardiology Division, Stuart Medical Group, Brockton, MA, USA

DOI 10.1007/978-1-4471-7290-1_21
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180 J. Weinstock and C. Clyne
EPS are indicated in patients with recurrent supraventricular tachycardia (narrow

QRS complex <120 ms), to better define the mechanism of the arrhythmia and for
selection of the appropriate therapy, either medical or ablation. Wide complex
tachycardias (wide QRS >120 ms) may be a result of either supraventricular arrhyth-
mias with intraventricular conduction delay (aberration), pre-excitation in the
Wolff-Parkinson-White syndrome, or ventricular tachycardia. When the mechanism
of documented arrhythmias is not clear on a surface ECG, EPS are indicated to
define the mechanism and guide therapy. Non-invasive programmed stimulation
(via an ICD) is indicated in patients who have ventricular arrhythmias, in whom
prescription of new antiarrhythmic medications may alter the characteristics of the
tachycardia, which affects the programming of their ICD.
Indications for EPS in patients with Wolff-Parkinson-White syndrome (WPW)
include patients in whom ablation of an accessory pathway is planned, and patients
with WPW manifest on a surface ECG who suffer a cardiac arrest or syncope.
Asymptomatic patients with WPW who have a family history of sudden cardiac death,
or who engage in high risk occupations, may require EPS, for risk stratification, and to
determine the best therapy if required, including pharmacologic or ablation therapies.
In patients with left ventricular dysfunction, non-sustained ventricular tachycar-
dia can be a risk factor for sudden cardiac death. EPS with ventricular stimulation is
indicated in patients with non-sustained ventricular tachycardia, coronary artery
disease, and left ventricular dysfunction for risk stratification, where if inducible for
ventricular arrhythmias, patients may benefit from implantation of a cardiac defi-
brillator. In patients with non-ischemic cardiomyopathy, the results of ventricular
stimulation are not predictive of risk. Patients with highly symptomatic, drug resis-
tant, uniform premature ventricular contractions; or non-sustained ventricular
tachycardia (with or without structural heart disease) may undergo and EPS to
localize the arrhythmia, and allow for ablation.
EPS are indicated in patients with syncope and structural heart disease in whom
the cause of syncope is unknown after routine evaluation. Additionally, patients
without structural heart disease who have recurrent unexplained syncope despite an
appropriate non-invasive workup may require EPS to assist in the diagnosis. EPS
are indicated in patients with recurrent palpitations in whom repeated efforts to
obtain electrocardiographic recordings have failed, or in patients in whom palpita-
tions preceded a syncopal event.
Contraindications
As with most intravascular cardiac procedures, EPS are contraindicated in the pres-
ence of significant coaguloapathies or known obstruction to venous access. EPS
should not be performed in the setting of hemodynamic instability, acute exacerba-
tions of heart failure, systemic infection, and respiratory distress. Additionally, EPS
is contraindicated in patients with left main coronary disease, a large burden of car-
diac ischemia, severe aortic stenosis, acute myocardial infarction, or unstable angina.
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21 Electrophysiologic Testing 181
Equipment
Equipment required to perform EPS, is similar to other cardiac catheterization

equipment and includes a fluoroscopic unit, a patient table suitable for radiography,
a physiologic recorder and display for hemodynamic, surface electrocardiography
and intracardiac recordings, and equipment for intravascular access. Equipment for
emergencies such as an external defibrillator, tools for airway support, and emer-
gency medications should be easily available in the room in which the procedure is
performed.
Unique to EPS are a programmable stimulator, a junction box, and electrode
catheters. The stimulator is a device that is capable of delivering accurately timed
(within 1 ms) stimuli via intracardiac catheters triggered either by previously paced
beats or intrinsic beats. Multiple stimuli can be delivered with complex timing
sequences. The junction box acts as a common location for catheters to connect to
the recording and pacing equipment. Specialized catheters are used which have a
variable number of electrode pairs on their ends, to both record intracardiac electri-
cal activity and deliver pacing stimuli to the heart. Some electrophysiology labora-
tories are equipped with additional equipment such as 3-D mapping systems that
assist in the diagnosis and localization of arrhythmias, and specialized ablation
catheters and generators (radiofrequency and cryo-thermal energies) for delivery of
catheter directed energy that destroys the arrhythmia focus.
Technique
The patient is brought to the electrophysiology laboratory in the fasting state and the
sites of venous access are sterilized with either betadine or chlorhexadine, after
which the patient is draped. General anesthesia is rarely used for diagnostic EPS, as
the vast majority of procedures can be achieved by conscious sedation with the use
of benzodiazepines and other drugs. General anesthesia may be employed for lon-
ger procedures such as atrial fibrillation or ventricular tachycardia (VT) ablations.
The sites of access are almost always the femoral veins, with only the rare need for
arterial access. Occasionally access is gained from the upper extremity, the subcla-
vian, or internal jugular veins, either because of a contraindication to the femoral
approach, or for ease of placement of a particular catheter, usually the coronary
sinus, which sometimes can be difficult from an inferior approach.
Venous access is gained via the Seldinger technique, and a series of sheaths are
placed intravenously. Through these sheaths a number of multipolar electrode cath-
eters are positioned under fluoroscopy in standard locations in the heart. Between 2
and 4 catheters can be used for an EPS, depending on the clinical scenario. Standard
catheter positions include the high lateral right atrium, the His bundle position, and
right ventricular apex (Fig. 21.1). A complete ventricular stimulation protocol also
includes the repositioning of the right ventricular catheter in the right ventricular
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HRA
His
HRA
His
RVA
RVA
Fig. 21.1 AP and Lateral views of cardiac silhouette with three diagnostic (quadripolar) catheters
placed in the high right atrium (HRA), across the tricuspid annulus for His bundle recording (His),
and in the right ventricular apex (RVA)
outflow tract- below the pulmonic valve. If the EPS is designed to specifically diag-
nose or induce supraventricular arrhythmias (SVT), an additional multipolar cath-
eter is usually positioned within the coronary sinus from the right atrium. If needed,
access to the left atrium and ventricle, may be achieved via a transseptal puncture of
the intra-atrial septum, or retrograde across the aortic valve via the femoral artery
and aorta.
A basic EPS consists of a standard protocol that assesses baseline characteristics
of the conduction system followed by attempted induction of arrhythmias. EPS
begins with the measurement of baseline conduction intervals beginning with those
on the surface electrocardiogram such as PR interval, and QRS width, and includes
the intra-cardiac intervals measuring the time for conduction from the atrium to the
His bundle deflection (AH interval), and from the His bundle deflection to the ven-
tricular activation deflection (HV interval) (Fig. 21.2).
Pacing maneuvers are employed to assess sinoatrial (SA) node function and con-
duction properties from the atrium to ventricle (AV conduction), from the ventricle
back to the atrium (VA conduction), and of the atrio-ventricular node (AVN)-
including the rate at which the AVN displays both antegrade and retrograde
Wenkebach and 2:1 conduction block. Introduction of premature atrial stimuli is
performed in a standard fashion to further define the arrhythmogenic substrate (dual
AVN pathways; accessory pathways), and to expose various forms of SVT’s (AV
nodal reentry, AV reentry, atrial arrhythmias). These pacing maneuvers also help to
define the refractoriness of the AV node, and to characterize the antegrade conduction
properties of an existing accessory pathway. Similar maneuvers are performed from
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II s
aVR
V1
V6
HRA
HIS
HBEP
Atrium
HISMID
Ventricle
HBED
RVA
Fig. 21.2 Recording of sinus rhythm during an electrophysiology study. The top six tracing are
from the surface electrocardiogram, the next five lines are intra-cardiac recordings from the high
right atrium (HRA), proximal His bundle (HBEP), mid His bundle (HISMID), distal His bundle
(HBED) and right ventricular apex (RVA). The recording speed is 50 mm/s. The deflections on the
individual catheters are labeled as atrium, His bundle, and ventricle, corresponding to sensed depo-
larization of each structure
the ventricle (s) to characterize ventricular conduction and detect ventricular

arrhythmias (VT, VF).
Various pacing maneuvers are performed in a variety of locations in an attempt
to induce supraventricular or ventricular tachycardia. Extra-stimuli are delivered in
increasing numbers [1–3] and prematurity after a drive train of eight beats from
multiple sites (RA, RVA, RVOT, +/−CS/LA) in an attempt to induce an arrhythmia.
The administration of drugs such as epinephrine, isoproterenol or atropine is often
added to standard induction protocols to increase the chance of induction. Optimal
therapy (drug, ablation, or device) can be planned if an arrhythmia is reproduced.
Hemostasis is achieved with manual pressure at the end of the procedure after the
catheters and sheaths are removed.
Data Interpretation
Abnormal sinus node function indicated by a long sinus node recovery time (the
interval following atrial pacing after which the sinus node fires) in combination with
unexplained syncope is an indication for a permanent pacemaker.
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A prolonged HV interval (≥100 ms), or easily induced block in the His-Purkinje

system (infra-Hisian) is a relative indication for a permanent pacemaker as it pre-
dicts a high likelihood of progressing to high degree AV block.
The presence of two AV nodal pathways with atrial pacing maneuvers suggests
AV nodal reentry tachycardia as the etiology of a supraventricular arrhythmia in
symptomatic patients.
Induction of monomorphic VT in a patient with unexplained syncope identifies a
cause for the syncope, and an indication for an ICD.
The reproducible induction of a supraventricular tachycardia in the electro-
physiology laboratory allows for a variety of pacing maneuvers to be performed
during the tachycardia. These maneuvers in combination with the initiation and
termination characteristics of the arrhythmia allow for an exact diagnosis of the
arrhythmia by careful analysis of the intracardiac recordings. Most supraventricu-
lar tachycardias are amenable to relatively safe and effective ablation procedures,
which can be performed in the same session [4]. Atrial flutter, AV nodal reentry
tachycardia, atrioventricular reciprocating tachycardia (WPW), and atrial tachy-
cardia are examples of supraventricular tachycardias that can be cured with
ablation.
Ventricular tachycardias may be characterized and identified by their location,
morphology, rate and induction characteristics. Sustained monomorphic ventricular
tachycardia is a more specific finding than polymorphic ventricular tachycardia or
ventricular fibrillation. Specificity is greatest with induction at the right ventricular
apex with low number of slower extrastimuli. The specificity decreases as the num-
ber and rapidity of extrastimuli increase. Localization of the tachycardia via 3-D
mapping techniques allows for the ablation of stable VT’s in appropriate ablation
candidates.
Complications
Bleeding and hematoma formation either superficially or in deep tissue (retroperito-

neum) is a potential complication of EPS. Venous thromboembolism (DVT/PE)
occurs in approximately 0.05 % of EPS procedures. The risk of arterial thromboem-
bolism (peripheral arterial embolus, CVA) increases when catheters are placed in
the left atrium or left ventricle making anticoagulation necessary during the proce-
dure. Cardiac tamponade as a result of cardiac perforation by electrode catheters
occurs in approximately 0.08 % of studies, but is higher if ablation is performed.
The risk of death from EPS is rare despite the routine induction of life-threatening
arrhythmias, as the response to such events in such a controlled setting results in a
rapid effective response.
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II
AVF
V1
AH AH AH AH AH
HBE
V V
Fig. 21.3 Electrophysiology study recording of a patients with syncope and type 2nd second-
degree heart block. The first three tracings are surface leads, HBE is the electrogram recorded at
the His bundle. An A (atrial) deflection is followed on each occasion by an H (His) deflection. Only
the first and fourth atrial impulse conduct to the ventricle signified by V. The remainder of the atrial
impulses block at the infra-Hisian level
Clinical Vignettes
Case #1
A 76-year-old man presented with recurrent syncope, and a left bundle branch block
on ECG. EPS revealed block below the bundle of His (Fig. 21.3). A permanent pace-
maker was implanted, and his syncope did not recur.
Case #2
A 62-year-old man with a remote myocardial infarction, reduced left ventricular

ejection fraction (40 %), presented with recurrent syncope. Ventricular tachycardia
was induced during an electrophysiology study (Fig. 21.4). An ICD was implanted
and he subsequently received appropriate shocks for ventricular arrhythmias.
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Fig. 21.4 Tracing from an electrophysiology study during induction of ventricular tachycardia.
The first five recordings are surface ECG, followed by RA (right atrium), HBP (His bundle proxi-
mal), HBM (His bundle mid), HBD (His bundle distal) and RVA (RV apex). The first eight QRS
complexes result from ventricular pacing, followed by two premature stimuli, which induced ven-
tricular tachycardia. Rapid ventricular pacing terminates the tachycardia
References
1. Josephson ME. Clinical cardiac electrophysiology: techniques and interpretation. 3rd ed.
Philadelphia: Lippincott Williams and Wilkins; 2002.
2. Fogros RN. Electrophysiologic testing. 3rd ed. Cambridge: Blackwell Publishing; 1999.
3. Zipes DP, Dimarco JP, Gillette PC, et al. Guidelines for clinical electrophysiologal and catheter
ablation procedures. J Am Coll Cardiol. 1995;26:555–73.
4. Huang SK, Miller JM. Catheter ablation of cardiac arrhythmias. 3rd ed. Philadelphia: Elsevier
(Saunders); 2015.
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Chapter 22
Temporary Transvenous Pacing
Alawi A. Alsheikh-Ali and Mark S. Link
Indications
Temporary cardiac pacing is generally indicated for the acute management of seri-
ous and often symptomatic bradyarrhythmias, that are refractory to medical therapy
[1]. Several approaches to temporary pacing are available, including transvensous,
transcutaneous, epicardial, and transesophageal. Compared to the other modalities,
the transvenous approach is the most stable and readily available option, with the
unique ability for selective atrial or ventricular pacing. Conversely, this approach is
associated with a variety of complications, and its safe and effective use requires
considerable knowledge and technical skill.
Acute myocardial infarction (AMI) is associated with several conduction distur-
bances, some of which may necessitate temporary transvenous pacing [1]. Generally,
temporary pacing should be considered in any patient with AMI and a bradyarrhythmia
associated with symptoms or hemodynamic compromise, and those asymptomatic
with anterior AMI and alternating bundle branch block, Mobitz II or higher atrioven-
tricular (AV) block. Indications for temporary transvenous pacing in AMI are based on
the status of AV nodal and intraventricular conduction, as outlined in Table 22.1. The
most ominous sign requiring temporary transvenous pacing in AMI is alternating left
and right bundle branch block, which constitutes a Class I indication regardless of the
status of AV nodal conduction. Likewise, temporary transvenous pacing in AMI is
indicated when Mobitz II second-degree AV block is present, regardless of the status of
intraventricular conduction. Other indications for temporary transvenous pacing in
AMI are shown in Table 22.1. In general, if the indications for temporary pacing persist
for 5–7 days after an AMI, a permanent pacemaker should be considered.
A.A. Alsheikh-Ali, MD (*) • M.S. Link, MD

Cardiac Arrhythmia Center, Tufts Medical Center,
Tufts University School of Medicine, Boston, MA, USA
e-mail: [email protected]; [email protected]

DOI 10.1007/978-1-4471-7290-1_22
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188 A.A. Alsheikh-Ali and M.S. Link
Table 22.1 Recommendations for temporary transvenous pacing in acute ST-elevation myocardial
infarction
Mobitz I Mobitz II
Normal AV First-degree second- second-
conduction block degree block degree block
Normal intraventricular conduction III III III IIa
Old or new fascicular block III III III IIa
Old bundle branch block III IIb IIb IIa
New bundle branch block IIb IIa IIa I
Fascicular block + RBBB IIb IIa IIa I
Alternating RBBB + LBBB I I I I
In the absence of an AMI, temporary transvenous pacing should be considered in

any patient presenting with acute symptomatic bradyarrhythmia refractory to medical
therapy until the offending cause is withdrawn (e.g., beta-blocker, calcium channel
blocker, digoxin) and appropriate evaluation for structural or ischemic heart disease
and the need for permanent pacing is completed. Other clinical situations where tem-
porary transvenous pacing should be considered include advanced AV block associ-
ated with Lyme carditis. Given the reversible nature of bradyarrhthmias in Lyme
disease, temporary rather than permanent pacing should be considered if needed.
Temporary transvenous pacing is also used after the removal of an infected permanent
pacemaker in patients who are deemed pacemaker dependent. A temporary pacer-
maker is placed until the infection is treated with intravenous antibiotics, after which
it is replaced with a new permanent pacer. Similarly, temporary transvenous pacing
may be indicated in patients with acute endocarditis (especially with aortic valve
involvement) who show signs of conduction disturbance (advanced AV block or new
bundle branch block). In addition, prophylactic transvenous pacing should be consid-
ered during right heart catheterization or right ventricular endomyocardial biopsy in
patients with existing left bundle branch block, given the associated risk of traumatic
right bundle branch block during the procedure leading to completer heart block.
Contraindications
The only absolute contraindication to temporary transvenous pacing is refusal by a

competent patient. Relative contraindications include a bleeding diathesis that can-
not be corrected for safe placement of a temporary transvenous pacer. A decision
regarding temporary transvenous pacing depends on the specific clinical situation
including the nature of the underlying arrhythmia and availability of other tempo-
rary pacing modalities (e.g., transcutaneous or transesophageal). The presence of a
mechanical tricuspid valve also precludes the safe placement of a right ventricular
temporary pacer although in these situations left ventricular pacing via the coronary
sinus may be considered.
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22 Temporary Transvenous Pacing 189
Equipment
Temporary transvenous pacing is achieved through intravenously placed catheter

electrodes (leads) that are in direct contact with the endocardium. Pacing leads
are connected to an external generator providing electrical current pulses to stim-
ulate the myocardium. Pacing leads are most commonly bipolar in configuration
in which both the cathode (negative pole) and anode (positive pole) are intracar-
diac near the tip of the lead. Unipolar configuration can also be used, in which
one pole, typically the anode, is extracardia. Pacing leads are either flexible with
an inflatable balloon near the tip to direct flow, or semi-rigid without a flow-
directing balloon. Semirigid catheters are easier to manipulate and can have pre-
formed distal preformed curvatures for easier manipulation and positioning.
Once positioned, the lead is connected to an external generator through which
pacing rate and mode, sensitivity, and current output can be adjusted. Alternatively,
a permanent screw-in pacing lead can be introduced and then attached to a per-
manent pacing generator that is securely taped outside the body. This temporary
arrangement provides the most lead stability, and allows for prolonged pacing
and safe patient ambulation. For any patient in which temporary pacing may be
needed for some time (i.e., while treating an infected pacemaker) a permanent
screw in lead should be strongly considered. This arrangement is also preferable
for atrial pacing.
Technique
As with any procedure involving transvenous insertion of a foreign body, standard

sterile techniques should be followed. An external defibrillator with pacing capabili-
ties should be present in the room during lead insertion or manipulation. The right
internal jugular vein provides the most rapid and direct route for proper transvenous
pacing lead positioning. Subclavian venous access can be used, but carries the
added risk of a pneumothorax and injury to the subclavian artery, and is typically
saved for a future permanent pacemaker should the patient need one. Femoral vein
access can also be used, but carries the added risk of venous thrombosis and a poten-
tially higher infection rate. For positioning in the right atrium, a J-curve configura-
tion is typically used, and the lead is typically advanced to the level of the tricuspid
valve, and then withdrawn back gently until it hooks on the right atrial appendage.
For right ventricular positioning, the lead is advanced through the tricuspid valve
either directly with the tip first, or after formation of a loop in the right atrium under
fluoroscopy, which is then advanced through. Once in the right ventricle, gentle
advancement and torque is required to reach the apex (counter-clockwise torque if
coming in from the superior vena cava, or clockwise if from the inferior vena cava).
Once the lead is positioned, appropriate sensitivity and output are confirmed (see
below), then the lead is sutured to the skin, and covered with sterile dressing.
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Ideally, lead advancement is performed under fluoroscopic guidance to ensure

appropriate positioning and minimize risk of cardiac perforation. However, electro-
cardiographic guidance can be used, whereby the lead is connected to an ECG while
being advanced. A large ventricular electrogram indicates presence in the ventricle,
while development of ST segment elevation indicates contact with ventricular endo-
cardium. Pacing leads can also be advanced under echocardiographic guidance uti-
lizing the apical or subxiphoid windows for best visualization of the right atrium
and ventricle. Under emergency conditions, a pacing lead can be advanced blindly
while connected to a generator set to highest output until ventricular capture (paced
QRS) is seen. Electrocardiographically, a paced QRS originating from the right
ventricular apex should have a left bundle branch block morphology with superior
axis. A right bundle branch morphology most commonly indicates pacing from the
coronary sinus or left ventricle (i.e., perforation into the left side). Regardless of the
guidance modality used, a chest x-ray should be obtained in all patients after a tem-
porary transvenous pacer to ensure appropriate positioning.
Data Interpretation
The term “sensitivity” as used for cardiac pacing relates to the amplitude (often in mV)
of the P wave or R wave as seen by the intracardiac electrode in the atrium or ventricle
respectively. Sensing threshold (the amplitude above which intrinsic activity is not
detected) can be determined by setting the pacemaker to a rate lower than the intrinsic
rate, and then lowering the sensitivity (increasing the amplitude on the mV scale) until
pacing occurs. Pacing occurs at the sensing threshold because the pacemaker does not
“see” the intrinsic beat. Sensitivity is then set at 25–50 % the sensing threshold. High
amplitude is desired (>1 mV for P wave, and >5 mV for R wave), to allow for a comfort-
able sensitivity safety margin at which the pacemaker can reliably sense intrinsic activ-
ity without running the risk of sensing low amplitude “noise” (i.e., oversensing). Pacing
(output) threshold can be determined by setting the pacemaker to a rate higher than the
intrinsic rate at low output, and then increasing the output current gradually until myo-
cardial capture (pacing spike followed by a QRS complex) occurs. Optimal pacing
threshold is less than 1 mA. Output is typically set at 3–5 times the pacing threshold to
allow for any temporal changes in pacing threshold. Both sensing and pacing thresholds
should be checked daily and sensitivity and output changed accordingly.
Complications
Complications from temporary transvenous pacing are related to obtaining and

maintaining venous access, intracardiac catheter manipulation and retaining an intra-
vascular foreign body [2]. In addition, these leads can perforate the myocardium at
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any time after insertion. Risks specific to venous access include bleeding, vascular
arterial injury, pneumothorax (with subclavian or internal jugular access), air embo-
lism, cardiac perforation including tamponade, pericarditis, and venous thrombosis/
thrombophlebitis (more common with femoral vein approach). Intracardiac catheter
manipulation carries the risk of inducing atrial or ventricular tachyarrhythmias.
While bacteremia can be demonstrated in many patients with temporary transvenous
pacers, clinical infection (including sepsis) is much less common occurring in less
than 5 % of patients.
Clinical Vignettes
Case 1
A 50 year old woman with diabetes mellitus, hypertension was noted to be brady-
cardic with a heart rate of 40 beats per minute during a routine colonoscopy. An
electrocardiogram demonstrated complete heart block. She reported an episode of
syncope 1 week prior. Given her risk factor profile, work up for coronary disease
and structural heart disease was ordered.
While awaiting the ordered workup and given her recent syncope, a temporary
transvenous pacer with a screw in lead was placed through a right internal jugular
venous approach (Fig. 22.1). A dipyridamole myocardial perfusion scan was nor-
mal, and a transthoracic echocardiogram revealed no structural heart disease with
a left ventricular ejection fraction of 60 %. A new left sided permanent dual cham-
ber pacemaker system was placed through a left subclavian venous approach
(Fig. 22.2a, b) and the temporary pacer was removed.
Fig. 22.1 Temporary

transvenous screw-in
pacing lead is seen placed
through right internal
jugular vein. The generator
(outside the body) is seen
next to the right shoulder
ERRNVPHGLFRVRUJ
a b
Fig. 22.2 (a, b) PA (2A) and lateral (2B) chest radiographs. The temporary pacer has been
removed and a new permanent dual chamber pacemaker through the left subclavian vein is in
place. Note the anterior orientation of both pacing leads indicating appropriate positioning. A
posterior orientation of the ventricular lead would indicate placement in the coronary sinus
Case 2
An 84 year old female with hypertension and dyslipidemia presented with acute
pulmonary edema and respiratory distress requiring intubation. Her electrocardio-
gram showed anterior Q waves in leads V1–V5. A transthoracic echocardiogram
showed a left ventricular ejection fraction of 30 %. The patient was noted to have
intermittent episodes of complete heart block with a wide QRS complex escape
rhythm around 30 beats per minute.
A temporary non-screw in pacing lead was placed urgently through a left subcla-
vian approach (Fig. 22.3). Because of recurrent fevers, and in anticipation of a pro-
longed hospitalization, a new temporary screw-in lead connected to an external
generator was placed through the right internal jugular vein, and the old non-screw
in lead removed (Fig. 22.4). Once her infection was treated, a permanent pacemaker
was placed and the temporary one removed.
Fig. 22.3 Temporary

transvenous non-screw-in
pacing lead is seen placed
through the left subclavian
vein (white arrow). A
pulmonary artery catheter
is also seen placed through
the right internal jugular
vein (red arrow)
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Fig. 22.4 The temporary

non-screw in pacer has
been removed and a new
screw-in lead is seen (white
arrows) placed through the
right internal jugular vein
and attached to an external
generator
References
1. Epstein AE, DiMarco JP, Ellenbogen KA, Estes NA, Freedman RA, Gettes LS, Gillinov AM,
Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH,
Silka MJ, Stevenson LW, Sweeney MO. ACC/AHA/HRS, 2008 guidelines for device-based
therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology/
American Heart Association task force on practice guidelines (writing committee to revise the
ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiar-
rhythmia devices) developed in collaboration with the American Association for thoracic sur-
gery and society of thoracic surgeons. J Am Coll Cardiol. 2008;51:1–62.
2. Francis GS, Williams SV, Achord JL, Reynolds WA, Fisch C, Friesinger 2nd GC, Klocke FJ,
Akhtar M, Ryan TJ, Schlant RC. Clinical competence in insertion of a temporary transvenous
ventricular pacemaker. A statement for physicians from the ACP/ACC/AHA task force on
clinical privileges in cardiology. Circulation. 1994;89(4):1913–6.
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Chapter 23
Cardiac Pacemakers
Constancia F.C. Macatangay
Currently, three approaches to permanent cardiac pacing are in common use. Single-
chamber pacemaker is a device wherein one pacing lead is implanted in either the
right atrium or right ventricle. Dual-chamber pacemaker has two pacing leads, one in
the right ventricle and one in the right atrium, this is the most commonly used type
of pacemaker. Biventricular pacemaker or cardiac resynchronization therapy (CRT)
is a device wherein in addition to single- or dual-chamber right heart pacing leads, a
third lead is advanced to the coronary sinus for left ventricular epicardial pacing.
Indications
The decision to implant a permanent pacemaker is based on the association of

symptoms with a bradyarrhythmia, the location of the conduction abnormality, and
the absence of a reversible cause.
A careful history taking and documentation of cardiac rhythm, with either an
electrocardiogram or ambulatory monitoring, should be done. Symptoms include
dizziness, lightheadedness, syncope, fatigue, and poor exercise tolerance. The direct
correlation between symptoms and bradyarrhythmia will increase the likelihood
that the pacemaker therapy would result in clinical improvement.
The most common indications for permanent pacemaker implantation are sinus
node dysfunction (SND) and high-grade or symptomatic atrioventricular (AV)
block. SND refers to abnormalities in sinus node and atrial impulse formation and
propagation. It is primarily a disease of the elderly and is thought to be due to senes-
cence of the sinus node and atrial muscle. SND encompasses a wide array of
C.F.C. Macatangay, MD (*)

520 East 70th Street, Starr 4, New York, NY 10021 USA

DOI 10.1007/978-1-4471-7290-1_23
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196 C.F.C. Macatangay
abnormalities which include: persistent sinus bradycardia and chronotropic incom-

petence without identifiable causes, paroxysmal or persistent sinus arrest with
replacement by subsidiary escape rhythms in the atrium, AV junction, or ventricular
myocardium, and “tachy-brady syndrome”. There is no evidence that cardiac pacing
prolongs survival in patients with sinus node dysfunction.
Type II second-degree AV block is characterized by fixed PR intervals before and
after blocked beats and is usually associated with a wide QRS complex. It is usually
infranodal (either intra- or infra-His), especially when the QRS is wide, and typically
indicates diffuse conduction system disease. Thus, this type of block constitutes an indi-
cation for pacing even in the absence of symptoms. Symptoms are frequent, prognosis
is compromised, and progression to third-degree AV block is common and sudden.
Third-degree AV block (complete heart block) is defined as absence of AV conduction.
Bifascicular block refers to ECG evidence of impaired conduction below the AV
node in the right and left bundles. Please refer to Tables 23.1, 23.2, and 23.3 for a
full listing of all the indications for pacemaker pacing in SND, AV block, and
chronic bifascicular block.
Pacemaker may also be indicated in neurocardiogenic syncope in which there is a
severe or persistent component of bradycardia and more conservative therapeutic
attempts have failed. There are other special circumstances which require permanent
cardiac pacing: after the acute phase of myocardial infarction, after cardiac transplanta-
tion, in sleep apnea syndrome, infiltrative disorders, and neuromuscular disorders [1].
Contraindications
Once it has been established that the bradycardia or a conduction disorder warrants
permanent pacing, there are a few contraindications for the actual permanent pace-
maker insertion. These include local infection at implantation site and/or active
systemic infection with bacteremia.
In general, pacemakers are not indicated for asymptomatic patients. Symptoms
due to sinus node dysfunction have to occur during the documented episodes of bra-
Table 23.1 Indications for permanent pacing in sinus node dysfunction [1, 2]
Strength of
Indication indication
Sinus node dysfunction with documented symptomatic bradycardia, including Class I
frequent sinus pauses that produce symptoms
Symptomatic chronotropic incompetence Class I
Symptomatic sinus bradycardia that results from required drug therapy for Class I
medical conditions
Sinus node dysfunction with heart rate less than 40 bpm when a clear association Class IIa
between significant symptoms consistent with bradycardia and the actual presence
of bradycardia has not been documented
Syncope of unexplained origin when clinically significant abnormalities of sinus Class IIa
node function are discovered or proved in electrophysiological studies
Minimally symptomatic patients with chronic heart rate less than 40 bpm while Class IIb
awake.
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23 Cardiac Pacemakers 197
Table 23.2 Indications for permanent pacing in acquired atrioventricular block in adults [1]
Indication Strength of indication
3rd degree and advanced 2nd degree AV block at any anatomic level Class I
associated with bradycardia with symptoms (including heart failure) or
ventricular arrhythmia presumed to be due to AV block
associated with arrhythmias and other medical conditions that require
drug therapy that results in symptomatic bradycardia
3rd degree and advanced 2nd degree AV block at any anatomic level in Class I
awake, symptom-free patients in sinus rhythm, with documented
periods of asystole greater than or equal to 3.0 s, or any escape rate
<40 bpm, or with an escape rhythm that is below AV node
3rd degree and advanced 2nd degree AV block at any anatomic level in Class I
awake, symptom-free patients with atrial fibrillation and bradycardia
with one or more pauses of at least 5 s or longer
associated with postoperative AV block that is not expected to resolve
after cardiac surgery
after catheter ablation of the AV junction
associated with neuromuscular diseases with AV block
2nd degree AV block with associated symptomatic bradycardia Class I
regardless of type or site of block
Asymptomatic persistent 3rd degree AV block at any anatomic site Class I
with average awake ventricular rates of 40 bpm or faster if
cardiomegaly or LV dysfunction is present or if site of block is below
the AV node
2nd or 3rd degree AV block during exercise in the absence of Class I
myocardial ischemia
Persistent 3rd degree AV block with an escape rate greater than 40 bpm Class IIa
in asymptomatic adult patients without cardiomegaly
Asymptomatic 2nd degree AV block at intra- or infra- His levels found Class IIa
at electrophysiological study
1st or 2nd degree AV block with symptoms similar to those of Class IIa
pacemaker syndrome or hemodynamic compromise
Asymptomatic type II 2nd degree AV block with a narrow QRS Class IIa
Neuromuscular diseases with any degree of AV block (including 1st Class IIb
degree AV block), with or without symptoms
AV block in the setting of drug use and/or drug toxicity when the block Class IIb
is expected to recur even after the drug is withdrawn
dycardia. It is of utmost importance to assess for the etiology of the bradycardia:

bradyarrhythmia due to a non-essential drug therapy would require drug therapy
cessation, and if due to reversible cause (e.g., Lyme disease, increased vagal tone,
hypoxia in sleep apnea syndrome in absence of symptoms), would require treatment
of underlying cause. Finally, an appropriate diagnosis of the type or level of block is
mandatory. Asymptomatic 1st degree, type I 2nd degree AV block at the supra-His
(AV node) level, and fascicular block without AV block, do not need a pacemaker.
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Table 23.3 Indications for permanent pacing in chronic bifascicular block [1]
Strength of
Advanced 2nd degree AV block or intermittent 3rd degree AV block Class I
Type II second-degree AV block Class I
Alternating bundle-branch block Class I
Syncope not demonstrated to be due to AV block when other likely causes have Class IIa
been excluded, specifically ventricular tachycardia
Incidental finding at electrophysiological study of a markedly prolonged HV Class IIa
interval >100 ms in asymptomatic patients
Incidental finding at electrophysiological study of pacing-induced infra-His block Class IIa
that is not physiological.
Neuromuscular diseases with bifascicular block or any fascicular block, with or Class IIb
without symptoms
Equipment
The basic equipment required for a permanent pacemaker insertion includes: fluoro-
scope, topical anesthesia (1–2 % lidocaine or bupivacaine), instrument tray, pacing
system analyzer, introducer kit, suture material, electric cautery, external pacemaker,
antimicrobial flush and saline for pocket irrigation. A single-plane fluoroscopy using
anteroposterior, 30° right anterior oblique, and 45° left anterior oblique views is used.
A pacemaker system consists of two major components: a pulse generator and one or
more electrodes. The pulse generator (Fig. 23.1) is the “battery” component of the
pacemaker and it provides the electrical impulse for the myocardial stimulation. The
electrodes, also known as “leads” (Fig. 23.2a), deliver the electrical impulse from the
generator to the myocardium. Currently, the most common cardiac pacing system
utilizes transvenous electrodes (leads). However, there are certain clinical situations
wherein transvenous leads are not possible (i.e., infection, venous thrombosis/steno-
sis). In these situations, the epicardial or leadless pacing systems may be considered.
A full discussion of these types of pacing system is beyond the scope of this chapter.
Technique
The implantation usually involves a combination of local anesthesia and conscious

sedation. The pacing generator is typically placed subcutaneously, superficial to the
pectoralis, however, under certain conditions, it may also be placed subpectoral/
infra-mammary, or intra-abdominal (i.e., surgically via thoracotomy).
Antibiotic prophylaxis, either with cefazolin or vancomycin, is a standard for
device implantation. A central vein: subclavian, internal jugular, or axillary vein, is
ERRNVPHGLFRVRUJ
Fig 23.1 Example of a

pacemaker generator
Fig. 23.2 (a) Example of an intravenous lead. (b) Two types of lead tips: helical screw (above)
and grappling hook (below)
ERRNVPHGLFRVRUJ
Fig. 23.3 Chest radiograph PA and lateral of a patient with dual chamber pacemaker
access via percutaneous approach. A venous cut down of the cephalic vein may also
be done. After venous access is obtained, a guidewire is advanced and subsequently,
a sheath and dilator are advanced. The pacemaker lead is then advanced to the
chamber of interest (i.e., right atrium, right ventricle). Usually, the ventricular lead
is positioned before the atrial lead to prevent its dislodgment.
Once the correct lead positioning is confirmed, lead is affixed to the endocar-
dium either passively with tines (grappling hook) or actively via a helical screw
located at the tip (Fig. 23.2b). Pacing and sensing thresholds and lead impedances
are measured with the pacing system analyzer. Pacing is also performed at 10 V to
assess for diaphragmatic stimulation. After confirmation of lead position and
threshold, the proximal end of the lead (s) is then secured to the underlying tissue
and connected securely to the pulse generator. The pacemaker pocket is usually
irrigated with antimicrobial solution. The incision is closed in layers with absorb-
able sutures and skin with either adhesive strips or skin glue. An arm sling is
applied to the unilateral arm for 12–24 h to limit movement. A post-procedure
chest radiograph is usually done for lead position confirmation and to rule out
pneumothorax (Fig. 23.3). On the following day, postero-anterior (PA) and lateral
chest radiographs will again be done to confirm lead positions and exclude any
delayed pneumothorax.
Data Interpretation
A universal pacing code system, also known as NBG pacemaker code, is used to
facilitate the understanding of pacemakers. It describes the five-letter code for oper-
ation of implantable pacemakers and defibrillators.
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Position I reflects the chamber (s) paced. “A” indicates the atrium, “V” indicates
the ventricle, and “D” means dual chamber (i.e., both atrium and ventricle).
Position II refers to the chamber (s) sensed. The letters are the same as those for the
first position: “A”, “V”,or “D”. An addition option “O” indicates an absence of
sensing. If a device is programmed in this mode, it will pace automatically at a
specific rate, ignoring any intrinsic rhythm.
Position III refers to how the pacemaker responds to a sensed event. “I” indicates
that a sensed event inhibits the output pulse and causes the pacemaker to recycle
for one or more timing cycles. “T” indicates that the output pulse is triggered in
response to a sensed event. “D” indicates dual modes of response and is restricted
to dual chamber systems.
Position IV reflects rate modulation, also known as rate adaptive or rate responsive
pacing. “R” indicates that the pacemaker has rate modulation and incorporates a
sensor to adjust its programmed paced heart rate in response to patient’s activity.
“O” indicates that rate modulation is either unavailable or disable.
Position V is rarely used and specifies only the location of multisite pacing or absence
thereof. Multisite pacing is defined as stimulation sites in both atria, both ventri-
cles, more than one stimulation site in any single chamber, or a combination of
these. “O” indicates no multisite pacing. “A” means multisite pacing in the atria.
“V” means multisite pacing in the ventricles, and “D” for both atrium and ventri-
cle. The most common application of multisite pacing is biventricular pacing.
Complications
Although considered a minimally invasive procedure, the incidence of complica-

tions in modern pacing therapy is still substantial. Permanent pacemaker placement
poses various risks ranging from minor to serious life-threatening complications.
These complications may be classified according to severity (minor or major), com-
ponent of pacing system involved (lead, generator/pocket, patient), or to timing of
occurrence: in-hospital or acute, sub-acute, or late.
Acute complications occur peri-procedural or in-hospital. Pneumothorax may
occur in 1–3 % in patients undergoing pacemaker implantation. Due to this known
complication, chest radiographs are performed immediately after, and often, the day
after the procedure. Vascular access complications may also occur. Direct subcla-
vian vein punctures are associated with a higher incidence of pneumothorax and
lead damage from subclavian crush syndrome. The axillary venous puncture
approach and cephalic venous cut down, on the other hand, are associated with
lower incidence of pneumothorax and lead damage. Myocardial perforation has
been reported to occur in 1 % of patients, with the asymptomatic subclinical perfo-
ration occurring to as much as 15 %. Device pocket hematoma is also a common
complication. It has an incidence of approximately 5 %, with a higher incidence in
patients on anticoagulation or antithrombotic medications. Finally, in-hospital death
generally occurs in less than 1 % of pacemaker implantations [3].
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Subacute post-implantation complications occur after hospital discharge and less

than 30 days after placement. During this period, several types of pacemaker and
lead function/failures have been reported: failure to capture, failure to output, under-
sensing, and inappropriate pacemaker rate [3].
Late complications occur more than 30 days after placement. The most common
complications include infection, device/lead advisories, lead function problems/
failures, venous thrombosis or stenosis. Localized infection involving the device
pocket may occur up to 60 % of the patients, with the rest presenting as endovascu-
lar infection. Device malfunction leading to device explantation occurs in <1 % of
patients. A rise in capture threshold may occur beyond 6 weeks of implantation. As
this threshold rises, it may exceed the maximum output of pulse generator. This
phenomenon is called “exit block”. Venous stenosis, less commonly thrombosis,
has also been reported after implantation of pacing leads [3].
Clinical Vignettes
Case 1
A 76 year old man with hypertension and dyslipidemia comes in for an annual
check-up. He is feeling well, active, and runs yearly in a marathon. His medications
include lisinopril and atorvastatin. His resting heart rate was found to be 43
beats/min with blood pressure of 120/75. An ECG was done which shows sinus
bradycardia 44 beats per minute, with normal PR and QRS intervals.
The most important feature in this patient’s history is the absence of any symp-
tom. It is a Class III recommendation to implant a permanent pacemaker for SND in
asymptomatic patients. ECG monitoring may be done should any symptom arise
and if there is a need to correlate it with bradyarrhythmia. Given the lack of symp-
toms and patient’s high level of activity, pacemaker is not indicated.
Case 2
A 68 year old woman with hypertension and coronary artery disease, presented to
the hospital for two episodes of syncope. She has been having palpitations and sev-
eral pre-syncopal episodes for 3 months. Upon arrival, patient is awake and alert.
A rhythm strip was obtained which showed atrial fibrillation with a ventricular rate
of 185 bpm. Her BP was 115/70. Metoprolol 2.5 mg IV was given and patient
became pre-syncopal. She then had a heart rate of 30 bpm and a BP of 90/60. An
hour later, she was again in atrial fibrillation with a ventricular rate of 170 bpm.
This association of paroxysmal atrial fibrillation and sinus bradycardia, accom-
panied by symptom, is worrisome for a “tachy-brady syndrome”, a type of sinus
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node dysfunction. Individuals with tachy-brady syndrome have diseased SA nodes

and often display exaggerated overdrive suppression. Given the patient’s symptoms
and sinus node dysfunction, a pacemaker is recommended.
References
1. Epstein AE, DiMarco JP, Ellenbogen KA, Freedman RA, Silka MJ, et al. ACC/AHA/HRS
2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the
American College of Cardiology/American Association task force of practice guideline. J Am
Coll Cardiol. 2013;61(3):e6–75.
2. Brignole M, Auricchio A, Baron-Esquivias G, Bordachar P, Boriani G, Vardaas PE, et al. 2013
ESC guidelines on cardiac pacing and cardiac resynchronization therapy: the task force on
cardiac pacing and resynchronization therapy of the European Society of Cardiology (ESC).
Developed in collaboration with the European Heart Rhythm Association (EHRA). Europace.
2013;15(8):1070–118.
3. Jeffrey L. Williams and Robert T. Stevenson (2012). Complications of Pacemaker Implantation,
Current Issues and Recent Advances in Pacemaker Therapy, Dr. Attila Roka (Ed.), InTech,
DOI: 10.5772/48682. http://www.intechopen.com/books/current-issues-and-recent-advances-
in-pacemaker-therapy/complications_of_pacemaker_implantation
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Chapter 24
Biventricular Pacing
Chris Healy and Juan F. Viles-Gonzalez
Introduction
As left ventricular (LV) systolic dysfunction progresses to clinical heart failure, it is

frequently accompanied by impaired electromechanical coupling. This may further
impair ventricular contractility. Prolonged interventricular and intraventricular con-
duction results in regional mechanical delay within the LV and can cause reduced
ventricular systolic function, functional mitral regurgitation, and ventricular remod-
eling/dilation. Modification of ventricular electromechanical delay with multisite
ventricular pacing (commonly called biventricular [BiV] pacing or cardiac resyn-
chronization therapy [CRT]) can improve ventricular systolic function, induce
favorable remodeling, decrease heart failure hospitalizations, and reduce mortality
[1, 2]. Currently, CRT is indicated for mortality reduction and symptom improve-
ment in patients with systolic heart failure and LV dyssynchrony as evidenced by a
wide QRS complex on electrocardiogram (EKG). Numerous markers of LV dys-
synchrony have been described, including a number of echocardiographic measure-
ments. However, the marker which best predicts outcomes following CRT is the
width/morphology of the QRS complex. As such, the strength of the indication for
CRT is dependent on a patient’s QRS duration and morphology as well as New York
Heart Association (NYHA) heart failure class.
C. Healy, MD • J.F. Viles-Gonzalez, MD (*)

University of Miami Miller School of Medicine, Miami, FL, USA

DOI 10.1007/978-1-4471-7290-1_24
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206 C. Healy and J.F. Viles-Gonzalez
Indications
Per the most recent ACC/AHA guidelines, the only Class I indication for CRT is for
patients in sinus rhythm with LV ejection fraction (LVEF) ≤35 %, a QRS duration
≥150 ms, left bundle-branch block (LBBB) morphology, and NYHA class II, III, or
ambulatory IV heart failure. Please refer to Table 24.1 for a full listing of all the
indications for CRT. It is important to note that all of these recommendations refer
to patients who are already on guideline directed medical therapy [3].
Contraindications
There are two circumstances under which CRT carries a Class III recommendation
(no benefit and may cause harm). These are patients who do not fulfill implant criteria
(NYHA class I or II symptoms, non-LBBB pattern, and QRS duration <150 ms) and
patients with estimated survival <1 year based on comorbidities and/or frailty [3].
Equipment
CRT devices, like the majority of cardiac implantable electronic devices, consist
of two basic components, the pulse generator and the leads (Fig. 24.1). There are
two main categories of CRT devices, BiV pacemakers and BiV ICDs. The
Table 24.1 Indications for cardiac resynchronization therapy

Strength of
Sinus rhythm, LVEF ≤35 %, LBBB, QRS duration ≥150 ms, and NYHA Class I
class II, III, or ambulatory IV symptoms
Sinus rhythm, LVEF ≤35 %, LBBB, QRS duration 120–149 ms, and NYHA Class IIa
class II, III, or ambulatory IV symptoms
Sinus rhythm, LVEF ≤35 %, non-LBBB pattern, QRS duration ≥150 ms, and Class IIa
NYHA class III or ambulatory IV symptoms
Atrial fibrillation, LVEF ≤35 %, patient requires ventricular pacing, and AV Class IIa
nodal ablation or pharmacologic rate control will allow near 100 %
ventricular pacing with CRT
LVEF ≤35 % and undergoing new or replacement device placement with Class IIa
anticipated requirement for significant (>40 %) ventricular pacing
Sinus, rhythm, LVEF ≤30 %, LBBB, QRS duration ≥150 ms, ischemic Class IIb
etiology of heart failure, and NYHA class I symptoms
Sinus, rhythm, LVEF ≤35 %, non-LBBB pattern, QRS duration 120–149 ms, Class IIb
and NYHA class III or ambulatory IV symptoms
Sinus, rhythm, LVEF ≤35 %, non-LBBB pattern, QRS duration ≥150 ms, Class IIb
and NYHA class II symptoms
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24 Biventricular Pacing 207
a b
Fig. 24.1 PA and lateral radiographic images of a biventricular implantable cardioverter defibril-
lator. PA (Panel a) and lateral (Panel b) chest x-rays showing a biventricular implantable cardio-
verter defibrillator. Both images show the device (thick white arrow) implanted in the left chest, the
atrial lead (thin white arrow) positioned in the right atrial appendage, the right ventricular lead
(thick black arrow) positioned in the right ventricular apex, and the left ventricular lead (thin black
arrow) positioned in a lateral branch of the coronary sinus
majority of devices implanted are BiV ICDs, as the majority of patients who are
candidates for CRT also have an indication for an ICD for primary prevention of
sudden cardiac death.
CRT devices are typically larger than standard pacemakers or ICDs. However,
even the largest devices are smaller than an average deck of playing cards. The
device contains two main components, the electronics that control the device func-
tion and a compact battery.
All CRT devices have at least two leads, and most have three leads. Typically there
is an atrial lead to facilitate AV synchrony, though in some circumstances this may not
be necessary (chronic atrial fibrillation). By definition, these devices must have two
ventricular leads. Typically one lead is placed in the right ventricular (RV) apex or
elsewhere in the RV along the interventricular septum. Unique to BiV devices, is the
presence of a pacing lead in the coronary sinus. The coronary sinus lead can have as
many as four pacing electrodes on it (Fig. 24.2). This allows for multiple possible pac-
ing vectors, so as to produce the most synchronous contraction of the LV.
Technique
Placement of a CRT device involves two procedural components, creation of the

pocket where the pulse generator will sit and placement of the leads. The procedure
is performed in a sterile environment (either an electrophysiology laboratory or an
operating room). The most common locations for the device pocket are the left and
right chest. The device is typically placed prepectorally. However, the device can
also be placed below the pectoralis muscle if necessary (thin patient, desire for bet-
ter cosmetic result, etc.). This results in a relative increase in the risk of
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Fig. 24.2 Radiographic

image of coronary sinus
lead. PA chest x-ray
showing a quadripolar lead
implanted in a lateral
branch of the coronary
sinus. Note the four pacing
poles marked by the black
arrows. This allows for
numerous possible pacing
configurations
post-procedure bleeding. The device can be placed in the abdomen instead of the
chest wall when necessary, though this is uncommon.
Whenever possible, all leads are placed via the transvenous route. Typically access
is obtained into the axillary or subclavian vein and the right atrial (RA) and RV leads
are passed via the superior vena cava to their ultimate locations. The coronary sinus
lead is typically the most challenging lead to place. First, a guiding catheter is placed
via the RA into the coronary sinus. Then, a balloon-tipped catheter is advanced through
the guiding catheter into the coronary sinus. With the balloon inflated in the proximal
coronary sinus, a venogram of the coronary sinus is obtained. This provides anatomical
information, so that the most ideal branch of the coronary sinus for lead placement can
be determined. The branch which allows for the most lateral location of the lead is
commonly chosen. Next, a wire is advanced through the guiding catheter and posi-
tioned in the chosen coronary sinus branch. The coronary sinus lead is then advanced
over the wire to its ultimate location. As with any pacing system, all leads must be
tested after placement for adequate sensing, impedance, and pacing thresholds.
Occasionally, the leads cannot be placed in adequate locations for various reasons
(central venous stenosis, unfavorable coronary sinus anatomy, etc.). In these circum-
stances, patients may require epicardial lead placement via an open, surgical approach.
When all leads have been placed, they are connected to the device which is
secured in the pocket and the incision is closed.
Data Interpretation
The most important response to placement of a CRT device is the patient’s func-
tional capacity. Many coronary sinus leads have multiple electrodes, and if a patient
has a suboptimal response to CRT a different pacing vector for the coronary sinus
lead can be chosen. Different protocols exist for echocardiographic or SPECT
guided CRT optimization. However, data on these approaches is currently limited.
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24 Biventricular Pacing 209
Complications
Placement of a CRT device is an invasive procedure that carries the risk of serious
and possibly life threatening complications. The most common complications
include device infection and bleeding at the incision site or in the pocket. Bleeding
can typically be controlled with the use of a pressure dressing, but occasionally
large pocket hematomas require drainage. Infection is a more serious complication,
and complete extraction of all device components is recommended whenever
possible in addition to antibiotic therapy.
Less common complications include injury to the SVC or other major blood ves-
sels; perforation of the RA, RV, interventricular septum, or coronary sinus; pericar-
dial effusion; cardiac tamponade; arrhythmia; and death. Pericardial effusions can
usually be treated conservatively with observation. However, if there is evidence of
cardiac tamponade, percutaneous drainage is required. In rare cases, emergent sur-
gery may be necessary.
Clinical Vignettes
Case 1
A 55 year old man with ischemic cardiomyopathy of 4 years duration presents to

clinic. He reports stable DOE with walking one block. His medications include
lisinopril, metoprolol, aspirin, simvastatin, spironolactone, and furosemide. He had
a single lead ICD placed 2 years ago for primary prevention of sudden cardiac
death. His EKG shows sinus rhythm with a LBBB and a QRS duration of 153 ms.
His echocardiogram shows a LVEF of 25 %.
The key question is: What is the most appropriate next step? It is premature for
referral for transplant or to consider hospice and adding additional medical therapy,
such as with an ARB, is unlikely to provide much benefit.
The best course would be to upgrade the device to a BiV system. He has a Class
I indication for CRT (systolic heart failure, NYHA class III, sinus rhythm, LBBB,
QRS ≥ 150 ms, and EF ≤ 35 %).
Case 2
In which of the following patients undergoing device implantation would implanta-

tion of a CRT device be reasonable?
A. 85 year old man referred for AAI pacemaker implantation for the treatment of
symptomatic sick-sinus syndrome
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B. 56 year old woman with nonischemic cardiomyopathy, LVEF of 25 %, and a

QRS duration of 95 ms referred for ICD implantation for the primary prevention
of sudden cardiac death
C. 45 year old man with nonischemic cardiomyopathy and LVEF 40–45% referred
for dual-chamber pacemaker implantation in complete heart block
D. None of the above
The correct answer is C, a 45 year old man with nonischemic cardiomyopathy
and LVEF 40–45% referred for dual-chamber pacemaker implantation in complete
heart block. He already has evidence of cardiomyopathy (EF 40–45 %) and he
would be expected to pace nearly 100 % of the time (complete heart block). He
would be at risk of deterioration in his EF from chronic RV pacing, and thus it
would be reasonable to consider a CRT device. The first patient’s indication for a
pacemaker is sick-sinus syndrome and thus he would not be expected to pace the
ventricle. The second patient has a narrow QRS and no pacing indication. Neither
of these patients would likely benefit from CRT.
References
1. Moss AJ, Hall WJ, Cannom DS, Klein H, Brown MW, et al. Cardiac-resynchronization therapy
for the prevention of heart-failure events. N Engl J Med. 2009;361(14):1329–38. PMID:
19723701.
2. Cleland JG, Daubert JC, Erdmann E, Freemantle N, Gras D, et al. The effect of cardiac
resynchronization on morbidity and mortality in heart failure. N Engl J Med. 2005;352(15):
1539–49. PMID: 15753115.
3. Epstein AE, DiMarco JP, Ellenbogen KA, Estes 3rd NA, Freedman RA, et al. 2012 ACCF/
AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for device-
based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology
Foundation/American Heart Association task force on practice guidelines and the heart rhythm
society. J Am Coll Cardiol. 2013;61(3):e6–75. PMID: 23265327.
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Chapter 25
Implantable Cardioverter Defibrillators (ICD)
Camilo A. Gomez
Implantable cardioverter-defibrillators (ICD) are devices designed for the prevention

of sudden cardiac death (SCD) in selected patients. SCD often occurs as a conse-
quence of malignant ventricular arrhythmias as ventricular tachycardia (VT) or VT
that degenerated in ventricular fibrillation (VF). Current ICD’s are capable to deliver
multiple therapies, which incorporate antitachycardia pacing (ATP), cardioversion,
and defibrillation, also provide support in episodes of bradycardia or heart block
with a rate-response pacing and automatic switching mode function. Modern devices
are able to provide resynchronization therapy, an important option in selected
patients requiring advanced heart failure therapies [1].
Indications
ICD’s are currently indicated for the prevention of SCD. In survivors of VT/VF
cardiac arrest, ICD’s are the optimal treatment for “secondary prevention” of
patients. ICD’s are also recently used as “primary prevention” in patients who are
considered to be at high risk for VT/VF.
The use of ICD as secondary prevention is supported by multiple randomized
controlled trials and has the benefit in patients with marked reduction of left ven-
tricular function. The use of ICD for primary prevention currently represents more
than 80 % of its implantation.
There are other high risk conditions that are known to be associated with SCD,
as patients with structural heart disease or inherited channelopathies.
C.A. Gomez, MD
Division of Cardiology, University of Miami Miller School of Medicine,
Jackson Memorial Hospital, 1611 NW 12 Ave,
Central Bldg. Rm. 409, Miami, FL 33136, USA

DOI 10.1007/978-1-4471-7290-1_25
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212 C.A. Gomez
Consideration of ICD therapy, particularly those for primary prevention apply

only to patients who are receiving optimal medical therapy, have a reasonable
expectation of survival with good functional status for more than 1 year, and an
independent risk assessment, including patient preference (See Table 25.1) [2, 3].
Table 25.1 ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities
CLASS I INDICATIONS evidence and/or general agreement that ICD’s are useful and
effective
1. Survivors of cardiac arrest due to ventricular fibrillation or hemodynamically unstable
sustained VT after evaluation to define the cause of the event and to exclude any completely
reversible causes
2. Structural heart disease and spontaneous sustained VT, whether hemodynamically stable or unstable
3. Syncope of undetermined origin with clinically relevant, hemodynamically significant
sustained VT or ventricular fibrillation induced at electrophysiological study
4. LVEF less than or equal to 35 % due to prior myocardial infarction who are at least 40 days
post–myocardial infarction and are in NYHA functional Class II or III
5. Nonischemic dilated Cardiomyopathy who have an LVEF less than or equal to 35 % and who
are in NYHA functional Class II or III
6. LV dysfunction due to prior myocardial infarction who are at least 40 days post–myocardial
infarction, have an LVEF less than or equal to 30 %, and are in NYHA functional Class I
7. Nonsustained VT due to prior myocardial infarction, LVEF less than or equal to 40 %,
and inducible ventricular fibrillation or sustained VT at electrophysiological study
CLASS IIa INDICATIONS conflicting evidence about the usefulness of ICD therapy,
with the weight of evidence/opinion in favor of usefulness/efficacy
1. Reasonable for patients with unexplained syncope, significant LV dysfunction, and
nonischemic cardiomyopathy
2. Reasonable for patients with sustained VT and normal or near-normal ventricular function
3. Reasonable for patients with hypertrophic cardiomyopathy who have 1 or more major risk
factor for SCD
4. Reasonable for the prevention of SCD in patients with arrythmogenic RV dysplasia who have
1 or more risk factors for SCD
5. Reasonable to reduce SCD in patients with long-QT syndrome who are experiencing syncope
and/or VT while receiving beta blockers
6. Reasonable for non hospitalized patients awaiting for transplantation
7. Reasonable for patients with Brugada syndrome with syncope or who have documented VT
that has not resulted in cardiac arrest
8. Reasonable for patients with catecholaminergic polymorphic VT who have syncope and/or
documented sustained VT while receiving beta blockers
9. Reasonable for patients cardiac sarcoidosis, giant cell myocarditis, or Chagas disease
CLASS IIb INDICATIONS usefulness/efficacy is less well established by evidence/opinion
1. Considered in patients with nonischemic heart disease who have an LVEF of less than or
equal to 35 % and who are in NYHA functional class I
2. Considered for patients with long-QT syndrome and risk factors for SCD
3. Considered in patients with syncope and advanced structural heart disease in whom through
invasive and noninvasive investigations have failed to define a cause
4. Considered in patients with a familial cardiomyopathy associated with SCD
5. Considered in patients with LV noncompaction
From Ref. [1]
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25 Implantable Cardioverter Defibrillators (ICD) 213
Table 25.2 CLASS III conditions for which there is a general agreement that ICD’s are not useful
and possibly harmful
1. Not indicated for patients who do not have a reasonable expectation of survival with an
acceptable functional status for at least 1 year, even if they meet ICD implantation criteria
2. Not indicated for patients with incessant VT or VF
3. Not indicated in patients with significant psychiatric illnesses that may be aggravated by
device implantation or that may preclude systematic follow-up
4. Not indicated for NYHA class IV patients with drug-refractory congestive heart failure who
are not candidates for cardiac transplantation or CRT-D
5. Not indicated for syncope of undetermined cause in a patient without inducible ventricular
tachyarrhythmias and without structural heart disease
6. Not indicated when VF or VT is amenable to surgical or catheter ablation (e.g., atrial
arrhythmias associated with the Wolff-Parkinson-White syndrome, RV or LV outflow tract
VT, idiopathic VT, or fascicular VT in the absence of structural heart disease)
7. Not indicated for patients with ventricular tachyarrhythmias due to a completely reversible
disorder in the absence of structural heart disease (e.g., electrolyte imbalance, drugs, or
trauma)
From Ref. [1]
Contraindications
Major ICD implantation contraindications are included in the ACC/AHA/HRS

guidelines (See Table 25.2). Other contraindications are: Hemodynamically unstable
patients, in the setting of acute myocardial ischemia or hypoxia, post coronary artery
bypass surgery, in the setting of active infection in the chest wall or bloodstream
infections, with electrolyte imbalances and with drug toxicities [2, 3].
Equipment
The physical components of the implanted system consist of:

1. ICD generator: consist of a battery, capacitor, DC-DC converter, a microprocessor,
and telemetry communication coils an their connections (Fig. 25.1).
2. Sensing and the pacing leads, and one or more high energy leads (also known as
electrodes). These elements deliver the three essential functions of the ICD,
detection, tachycardia therapy and bradycardia pacing (Fig. 25.2) [3, 4].
Technique
Implantation of the ICDs system involves its subcutaneous insertion, positioning

of the leads and finally testing the sensing and pacing functions. Usually are
implanted in the left pre-pectoral area with the purpose to create a left-to-right
vector for defibrillator shocks, the right pectoral area may be used in selected
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214 C.A. Gomez
Fig. 25.1 ICD generator

that is implanted
subcutaneously in the
prepectoral region, it is
replaced when battery ends
life. Has and has an upper
portion with connectors
were the leads are attached
Fig. 25.2 Different examples of leads that has pacing and sensing capabilities, which exist in dif-
ferent shapes according the chamber were they are placed (atrium or ventricles) and distal portions
with different end tip electrodes for active or passive fixation
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left-handed patients or when left venous access is impeded, in cases of infection

or any other abnormalities. Initially with an standard sterile technique, an incision
is made in the left pre-pectoral area, the subclavian, cephalic or both veins are
dissected, once the vein (s) are exposed leads can be inserted transvenously.
Cephalic vein access is preferred over subclavian because carries a smaller risk of
arterial puncture, pneumothorax and subclavian crush injury at long term, which
occur when the inserted leads are trapped within the subclavius muscle or the
costoclavicular complex. Once the vein is incised the leads are advanced under
fluoroscopic guidance into the right heart until reach the pulmonary artery. then
the lead is pulled back and fixed in the right ventricle (RV) apex. Subsequently
lead positioning, electrocardiogram stability and adequate sensing and pacing
parameters are confirmed. When dual-chamber ICD are implanted require the
insertion of an additional atrial lead, it is placed following the insertion of the
ventricular lead, and should be placed in the high right atrium or in the superior
aspect of the atrial appendage to avoid cross-talk between atrial stimuli and the
ventricular detection circuits. The sleeve of the lead is anchor using silk sutures to
the surrounding muscular fascia.
After vascular access, a pocket is created were the generator will be seated,
it should be of adequate size for the device to avoid device erosion, migration
or seroma formation, it is usually on the medial aspect anterior to the plane of
the pectoral fascia, it should be inferior to the clavicle and in a medial position
to avoid restriction of movement of the shoulder and the arm. The leads then
are connected to the generator header, insertion in the correct ports and
securely connection is verified, pocket is clean for tissue, secretions and blood
that may be interposed. An antibiotic solution is used to irrigate the port and
the generator is placed in the pocket. Device is tested for sensing, pacing and
DFT, once adequate device function is confirmed the pocket is closed with
sterile suture.
Patient’s arm is placed in a sling, lead position is confirmed by immediate postop
chest x ray and also to rule out complications as pneumothorax. Before discharge
postero-anterior and lateral chest x ray are performed (Fig. 25.3) [4, 5].
Data Interpretation
Patients are follow up with routine clinical visits usually at quarterly intervals.
Devices are interrogated to evaluate its function, battery depletion, alarms and
events. Also gives the advantage of monitoring comorbidities measuring physiolog-
ical parameters in conditions as heart failure and atrial fibrillation. Furthermore
there are devices with remote internet based functions that permits automatically
transmit stored data by wireless telemetry.
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216 C.A. Gomez
Fig. 25.3 X-ray of a

patient post single chamber
ICD implantation. All parts
of the ICD system can be
appreciated, the generator
with a single lead directed
and attached in position at
the apex of the right
ventricle
Complications
• Surgical related: Ranges between 3 and 5 % for single or dual-chamber ICDs.

Complications are similar to those of pacemaker implantation: cardiac perfora-
tion, tamponade, vascular perforation, pneumothorax, hematoma, infection and
lead dislodgment. Pulse generator changes adds a 1–4 % risk of infection, and
complications can increase up to 15 % when a new transvenous lead is added at
the time of replacement.
• Late complications: less than 4 % and include lead fracture, generator migration/
erosion, generator failure, thrombosis, and complications related to defibrillation
testing as myocardial or cerebral ischemia, electromecanical dissociation and
refractory VF (4, 6).
Clinical Vignettes
Case 1
A 55 year old male was admitted with substernal chest pain radiated to the left arm
for 30 min. Vitals at admission were blood pressure of 88/50, heart rate of 98 and
respiratory rate of 22. The electrocardiogram showed ST elevation in anterior leads
(V1–V4), troponin was found elevated. Emergent cardiac catheterization was per-
formed with percutaneous intervention of a completely occluded left anterior
descending artery by a thrombus. Post MI echocardiogram showed an ejection frac-
tion of 15–20 % with severe akinesis of the anterior wall. The patient was discharged
with dual antiplatelet agents, beta blocker, statin and ace- inhibitor. Forty days post
MI was seen in the clinic, echocardiogram was performed and showed an EF of
20–25 %.
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The patient has cardiomyopathy, with an EF less than 35 % and is 40 days post
MI, is functional class II and therefore should received an ICD for primary preven-
tion of SCD.
Case 2
A 30 year old male with no known medical conditions, suddenly collapse at home,
CPR was started by one of his family members. When EMS arrived at the scene, he
was found with ventricular fibrillation and was shocked 2 times before the return of
spontaneous circulation. He was taken to the hospital, and admitted to the cardiac
intensive care unit. Initial echocardiogram showed and EF of 10 % with global
hypokinesis post cardiac arrest. He progressively recovered over the following 2
weeks without neurological deficits, but the cause of cardiac arrest couldn’t be clar-
ify after extensive cardiac workup. Repeat echocardiogram showed an EF of 55 %
with a normal ventricular wall motion.
An ICD is indicated in patients such as this, who are survivors of cardiac arrest
due to VF or hemodynamically unstable sustained VT after evaluation to define the
cause of the event and to exclude any completely reversible causes.
References
1. Miller J, Yousuf O, Berger R. The implantable cardioverter-defibrillator: an update. Trends

Cardiovas Med. 2015;25:606–11.
2. Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS 2008 guidelines for device-
based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology/
American Heart Association task force on practice guidelines (writing committee to revise the
ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiar-
rhythmia devices) developed in collaboration with the American Association for thoracic sur-
gery and society of thoracic surgeons. J Am Coll Cardiol. 2008;51(21):e1–62.
3. Griffin B, Callahan T, Menon V, et al. Manual of cardiovascular medicine. Philadelphia:
Lippincott Williams & Wilkins; 2013.
4. Swerdlow C, Friedman P. Cardiac electrophysiology: from cell to bedside. Philadelphia:
Elsevier; 2014.
5. Ellenbogen KA, Kay GN, Lau C, et al. Clinical cardiac pacing, defibrillation and resynchroni-
zation therapy. Philadelphia: Elsevier Saunders; 2011.
6. Lee D, Krahn A, Healey J, et al. Evaluation of early complications related to de novo cardio-
verter defibrillator implantation. J Am Coll Cardiol. 2010;55:774–82.
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Chapter 26
Pacemaker Interrogation and Programming
D. Michael Farmer and Munther Homoud
Introduction
Pacemaker programming and interrogation is essential not only in the immediate

post-implantation period, but also at regular follow-up visits throughout the life of
the pacemaker. The implantation of a pacemaker follows a clinical event and it is
incumbent upon the physician implanting the device to insure that the device has
met its clinical goals. Current pacemakers are endowed with a variety of features to
help meet the aforementioned requirement. Hence, patients with pacemakers should
be seen regularly and their pacemakers should be interrogated with each visit.
Indications
Pacemaker function post-implant should be observed on cardiac telemetry prior to

discharge. In patients who are not pacemaker dependent, an electrocardiogram per-
formed with a magnet applied against the pacemaker will elicit a pacing spike from
the chamber being paced.
Following discharge, patients are often seen 1–2 weeks after the implant to assess
the site of the incision. The patient will then follow-up in an outpatient setting for
pacemaker interrogation in 6 weeks. This follow-up is important because it assesses
the rise and subsequent decline in pacing thresholds. The pacemaker generator out-
puts can then be programmed to outputs lower than those programmed at implant.
D.M. Farmer, MD
Cardiac Electrophysiology Laboratory, Mount Auburn Hospital, Cambridge, MA, USA
M. Homoud, MD (*)
New England Cardiac Arrhythmia Center, Tufts Medical Center, Boston, MA, USA

DOI 10.1007/978-1-4471-7290-1_26
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220 D.M. Farmer and M. Homoud
This process preserves generator battery life while providing an adequate safety
margin for expected fluctuations in the pacing thresholds.
After this initial outpatient interrogation is performed, Medicare and Medicaid
guidelines allow for dual chamber devices to be followed up every 6 months. Patients
with single chamber pacemakers who are not pacemaker dependent may follow-up on
an annual basis. During these visits, the original indications for pacemaker implant, as
well as the need for modification of the existing pacemaker system should be assessed.
Modifications may include the need to adjust the lower pacing rate, the upper tracking
rate, or the AV interval. The activity sensor may need to be turned on if the patient is
complaining of fatigue. The sensor parameters should be tested in the pacemaker
clinic by observing the patients’ heart rate response to graded activity. The develop-
ment of new clinical events such as heart failure or the recovery from an acute myo-
cardial infarction may prompt an upgrade of the pacemaker to an implantable
cardioverter defibrillator (ICD) or a pacemaker capable of biventricular pacing.
Beyond routine follow up, certain events warrant interrogation of a pacemaker.
Pacemaker interrogation should be performed when a clinical event has occurred
that could have been cause by pacemaker malfunction, e.g. syncope, or when a
clinical event can be further delineated by intra-cardiac electrograms that can be
retrieved during pacemaker interrogation. Intra-cardiac electrograms retrieved from
pacemakers can be useful in differentiating supraventricular tachycardias from ven-
tricular tachycardias, as well as excluding arrhythmias as a source of syncope in
patients with a pre-existing pacemaker.
A variety of procedures performed in the hospital may interfere with the pace-
maker’s normal function or may damage a pacemaker. The pacemaker should be
interrogated before and after certain types of procedures are completed. Examples of
such procedures include radiofrequency ablation, cardioversion, diathermy, electro-
convulsive therapy (ECT) and lithotripsy. Patients scheduled for surgery who are
pacemaker dependent should have their pacemakers programmed to an asynchro-
nous mode if the use of diathermy is anticipated. This would eliminate the fear that
diathermy would inhibit pacing. The patient should be continuously monitored in
case asynchronous pacing induces an arrhythmia. At the time of this writing, MRI
scanning in patients with pacemakers should be restricted to patients who have
received pacemakers and leads that have been approved for conditional use in the
MR environment. It is important for the provider ordering the MRI confirm that the
patient not have an older, non MRI compatible lead before proceeding with the study.
If a patient with a pacemaker lacking conditional approval inadvertently has an MRI
performed, the pacemaker should be promptly interrogated to determine its status.
Equipment
Pacemaker interrogation requires company-specific device programmers.

Pacemaker interrogation and programming cannot occur between products from
two different device companies. Although, there are several pacemaker companies
ERRNVPHGLFRVRUJ
26 Pacemaker Interrogation and Programming 221
Fig. 26.1 Pacemaker

interrogation
(Medtronic®, Boston Scientific®, Biotronik® and St. Jude Medical®) widely

used in the US, the techniques for pacemaker interrogation and concepts for pace-
maker data interpretation are similar. Each programmer is equipped with a pro-
gramming head, surface ECG leads, power cord, printer, and touch-screen
programmer (Fig. 26.1). Clinics where pacemaker interrogation is performed must
be equipped with an external defibrillator in the rare event the patient develops a
life threatening arrhythmia.
Technique
Pacemaker interrogation can be performed in either the sitting or supine position.

ECG surface leads should be connected to the patient and the programmer using
the device specific electrodes. The pacemaker programming head should be
placed over the patient’s pacemaker. The pacemaker is usually located in either
pectoral region, or rarely in the abdomen. The programming head should be posi-
tioned in a stable manner, such that constant telemetry can be maintained between
the device and programmer. Once the programmer is turned on, interrogation can
then proceed. Many newer programmers have automated follow up algorithms
that proceed once prompted by the operator.
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Data-Interpretation
Once device interrogation has occurred, baseline data should be ascertained and
lead testing should be performed. This data and testing results are essential in
evaluating a variety of pacemaker malfunctions. All available data should be sys-
tematically retrieved and evaluated during each pacemaker interrogation. The core
of this evaluation includes battery life, lead impedances, as well as capture and
sensing thresholds. The underlying rhythm of the patient, as well as lead configura-
tion (unipolar or bipolar) should also be determined. In addition, most pacemakers
have stored electrogram events that need to be retrieved and evaluated at each
interrogation.
Battery Status
Pacemaker battery status should be evaluated with each interrogation. At the

beginning of life (BOL) the battery voltage is approximately 2.8 V (specific val-
ues vary from manufacturer to manufacturer), and pacemaker behavior is as pro-
grammed. Over the life of the pacemaker, the battery reaches elective replacement
indicators (ERI). At ERI, the battery voltage is reduced, but still able to support
most if not all of the pacemaker functions. At this point, generator replacement
should be scheduled in weeks to months depending upon the degree of depen-
dence upon the pacemaker. As voltage reduces further, battery end of life (EOL)
is reached. At this junction, the voltage is unable to support basic pacer function,
and immediate generator change is required. It usually takes 3–6 months for the
pacemaker battery to reach EOL status after the battery reaches ERI. Another
parameter used to determine the pacemaker’s battery status is the battery’s imped-
ance. As the battery voltage declines, the battery impedance rises.
Lead Impedance
While different leads offer differ impedances, once a lead is implanted, the fluc-
tuation of impedance is very narrow. The lead impedance of each implanted lead
should also be measured during each interrogation. Lead impedance is the sum of
all factors that retard current flow. Very high lead impedances suggest the exis-
tence of lead fractures or a loose connection in the device header (between the
lead pin and the set screw). Very low lead impedances suggest insulation failure.
The change in impedance from a previous recording is more important than the
absolute value of the lead impedance. Changes greater than 300 Ω are abnormal
and should prompt further evaluation.
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Sensing and Pacing Thresholds
Although many devices have automated evaluations of pacing and sensing thresh-
olds, many require manual pacing and sensing threshold determinations. Sensing is
the ability of the pacemaker to detect and respond to intrinsic atrial and ventricular
activity. Sensing thresholds are unable to be assessed without the presence of native
atrial and/or ventricular activity. Most current programmers will automatically
check the amplitude of the underlying atrial or ventricular electrograms by tran-
siently inhibiting pacing or lowering the pacing rate in the respective chambers.
This would allow the emergence of the underlying rhythm and measurement of its
amplitude as sensed by the pacemaker in its respective chamber. Two other tech-
niques can be used used to evaluate sensing thresholds if the programmer lacks the
automated mode. One technique involves recording telemetered electrograms and
measuring peak-to-peak amplitudes of the resulting signal. The more common tech-
nique utilized in both automated and semi-automated fashions, is to progressively
reduce the sensitivity setting of the pacemaker until an inappropriate spike is deliv-
ered indicating that the pacemaker no longer senses an intrinsic electrical activity in
the chamber being tested. To use this method to assess ventricular sensing manually,
the pacing rate needs to be programmed to a rate below the patient’s intrinsic heart
rate. The patient’s dependency upon the pacemaker can also be assessed during this
maneuver. By programming the ventricular chamber to a less sensitive mode
(increasing the millivolt values) in the VVI mode the sensitivity value (in mV) at
which an inappropriate pacer output is displayed corresponds to the sensing thresh-
old of the ventricle. Atrial sensing thresholds can be manually determined in a simi-
lar fashion.
The capture threshold is the lowest pacing output that results in consistent cap-
ture of myocardium. This capture threshold is a measurement of the least amount of
energy that is required to consistently cause myocardial depolarization. This energy
is a function of current, voltage and pulse duration or width. Capture is reported in
both voltage and pulse duration. Both of these parameters can be independently
programmed. When determining capture threshold it is most commonly reported as
voltage threshold at a given pulse duration. It can also be reported as pulse duration
threshold at a given voltage. The relationship between these two parameters is
defined as the strength-duration curve. The curve is automatically created after
threshold testing with some Medtronic devices (Fig. 26.2). Manually, capture
threshold is determined by pacing the desired chamber at a rate higher than the
intrinsic rate while progressively decreasing the output (amplitude or pulse dura-
tion) until capture is lost (Fig. 26.3). The lowest voltage at which capture consis-
tently occurs is the capture threshold. Conversely, capture threshold can be testing
by progressively decreasing pulse duration. In most patients, especially those who
are pacemaker dependent, programming should provide a 2:1 safety margin in volt-
age threshold. Some pacemaker systems automatically monitor capture thresholds
and automatically adjust the output based on detected changes.
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Fig. 26.2 Strength-

duration curve
Fig. 26.3 Capture threshold determination. With decreasing output voltage, capture is lost at
2.7 V, noted by absence of ventricular capture at the right side of the electrogram
The basics of pacemaker interrogation are the assessment of battery voltage, lead
impedances, sensing thresholds, and capture thresholds. During each pacemaker
evaluation it is also important to evaluate all baseline programmed parameters.
These parameters include pacing mode, lower rate limit, upper rate limit, AV delay,
voltage output, and sensitivity. The inadvertent exposure to eletromechanical inter-
ference may result in inadvertent programming of various pacing parameters.
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Event Markers and Electrograms
Current devices all have the capability for electrogram storage. Event markers are
displayed on the programmer screens and intracardiac electrograms. These event
markers report behavior of the pacemaker in regards to paced and sensed events
using alphanumeric labeling. The interpretation of these markers during real-time
evaluation as well as in the assessment in the evaluation of stored events is crucial
in the pacemaker interrogation.
Rate-Adaptive Pacing and Mode Switching
Two additional basic concepts are important to evaluate during pacemaker program-
ming. The DDDR or VVIR modes are rate-adaptive pacing modes. Rate adaptive-
pacing provides a heart rate response to meet the increased metabolic requirements for
those patients with chronotropic incompetence during physical activity. Commercially
available sensors include accelerometers that respond to upper body movement or
minute ventilation that responds to changes in transthoracic impedance. They attempt
to provide input to the pacemaker modulating the heart rate to meet the body’s meta-
bolic requirements. Specific algorithms then convert this data to a heart rate response
in attempt to simulate the heart’s normal response. Programming the DDDR or VVIR
mode to DDD or VVI, respectively, can turn off these sensors.
Most patients known to have supraventricular tachycardias, especially atrial fibrilla-
tion, have mode switching programmed on. Without mode-switching algorithms, inap-
propriate tracking of rapid atrial activity would cause pacing at the upper rate limit.
When rapid atrial activity occurs, as in atrial fibrillation, the pacing mode is switched
from the DDDR to VVIR or DDIR mode depending on pre-programmed parameters.
Troubleshooting
The two following clinical vignettes give two examples of how pacemaker interro-
gation can be useful in clinical diagnosis. Figure 26.4 is a real time intra-cardiac
electrogram with event markers from an 82-year-old patient s/p permanent pace-
maker who presented to pacemaker clinic for routine follow-up. The intracardiac
electrograms reveal atrial undersensing as clearly indicated by the absence of atrial
channel markers when native activity is present. By decreasing the sensing millivolt
value, the sensitivity is increased and normal pacing function resumed.
Figure 26.5 is a real time intracardiac electrogram from a patient s/p a single
chamber device who was found to have pauses on telemetry while being hospital-
ized for an episode acute renal failure. Event markers revealed evidence of failure to
capture. Voltage output was subsequently increased. This maneuver coupled with
the resolution of electrolyte abnormalities restored normal pacemaker activity.
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Fig. 26.4 Intermittent ventricular capture
Fig. 26.5 Atrial undersensing: atrial activity is present, but is intermittent on the channel markers
at bottom
ERRNVPHGLFRVRUJ
Clinical Vignettes
Case 1
A 35 year old man with complete AV block, pacemaker dependency, contacts the
pacemaker clinic to inform them that earlier in the day he had an unheralded synco-
pal episode. This resulted in a laceration on his forehead. The day before, he reported
two presyncopal spells. He had never had any prior episodes. He is known to have
had obstructive hypertrophic cardiomyopathy and left bundle branch block and had
undergone alcohol septal ablation 5 years ago. The procedure was followed by the
development of complete AV block requiring the implantation of a pacemaker.
Upon interrogation of his pacemaker, the RV pacing threshold was seen to have
climbed from 0.7 volts at 0.4 ms. measured 4 weeks ago to 5.2 volts at 0.4 ms.
Furthermore, the PM interrogation intermittently registered high right ventricular
lead impedances. Pacemaker interrogation does not show that he has had any ven-
tricular arrhythmias. His underlying rhythm is sinus with complete AV block and no
escape greater than the lowest pacing rate the pacemaker could be programmed to.
Elevation of pacing impedance when coupled with elevation of pacing threshold in
a lead that has not been recently implanted, raises the concern for a fractured lead.
The unheralded syncopal episode along with the two preceding presyncopal spells,
point to a recent fracture. The patient is pacemaker dependent, and was admitted so
that a new lead could be implanted. While awaiting lead implantation, the imped-
ance and pacing threshold of the RV lead can be tested in unipolar mode. If the
pacing threshold and impedance are within normal in the unipolar mode, a tempo-
rary pacemaker can be avoided. This observation points to fracture of the outer coil.
In this patient, a chest X-ray demonstrated the fracture.
Case 2
Seven years after a 78-year old hypertensive male patient receives a dual chamber
pacemaker for complete AV block he contacts the PM clinic complaining of a 1-week
history of fatigue and shortness of breath. Examination reveals an otherwise healthy
man with a BP 110/70 mmHg and a pulse 65 bpm. An electrocardiogram demon-
strates sinus rhythm, complete AV block and ventricular pacing at 65 bpm in a VVI
mode. Given the age of this pacemaker, the battery most likely crossed the elective
replacement interval (ERI). Pacemakers are programmed to revert to a mode that
would consume less energy, slowing down impending battery depletion, conse-
quently, the shift to the VVI mode. However, upon losing atrioventricular synchrony,
symptoms not unlike those of heart failure can be provoked. Once a new, dual cham-
ber PM was implanted, the patient’s symptoms were completely relieved.
ERRNVPHGLFRVRUJ
Suggested Reading
1. Kenneth A. Ellenbogen MD, Bruce L. Wilkoff MD, G. Neal Kay MD, Chu-Pak Lau MD and
Angelo Auricchio MD, PhD. Clinical Cardiac Pacing, Defibrillation and Resynchronization
Therapy. 5th ed. Philadelphia: Elsevier; 2017:1031–063.
2. Ellenbogen KA, Kaszala K. Cardiac pacing and ICDS. 6th ed. Hoboken: Wiley Blackwell
Publishing; 2014:272–322.
3. Kusumoto FM, Goldschlager NF. Cardiac pacing for the clinician. 2nd ed. New York: Springer;
2008:647–694.
ERRNVPHGLFRVRUJ
Chapter 27
Cardioversion and Defibrillation
Aaron E. Brice
Cardioversion and defibrillation are both techniques of terminating cardiac

arrhythmias. Direct current (DC) cardioversion uses the discharge of electrical
energy through the myocardium to terminate certain arrhythmias. In DC cardio-
version shock delivery is synchronized with the QRS complex to avoid provoking
ventricular fibrillation (VF). If a shock is given during the vulnerable refractory
period of ventricular repolarization, VF may result [1]. In comparison defibrilla-
tion uses no synchronization and the shock is given randomly in the cardiac cycle.
Monophasic and biphasic waveforms have been shown to be effective in cardio-
version and defibrillation. In the use of biphasic waveforms current polarity
becomes reversed which more consistently terminates arrhythmias with less
energy delivered.
Indications
Cardioversion is effective in eliminating arrhythmias caused by a reentrant circuit

by depolarizing all tissue in the circuit and inducing a refractory period which
breaks the circuit. Cardioversion is therefore only indicated for specific arrhythmias
(Table 27.1). Defibrillation may be employed in cardiopulmonary resuscitation and
is indicated for VF, pulseless ventricular tachycardia (VT), and polymorphic VT. In
cases of hemodynamic instability, angina, or heart failure caused by tachyarrhyth-
mias immediate shocks are indicated. In the absence of such features cardioversion
may be done electively. Appropriate timing of cardioversion, use of vagal maneu-
vers, and medications including antiarrhythmics are specific for each arrhythmia.
A.E. Brice, MD
University of Miami Miller School of Medicine, 1611 NW 12th Ave,
Central Building Suite 600-D, Miami, FL 33136, USA

DOI 10.1007/978-1-4471-7290-1_27
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230 A.E. Brice
Table 27.1 Type of arrhythmia and response to cardioversion/defibrillation [1]

Reentrant (shockable) Ventricular fibrillation
Most ventricular tachycardias
Atrial fibrillation
Atrial flutter
AV reentrant tachycardia (AVRT)
AV nodal reentrant tachycardia (AVNRT)
SA nodal reentrant tachycardia
Automatic (not shockable) Sinus tachycardia
Junctional tachycardia
Atrial tachycardia
Accelerated idioventricular rhythm
Contraindications
There are few absolute contraindications to cardioversion and defibrillation. Patients

with digitalis overdose or electrolyte abnormalities including hypokalemia are at
increased risk of developing VF or VT with cardioversion. The procedure should be
deferred if possible until these are corrected. Atrial fibrillation of unknown or pro-
longed duration should not be cardioverted without first taking appropriate steps to
reduce risk of thromboembolism. Caution must be taken in patients with severe
disease of the cardiac conduction system as a shock may precipitate bradyarrhyth-
mia and temporary pacing capabilities should be on hand. Sinus tachycardia may be
a physiologic response to a specific cause such as hypotension and should not be
confused with a rhythm treatable with cardioversion.
Patients with implantable cardioverter/defibrillators (ICD) or pacemakers can
undergo DC cardioversion but the electric charge may disrupt computer program-
ming or damage the device. If cardioversion is performed interrogation must be
completed afterward. Pregnancy also is not a contraindication to cardioversion or
defibrillation but fetal heart rate should be monitored during the procedure.
Equipment
External cardioversion and defibrillation normally employ pads or paddles that are
pressed to the skin and connected by cables to a case housing the computer, energy
source, and cardiac monitor (Fig. 27.1). Devices manufactured prior to 2000 nor-
mally use monophasic waveforms and those made after use biphasic waveforms.
Electrode types include handheld paddles that use electrically conductive gel and
self-adhesive pads which stick to the patient’s skin [2].
Equipment for monitoring heart rhythm and vital signs should be available along
with supplies needed for an emergency response including a code cart for advanced
cardiac life support, temporary pacing, and airway equipment. Supplemental
ERRNVPHGLFRVRUJ
27 Cardioversion and Defibrillation 231
Fig. 27.1 Portable

cardioverter/defibrillator
oxygen should be present. Clippers for removing excess hair may be necessary for
application of adhesive pads and to reduce electrical impedance. If procedural seda-
tion is to be performed the appropriate sedative and analgesic agents must be
available.
Technique
Intravenous access, cardiac telemetry, and vital signs monitoring must be present
throughout the procedure. A 12-lead electrocardiogram should be done prior to and
following cardioversion. To reduce the risk of aspiration patients should not eat or
drink for at least 6 h before elective cardioversion. Supplemental oxygen should be
removed prior to discharge of any electrical energy due to the risk of fire.
Procedural sedation is commonly performed as cardioversion may cause pain,
anxiety, and unpleasant memories. Commonly used agents with initial dose in mg/
kg include midazolam (0.02–0.03), fentanyl (0.5–1.0), etomidate (0.1–0.15), ket-
amine (1.0–2.0), and propofol (0.5–1.0).
Proper electrode placement is important for successful cardioversion as this
determines the pathway of current [3]. Pads are primarily placed in two positions,
antero-lateral and antero-posterior (Fig. 27.2). If an ICD or pacemaker is present
pads or paddles should not be placed directly over the device and the antero-posterior
position may be favored. Pad placement should also avoid breast tissue.
The initial amount of energy selected will depend on the arrhythmia being treated
(Table 27.2). Higher energy levels have greater effectiveness in terminating the
arrhythmia but are more likely to result in complications. The lowest energy should
be used that is effective in eliminating the abnormal rhythm.
The synchronization function should be selected for cardioversion and the car-
diac monitor should be checked to verify the arrhythmia is still present. The
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232 A.E. Brice
Fig. 27.2 Correct pad placement
Table 27.2 Suggested initial energy for cardioversion/defibrillation [1]

Arrhythmia Biphasic waveform Monophasic waveform
Atrial fibrillation 120–200 J 200 J
Atrial flutter 50–100 J 50–100 J
AVNRT, AVRT 50–100 J 50–100 J
Monomorphic VT with pulse 100 J 100 J
Polymorphic VT and pulseless VT 120–200 J 360 J
Ventricular fibrillation 120–200 J 360 J
capacitor may then be charged and all personnel should be cleared and avoid contact
with the patient or bed. The clinician may then manually press the button to dis-
charge a shock. The monitor should be checked after shock delivery to verify termi-
nation of the arrhythmia. If the arrhythmia is still present the energy level should be
escalated in a stepwise fashion and repeat shock delivered with a minimum of
1 minute between shocks.
Data Interpretation
If the device cannot synchronize with the QRS complex the electrical deflections
may be too small to capture and the clinician should reposition the pads placing
them closer to the patient’s heart.
When evaluating the post cardioversion electrocardiogram temporary ST eleva-
tions and depressions or T wave changes may be noted. This usually occurs in the
absence of cardiac biomarker elevation and is a nonspecific finding rarely due to
myocardial injury [4].
Cardiac monitoring commonly displays arrhythmias after cardioversion.
Malignant arrhythmias such as VF and sustained VT must be quickly recognized
ERRNVPHGLFRVRUJ
27 Cardioversion and Defibrillation 233
and treated with defibrillation. Sinus arrest and other bradyarrhythmias may occur
but are usually of short duration; if persistent, cardiac pacing may be required.
Complications
Transcutaneous discharge of electrical energy may result in pain and first-degree

burns at the site of shock delivery and is related to the amount of energy used. Good
contact with the defibrillator pad/paddle and skin is essential. Improper pad place-
ment and use of monophasic waves increase this risk. Cutaneous burns may be best
treated with a cream, such as Silvadene. Myocardial necrosis may manifest as a
small elevation in cardiac biomarkers. This is usually due to high energy discharge.
Thromboembolism is a risk in patients with atrial fibrillation or atrial flutter
treated with cardioversion. Risk is reduced with 4–6 weeks of anticoagulation or
transesophageal echocardiogram confirming absence of clot in the left atrium.
Hypotension may be seen after cardioversion and is usually brief and responsive
to IV fluids. Pulmonary edema is infrequently encountered and may be due to left
ventricular dysfunction or decreased atrial mechanical activity after shock.
Clinical Vignettes
Case 1
A 67-year-old man is brought to the emergency department by his wife for worsening
weakness, shortness of breath, and palpitations. He believes his symptoms began
about 2 days ago but is not certain. He has diabetes and heart failure with an ejec-
tion fraction of 45 % measured 4 months ago. His medications are carvedilol, lisino-
pril, and metformin. On physical exam he is afebrile, blood pressure is 74/52, heart
rate is 122, respiratory rate is 32, and oxygen saturation is 82 % on face mask.
Cardiac exam discloses an irregularly irregular rhythm and on lung auscultation
rales can be heard bilaterally. Laboratory studies are pending. Electrocardiogram
shows an irregularly irregular narrow complex tachycardia.
This patient has atrial fibrillation with rapid ventricular response that is hemody-
namically unstable. Synchronized DC cardioversion should be quickly delivered.
He is hypotensive and ventricular rate control with a nondihydropyridine calcium
channel blocker or beta blocker should not be attempted. Unlike the present case, an
elective transesophageal echocardiogram or prolonged anticoagulation are pre-
ferred, when feasible, to reduce the risk of thromboembolism in stable patients with
atrial fibrillation for more than 48 hours. However, immediate synchronized cardio-
version is indicated in unstable and symptomatic patients.
ERRNVPHGLFRVRUJ
234 A.E. Brice
Fig. 27.3 Case 2 cardiac

monitor display
Case 2
A 52-year-old woman undergoes elective cardiac catheterization for evaluation of

coronary artery disease. No obstructive lesions are found but after the procedure
while in the periopertive area she develops chest pain, palpitations, and severe anxi-
ety. On physical exam she is afebrile, blood pressure is 105/72, heart rate is 180,
respiratory rate is 22, and oxygen saturation is 96 % on room air. She appears ner-
vous and cardiopulmonary exam reveals a rapid heartbeat but is otherwise unre-
markable. Serum chemistries are normal. Her cardiac monitor is examined and is
shown in Fig. 27.3. Electrocardiogram prior to catheterization shows normal sinus
rhythm with QTc interval of 410.
This patient has spontaneous polymorphic VT with a normal QT interval. This may
be seen in the setting of structural heart disease, familial syndromes, or coronary
artery disease. She currently has stable blood pressure but may decompensate and
should be shocked with an unsynchronized defibrillation energy level of 120–200 J. In
comparison recommendations for initial energy selection in monomorphic VT with a
pulse are 100 J synchronized. Polymorphic VT is classified according to presence or
absence of QT prolongation. She does not have polymorphic VT with prolonged QT
interval or torsades de pointes which is responsive to magnesium.
References
1. Link MS, Atkins DL, Passman RS, et al. Part 6: electrical therapies: automated external
defibrillators, defibrillation, cardioversion, and pacing: 2010 American Heart Association
Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.
Circulation. 2010;122:S706.
2. Roberts JR, Custalow CB, Thomsen TW, Hedges JR. Defibrillation and cardioversion. In:
Roberts and hedges’ clinical procedures in emergency medicine. 6th ed. Philadelphia: Elsevier
Saunders; 2014.
3. Botto GL, Politi A, Bonini W, et al. External cardioversion of atrial fibrillation: role of paddle
position on technical efficacy and energy requirements. Heart. 1999;82:726.
4. Irwin RS, Rippe JM, Lisbon A, Heard SO. Cardioversion and defibrillation. In: Procedures,
techniques and minimally invasive monitoring in intensive care medicine. 4th ed. Philadelphia:
Wolters Kluwer; 2008.
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Part IV
Interventional Cardiology
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Chapter 28
Coronary Angiography
Nima Aghili, Edouard Daher, and Carey Kimmelstiel
Introduction
Coronary angiography remains the gold standard for evaluation of ischemic heart
disease. For more than 50 years, cardiac catheterization and the invasive evaluation
of coronary arteries has defined the role of a cardiologist and serves as the diagnos-
tic backdrop for coronary intervention and myocardial revascularization.
Indications
Coronary angiography is performed most commonly after non-invasive tests have

shown the presence of coronary artery disease (CAD) in patients presenting with
symptoms of chest pain, despite medical therapy. These noninvasive tests could be
conclusive as to the presence of CAD, and in that case, angiography is performed to
accurately define the coronary arterial anatomy and whether any defined stenoses
are suitable for revascularization to achieve symptom relief. In the case of indeter-
minate non-invasive tests results, coronary angiography is frequently performed
N. Aghili, MD
Tufts Medical Center, 750 Washington Street, Boston, MA 0.2111, USA
E. Daher, MD
Eastlake Cardiovascular Associates, 24211 Little Mack, St. Clair Shores, MI 48080, USA
C. Kimmelstiel, MD (*)

DOI 10.1007/978-1-4471-7290-1_28
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238 N. Aghili et al.
when the index of suspicion for CAD remains high. Occasionally, patients are
referred for coronary angiography in the setting of an emergency such as acute coro-
nary syndromes such as myocardial infarction or unstable angina. Coronary angiog-
raphy is performed in patients with newly diagnosed cardiomyopathy and in cases
of valvular or congenital heart diseases to evaluate for concomitant CAD that might
affect the therapeutic management of these patients, especially when surgical cor-
rection is planned. Coronary angiography is also indicated in recipients of heart
transplant to evaluate for “cardiac allograft vasculopathy” (CAV) which can affect
up to 50 % of patients during the first 10 years following transplantation [1].
Contraindications
The only absolute contraindication for performing coronary angiography, is a men-

tally competent patient that refuses to consent for the procedure. More commonly,
there are relative contraindications for this procedure when the risk of coronary
angiography outweighs the benefit. These include, but are not limited to uncon-
trolled hypertension, uncontrolled ventricular arrhythmias, severe electrolyte
abnormalities, severe bleeding diathesis, history of contrast intolerance, renal
insufficiency, a non-cooperative patient, or one with a febrile condition that has not
been treated. These conditions should be assessed carefully against the potential
benefit of cardiac catheterization. These issues can mostly be addressed and coro-
nary angiography then performed safely once they are corrected or adequately
treated. Of note, a patient that has renal insufficiency but is already contemplating
or undergoing dialysis does not have contraindications for proceeding with coro-
nary angiography. Moreover, in cases where coronary angiography is urgent, such
as in patients presenting with an acute coronary syndrome, coronary angiography
should not be delayed. Instead, efforts should be concentrated on minimizing the
risks associated with the relative contraindications, therefore decreasing the risk of
complications.
Equipment
The fluoroscope and the hemodynamic monitor are the basic components required
to perform a coronary angiogram. Hemodynamic monitoring is performed continu-
ously during the procedure to monitor central and peripheral aortic pressure as well
as heart rate and rhythm. The fluoroscope includes an x-ray tube and generator, and
the image intensifier (Fig. 28.1). The fluoroscope is mounted on a C-arm that rotates
around the patient in a half circle of 180° while the patient is lying supine on the
table. Some labs are equipped with dual x-ray tubes and image intensifiers at a 90°
angle, so that orthogonal views of the coronary arteries can be imaged simultane-
ously, thus reducing procedural time as well as minimizing contrast and radiation
ERRNVPHGLFRVRUJ
28 Coronary Angiography 239
Fig. 28.1 Fluoroscopic

unit
exposure to the patient. A contrast power injector is utilized for ventriculography

and aortography when these procedures are performed.
Images are captured using equipment that store images in a digital format where
they can be displayed off line for further viewing and analysis and where reports are
generated. The hemodynamic data acquired during the case are also digitally stored
(Fig. 28.2). Disposable equipment come in sterile packaging. These include various
supplies such as syringes, needles, wires, manifolds, sutures, clamps, bowls, gauze,
drapes, towels, and catheters (Fig. 28.3). A code cart needs to always be present in
the angiography suite in the event of an emergency such as a cardiac arrest or a
cardiac arrhythmia that requires resuscitation of the patient.
Technique
Coronary angiography is performed via access to the femoral, radial or brachial

artery. For the femoral approach, which is still the dominant route utilized in the
United States, under sterile conditions, the groin is prepped and local anesthesia is
applied. A needle is used to access the femoral artery through which a wire is
advanced into the aorta. Fluoroscopy is used briefly to confirm the position of the
wire in the aorta and the needle is exchanged over the wire for a sheath, usually 5 or
6 F, which is inserted into the femoral artery where catheter exchanges can then be
ERRNVPHGLFRVRUJ
Fig. 28.2 Example of an

aortic pressure tracing
during a cardiac
catheterization
made. The radial approach requires testing the patency of ulnar artery by perform-
ing an Allens’s test [2] prior to the procedure. This is done, because placement a
catheter can result in thrombosis or rarely injury to the radial artery. Therefore the
test is used to reduce the risk of hand ischemia ensuring adequate collateral flow
from the ulnar artery. The Allen’s test is performed by having the patient clench
their fist. The, physician then applies occlusive pressure to both the ulnar and radial
arteries, to obstruct blood flow to the hand. The patient then opens their hand, and
the patient’s fingers are observed to ensure that they have blanched. The physician
then releases the occlusive pressure on the ulnar artery to determine its patency and
adequate perfusion to the hand in the event of radial artery occlusion. Reversal of
blanching and return of normal hand coloration or flushing the hand within 5–15 s
indicates adequate perfusion of the hand by the ulnar artery allowing for use of the
radial approach. Once the radial sheath is inserted a wire is advanced through the
sheath to ascending aorta.
Irrespective of the route of arterial access, once the sheath is placed, a preformed
catheter (Fig. 28.3) is then advanced over the wire, with fluoroscopy guidance
through the sheath into the ascending aorta. A number of different catheters are used
to selectively engage the left and right coronary arteries. Once selectively engaged,
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a b c d
e f g
Fig. 28.3 Example of different coronary (a–f) and left ventricular (g) catheters. A Judkins left, B
Judkins right, C Modified Amplatz Right, D Amplatz Left, E Multi-purpose, F Jacky, G Pigtail
iodinated contrast is injected at a rate of 5–7 cc/s and cineangiography is performed

in multiple angulated views with different obliquities to capture the major coronary
arteries and their branches in orthogonal views for the detection of coronary steno-
ses. Frequently, a pigtail catheter is used to perform left ventriculography as well as
aortography to assess left ventricular systolic function, the presence and severity of
mitral and aortic regurgitation. If a right heart catheterization is being performed at
the same time, the assessment of mitral and aortic stenosis can be performed as
well. The pigtail catheter is positioned in the proximal aorta, above the coronary
arteries when performing aortography and is otherwise advanced across the aortic
valve into the left ventricle to perform left ventriculography or perform the hemo-
dynamic assessment of stenotic left sided heart valves. For imaging, the pigtail cath-
eter is connected to a power injector that is programmed to deliver contrast at a
specific rate and volume into the aorta or left ventricle. The catheter has several
sideholes and the distal end of the catheter is curved – both properties lend them-
selves to atraumatic contrast delivery while minimizing trauma to the area where it
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resides. After all views are obtained, the catheters are withdrawn from the body
through the access sheath.
Upon completion of the cardiac catheterization the access sheath is removed. In
the case of femoral access cases, frequently, vascular closure devices are used to aid
in achieving hemostasis. The totality of the data suggests that these devices might
reduce the incidence of bleeding, albeit at a greater financial cost as opposed to not
using them. If these devices cannot be deployed, then manual compression is applied
for approximately 20 min to provide hemostasis. Patients are then asked to remain
supine at bed rest for a period of approximately 4 h. Radial sheaths are removed
with the use of compression bands. These bands proved pneumatic compression of
the radial artery and are deflated after 1–2 h. Vital signs should be done routinely as
part of standard post-procedural care. Special attention should be given to the distal
lower extremity pulses where the access was obtained.
Data Interpretation
There are three main coronary arteries (Fig. 28.4). The left main coronary artery
takes its origin from the superior portion of the left coronary sinus and then
divides into two main branches that usually supply blood to the left ventricle:
the left anterior descending artery (LAD) along with its diagonal and septal
branches supply the anterior, anterior septal, apical and anterolateral left
Fig. 28.4 Normal coronary anatomy: Left image: Left main bifurcates into Left Anterior
Descending artery (1) and Left Circumflex (2). The LAD gives rise to diagonal branches (3) and
the LCx gives rise to the obtuse marginal branch (4). In approximately 10 % of the population, the
posterior descending artery (5) arises from the left circumflex artery as opposed to the RCA. Right
image: Right Coronary Artery (6)
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ventricular (LV) walls, The left circumflex artery (LCX) along with its obtuse
marginal branches supply the lateral LV wall. In 10–15 % of patients, the LCX
gives rise to the posterior descending artery (PDA) which supplies blood to the
inferior LV wall. The right coronary artery takes its origin from the right aortic
sinus and supplies the right ventricle through its RV branches, and usually the
inferior and the posterior walls of the LV through the PDA and posterior LV
branches respectively.
Coronary angiograms are performed to determine the percent diameter ste-
nosis of coronary arteries. This is done by measuring the diameter of the ste-
nosed vessel and dividing it by diameter of the normal reference reference
vessel. Coronary arteries should be imaged in at least two orthogonal views to
most accurately gauge stenosis severity. Visual assessment of a stenosis is most
commonly done in the laboratory in daily practice and stenoses greater than
70 % are considered significant [3]. However, the decision of which coronary
lesion is responsible for a patient’s ischemia is not always certain. Therefore,
there are other modalities that can be used as adjuncts to coronary angiography
which aid in establishing which coronary lesion is significant. These include
imaging techniques such as intravascular ultrasound (IVUS) [4] and optical
coherence tomography (OCT) [5] or functional assessment with fractional flow
reserve (FFR) [6]. FFR measures the pressure ratio across a coronary artery
stenosis at maximal hyperemia to determine the likelihood that the stenosis is
responsible for an ischemic syndrome.
In the presence of totally occluded vessels or highly stenotic coronary arteries,
evaluation of the supply of the distal coronary bed by collaterals (Fig. 28.5) should
be done when performing cineangiography. The vessel of origin and degree of col-
lateralization can be used to guide decision making regarding possible revascular-
ization strategies.
The coronary microvasculature is assessed semi-quantitatively by assessing
the ‘Thrombolysis In Myocardial Infarction’ (TIMI) flow in the respective coro-
nary artery. TIMI flow is graded from 0 which is defined as no perfusion to 3
which indicates normal flow which fills the distal coronary bed briskly and com-
pletely [7].
Finally, left ventricular function can be quantified visually and quantitatively
through power injection of contrast media into the LV on average at 12–15 cc/s for
a total of 35–45 cc of contrast media with the pigtail catheter in the LV. Left ven-
triculography (Fig. 28.6) can be done in two views simultaneously in angiographic
suites equipped with biplane capacity. Assessment of the degree of mitral regur-
gitation is feasible during left ventriculography with its severity graded visually
from 1+ to 4+. Similarly, aortography (Fig. 28.7) can be performed to evaluate the
severity of aortic insufficiency and for the assessment of structural and congenital
heart disease that involves the aorta. Aortography can also be used to locate coro-
nary bypass grafts that have not been seen by selective injection techniques.
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Fig. 28.5 The importance of coronary collateral vessels. (a) Site of total occlusion of the LAD
(***) which reconstitutes distally (arrow) from left-sided collateral vessels. (b) The same patient
has a significant stenosis of the left circumflex artery (arrow). (c) The RCA of the same patient is
occluded proximally (star) and reconstitutes through bridging collaterals (arrow). (d) The conus
branch of the RCA gives rise to collaterals (*) to the occluded LAD (arrow). This patient’s ven-
triculography is depicted in diastole (e) and systole (f) showing an overall normal ejection fraction
which is most likely due to the maintenance of myocardial perfusion from collateral blood flow
Fig. 28.6 Left

ventriculogram in an RAO
projection in a patient with
stress induced
cardiomyopathy showing
apical ballooning
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Fig. 28.7 Aortography in

a patient with a descending
aortic coarctation (arrow)
Complications
Coronary angiography is for the most part a relatively safe procedure with a low
risk of complications in the average population, however they still do occur.
Fortunately, the risk of major complications in current practice is <1 %. The risk
varies according to patient characteristics. Patients with an acute coronary syn-
drome, congestive heart failure, severe vascular disease, left ventricular dysfunc-
tion, severe three vessel coronary artery disease, critical valvular heart disease,
prior stroke, and history of renal insufficiency are at higher risk for complications
compared to other patients. Major complications include the risk of death, myocar-
dial infarction, and stroke which typically occur in <0.5 % of the cases. Other vas-
cular complications including major thrombosis, bleeding requiring transfusion,
pseudoaneurysm or arteriovenous fistula occur in <1 % of cases. Minor complica-
tions including transient supraventricular arrhythmias, minor bleeding at access
sites, fever, and hypotension occur in <3 % of cases. Transient increase in creati-
nine is believed to occur in at approximately 5 % of patients. Allergic reactions to
dye occur in about 1 % of patients. A morbid complication of coronary angiogra-
phy and heart catheterization is systemic cholesterol embolization that occurs in
<0.2 % of cases but has severe consequences such as renal failure and bowel isch-
emia/infarction.
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Clinical Vignettes
Case 1
A 44 year old male with a history of diabetes, hypertension and smoking presented
with chest pain at rest. His electrocardiogram revealed ST elevation in the lateral
leads. He was emergently referred to the cardiac catheterization laboratory.
Coronary angiography was performed through a radial approach and docu-
mented proximal thrombotic occlusion of the LCX (Fig. 28.8). The patient under-
went uneventful primary angioplasty and stenting of the occluded LCX and made
an uneventful recovery.
Fig. 28.8 Case 1 catheterization images. (a) LAO caudal view shows the LAD (*) and thrombotic
occlusion of the LCX (arrow); (b) AP caudal view also shows the LAD (*) and thrombotic occlu-
sion of the LCX ; (c) RAO cranial view before injecting contrast depicts residual staining from
prior injection in the LCX due to thrombus; (d) LAO cranial view of the RCA
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Case 2
A 64 year old man with multiple cardiac risk factors including hypertension, hyper-
lipidemia, known coronary artery disease, and a previous history of smoking pre-
sented with increasing angina which was unsuccessfully treated with multiple
anti-anginal medications. He was referred for a stress test that revealed a large
infero-lateral ischemic defect.
The coronary angiogram documented a critical stenosis in the mid LCX
(Fig. 28.9). The mid LCX lesion was stented with a single drug-eluting stent and the
patient was afforded complete relief of his angina.
Fig. 28.9 Case 2 angiography. (a) AP caudal view showing the LAD (*) and the LCX (+); (b)
RAO caudal view showing the stenosis in the LCX (arrow); (c) LAO caudal view also shows the
proximal LAD (*) and the LCX (+) with the critically stenotic segment (arrow); (d) LAO Cranial
view of the RCA in this patient
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References
1. Weis M, von Scheidt W. Cardiac allograft vasculopathy; a review. Circulation.

1997;96:2069–207.
2. Greenwood MJ, Della-Siega AJ, Fretz EB, et al. Vascular communications of the hand in
patients being considered for transradial coronary angiography: is the Allen’s test accurate?
J Am Coll Cardiol. 2005;46:2013–7.
3. Klein LW, Weintraub WS, Agarwal JB, Schneider RM, Seelaus PA, Katz RI, Helfant
RH. Prognostic significance of severe narrowing of the proximal portion of the left anterior
descending coronary artery. Am J Cardiol. 1986;58(1):42–6.
4. Nishioka T, et al. Clinical validation of intravascular ultrasound imaging for assessment of
coronary stenosis severity. J Am Coll Cardiol. 1999;33(7):1870–8.
5. Gonzalo N, et al. Morphometric assessment of coronary stenosis relevance with optical coher-
ence tomography: a comparison with fractional flow reserve and intravascular ultrasound.
J Am Coll Cardiol. 2012;59(12):1080–9.
6. Pijls NHJ, et al. Fractional flow reserve; a useful index to evaluate the influence of an epicardial
coronary stenosis on myocardial blood flow. Circulation. 1995;92:3183–93.
7. The TIMI Study Group. The Thrombolysis in Myocardial Infarction (TIMI) trial: phase I find-
ings. N Engl J Med. 1984;33:523–30.
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Chapter 29
Coronary Blood Flow Measurements
Morton J. Kern
Introduction
Measuring coronary blood flow and pressure provides unique information that com-
plements the angiographic evaluation and facilitates decision-making regarding
therapy. Precise quantification of stenosis severity by angiography is limited by the
inability to provide accurate two or three dimensional resolution on coronary “lumi-
nograms”. The limitations of coronary angiography have been well documented by
comparisons to intravascular ultrasound and ischemic stress testing. Direct mea-
surement of coronary blood flow velocity and distal perfusion pressures allow the
interventional cardiologist to have a complete assessment of both coronary anatomy
and physiology.
Coronary pressure and flow relationships can identify the ischemic potential of a
stenosis (Fig. 29.1). Angiography (upper left) shows geometry of lesion responsible
for pressure (P) and flow (Q) reductions associated with ischemia. Two lesions of
the same dimension can have markedly different P-Q relationships (lower left).
Fractional flow reserve (FFR) is calculated from distal pressure/proximal pressure
ratio at maximal hyperemia (upper right). Coronary flow reserve is calculated from
ratio of maximal hyperemic average velocity to baseline velocity (lower right).
M.J. Kern, MD, MFSCAI, FAHA, FACC

Veterans Administration Long Beach Health Care System,
University of California, Irvine, CA, USA

DOI 10.1007/978-1-4471-7290-1_29
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250 M.J. Kern
Fig. 29.1 Angiography (upper left) shows geometry of lesion responsible for pressure (P) and
flow (Q) reductions associated with ischemia. Two lesions of the same dimension can have mark-
edly different P-Q relationships (lower left). FFR is calculated from distal pressure/proximal pres-
sure ratio at maximal hyperemia (upper right). Coronary flow reserve is calculated from ratio of
maximal hyperemic average velocity to baseline velocity (lower right)
The hemodynamic significance of a given stenosis, as determined by the pres-

sure-flow relationship, can be measured and incorporated into clinical discussion
using sensor angioplasty guidewires. A hemodynamically significant coronary
lesion is associated with one or more of the following parameters which have been
correlated to provokable myocardial ischemia:
1. For Coronary Doppler,
(a) Poststenotic absolute coronary flow reserve (CVR) <2.0
(b) Relative coronary flow reserve (rCVR) <0.8
(c) Proximal to distal flow velocity ratio (P/D) <1.7
(d) Diastolic to systolic velocity ratio (DSVR) <1.8
2. For Coronary pressure, the hyperemic translesional pressure ratio, also known as
the FFR has a treat/no treat threshold of <0.80 to treat for best outcomes. An
ischemic threshold of <0.75 has a 90 % sensitivity and 90 % specificity for cor-
respondence to stress testing [1]
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29 Coronary Blood Flow Measurements 251
Indications
Indications for performing coronary physiologic measurements include those lesion

subsets whose clinical relevance is uncertain following angiography. These include
intermediate severity stenosis, assessment of culprit lesions in patients with multivessel
coronary artery disease and guiding therapy in patients with tandem lesions or diffuse
disease in an epicardial vessel. Coronary physiologic studies are useful in areas poorly
studied angiographically eg. ostia and bifurcations, and can also be used to assess prog-
nosis following stent implantation. Coronary physiologic testing is useful in assessing
ischemic potential of patients with prior myocardial infarction (MI), in patients with
treated unstable coronary syndromes and to assess the collateral circulation. Table 29.1
summarizes the indications for using coronary physiologic measurements.
Contraindications
The contraindications to physiologic measurements are few. According to current

guidelines, no physiologic measurement (FFR/CVR) is needed for clinical decisions
when the clinical, angiographic and objective ischemia markers are concordant for
Table 29.1 Indications for physiologic measurements in the catheterization laboratory

Coronary pressure measurements
1. Assessment of Intermediate stenosis in one or more coronary arteries (including left main)
2. In patients with multivessel disease, determination of one or more target stenoses (either
serially or in separate vessels)
3. Evaluation of ostial or distal left main and ostial right lesions, especially when these regions
can not be well visualized by angiography
4. Guidance of treatment of serial stenoses in a coronary artery
5. Determination of significance of focal treatable region in vessel with diffuse coronary artery
disease
6. Determination of prognosis after stent deployment
7. Assessment of stenosis in patients with previous (non-acute) myocardial infarction
8. Assessment of lesions in patient with treated unstable angina pectoris
9. Assessment of the collateral circulation
(NOTE: For STEMI, not useful for acute IRA lesion assessment <6 days after MI)
Coronary Doppler flow
1. Assessment of Microcirculation
2. Endothelial function testing
3. Myocardial viability in acute myocardial infarction
Combined coronary pressure and Doppler flow velocity
1. Assessment of intermediate stenosis
2. Assessment of the microcirculation
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252 M.J. Kern
the diagnosis. Other contraindications include the inability to use anticoagulation for
angioplasty sensor wire placement, unstable clinical syndromes (relative contraindi-
cation) and unsatisfactory hemodynamic recording equipment [2].
Equipment
Intracoronary physiologic measurements are made with standard angioplasty equip-

ment and techniques. Doppler flow velocity can be measured using a Doppler-
tipped angioplasty guidewire. This guidewire is a 175 cm long, 0.014 in. diameter,
flexible, steerable wire with a piezoelectric ultrasound transducer integrated into the
tip (FloWire; Volcano Therapeutics, Del Mar, CA)
Several companies make pressure wire/catheter products. Unique handling char-
acteristics arise from special construction of the device. Current pressure wire sen-
sors are either piezo-electric or optical. Pressure wires also differ from regular
workhorse wires having to incorporate the thin wires or optical fibers that transmit
the pressure signals (Fig. 29.2).
Technique
After diagnostic angiography or during angioplasty, the sensor guidewire is passed

through an angioplasty Y-connector attached to a diagnostic or guiding catheter.
(Note: Side holes in large diameter guiding catheters have been used to alleviate
catheter related partial obstruction of the coronary ostium. Side hole guiding cath-
eters required an approximate doubling of the intracoronary (IC) adenosine dose
due to loss of drug from the side holes during instillation.) Intravenous (IV) hepa-
rin 40–70 units/kg and IC nitroglycerin (100–200 μg) are given several minutes
before the guidewire is advanced into the artery.
For flow velocity, the sensor tip is advanced at least 5–10 artery-diameter
lengths (>2 cm) beyond the stenosis to measure velocity in a region of re-estab-
lished laminar flow. Resting flow velocity data are recorded. Induction of coro-
nary hyperemia by IC or IV adenosine is performed, continuously recording
through peak hyperemic flow velocity. Coronary flow velocity reserve, CFVR is
computed as maximal hyperemic to basal average peak velocity (APV). Poor
Doppler signal acquisition may occur in 10–15 % of patients even within normal
arteries. Like transthoracic echo Doppler studies, the operator must adjust the
guidewire position (sample volume) to optimize the velocity signal [3].
For translesional pressure (FFR) measurements, the wire pressure is first matched
to the guide catheter pressure in the central aortic location, and then the wire is
advanced into the artery beyond the stenosis. Baseline pressure is recorded, followed
by induction of coronary hyperemia with IC or IV adenosine, continuously recording
both guide catheter and sensor-wire pressures. FFR is computed Pressuredistal/
Pressureaorta at maximal hyperemia. Pressuredistal is recorded from the pressure wire,
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Pressure Wire
Technology Micro-Catheter Technology Optical Fiber Technology
Electric wires (+, −, ground) Optical fiber
• Acist Medical • Opsens wire

• St. Jude Medical
– Rapid – Nitinol
– Wireless pressure construction
Exchange
transmission
– Use of best – Optical tech
– Temperature sensing
personal • Boston Scientific
– CFR guidewires
– Best conventional
– Absolute Flow – Optical tech wire
• Volcano Therapeutics
– Optical tech
– Pressure/Flow Combo
– Sync Vision
– iFR
Fig. 29.2 Comparisons of available pressure wires. Sensor Wire/Catheter Construction and spe-
cial features of current pressure wire and microcatheters systems for FFR. Left standard wire core
surrounded by thin transmission and ground wires for piezo-resistive transducer signal. Center
shape of Rxi microcatheter. Right nitinol or cobalt chromium wire core around central optical
fiber to transmit pressure signal. Increase in core dimension and concentricity produces increase
torque. Piezo-electric wires have core wire (Steel, Thin, low torque) compared to optical wires
with hollow wire (nitinol or Cobalt Chromium, larger, high torque. From Kern MJ. Cath Lab
Digest, May 2016)
Pressureaorta is recorded from the guide catheter that delivers the pressure wire.
Pressure signal artifacts may be reduced by careful attention to technique.
Stenosis severity should always be assessed using measurements obtained during
maximal hyperemia. Adenosine is the most common agent for hyperemia. It has a
short half-life, with a return to basal flow within 30–60 s after cessation of infusion.
IV and IC adenosine are very well tolerated with ~10 % drop in mean arterial pres-
sure but may be accompanied by short lived symptoms of dyspnea or chest burning.
Although transient, AV block may rarely occur at higher IC doses in the RCA. IV
adenosine uses weight-adjusted dosing (140 mcg/kg/min), and is required for the
evaluation of ostial lesions or for the assessment of diffuse disease during pullback
recordings. Compared to IC, IV administration has a higher incidence of side effects
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254 M.J. Kern
such as flushing, chest tightness, bronchospasm, nausea, and transient AV block or

bradycardia. IC adenosine doses that produced maximal hyperemia equivalent to IV
adenosine are 50–100 mcg for the right coronary artery, 100–200 mcg for the left
coronary artery produces [4].
Alternative to adenosine includes Regadenson, an α2A adenosine receptor
agonist that induces coronary vasodilatation and increased myocardial blood
flow in a manner reportedly equivalent to adenosine with fewer adverse effects
and IC nitroprusside. Regadenoson has a half-life of 2–3 min in the initial phase,
30 min in the intermediate phase and 2 h in the terminal phase. It is administered
as single intravenous bolus (0.4 mg), and thus may be easier to use, but its cost
and prolonged effect may complicate the measurement of multiple lesions or
arteries [5].
IC nitroprusside can be an alternative to IC adenosine. Serial doses of IC nitro-
prusside (boluses of 0.3, 0.6, and 0.9 mcg/kg) [6] produced equivalent coronary
hyperemia with a longer duration (about 25 %) compared with IC adenosine. IC
nitroprusside (0.9 mcg/kg) decreased systolic blood pressure by 20 % with minimal
change in heart rate, whereas IC adenosine had no effect on these parameters. IC
nitroprusside, in doses commonly used for the treatment of the no-reflow phenom-
enon, can produce coronary hyperemia suitable to measure FFR without detrimen-
tal systemic hemodynamics.
A summary of pharmacologic hyperemic agents for cath lab measurements is
provided in Table 29.2.
Data Interpretation
Ischemic Thresholds of Coronary Physiologic Measurements
An FFR of <0.75 identified coronary stenoses in patients with inducible myocardial

ischemia, with high sensitivity (88 %), specificity (100 %), positive predicted value
(100 %), and overall accuracy (93 %). An CFR of <2.0 corresponded to reversible
myocardial perfusion imaging defects with high sensitivity (86–92 %), specificity
(89–100 %), predictive accuracy (89–96 %), and positive and negative predictive
values (84–100 % and 77–95 %), respectively [7, 8].
Multivessel Coronary Artery Disease
Data from multiple recent clinical trials [9–11] strongly support the concept that
patients with multivessel CAD benefit from appropriately guided physiologic
guided revascularization with an FFR >0.80 associated with exceptionally good
prognosis treated with optimal medical therapy alone. FFR in and around the gray
zone important prognostic value, especially in proximal lesions and confirm that
FFR ≤0.80 is valid to guide clinical decision making [10].
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Table 29.2 Hyperemic agents used for coronary physiology assessment

Agent Route Dose Comments
Adenosine IV 140 μg/kg per Reference standard. Side effects include dyspnea
infusion min and chest pain. Prolonged hyperemia allows
pressure wire pullback
Adenosine IC bolus >100 μg Easy to use, inexpensive, no significant side
effects. Transient heart block at high doses.
Hyperemia lasts only 10–15 s
Adenosine IC 240–360 μg/min Inconvenient set-up. Fewer side effects compared
infusion with IV infusion. Prolonged hyperemia allows
pullback. Not well-validated
Regadenoson IV bolus 400 μg Convenient, single IV bolus. Expensive. Side
effects similar to IV adenosine but less severe
and briefer. Hyperemia lasts 20 s–10 min
Papaverine IC bolus 10–20 mg Easy to use, inexpensive. Rare, but significant
side effect of polymorphic VT. Hyperemia lasts
30 s, allowing pullback
Nitroprusside IC bolus 0.3–0.9 μg/kg Easy to use, inexpensive. Major side effect is
hypotension. Hyperemia lasts 50 s allowing
pullback. Not well-validated
Dobutamine IV 50 μg/kg/min Inconvenient as it takes time for onset on offset.
infusion Side effects includes palpitations and
hypotenstion. Not well-validated
Nicorandil IC bolus 2 mg Not available in United States. Fewer side effects
compared with IV adenosine. Hyperemia lasts 30
s. Not well-validated
From Fearon [12]
FFR indicates fractional flow reserve, IC intracoronary, IV intravenous, and VT ventricular tachy-
cardia
Left Main Coronary Artery Assessment
Numerous studies support FFR use for assessment of left main (LM) coronary steno-
ses (Table 29.3). For complex LM disease with downstream significant LAD or CFX
stenosis, the data from in vitro, animal, and human studies of LM stenosis demon-
strate that in most cases, downstream disease does not have a clinically significant
impact on the assessment of FFR across an intermediate LM stenosis. Downstream
stenoses in the LAD or LCx have to be both severe (i.e. FFR <0.60) and proximal to
have a marked effect on the LM FFR. In these situations, IVUS assessment of the
LM with a threshold minimal luminal area of <6.0 mm2 is recommended [13].
Acute Myocardial Infarction
Acute myocardial injury produces transient microvascular dysfunction to various

degrees and impairs maximal coronary hyperemia depending on the reduction of
myocardial mass, reducing the flow across a stenosis. After the patient
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256 M.J. Kern
Table 29.3 Left main revascularization outcomes and FFR

N Overall survival
FFR FU (months) Defer
First author Defer Surgical cut off mean group Surgical
(Ref. #) Total group group value duration (%) group (%)
Bech et al. [14] 54 24 30 0.75 29 ± 15 100 97
Jasti et al. [15] 51 37 14 0.75 25 ± 11 100 100
Jiménez- 27 20 7 0.75 26 ± 12 100 86
Navarro et al.
[16]
Legutko et al. 38 20 18 0.75 24 ± 12 100 89
[17]
Suemaru et al. 15 8 7 0.75 33 ± 10 100 100
[18]
Lindstaedt et al. 51 24 27 0.75 29 ± 16 100 81
[19]
Hamilos et al. 213 138 75 0.80 35 ± 12 90 85
[20]
Total or (mean) 449 271 178 – (28 ± 13) (95)* (89)
From Puri et al. [13]
FFR fractional flow reserve, FU duration of follow-up, ULMCA un protected left main coronary
artery
*
p = NS compared with surgical group
recuperates, myocardial recovery may increase coronary flow, and higher flow
would lower the FFR, perhaps below the ischemic threshold thus changing a treat-
ment decision from that made during the acute event. As a result FFR of a vessel
(i.e. a lesion different from the culprit lesion, but in the same vessel) that is
involved in a ST-elevation myocardial infarction or large non-NSTEMI can result
in a false-negative result. FFR has been demonstrated to be accurate after 4–6
days, and in most unstable angina patients and small NSTEMI patients. FFR of
most non-culprit lesions at a distance from the infarct related artery, has also been
shown to be accurate. Trials that have evaluated the use of FFR in ACS are sum-
marized in Table 29.4.
Complications
The complications of coronary physiologic measurements are the same as those

related to diagnostic coronary angiography and less than those associated with coro-
nary angioplasty. The major safety considerations are those involving guiding cath-
eter/wire vessel trauma (not different from regular angioplasty wires), thrombus, or
coronary vasospasm. The incidence of such complications are <0.01 %. The use of
vasodilators, such as adenosine, may be associated with bradycardia and
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29
Table 29.4 FFR and ACS trials

Author N
Acute MI Culprit vessel Unreliable Tamita 33 STEMI Mean FFR after successful PCI was higher (0.95 ± 0.04) than in ref group
2002 of stable angina patients (0.90 ± 0.04, p = 0.002) despite identical IVUS
paramaters, likely reflecting microvascular stunning & dysfunction
Acute MI Non-culprit Reliable Ntalianis 75 STEMI, 112 non-culprit lesions measured acutely and 35 ± 24 days later. Only 2
vessel 2010 26 NSTEMI lesions had clinically meaningful change – FFR >0.80 during the acute
episode and <0.75 at follow-up
Recent MI Culprit vessel Reliable De 57 Acute MI FFR after acute MI (≥6 days, mean 20 days) compared to SPECT before
Bruyne with viable and after PCI. FFR <0.75 had high sensitivity (87 %) and specificity
2001 myocardium on (100 %) for detecting ischemia on true positive/negative SPECT. BCV
LVgram for FFR 0.78. Inverse correlation between FFR and LVEF – for a similar
degree of stenosis, FFR depends on mass of viable myocardium
Coronary Blood Flow Measurements
Recent MI Culprit vessel Reliable Samady 36 STEMI, FFR after acute MI (STEMI ≥3 days, NSTEMI ≥2 days, mean 3.7 days)
2006 12 NSTEMI compared to SPECT at 11 weeks. FFR ≤0.75 had high sensitivity (88 %),
specificity (93 %), and overall accuracy (91 %) for detecting reversibility
on true positive/negative SPECT. BCV for FFR 0.78
Recent MI Non-culprit FFR-guided Potvin 125 ACS, 201 consecutive pts (62 % unstable angina, NSTEMI, or >24 h after
vessel PCI = good 2006 60 SIHD, STEMI) with ~50 % stenosis in which PCI was deferred based on FFR
clinical outcomes 16 Atypical CP ≥0.75. No difference in clinical outcomes between ACS and stable
angina pts
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Recent MI FFR-guided Fischer 35 ACS FFR-guided PCI of intermediate lesions (50–70 %). Deferring PCI for
PCI = good 2006 FFR ≥0.75 in pts with recent ACS. Similar MACE rates at 12 months
clinical outcomes compared to pts without ACS
UA/ Culprit vessel FFR-guided Leesar 70 UA/ Recent NSTE-ACS with intermediate single-vessel lesion randomized to
NSTEMI PCI = good 2003 NSTEMI immediate FFR-guided PCI vs. post-angio SPECT. FFR-guided
clinical outcomes treatment reduced hospital stay & cost, with no increase in procedure
time, radiation exposure, or clinical event rates at 1 year
UA/ Culprit + Non- FFR-guided Tonino 326 UA/ FAME study. FFR-guided PCI vs. angiography-guided PCI for
NSTEMI Culprit vessel PCI = good 2011 NSTEMI multivessel disease. In subset of pts with recent NSTE-ACS,
clinical outcomes significantly lower MACE rate with FFR-guided PCI
257
258 M.J. Kern
hypotension. Overall, the clinical practice using sensor wire measurements with
pharmacologically induced hyperemia is safe with the benefit of valuable informa-
tion off setting the small risk of the invasive approach.
Clinical Vignettes
Case #1
69-year-old man with exertional angina presents for evaluation. Chest pain was sub-
sternal, radiated to the neck and left shoulder. It was relieved with rest and recently
responded to sublingual nitroglycerin. An exercise radionuclide perfusion imaging
study was positive for anterior reversible defects. Coronary angiography was per-
formed and showed a LAD and OM1 lesion (Fig. 29.3a, top; white arrow and *,
respectively). Because of anterior ischemia on stress testing, angioplasty and stent
placement was performed in the LAD (Fig. 29. 3b, top). For interest, FFR in the
LAD was 0.56 before angioplasty (Fig. 29.3a, bottom) and 0.94 after stent place-
ment (Fig. 29.4b, bottom).
The operator now approached the OM1 lesion. (fig, top (*)) The clinical options
included medical management, stent placement or FFR assessment and manage-
ment accordingly. Because there was no demonstrable ischemia, the operator
elected to perform FFR and provide a definite assessment of the ischemic potential
of the lesion. A sensor wire pull back was performed (Fig. 29.4) and indicated an
FFR of 0.86 and pull back pressure gradually increasing to 0.96 over the course of
the vessel. Medical Management was then instituted with annual follow-up.
Case #2
72-year-old woman with atypical chest pain occurring at rest and with exertion.
No stress testing was performed. Coronary angiography was performed and dem-
onstrated normal coronary arteriography with the exception of ostial left main
narrowing in one angiographic projection only (Fig. 29.5, arrow). The options for
management from this point forward included patient referral for immediate
bypass surgery,, perform FFR and/or IVUS while in the catheterization labora-
tory or discharge the patient from the catheterization laboratory and refer for
in-patient stress testing.
FFR was performed with intravenous infusion of adenosine (140 mcg/kg × 4 min)
and was abnormal at 0.68. IVUS also demonstrated a lesion cross-sectional area of
3.9 mm2 relative to a reference vessel area of 9.8 mm2 (Fig 29.5, right side). The
patient was referred for coronary bypass surgery.
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Fig. 29.3 (a) Top – Coronary angiogram showing lesions in the LAD (arrow) and first obtuse
marginal branch of the left circumflex artery (*). Bottom – FFR across the LAD lesion. (b) Top.
Angiogram showing the stented LAD. Bottom – FFR in the LAD following stenting
Fig. 29.4 Pull back FFR of the obtuse marginal lesion shown in figure 4, starting distally and
moving proximal to the lesion. The FFR distally of 0.86 is shown in the figure
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260 M.J. Kern
LM ostium Distal LM
MLA=3.9 MLA=9.8
Fig. 29.5 Left side – Coronary angiogram showing an eccentric left main lesion (arrow). Right
side – Intravascular ultrasound imaging of the ostium of the left main and the distal reference
vessel
References
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artery disease: 2-year follow-up of the FAME (Fractional Flow Reserve Versus Angiography
for Multivessel Evaluation) study. J Am Coll Cardiol. 2010;56:177–84.
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sure measurement. Catheter Cardiovasc Interv. 2000;49:1–16.
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in normal coronary vasodilatory reserve stratified by artery, gender, heart transplantation and
coronary artery disease. J Am Coll Cardiol. 1996;28:1154–60.
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studies of coronary physiology. Catheter Cardiovasc Interv. 2008;71(2):198–204.
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Cardiovasc Interv. 2014;83(3):369–74.
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nary sodium nitroprusside. Circulation. 2004;109:1236–43.
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for Multivessel Evaluation) study. J Am Coll Cardiol. 2010;56:177–84.
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B. The impact of downstream coronary stenosis on fractional flow reserve assessment of
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2015;8(3):398–403.
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Interv. 2015;8:e001942.
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bypass surgery for equivocal left main coronary artery disease. Heart 2001;86:547–52.
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flow reserve and intravascular ultrasound in patients with an ambiguous left main coronary
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17. Legutko J, Dudek D, Rzeszutko L, Wizimirski M, Dubiel JS. Fractional flow reserve assess-
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Chapter 30
Percutaneous Coronary Intervention
Yousef Bader, Manny C. Katsetos, and Carey Kimmelstiel
Introduction
There are over one million percutaneous coronary interventions (PCI) per-
formed each year in the United States. PCI refers to catheter- based procedures
that allow for improved perfusion through epicardial coronary arteries to the
myocardium. PCI originally referred to percutaneous transluminal coronary
angioplasty, a solely balloon-based procedure, but has since expanded to
include directional, rotational, orbital and extraction atherectomy, excimer
laser angioplasty, and most commonly, stent deployment. The devices used for
PCI are meant to relieve coronary stenoses by several mechanisms including
fracturing or debulking the atherosclerotic plaque and stretching the target
arterial segment. PCI is successful in reducing fatal and nonfatal ischemic
complications in patients with acute myocardial infarction and high-risk acute
coronary syndromes.
Y. Bader, MD (*)
M.C. Katsetos, MD
University of Connecticut, New Britain, CT, USA
C. Kimmelstiel, MD

DOI 10.1007/978-1-4471-7290-1_30
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264 Y. Bader et al.
Indications
PCI is indicated in patients whose clinical presentation is an acute coronary

syndrome including ST segment elevation myocardial infarction, non-ST seg-
ment elevation myocardial infarction, and unstable angina. It is also indicated in
those patients with angina pectoris and objective evidence of ischemia with one
or more high-grade coronary artery lesions who have failed medical therapy.
PCI is also indicated in patients who have a high burden of ischemia on stress
testing with favorable anatomy [1]. Several invasive tools are available to fur-
ther assess angiographically moderate stenoses. Fractional flow reserve (FFR) is
a measurement that can be obtained using a coronary pressure wire comparing
pressure distal and proximal to a stenosis during maximal hyperemia with an
agent such as adenosine. An FFR value less than 0.8 would be an indication to
intervene. Intravascular ultrasound is useful in further defining coronary anat-
omy and characterizing the plaque burden and morphology, eg. the presence of
calcification as well as quantitating the luminal area which can be useful in
selecting which devices and which size devices to be used in PCI. A luminal
area of less than 4 mm2 in the left anterior descending, left circumflex or right
coronary arteries is one indication to perform PCI. In the left main coronary
artery, a luminal area of less than 6 mm2 is considered indicative of significant
disease.
Contraindications
Contraindications to PCI can be divided into those related to patient character-

istics and those related to coronary anatomy. Patient factors such as a history of
recent gastrointestinal bleeding, intracranial hemorrhage, recent surgery or
bleeding diathesis are relative contraindications. Active life threatening bleed-
ing is an absolute contraindication to PCI. Coronary revascularization should
not be performed in asymptomatic patients with <50 % stenosis severity with-
out evidence of ischemia on objective testing which in the current era often
involves FFR determination. Coronary artery anatomy may also predict the
feasibility and success of PCI in a certain patient. Coronary calcification,
severe tortuosity, small reference vessel diameter (<1.5 mm), and diffuse
disease are all characteristics that may predict poor outcomes with
PCI. Consequently, a careful evaluation of lesion and patient characteristics
should be performed prior to embarking on PCI. In complex cases, a multidis-
ciplinary team approach is indicated to determine the best management strat-
egy for the patient (PCI versus coronary artery bypass grafting versus medical
therapy) [1, 2].
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30 Percutaneous Coronary Intervention 265
Equipment
Access
In order to perform a PCI the procedural planning and required equipment depends
upon access. Femoral, brachial and radial arteries are all potential access points for
intervention based on the operator’s preference and the patient characteristics.
Routine access is usually a 6 French sheath via the right radial or right femoral
artery. However, complex anatomy such as bifurcation lesions or heavily calcified
lesions may require a 7 French sheath and femoral access for guide catheter support
to more easily perform PCI with potentially higher-profile devices.
Guiding Catheter
Guiding catheters have larger inner lumen diameters than diagnostic catheters and
allow for the passage of guidewires, balloon catheters, and stents into the coronary
artery and across the lesion. These catheters are selected based on the size of the
ascending aorta, coaxial engagement of the coronary artery and the amount of
backup support required to perform the case safely and effectively. The most com-
monly used catheters are the Judkins left and right coronary guiding catheters.
Guiding catheters can be divided into active or passive manipulation catheters. The
Judkins left and Ikari left are active-type catheters, meaning a power position can be
employed by the operator to provide backup support. The Extra back up (EBU) and
Xtra backup (XB) are passive-type guides which provide support without the need
for operator manipulation. These may be easier to use but are associated with a
somewhat higher risk of left main dissection. For the right coronary artery, the Ikari
left can be used from the radial approach as an active-type guiding catheter. The
Amplatz left is a passive-type guiding catheter (Fig. 30.1).
Guidewires
Guidewires are usually 0.014 in-thickness wires that are advanced across a lesion in
the coronary artery and used as a rail to support the passage of devices. The guide-
wires are selected based on coronary anatomy and lesion morphology. Each guide-
wire must be flexible, steerable, as well as stiff enough to support advancing devices
past the lesion. Guidewires are characterized by their coating, their stiffness, and tip
load. When compared to hydrophobic wires, hydrophilic wires allow for easier pas-
sage across lesions but increase the risk of entering the subintimal space and small
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266 Y. Bader et al.
Fig. 30.1 This image shows six guiding catheters. (a) A JL-4 guiding catheter is used to engage
the left coronary artery and obtain images of the left coronary system in different projections. (b)
A Voda Left-3 catheter is used to engage the left coronary artery. It is particularly useful for provid-
ing enhanced support for LCx coronary interventions. (c) An Amplatz Left-1 catheter is a sup-
portive guide which can be used to engage the left coronary arteries and bypass grafts and
occasionally, the native right coronary artery. (d) A multipurpose-1 catheter can be shaped in the
body and used to engage any coronary or bypass graft. It is particularly useful for anomalous coro-
nary arteries. (e) An Amplatz Right 2 guiding catheter is useful in engaging the native right coro-
nary artery as well as anomalous right coronary arteries with an inferior take-off. (f) A JR-4
diagnostic catheter is used to engage the right coronary artery and obtain images of the right coro-
nary artery in different projections. This catheter can also be used to engage bypass grafts
branches. An operator usually has a “workhorse” wire, which is a safe wire that is
used routinely. A workhorse wire should be safe, durable, retain its tip shape, have
1:1 torquability, and offer moderate support for the delivery of devices. If the opera-
tor is unable to succeed using the workhorse wire, a different wire is used. The next
choice of wire depends on the specific barrier to success with the workhorse. If
more support is needed, upgrading to a wire with extra support such as a Choice
Extra Support, Grand Slam or HT Iron Man is recommended. If there is difficulty in
crossing the lesion, one may consider using a hydrophilic wire but these wires are
more likely to enter the subintimal space and are associated with a modestly higher
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Fig. 30.2 This is an image of a coronary wire. In (a–c) one can visualize different curves on the
wire to allow for access to the desired vessel. Wires are shaped based on the size and tortuosity of
the vessel and the angle at which the target vessel comes off the main branch
risk of perforation. If the difficulty is crossing the lesion because of insufficient tip
load in the case of a chronic total occlusion, one may move to a specialty wire such
as a Miraclebros 3–12 or a Confianza Pro 9–12 (Fig. 30.2).
Balloon Catheters
Balloon catheters are meant to perform lesion dilatation. When selecting a balloon,
the operator must decide on the diameter, length and compliance of the balloon. An
ideal balloon to artery ratio of 0.9–1.1 is needed to minimize the risk of dissection
and abrupt closure. There are three types of balloon catheters: over-the-wire, mono-
rail, and fixed wire balloon catheters.
Over-the-wire balloon catheters have a central lumen for the guidewire and
another lumen to allow for balloon inflation throughout the catheter. This system
has the advantage of maintaining coronary artery access with the guidewire distal to
the lesion while exchanging balloon and stent catheters. Guidewires can also be
exchanged without losing arterial access by pushing the balloon to the distal portion
of the artery. Because of the length of the two balloon lumens, additional personnel
are needed to aid in exchange of the catheters and guidewires.
The rapid-exchange or monorail balloon catheters have a short segment that con-
tains two lumens. One lumen, which runs the length of the catheter, is used for bal-
loon inflation, while the second lumen is shorter and contains the guidewire. This
creates a lower profile catheter and allows a single operator to exchange catheters
while maintaining distal wire protection. It also allows for the use of a shorter coro-
nary guidewire. These catheters however require more manipulation of the guide-
wires and balloon catheters by the operator.
The fixed-wire angioplasty balloon catheters have a balloon mounted on a cen-
tral hollow wire. The guidewire and the balloon cannot be advanced indepen-
dently of each other. The chief limitation of this catheter is that the balloon or wire
cannot be exchanged without losing access to the vessel. These devices are no
longer used.
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268 Y. Bader et al.
Stents
Stents are balloon-expandable scaffolds made of stainless steel or alloys and are
placed within the lesion. As with coronary balloons, stents are available in over-the-
wire or monorail designs. Stents are also selected based on their diameter and length.
Stents can be ‘bare-metal’ without a drug coating or ‘drug-eluting,’ that is, coated with
a medication that prevents neointimal hyperplasia with consequent restensois. The
first drug eluting stent (DES) was approved by the FDA in 2003 and currently there
are four generations of DES. Although drug-eluting stents decrease neointimal hyper-
plasia, or restenosis, they have historically required a longer duration of dual anti-
platelet therapy because of the increased risk of late stent thrombosis. This increase in
late stent thrombosis, has been markedly mitigated with design changes in later gen-
eration DES. Bioresorbable or bioabsorbable stents are novel products now widely
available in Europe, with one FDA-approved device in which the polymer which
delivers the drug is resorbed over several months. The hallmark of these stents is that
they are completely resorbed over time and this might conceivably counter some of
the perceived limitations of durable metallic stents. These limitations include late stent
thrombosis, the need for longer-term dual antiplatelet therapy, the metal scaffold inter-
fering with vascular remodeling and coronary vasomotion and also making future
surgical coronary artery bypass grafting (CABG) procedures more difficult [3–5].
Technique
Once a stenosis is identified, careful analysis of the clinical characteristics and coro-
nary anatomy is necessary to determine whether or not the patient would be best
served by percutaneous revascularization, CABG or medical therapy. A lesion clas-
sification system has been developed to categorize the anatomic risk of the lesion
undergoing intervention and is related to the likelihood of a successful procedure
(Table 30.1). A relatively newer scoring system called the Syntax score is used spe-
cifically to compare outcomes of PCI versus CABG surgery in multivessel disease.
Patients with a low Syntax score <22 do equally well with PCI whereas those with
a high Syntax score >34 tend to perform better with CABG surgery [1, 2].
After the decision to proceed with an intervention is made, a guiding catheter is
introduced through an arterial sheath, typically placed in the femoral, radial, or
brachial artery. The guiding catheter is then advanced into the aorta and the coro-
nary artery is cannulated so that the catheter is coaxial to the ostium of the coronary
artery. Guiding catheters have distinct shapes and are selected based on their ability
to provide adequate backup support for advancing equipment into the coronary
artery relative to its take-off from the aorta.
Before advancing guidewires into the coronary arteries, the patient should be
started on an intravenous anticoagulation regimen. In general, the adequacy of
procedural anticoagulation ia guided by the activated clotting time (ACT) which
should be usually be >300 s with the use of IV heparin. The ACT has limited utility
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Table 30.1 Classification system describing lesion characteristics related to the likelihood of a
successful PCI
Low risk Moderate risk High risk
Discrete (length <10 mm) Tubular (length 10–20 mm) Diffuse (length >20 mm)
Concentric Eccentric Total occlusions >3 months old
and/or bridging collaterals
Non-angulated segment Moderately angulated Extremely angulated segments
(<45°) segment (45–90°) (>90°)
Non-tortuous Moderate tortuosity Excessive tortuosity
Little or no calcification Moderate calcification Heavy calcification
No major side branch Bifurcation lesions requiring Inability to protect major side
involvement double guidewires branches
Little or no calcification Moderate calcification Heavy calcification
Absence of thrombus Some thrombus is present Degenerated vein grafts with
friable lesions
Not ostial in location Ostial in location
in guiding PCIs in which the direct thrombin inhibitor bivalirudin is utilized. All
PCIs require the administration of antiplatelet therapy as post procedural stent
thrombosis is disproportionately influenced by platelet functions. Most usually,
dual antiplatelet therapy with aspirin and an ADP receptor antagonist (eg. clopido-
grel, prasugrel, ticagrelor) are administered at the time of PCI and for 1 year, or even
longer in selected patients. A 0.014 in. guidewire is placed in the catheter via a
Y-connector (Tuohy-Borst or Copilot) and is maneuvered past the stenosis under
fluoroscopic guidance. The guidewire is advanced as far distally into the vessel as
needed to support balloon advancement.
Once the lesion is crossed with the guidewire, the balloon catheter is advanced,
using the guidewire, as a rail to the target lesion. The balloon is then inflated at the
stenosis thereby dilating the lesion. Contrast is then injected through the guide cath-
eter to assess the result of predilation and coronary blood flow. The balloon can be
used at this time to help assess, the length of stent required.
A stent is then advanced through the guiding catheter to the target lesion. The
stent is deployed at a pressure that will maximize stent expansion within the lesion
without causing vascular dissection at the margins of the stent or the much less com-
mon complication of perforation. The stent catheter is then removed following stent
implantation in the artery. The stent is visualized through a contrast injection to
determine if it is properly deployed. Although direct stenting without balloon predi-
lation can be performed, not all lesions are amenable to this technique. Lesions
which are calcified and tortuous may prevent optimal stent implantation and should
be predilated with a balloon catheter. Intravascular ultrasound can also be used to
verify adequate deployment of the stent by visualizing the relationship of the stent
struts to the vessel wall. If the stent does not appear to be fully expanded, a non-
compliant balloon may then be advanced into the stent and inflated to fully expand
it and better appose the stent against the arterial wall.
Several lesion types represent higher-risk anatomic subsets for intervention and
require specific techniques to help ensure optimal procedural and clinical results.
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270 Y. Bader et al.
Bifurcation Lesions
Bifurcation lesions usually refer to a diseased arterial segment which involves a par-
ent and sidebranch vessel. PCI in these cases should be approached prudently in
order to preserve the parent vessel and side branch. If the side branch is a large
diameter vessel and there is critical disease within the proximal vessel, then bifurca-
tion stenting should be strongly considered. When the side branch is free of or mini-
mally diseased, provisional stenting is preferable. This refers to the situation when
the parent vessel is stented across the origin of the side branch. The side branch is
only rewired for ballooning or stenting if there is reduced flow or if the patient has
ischemic symptoms referable to flow obstruction in the side branch. If bifurcation
stenting is going to be performed, several approaches have been described and the
choice of which approach is employed is based on the angle between the side branch
and parent vessel as well as other factors.
Saphenous Vein Graft Intervention
Another challenging lesion subset for PCI are those in degenerated saphenous vein
bypass grafts. These lesions are at elevated risk of distal embolization into the native
coronary vasculature during balloon and stent inflation and can cause no reflow
phenomenon – the occurrence of impedance to blood flow to ischemic tissue fol-
lowing the relief of coronary occlusion, presumably due to microvascular obstruc-
tion. Due to the high thrombotic burden present in the diseased graft, a distal
protection device (Guardwire, Filterwire, etc) should be used, when feasible, to
prevent or decrease any downstream debris embolization. The distal protection
device is then retrieved and can be assessed for the presence of debris. Intracoronary
medications such as nitroprusside and verapamil can also be delivered prophylacti-
cally in an effort to prevent no reflow and potentially as a treatment should it occur.
Calcified Lesions
Severe calcified stenoses are associated with decreased success rates and increased
risk of complications such as dissection with balloon inflation. Techniques such as
rotational atherectomy can debulk the calcified lesion through the use of a high
speed (150,000 rpm) diamond tip burr. Orbital atherectomy is a newer technology
which is also effective in pretreating calcified lesions to allow for easier delivery of
balloons and stents. Orbital atherectomy is contraindicated however for aorto-ostial
lesions. These devices debulk calcium, thereby enhancing vascular compliance
allowing the diseased segment to be stented.
For patients undergoing high risk PCI with compromised left ventricular func-
tion, ongoing ischemia, or in cardiogenic shock, the operator should consider the
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implantation of a mechanical support device such as an intra-aortic balloon pump or

an Impella.
Once a satisfactory revascularization result is achieved, the artery is imaged in
several views demonstrating the result. The guidewire is then removed. A coronary
angiogram after wire removal should be performed to ensure there is no distal per-
foration and to assess vascular anatomy without wire-induced straightening arti-
facts. The guide catheter is then removed and the arterial sheath should then be
removed and hemostasis achieved either via manual compression or with the aid of
a vascular closure device.
Post PCI, the patient should be monitored for recurrent myocardial ischemia
until discharge. All patients should be made to understand the importance of
adhering to recommended medical therapies, including anti-platelet therapies and
risk factor modification proven to reduce morbidity and mortality form coronary
artery disease.
Data Interpretation
Angiographic success after percutaneous coronary intervention is defined as

decreasing the stenosis diameter reduction to <20 % with TIMI-3 flow. Additionally
there should be clinical signs of success with relief of signs and symptoms of myo-
cardial ischemia post procedure.
Complications
Acute vessel closure is an important complication of percutaneous coronary inter-

vention and can be caused by dissection, thrombus formation, and spasm. If the
target vessel remains closed, then the impaired blood flow can result in hypotension,
myocardial infarction, arrhythmia and death. With the advent of coronary stenting
and adjunctive pharmacologic therapy, the incidence of acute closure has markedly
decreased.
Increased mortality of percutaneous coronary interventions has been associated
with advanced age, female gender, diabetes, prior myocardial infarction, multives-
sel disease and a large area of myocardium at risk. The combined risk of death,
nonfatal myocardial infarction, stroke, and emergent bypass surgery during PCI is
approximately 1 %.
The most common complication for patients undergoing PCI, however, is
bleeding at the arterial puncture site. This may occur in 1–3 % of all cases.
Radial access for PCI has been associated with a lower incidence of vascular
complications and there are some reports of decreased mortality when radial
approach is used for STEMI patients. Moreover, patients with renal insuffi-
ciency may develop worsening renal function secondary to the use of iodinated
contrast.
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272 Y. Bader et al.
Restenosis has been a major determinant of event free survival following coro-
nary intervention and results from elastic recoil and neointimal hyperplasia of the
artery. Clinical factors such as diabetes, unstable angina, history of prior restenosis
and procedural factors such as smaller minimal lumen diameter and smaller acute
gain of the target vessel are predictors of restenosis. With the advent of the antipro-
liferative drug eluting stents, the incidence of in-stent restenosis has substantially
decreased.
Clinical Vignettes
Case 1
A 60 year old female with Type II diabetes presented to the emergency room
with 1 h of chest pain radiating to the jaw and left arm. ECG demonstrated ST
elevation in leads II, III, and avF. The patient was given aspirin, lopressor, IV
Heparin.
The patient was taken emergently to the cardiac catheterization lab and was
found to have a 100 % occlusion in the right coronary artery (Fig. 30.3). A JR 4
guiding catheter was placed in the ostium of the right coronary artery and a guide-
wire was advanced through the target lesion. The lesion was dilated with a balloon
(2.0 × 12 mm). A drug eluting stent (3.25 × 20 mm) was then deployed. Angiography
demonstrated 0 % residual stenosis (Fig. 30.4).
Fig. 30.3 This is a view of

the right coronary artery in
a left anterior oblique
projection which shows a
completely occluded mid
RCA
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Fig. 30.4 This is an LAO

projection of the
revascularized RCA
Case 2
A 55 year old male smoker with dyslipidemia presents for an outpatient cardiac cath-
eterization for worsening chest pain with exertion. The patient exercised for 7 min on
the Bruce protocol, developed angina with 2 mm ST depression in the precordial
ECG leads with a large moderately reversible anterior defect with nuclear imaging.
Angiography revealed a significant stenosis at the LAD/Diagonal bifurcation
with a 90 % mid left anterior descending coronary artery lesion and a 95 % Diagonal
coronary artery lesion (Fig. 30.5). A balloon catheter (2.0 × 12 mm) was advanced
Fig. 30.5 This is an RAO

cranial projection of the
left coronary system. Once
can see that there is a
lesion involving the LAD
and Diagonal coronary
arteries with an 90 %
stenosis in the LAD and
95 % stenosis in the
diagonal branch
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274 Y. Bader et al.
a b
Fig. 30.6 This demonstrates the bifurcation stenting during and after revascularization. A mini-
crash technique was used. (a) A stent is positioned in the diagonal and a second stent placed in the
LAD. The diagonal stent is deployed and the balloon and wire are withdrawn. Next the LAD stent
is fully deployed. After that the diagonal branch is rewired and kissing balloon inflation is per-
formed. (b) The final result after post dilation
over a guidewire and was inflated at both lesions. A crush technique was used to
treat the lesions with a 2.5 × 20 DES to the Diagonal branch and 3.0 × 24 DES to the
LAD (Fig. 30.6).
References
1. Levine G, Bates E, Blankenship J, et al. 2011 ACCF/AHA/SCAI guideline for percutaneous

coronary intervention. Circulation. 2011;124:e574–651.
2. Serruys P, Morice M, Kappetein P, et al. Percutaneous coronary intervention versus coronary-
artery bypass grafting for severe coronary artery disease. N Engl J Med. 2009;360:961–72.
3. Kereiakes DJ, Yeh RW, Massaro JM, et al. Stent thrombosis in drug-eluting or bare-metal
stents in patients receiving dual antiplatelet therapy. JACC Cardiovasc Interv.
2015;8:1552–62.
4. Garg S, Serruys P, et al. Coronary stents, current status. J Am Coll Cardiol. 2010;56(10s):S1–42.
5. Hilliard AA, From AM, Lennon RJ, et al. Percutaneous revascularization for stable coronary
artery disease: temporal trends and impact of drug-eluting stents. J Am Coll Cardiol Intv.
2010;3:172–9.
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Chapter 31
Alcohol Septal Ablation
Carey Kimmelstiel
Indications
Hypertrophic obstructive cardiomyopathy (HOCM) is a relatively common genetic

disorder that exhibits wide variability in its clinical expression. Symptomatic
patients most frequently experience exertional dyspnea, chest pain, fatigue and,
occasionally, orthopnea or nocturnal dyspnea. Five to 10 % of symptomatic patients
with HOCM are refractory to medical therapy (typically beta blockers and heart rate
lowering calcium antagonists) and may require mechanical approaches targeting
relief of obstruction and mitral regurgitation. Previously, mechanical approaches
were limited to surgical myectomy, however, since the late 1990s increasing experi-
ence with a percutaneous technique, alcohol septal ablation, has become a widely-
used alternative to surgical myectomy.
General indications for alcohol septal ablation include patients with severe
symptoms – New York Heart Association class III or IV, refractory to maximal drug
therapy with a left ventricular outflow gradient ≥ approximately 50 mmHg at rest or
after provocation, with a basal septal thickness ≥17 mm as measured with echocar-
diography or MRI [1].
Contraindications
Relative contraindications to performing alcohol septal ablation include coexistent

abnormalities that are best treated surgically – eg. multivessel coronary artery dis-
ease and especially mitral valve or papillary muscle/mitral apparatus abnormalities
C. Kimmelstiel, MD

DOI 10.1007/978-1-4471-7290-1_31
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276 C. Kimmelstiel
that contribute to mitral regurgitation and/or left ventricular outflow tract obstruc-
tion. These patients, who comprise approximately one-third of the HOCM
medication-refractory population, should be referred for surgical myectomy, at
which time, coexisting abnormalities can be addressed.
Equipment
Alcohol septal ablation uses standard coronary intervention equipment (Fig. 31.1):
a coronary guide catheter, guide wire and angioplasty balloon along with a pulmo-
nary artery catheter to measure pulmonary pressures and an end-hole pigtail or halo
catheter to measure the left ventricular pressure. Comparison of the left ventricular
pressure to the central aortic pressure determines the left ventricular outflow gradi-
ent. All patients have a temporary pacemaker placed at the right ventricular apex.
Transthoracic echocardiography is used in all cases to guide ablation.
Technique
Alcohol septal ablation is performed in the cardiac catheterization laboratory. A

right and left heart catheterization are performed at which time pulmonary capillary
wedge and pulmonary arterial pressures are measured. Left ventricular outflow gra-
dients are measured, usually with an endhole pigtail or halo catheter so as to be able
Fig. 31.1 Equipment/

catheters used in alcohol
septal ablation. TPM
temporary pacemaker,
CGC coronary guide
catheter, PAC pulmonary
artery catheter, CGW
coronary guide wire, CBC
coronary balloon catheter,
Halo Halo left ventricular
catheter
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31 Alcohol Septal Ablation 277
to record pressure at a precise location within the left ventricle with a catheter whose
shape makes entrapment unlikely. Determination of the left ventricular outflow gra-
dient is accomplished by comparing the left ventricular pressure to the central aortic
pressure as recorded usually from the coronary guide catheter (Fig. 31.2). It is
important to establish the gradient that will be followed to judge procedural efficacy
and to establish, with the aid of echocardiography, that the location of obstruction to
left ventricular outflow is subaortic. For those patients in whom the outflow gradient
is either absent or small at rest, the magnitude of provocable obstruction is most
appropriately determined with exercise. If exercise is not feasible, Valsalva maneu-
ver or post-PVC beats are employed.
Prior to proceeding with alcohol infusion, all patients have a temporary pace-
maker placed in the apex of the right ventricle as a precaution against the occurrence
of complete heart block following alcohol injection. This is usually placed from the
right internal jugular vein, as this is a stable route allowing for maintenance of
proper positioning following the procedure.
Coronary angiography is performed to assess for the presence or absence of athero-
sclerotic epicardial coronary artery disease and to identify potential target septal per-
forator branches, which most often originate from the left anterior descending (LAD)
coronary artery. Most practitioners employ myocardial contrast echocardiography,
which involves two dimensional echocardiographic imaging during the infusion of
1–2 mL of echo or angiographic contrast through the lumen of an inflated balloon dila-
tation catheter. This technique enhances the efficacy and safety of the procedure by
avoiding septal branches that supply areas of myocardium distant to the targeted
region, limiting the number of vessels intervened on, thereby reducing the amount of
alcohol used which aids in preventing the complication of complete atrioventricular
Fig. 31.2 Left ventricular outflow gradients before and following alcohol septal ablation. Before
ablation, the gradient is 170 mmHg. Note the bifid aortic waveform, highly suggestive of dynamic
outflow obstruction with a narrow pulse pressure. Following ablation, the gradient has been
reduced to 20 mmHg. The aortic waveform no longer exhibits a bifid contour and the pulse pres-
sure has increased
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278 C. Kimmelstiel
Fig. 31.3 Echocardiographic view during alcohol septal ablation. Panel A demonstrates the ante-
rior leaflet of the mitral valve (arrows) making contact with the basal portion of the anterior inter-
ventricular septum (*) during systole. Ao aortic valve, LV left ventricle, LA left atrium. Panel B is
alcohol (arrowheads) in basal anterior septum including the area where the anterior mitral leaflet
makes contact (*)
block. The targeted myocardial region for ablation is that area of the basal septum
where contact is made with the anterior leaflet of the mitral valve (Fig. 31.3) [2].
Once the target vessel or branch has been identified, angiographic contrast is
injected through the coronary guide catheter and through the distal port of the
inflated balloon catheter in the septal vessel. This is done to ensure that the inflated
balloon completely occludes the septal vessel, so that upon injection, alcohol cannot
leak back into the LAD, which is a potentially disastrous complication. Myocardial
contrast echocardiography has taught us that contrary to what was originally
thought, the entire septal branch need not be ablated in order to obtain a satisfactory
hemodynamic result (Fig. 31.4).
Alcohol septal ablation is accomplished by injection of usually 1–2 mL of
96–98 % ethanol into the target septal branch. The alcohol is injected slowly, at a
rate of approximately 1 mL/min. This is done to minimize complications, especially
high-degree atrioventricular block. Immediately prior to alcohol injection, intrave-
nous analgesia is administered in an effort to mitigate the pain associated with
alcohol-mediated myocardial necrosis. During and immediately following alcohol
infusion, the patient is scrupulously monitored looking for QRS widening, ST
segment changes, the occurrence of complete heart block and for signs of hemody-
namic deterioration.
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Fig. 31.4 Pre-ablation panel: Coronary angiogram showing the basal septal branch of the first
septal perforator (arrow) which was documented by myocardial contrast echocardiography to be
the target for alcohol ablation. Post-ablation panel: Ablated basal septal branch (arrow) following
the slow injection of 1.25 cc of alcohol
Following alcohol septal ablation, patents remain in the coronary care unit for
approximately 24 h, predominantly for monitoring, especially as relates to detecting
ventricular arrhythmias and complete heart block. In general, if the patient has not
required pacing, the temporary pacemaker is removed.
Data Interpretation
As a general rule, alcohol septal ablation is considered successful when an acute

reduction in the resting or provoked left ventricular outflow gradient of greater than
50 % or to less than 20 mmHg has been achieved (Fig. 31.2). Comprehensive pres-
sure sampling is usually performed given the dynamic nature of the left ventricular
outflow gradient in HOCM. Frequently, the initial improvement in the outflow gra-
dient appears to be lost on follow-up Doppler study the day following the proce-
dure. The immediate gradient reduction is likely secondary to alcohol-induced
septal necrosis and stunning, an effect which can be evanescent and is distinct from
the permanent septal thinning and remodeling which is associated with progressive
and long-lived gradient reduction seen on long-term follow-up.
To date, there have been no randomized studies comparing alcohol septal abla-
tion to surgical myectomy in patients with medication-refractory HOCM. Meta-
analyses of large observational series have suggested that septal ablation and
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280 C. Kimmelstiel
myectomy are comparable in terms of long-term survival and symptomatic relief

with septal ablation leading to a higher rate of permanent pacemaker implantation
[3–6]. There are suggestions that patients undergoing septal ablation have higher
residual gradients as compared to patients treated surgically, however, the clinical
significance of this finding is not clear.
Complications
The risk of procedural mortality following alcohol septal ablation is low. Recent
series have reported in-hospital mortality of less than 1 % [3–6]. The reduction in
procedural mortality over the years has paralleled the decline in the volume of alco-
hol used to accomplish gradient reduction. Approximately 75 % of the patients
undergoing alcohol septal ablation will develop a right bundle branch block follow-
ing the procedure which is in contrast to patients undergoing surgical myectomy
who almost universally develop a left bundle branch block.
The most frequent complication of alcohol septal ablation is complete heart block.
The decision to implant a permanent pacemaker in patients with heart block involves
a clinical assessment of risk of recurrence and/or permanence of the heart block
involving clinicians caring for the patient which usually involves electrophysiologic
consultation. There is some variability in the threshold for pacemaker implantation,
with a current frequency in the United States of approximately 10–15 % of ablation
patients. There is a higher frequency of heart block and pacemaker implantation in
the elderly given their higher frequency of intrinsic conduction system disease.
The most feared complication of septal ablation is the application of alcohol
outside of the myocardial region targeted by myocardial contrast echocardiography.
This can occur when alcohol leaks down the LAD through a nonocclusive balloon
or when alcohol enters collateral channels (which may be below fluoroscopic imag-
ing resolution) leading away from the targeted septal branch. The obvious result is
infarction in an unintended myocardial region. The consequences depend on the
involved area of myocardium and the volume of alcohol entering this region.
Patients experiencing this complication may exhibit rapid clinical deterioration due
to widespread acute myocardial infarction often with consequent pulmonary con-
gestion. Mitral and tricuspid regurgitation as well as ventricular tachyarrhythmias
are also possible in this subset of patients. Echocardiography, which is readily avail-
able during this procedure, is a key aid in confirming this diagnosis. Other rare coro-
nary complications include coronary dissection, perforation, and thrombosis.
A potential longer-term complication of alcohol septal ablation is the facilitation
of ventricular arrhythmias. Alcohol septal ablation does induce intramyocardial scar
formation in a population of patients already prone to reentrant ventricular
arrhythmias raising the possibility that the induced septal infarct could enhance the
likelihood of sudden death in some patients. This concern has not, to date been real-
ized as interrogation of defibrillators, implanted for primary prevention in HOCM
patients undergoing septal ablation has not documented any signal for an increased
ERRNVPHGLFRVRUJ
incidence of ventricular arrhythmias. Comparative analyses have similarly shown

no increase in the incidence of sudden cardiac death in ablation patients when com-
pared with similar populations undergoing surgical myectomy.
Clinical Vignette
A 67 year old, morbidly obese man with a history of prior coronary bypass surgery,
COPD and obstructive sleep apnea presented with an 8 month history of progres-
sive dyspnea on exertion, NYHA Class III in severity which severely limited his
normal daily activities. Physical exam documented a bifid carotid pulse and a loud
apical systolic murmur which increased by 1 grade following a Valsalva maneuver.
Echocardiography revealed hyperdynamic left ventricular systolic function, basal
septal hypertrophy with a thickness of 21 mm consistent with a diagnosis of hyper-
trophic cardiomyopathy. There were no noted abnormalities of the mitral valve or
the subvalvular apparatus. Continuous wave Doppler study estimated an 80 mmHg
subaortic gradient due to dynamic systolic anterior motion of the mitral valve with
basal septal contact. Coronary artery angiography documented patent grafts to the
distal LAD, right and left circumflex arteries. The LAD was occluded in its mid seg-
ment after the second diagonal branch.
Medical management with escalating doses of β-blocking agents and verapamil
were ineffective in relieving the patient’s symptoms. Due to prior coronary bypass
surgery, medical comorbidities and patient preference ASA was recommended. The
patient was referred to the cardiac catheterization laboratory where a 100 mmHg
resting left ventricular outflow gradient was documented. Myocardial contrast echo-
cardiography identified a basal branch of the first large septal perforating branch of
the LAD as supplying the basal septum at the site of contact with the anterior leaflet
of the mitral valve. Following the slow infusion of 1.25 mL of alcohol, the resting
gradient was reduced to 20 mmHg. The patient required temporary pacing for
10 min following the injection of alcohol, but sinus rhythm returned shortly thereaf-
ter, albeit with the emergence of a right bundle branch block. Permanent pacemaker
implantation was not required. On follow-up 3 months later, the patient reported
marked clinical improvement with NYHA Class I symptoms. Echocardiography
with Doppler study documented that the basal septum had remodeled to a maximal
thickness of 17 mm with a resting outflow gradient of 20 mmHg.
References
1. Kimmelstiel CD, Maron BJ. Role of percutaneous septal ablation in hypertrophic obstructive
cardiomyopathy. Circulation. 2004;109:452–5.
2. Lakkis NM, Nagueh SF, Kleiman NS, Killip D, He Z-X, Verani M, Roberts R, Spencer
WH. Echocardiography-guided ethanol septal reduction for hypertrophic obstructive cardio-
myopathy. Circulation. 1998;98:1750–5.
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282 C. Kimmelstiel
3. Jensen MK, Almaas VM, Jacobsson L, Hansen PR, Havndrup O, Aakhus S, Svane B, Hansen
TF, Kober L, Endresen K, Eriksson MJ, Jorgensen E, Amlie JP, Gadler F, Bundgaard H. Long-
term outcome of percutaneous transluminal septal myocardial ablation in hypertrophic obstruc-
tive cardiomyopathy. A Scandinavian multicenter study. Circ Cardiovasc Interv. 2011;4:
256–65.
4. Sorajja P, Ommen SR, Holmes DR, Dearani JA, Rihal CS, Gersh BJ, LennonRJ NRA. Survival
after alcohol septal ablation for obstructive hypertrophic cardiomyopathy. Circulation.
2012;126:2374–80.
5. Nagueh SF, Groves BM, Schwartz L, Smith KM, Wang A, Bach RG, Nielsen C, Leya F,
Buergler JM, Rowe SK, Woo A, Munoz Maldonado Y, Spencer III WH. Alcohol septal abla-
tion for the treatment of hypertrophic obstructive cardiomyopathy: a multicenter North
American registry. J Am Coll Cardiol. 2011;58:2322–8.
6. Jensen MK, Prinz C, Horstkotte D, van Buuren F, Bitter T, Faber L, Bundgaard H. Alcohol
septal ablation in patients with hypertrophic obstructive cardiomyopathy: low incidence of sud-
den cardiac death and reduced risk profile. Heart. 2013;99:1012–7.
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Chapter 32
Transcatheter Closure of Atrial Septal Defects
and Patent Foramen Ovale
Francisco Garay, Qi-Ling Cao, and Ziyad M. Hijazi
Atrial Septal Defect
Secundum atrial septal defects (ASD) represent 6–10 % of all congenital cardiac
anomalies and are twice as frequent in females than males. ASD leads to a left to
right shunt which in turn produces right sided cardiac volume overload, increased
pulmonary blood flow and eventually pulmonary arterial hypertension and pulmo-
nary vascular disease. The closure of these defects can be achieved safely and effi-
ciently by transcatheter methods [1, 2].
Indications
Closure of this defect is indicated in patients with evidence of a significant hemody-

namic shunt which is usually documented by echocardiographically demonstrated
right ventricular and atrial enlargement. Clinically, this is evident by the presence of
a systolic ejection heart murmur with fixed splitting of S2. Patients may or may not
have overt symptoms, including shortness of breath, fatigue and palpitations.
F. Garay, MD (*)
Department of Pediatrics, Cardiac Catheterization Laboratory,
Catholic University, Santiago, Chile
Q.-L. Cao, MD
Echo Research Lab, Cardiac Program, Sidra Medical and Research Center, Doha, Qatar
Z.M. Hijazi, MD, MPH, FACC, MSCAU
Weill Cornell Medicine, New York, NY, USA
Cardiac Program, Sidra Medical and Research Center, Doha, Qatar

DOI 10.1007/978-1-4471-7290-1_32
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Contraindications
• The development of non-reactive pulmonary vascular disease. This is rare (about

5 % of patients) and usually occurs in adults older than 40 years of age. A pulmo-
nary vascular resistance indexed higher than 7 Wood units after a trial of vasodi-
lators, such as inhaled nitric oxide is a contraindication for closure.
• Systemic or local infection within 1 month of the procedure.
• Bleeding disorders or other contraindications to aspirin therapy, unless other
antiplatelet agents such as clopidogrel can be used for 6 months.
• Presence of intracardiac thrombus.
• Nickel allergy is a relative contraindication. This issue has not been a clinically
important one even in patients with documented nickel allergy.
• Patients with primum or sinus venosus types of atrial defects are in general, not
candidates for non-surgical closure.
Equipment
The Amplatzer® Septal Occluder (ASO) consists of 2 nitinol wire mesh discs con-
nected by a 3–4 mm waist (Fig. 32.1). The device size is determined by the diameter
of its connecting waist with available sizes ranging from 4 to 40 mm. The two flat
discs extend radially beyond the connecting waist to secure anchorage. The left
atrial disc is larger than the right atrial disc. Dacron polyester patches are sewn into
each disc and the connecting waist to increase thrombogenicity of the device. The
ASO is delivered through a sheath ranging from 6 to 12 F diameter and lengths of
60–80 cm which is advanced from the right femoral vein, through the right atrium
across the interatrial septum into the left upper pulmonary vein. The ASO is pushed
through the sheath by a delivery cable which is unscrewed when proper location and
deployment are documented.
Fig. 32.1 The Amplatzer Septal Occluder (right) and the Amplatzer PFO Occluder (left). Both
devices are made of Nitinol wire mesh
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32 Transcatheter Closure of Atrial Septal Defects and Patent Foramen Ovale 285
The Amplatzer® Sizing balloon is optional but recommended to facilitate correct

device sizing.
The Gore Helex Septal Occluder® is a low-profile device constructed from a
single nitinol wire with ePTFE bonded to the nitinol frame. The device is available
in 5 sizes, ranging in diameters of 15–35 mm. As recommendations for the use of
this device advise a ≥2:1occluder to defect diameter ratio, the Gore Helex is most
usually applied to pediatric patients.
Technique
One should review all previous data related to the patient and the defect to be closed
and ensure that appropriate devices and delivery systems are available. Aspirin
81–325 mg should be started 48 h prior to the procedure. Alternatively, clopidogrel
75 mg could be used.
The procedure is performed under either transesophageal echocardiography
(TEE) or intracardiac echocardiography (ICE) guidance. If TEE is used, due to the
length of the procedure and for patient’s comfort, the procedure should be done
under general endotracheal anesthesia. If the procedure is performed under ICE
guidance, mild sedation is given. The procedure is most often performed via femo-
ral venous access. Heparin is administered to maintain an activated clotting time
(ACT) above 200 s at the time of device deployment. Broad spectrum antibiotic
administration is recommended for the procedure (eg. cefazolin 1 g iv), the first
dose at the time of the procedure and two additional doses 6–8 h apart. Right heart
catheterization is performed to measure pulmonary artery pressure, calculate pul-
monary vascular resistance and shunt (Qp:Qs) ratio. The pulmonary vascular reac-
tivity can be evaluated if necessary. TEE or ICE (Figs. 32.2 and 32.3) images are
obtained to assess the ASD anatomy (location, size, additional defects and rims) [3].
It is important to fully evaluate the atrial septal anatomy as well as that of adjacent
structures to ensure that the device will be properly seated following deployment.
The angiographic catheter is advanced into the left atrium from the inferior vena
cava into the right upper pulmonary vein. An angiogram is then performed
(Fig. 32.4a) to evaluate the atrial septal length and shape. A stiff guide wire is
advanced just distal to the catheter tip (Fig. 32.4b). The angiographic catheter is
exchanged for a sizing balloon (Fig. 32.4c). The balloon is placed across the defect
under fluoroscopic and echocardiographic guidance and then inflated with diluted
contrast until the left-to-right shunt ceases as observed by color flow Doppler on
TEE or ICE. The indentations in the balloon made by the margins of the ASD are
measured on echocardiographic or fluoroscopic images (Fig. 32.4c). Usually the
echo measurements are more reliable than the fluoroscopic measurements. A device
approximately 1–2 mm larger than the measured sizing balloon diameter is selected.
The sizing balloon is removed and a delivery sheath is advanced over the super stiff
guide wire to the left upper pulmonary vein (Figs. 32.4d and 32.5b). Extreme care
must be exercised to not allow passage of air inside the delivery sheath.
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286 F. Garay et al.
Fig. 32.2 Transesophageal echocardiographic images obtained to assess the ASD anatomy. (a, b)
four chamber view without and with color Doppler demonstrating the ASD (arrow) and left-to-
right shunt. (c, d) short axis view without and with color Doppler demonstrating the ASD (arrow),
the anterior rim near the aortic valve and posterior rim (arrowhead). (e, f) bi caval long axis view
without and with color Doppler demonstrating the ASD (arrow), the superior rim near the superior
vena cava and inferior rim near the inferior vena cava (arrowhead). RA right atrium, LA left atrium,
RV right ventricle, LV left ventricle, SVC superior vena cava
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Fig. 32.4 Cine fluoroscopic images in a patient with a large secundum ASD during closure with
the Amplatzer device under intracardiac echocardiographic guidance. Black arrow is the AcuNav
catheter for intracardiac echocardiographic images. (a–h) were obtained in the hepatoclavicular
projection and the remaining images in straight frontal projection. (a) angiogram in the right upper
pulmonary vein demonstrating the left-to-right shunt through the ASD (arrow). (b) cine image
during passage of the guide wire (white arrow) through the ASD to the left upper pulmonary vein.
(c) cine image during balloon sizing demonstrating the “stop-flow” diameter of the defect (white
arrows). (d) cine image during passage of the delivery sheath (white arrow) to the left upper pul-
monary vein. (e) cine image during deployment of the left atrial disk (white arrow) in the left
atrium. (f) cine image during deployment of the right atrial disk (white arrow) in the right atrium.
(g) cine image immediately after the cable (white arrow) was released from the device. (h) final
angiogram in the right atrium in the showing good device position
Fig. 32.3 Intracardiac echocardiographic images obtained to assess the ASD anatomy. (a, b)
Septal view without and with color Doppler demonstrating the ASD (arrow) and left-to-right
shunt. (c, d) bi caval long axis view without and with color Doppler demonstrating the ASD
(arrow), the superior rim near the superior vena cava and inferior rim near the inferior vena cava
(arrowhead). (e, f) short axis view without and with color Doppler demonstrating the ASD (arrow),
the anterior rim near the aortic valve and posterior rim (arrowhead). Note, with ICE, the left atrium
is in the bottom of image and right atrium in toip which is in contrast with TEE images. RA right
atrium, LA left atrium, SVC superior vena cava
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288 F. Garay et al.
Fig. 32.5 Transesophageal echocardiographic images in the same patient as Fig. 32.2 demonstrat-
ing the steps of closure. (a) passage of guide wire (arrow) in 4-chamber view to the left atrium. (b)
passage of the delivery sheath (arrow) in 4-chamber view to the left atrium. (c) deployment of the
left atrial disk (arrow) in 4-chamber view in the left atrium. (d, e) device release (arrow) in
4-chamber view without and with color Doppler demonstrating good device position. (f–h) deploy-
ment of the right disk (arrow), device and assessment of position in short axis view without and
with color Doppler. Device looks good and no residual shunt. (i, j) bi caval view without and with
color Doppler demonstrating good device position
The device, attached to a delivery cable is advanced to the tip of the sheath. Then
the cable and delivery sheath are pulled back as one unit to the middle of the left
atrium. This position and the next steps are verified under fluoroscopy or TEE/ICE
(Figs. 32.4, 32.5 and 32.6). The left atrial disc is deployed by pulling back the sheath
maintaining the cable position and taking care of not to interfere with the atrial append-
age. Finally withdrawing the delivery shearth over the cable, the connecting waist and
the right atrial disc are deployed in the ASD itself and in the right atrium respectively.
Proper device position can be assessed by fluoroscopy where both discs are seen
parallel to each other and separated from each other by the atrial septum (Fig. 32.4h).
The echocardiogram (TEE/ICE) must demonstrate the presence of one disc in each
atrial chamber. If the position is uncertain or questionable, after all these maneu-
vers, the device can be recaptured and repositioned. After the position of the device
has been verified, the device is released from its delivery cable. Assessment of the
final result of the closure procedure is performed immediately with TEE or ICE, and
24 h later with transthoracic echocardiography.
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Fig. 32.6 Intracardiac echocardiographic images (ICE) during various stages of device deploy-
ment in the same patient as Fig. 32.3. (a–c) views between septal and bicaval views demonstrating
passage of guide wire (arrow) (a) delivery sheath (arrow) (b) and the 32 mm device inside the
sheath (arrow) (c). (d) deployment of the left disk (arrow) in the left atrium. (e) deployment of the
connecting waist (arrow) in the defect itself. (f) deployment of the right disk (arrow) in the right
atrium. (g) device release demonstrating good device position. (h) bicaval view showing good flow
in the superior vena cava and good device position
Patients are treated with daily aspirin for 6 months and endocarditis prophylaxis
when necessary for 6 months after the procedure. Full activity including competi-
tive and contact sports are allowed after 4 weeks of implantation.
Data Interpretation
Measurement of Qp:Qs ratio in the catheter laboratory is prone to errors, therefore,

evidence of the right-sided volume overload relies mainly on echocardiographic
findings. In adults older than 65 years and with large defects, it is prudent to mea-
sure the LA pressure during balloon occlusion of the defect to evaluate the LV
compliance. If an increase to > 18 mm of Hg in the LA pressure is observed, then a
LV conditioning treatment is started with anticongestive and afterload therapy for
48-72 hours prior to attempting the closure procedure [4].
Complications
Air embolism meticulous technique should be used to prevent air entry into the left
sided cardiac chambers which may result in coronary ischemia and stroke. Free flow of
blood from the sheath must be allowed, avoiding forceful negative pressure aspiration.
Device embolization if this occurs the device has to be removed either surgically or
by transcatheter snare techniques. One should avoid pulling the device across valves.
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290 F. Garay et al.
Prolapse of the left disc across the defect during deployment: especially in
patients with large defects and deficient antero/superior rims, resulting in left atrial
disc prolapse through the anterior/superior part of the ASD. Several technical
maneuvers can correct such malpositioning [5, 6]
Arrhythmias an increase in atrial arrhythmias occurs following the procedure, but
this is a transient phenomenon that usually resolves within 6 months. Heart block
has been rarely reported [7].
Right atrial and aortic root perforation Extremely infrequent (0.1 %). To minimize
this risk, device oversizing should be avoided [8].
Patent Foramen Ovale (PFO)
The foramen ovale is created by the overlap of septum primum and septum secun-
dum. Anatomic variants exist (flap type, tunnel type and PFO with aneurysmal sep-
tum primum). It has been described to remain probe-patent in 25 % of the population,
being a potential source of paradoxical emboli when a right-to-left shunting is pres-
ent. PFO has been demonstrated with a higher than normal prevalence in crypto-
genic stroke patients less than 55 years old and an association has been suggested
with an aneurysmal septum primum increasing this risk. Additionally, conditions
associated with elevated RA pressure (chronic pulmonary disease, recurrent pulmo-
nary embolus) and hypercoagulable states increase the potential for right-to-left
shunt and paradoxical emboli. In spite of medical management the risk of stroke
recurrence remains significant.
Several devices have been designed to specifically close PFO’s, however ASD
closure devices have also been used for PFO closure. The Amplatzer® PFO
Occluder is a self-expandable, double-disc device made from a Nitinol wire mesh
0.005–0.006 in. in diameter (Fig. 32.1). The two discs are linked together by a con-
necting waist 2 mm in diameter and 4 m in length. The discs are filled with polyester
fabric sewn securely to each disc by a polyester thread, that increases the device
closing ability. The device is similar in design to the ASD occluder, differing in that
the right atrial disc is larger than the left one.
Indications Patients with recurrent cryptogenic stroke due to presumed paradoxi-
cal embolus through a PFO and who have failed conventional medical therapy [9].
This procedure is usually performed off-label with an ASD device in the United
States as PFO closure has not yet been approved by the FDA. Randomized trials
have been negative in terms of the composite endpoint, but have suggested preven-
tion of recurrent paradoxical embolism-induced stroke in patients randomized to
device closure.
Contraindications The same as for secundum ASD closure.
Equipment The delivery system is similar to the ASD delivery system.
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Fig. 32.7 Intracardiac echocardiographic images to assess anatomy of the PFO in a patient who
sustained a stroke. (a, b) septal view without and with color Doppler demonstrating presence of a
PFO (arrow) with left-to-right shunt. (c, d) short axis view demonstrating the PFO (arrow) and
left-to-right shunt
Technique Similar to the ASD procedure [10]. A sheath is inserted into the fem-
oral vein. Heparin and antibiotics are administered. The procedure is performed
under general anesthesia or conscious sedation depending on the imaging modal-
ity used to guide deployment (TEE or ICE). Assessment of PFO anatomy and
rims (Fig. 32.7) should be performed (a minimal distance of 9 mm to the SVC and
to the aortic root is required to implant the device). In cases with an aneurysmal
septum a larger device is preferred. Unlike the ASD closure procedure, balloon
sizing is not performed. The device deployment is identical to ASD closure
(Fig. 32.8).
Data interpretation A contrast bubble study with and without Valsalva maneuver
under echocardiography or transcranial Doppler (TCD) is necessary to demon-
strate right-to-left interatrial shunting and is repeated at the end of the procedure to
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292 F. Garay et al.
Fig. 32.8 Intracardiac echocardiographic images in same patient as Fig. 32.7 during various
stages of device closure. (a, b) septal view without and with color Doppler demonstrating the PFO
(arrow). (c) contrast bubble study at rest showing passages of bubbles from right atrium to left
atrium. (d) passage of the delivery sheath (arrow) to the left atrium. (e) deployment of the left disk
of a 25 mm Amplatzer PFO device into the left atrium. (f) deployment of the right disk (arrow) in
the right atrium. (g) device has been released showing good position. (h) repeat contrast bubble
study showing negative result at end of Valsalva maneuver
document successful closure. Closure rates using the Amplatzer PFO device have
been over 95 % [10].
Complications
Right atrial and aortic root perforation Extremely infrequent. It has motivated the
company to introduce the septal measurements, emphasizing the distance of the free
right atrial wall from the defect and device.
Entrapment of prominent Eustachian Valve on the delivery cable it causes no prob-

lem with the deployment, however to avoid the avulsion of the Eustachian Valve, it
is suggested to advance the delivery sheath to the hub of the right disc prior to
releasing the cable from the device.
Clinical Vignettes
Case 1 (ASD Closure)
An asymptomatic 28year old female patient was diagnosed to have a secundum type
ASD. On a routine scheduled physical examination she was noted to have a widely
split S2 and a grade 2 systolic ejection murmur heard best at the left upper sternal
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border. The lungs were clear to auscultation. TEE revealed a large secundum ASD
measuring 26 mm with left-to-right shunting and evidence of right ventricle volume
overload. Cardiac catheterization performed under conscious sedation and ICE
guidance showed a significant left-to-right shunt with calculated Qp:Qs ratio of
4.1:1, the mean pulmonary artery pressure was 18 mm of Hg and PVR was 1.3
Wood units. ICE revealed a large ASD measuring 26 mm in diameter with left-to-
right shunt and a deficient anterior rim (Figs. 32.3 and 32.6).
A 32 mm Amplatzer septal occluder device was chosen and a 11 Fr Hausdorf long
sheath was used to deliver the device. ICE revealed complete closure. The patient was
discharged 24 h later with TTE showing proper device position and no residual shunt.
Case 2 (PFO Closure)
A 42-year old female patient chronically treated with aspirin, presented reporting the
sudden onset of right-sided weakness and dysarthria while driving her car. On exam-
ination, she was noted to be aphasic with a facial droop and right upper and lower
extremity hemiplegia. She was treated with heparin and aspirin with clinical resolu-
tion of most symptoms overnight. One day later, an MRI of the brain revealed an
infarct in the distribution of the left middle cerebral artery with evidence for a prior,
clinically unrecognized event in the right parietal cortex.. Work-up was remarkable
solely for a PFO with right-to-left shunting and an atrial septal aneurysm.
She was referred for device closure for recurrent stroke in the setting of anti-
platelet therapy. The procedure was done under ICE guidance (Fig. 32.7) and a
25 mm Amplatzer PFO device was successfully implanted (Fig. 32.8). Her ICE and
TCD were negative for residual shunt after the closure.
References
1. Harper RW, Mottram PM, McGaw DJ. Closure of secundum atrial septal defects with the
Amplatzer septal occluder device: techniques and problems. Catheter Cardiovasc Interv.
2002;57(4):508–24.
2. Omeish A, Hijazi ZM. Transcatheter closure of atrial septal defects in children & adults using
the Amplatzer Septal Occluder. J Interv Cardiol. 2001;14(1):37–44.
3. Hijazi Z, Wang Z, Cao Q, Koenig P, Waight D, Lang R. Transcatheter closure of atrial septal
defects and patent foramen ovale under intracardiac echocardiographic guidance: feasibility
and comparison with transesophageal echocardiography. Catheter Cardiovasc Interv.
2000;52(2):194–9.
4. Schubert S, Peters B, Abdul-Khaliq H, et al. Left ventricular conditioning in the elderly patient
to prevent congestive heart failure after transcatheter closure of atrial septal defect. Catheter
Cardiovasc Interv. 2005;64:333–7.
5. Wahab H, Bairam A, Cao Q, et al. Novel technique to prevent prolapse of the Amplatzer Septal
Occluder through large atrial septal defect. Catheter Cardiovasc Interv. 2003;60(4):543–5.
6. Dalvi B, Pinto R, Gupta A. New technique for device closure of large atrial septal defects.
Catheter Cardiovasc Interv. 2005;60:102–7.
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294 F. Garay et al.
7. Hill S, Berul C, Patel H, et al. Early abnormalities associated with transcatheter closure of
atrial septal defects using the Amplatzer septal occluder. J Interv Card Electrophysiol.
2000;4(3):469–74.
8. Amin Z, Hijazi Z, Bass J, et al. Erosion of Amplatzer Septal Occluder device after closure of
secundum atrial septal defects: review of registry of complications and recommendations to
minimize future risk. Catheter Cardiovasc Interv. 2004;63:496–502.
9. Landzberg MJ, Khairy P. Indications for the closure of patent foramen ovale. Heart.
2004;90(2):219–24.
10. Hong T, Thaler D, Brorson J, et al. Transcatheter closure of patent foramen ovale associated
with paradoxical embolisim using the amplatzer pfo occluder: initial and intermediate-term
results of the U.S. multicenter clinical trial. Catheter Cardiovasc Interv. 2003;60(4):524–8.
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Chapter 33
Balloon Valvuloplasty
Ted Feldman
Balloon valvuloplasty is used to treat stenotic lesions of the pulmonic, aortic, and
mitral valves. The patient populations appropriate for this procedure are highly
different for each of the three valve types. The major contraindication to balloon
valvuloplasty in any of these valve positions is severe valvular regurgitation.
Aortic Valvuloplasty
Indications
Balloon aortic valvuloplasty (BAV) is first choice therapy for aortic stenosis in chil-
dren and young adults, age 21 years or less. In older adult patients, it is infrequently
a first choice therapy because restenosis occurs in most patients between 6 months
and 2 years after the therapy is initially applied. It is indicated as a bridge to surgery
in hemodynamically unstable high-risk patients prior to aortic valve replacement,
for palliation in patients with serious comorbid conditions, and prior to noncardiac
surgery in some patients. The most common use of BAV in current practice is as a
bribge to TAVR for patients with debilitating symptoms or refractory heart failure.
It is also increasingly used for patients who are not candidates for either aortic valve
replacement surgery or TAVR, as a palliative treatment for temporary relief of
symptoms. It is not used as an alternative to aortic valve replacement. Patients are
selected on the basis of symptoms of angina, dyspnea or syncope in association with
echocardiographic evidence for aortic stenosis, usually with an aortic valve area
<0.8 cm2, although patients with valve area 0.8–0.9 cm2 are occasionally treated.
T. Feldman, MD
Cardiology Division, Evanston Hospital,
Walgreen Bldg 3rd Floor, 2650 Ridge Ave, Evanston, IL 60201, USA

DOI 10.1007/978-1-4471-7290-1_33
ERRNVPHGLFRVRUJ
296 T. Feldman
Contraindications
The major contraindications to BAV are the patient who is a candidate for aortic
valve replacement, and then among patients in whom BAV is desired, inability to
accomplish retrograde catheterization or contraindications to transseptal catheter-
ization are strong relative contraindications.
Equipment
10–14F sheaths for arterial or venous approaches

0.032 ̋ & 0.035 ̋ extra-stiff 260–300 cm length guidewires
Transseptal sheath & needle for antegrade BAV
Temporary pacemaker
PA catheter (Swan-Ganz)
percutaneous suture closure devices
18–24 mm balloon catheters with 120 cm shaft for retrograde BAV
26 mm Inoue balloon catheter for antegrade BAV
Techniques
The techniques for performing aortic valvuloplasty include the conventional

retrograde approach (Fig. 33.1) and the less frequently utilized antegrade trans-
septal approach [1]. Retrograde valvuloplasty requires a 10–12 French arterial
sheath. After placement of a large sheath, the valve is crossed retrograde, and a
balloon catheter ranging from 18 up to 24 mm diameter is passed retrograde
across the valve and inflated to relieve the stenosis. The balloon size is usually
estimated from the annulus diameter on transthoracic echo or the short axis of the
annulus diameter on TEE. Rapid right ventricular pacing is used as a method to
diminish balloon “watermelon seeding” during balloon inflations. Without this
adjunct, ventricular systole, especially in patients with preserved left ventricular
systolic function, ejects the balloon during attempts to inflate it in the stenotic
aortic valve. Burst pacing at between 140 and 200 beats per minute effectively
reduces cardiac output sufficiently to allow the balloon to be positioned stably for
inflations. Shorter balloons can thus be used, which diminishes the time of the
inflation-deflation cycle. Temporary pacing is also needed if there is underlying
bundle branch block.
The use of suture preclosure has diminished the challenges in managing the large
arterial puncture [2]. Using a single 10 French Perclose device or one or two 6
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33 Balloon Valvuloplasty 297
Fig. 33.1 Retrograde

BAV. A curved giudewire
is placed across the aortic
valve into the left
ventricular (LV) apex from
the retrograde femoral
arterial approach. A
temporary pacemaker is
used to pace the LV at
160–200 bpm while the
balloon is inflated
French Proglide devices, immediate hemostasis can be obtained in the vast majority
of patients, without any need to reverse the heparin anticoagulation.
Antegrade BAV have been described. A 14 French sheath can be placed in the
right femoral vein to allow transseptal access and antegrade passage of a wire loop
through the circulation, followed by balloon placement. Venous preclosure may be
used as well, which similarly simplifies the management of the large venous punc-
ture. Antegrade valvuloplasty may be performed with a conventional balloon or
with an Inoue balloon. The valve areas achieved with the Inoue device are signifi-
cantly greater than with a conventional balloon. The antegrade approach is more
complex technically, but has the advantages of eliminating the need for a large
arterial puncture, allowing more stable positioning of the balloon in the valve, and
facilitating the delivery of larger balloon into the valve orifice. Since the routine use
of rapid pacing the antegrade approach is rarely used.
Data Interpretation
Interpretation of hemodynamic data during the procedure is based on measurement

of transvalve pressure gradient and cardiac output with calculation of valve areas
(Fig. 33.2) [3]. Most patients have an initial aortic valve area between 0.4 and
0.8 cm2. Typical post-procedure results involve increases in valve area up to 0.9–
1.2 cm2. One standard definition of procedure success is a 50 % increase in valve
area or a 50 % decrease in mean transvalvular pressure gradient.
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298 T. Feldman
Fig. 33.2 Transaortic valve pressure gradient before and after BAV. The left panel shows a mean
gradient of 45 mmHg (shaded area), representing the difference between the left ventricular and
aortic pressures. The valve area was 0.6 cm2. After BAV the mean gradient has decreased to
12 mmHg, and the valve area has increased to 1.3 cm2. Aorta aortic pressure, LV left ventricular
pressure
Complications
Major complications of the procedure are vascular access complications, damage

to the aortic valve, or cardiac perforation. Large vascular sheaths are used for either
venous or arterial access. Bleeding complications can be common and transfusion
is needed in 25 % of patients when manual compression is used for arterial hemo-
stasis. Bleeding complications are minimized by the use of suture closure tech-
niques following the procedure. Some patients have dramatic hypotension and left
ventricular failure immediately following balloon inflations, which in some cases
leads to fatality on the catheterization laboratory table. Permanent pacemakers for
heart block are required in 1 % or 2 % of patients, especially if underlying bundle-
branch block is present to begin with. Hospital mortality is 5–8 % in this elderly,
highly sick patient population when BAV is done as primary therapy, and probably
less when BAV is done as a bridge to TAVR [4].
Clinical Vignette
An 84 year old man presents with CHF and is found to have aortic stenosis with a
Doppler estimated aortic valve area of 0.6 cm2. The transvalve mean and peak gradi-
ents are 54 and 76 mmHg, and left ventricular function is moderately depressed with
ejection fraction 40 %. He has a history of CABG at age 70 and then again at age 78
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years. The ECG shows atrial fibrillation with a rate of 85 bpm. Angiography shows a
patent LIMA to LAD, patent native RCA, and occluded native and graft circumflex sup-
ply. In addition he has chronic kidney disease and recently diagnosed lung cancer.
His STS risk score is 16 % and due his untreated cancer and frailty he is felt not to
be a candidate for TAVR. Thus, balloon valvuloplasty is an attractive palliative ther-
apy. BAV was performed using the antegrade approach. Right femoral venous 6F
access was obtained, and a 6F Closer S device was used to place a suture. Baseline
right heart pressures were measured. A 14F sheath was placed. After transseptal
puncture, baseline transaortic gradient was assessed & valve area calculated. A bal-
loon flotation was passed from LA to LV, and then antegrade across the aortic valve
into the descending aorta. A guidewire was passed through the balloon catheter and
snared in the descending aorta. The transseptal catheter was exchanged for a Inoue
26 mm balloon. This was passed over the wire to the aortic valve and inflated once to
accomplish valve dilatation. Final transaortic valve pressure gradients were measured
and valve area calculated. The 14F venous sheath was removed with pre-placed
suture closure. He was discharged from the hospital the next morning.
Pulmonic Valvuloplasty
Indications
Balloon valvuloplasty (PBV) is the treatment of choice for patients with pulmonic
stenosis. It is indicated for patients with pulmonic stenosis and symptoms of exer-
tional dyspnea, angina, syncope, or presyncope. Asymptomatic patients with normal
cardiac output and peak gradient greater than 50 mm should be treated as well.
Treatment is controversial in patients who are asymptomatic with normal cardiac
output and peak gradient between 30 and 50 mmHg. Asymptomatic patients with
gradients less than 30 mmHg should not be treated with balloon valvuloplasty. The
treatment is highly durable with clinical improvement in symptomatic relief in the
vast majority of patients lasting for decades [5–6].
Contraindications
The major contraindication is more than moderate pulmonic insufficiency.
Equipment
12–14 F sheaths for femoral venous access

Dual lumen catheter
0.035 ̋ & 0.038 ̋ extrastiff 260–300 cm length guidewires
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300 T. Feldman

22 & 24 mm balloon catheters with 120 cm shaft
26–30 mm Inoue balloon catheters
Technique
The procedure is performed via femoral venous access [7]. A guidewire is passed
across the stenotic pulmonic valve, and transvalve pressure gradient measured with
a dual lumen catheter. A balloon catheter is passed across the valve. It is important
to measure the valve annulus diameter using echocardiography prior to the proce-
dure so balloon sizing can be appropriate. A single large balloon is adequate in the
majority of patients. A balloon to annular diameter ratio of 1.2 is ideal. Occasional
patients require double balloon technique to achieve an adequate result. The Inoue
balloon may be used and is available in diameters up to 30 mm, which will be suit-
able for the majority of patients.
Data Interpretation
Transvalvular pressure measurement is used before and during the pressure to assess
the degree of stenosis. Gradient >50 mmHg at rest is typical. Valve areas are not
routinely reported for this procedure, but are useful to follow and should be mea-
sured in adult patients. After valvuloplasty the PA pressure changes little. Diminished
RV pressure is mostly responsible for the decreases in gradient.
Complications
The major complications include vascular access bleeding, which is not ordinarily
problematic because the access is venous. Pulmonic insufficiency may result and is
usually tolerated acutely [8].
Clinical Vignette
A 43 year old man presents with fatigue. After a heart mumur is noted he is
found to have congenital pulmoinc stenosis on echo. The mean gradient is esti-
mated to be 80 mmHg and there is no pulmonic regurgitation. There is RV
hypertrophy without chamber enlargement. The pulmonic annulus diameter
measured 23 mm.
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Right femoral 14 access was obtained. Arterial pressure was monitored by cuff.
Pressures were measured, and after the transpulmonic gradient was confirmed, a
28 mm Inoue balloon was passed into the valve and inflated twice. The balloon was
removed and a double lumen catheter passed back across the valve. Repeat pressure
measurement showed a decrease in transpulmonic gradient to 35 mmHg. The single
right femoral venous sheath was removed with manual compression. After 6 h of
bed rest the patient was ambulated and then discharged.
Mitral Valvuloplasty
Indications
Balloon mitral valvuloplasty is also referred to as balloon mitral valvotomy (BMV),

or percutaneous transvenous mitral commissurotomy (PTMC). BMV is indicated for
symptomatic patients with mitral valve area 1.5 cm2 or less and favorable valve mor-
phology [9]. The most important contraindication is left atrial thrombus seen on
transesophageal echo, which is necessary for screening all patients, in the absence of
moderate to severe mitral regurgitation. Favorable leaflet morphology is related to the
pliability of the leaflets, symmetry of commissural fusion, and the degree of leaflet
calcification and subvalvular deformity. Asymptomatic patients with valve area less
then 1.5 cm2 and pulmonary artery systolic pressure greater than 50 mm at rest or
60 mm with exercise, may be treated as well. Severely symptomatic patients with
highly calcified valves who are high risk for mitral valve replacement can be treated
as well. Treatment for asymptomatic patients with new atrial fibrillation is controver-
sial. Patients with mild mitral stenosis should not be treated with balloon valvotomy.
Contraindications
The most important contraindication for BMV is left atrial thrombus, which may be
seen in as many as 20 % of patients screened for the procedure, even among those
taking coumadin anticoagulation therapy. The addition of more intense anticoagu-
lant therapy will result in resolution of the thrombus in most patients within 6 t o 12
weeks, allowing performance of the procedure at a later time.
Technique
Numerous techniques exist, among them the double balloon technique, Inoue bal-
loon technique, metal commissurotome, and retrograde transarterial technique [10].
Dilatation is usually performed via an antegrade approach using transseptal punc-
ture. The most commonly used device for catheter mitral valvotomy worldwide is
the Inoue balloon catheter. This is a novel single balloon that inflates in three stages
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302 T. Feldman
Fig. 33.3 Sequence of balloon inflation for Inoue technique BMV. (a) Partially inflated Inoue bal-
loon, across the mitral valve, in the left ventricle. (b) the balloon is pulled back to engage the mitral
leaflets and (c) fully inflated to split the valve commissures
(Fig. 33.3). After the balloon is passed into the left atrium, the front portion is
inflated in the manner a pulmonary artery catheter is inflated, and then the balloon is
maneuvered across the mitral valve. This is accomplished with the aid of a steering
stylette with a preformed anterior curve. The balloon is pulled back until it engages
the stenotic mitral orifice. As the balloon is inflated, the middle section opens, apply-
ing pressure to the commissures. The balloon may be inflated with increasing vol-
umes of contrast with resultant increases in diameter. After each balloon inflation
the pressure gradient can be measured and mitral regurgitation assessed either by
echocardiographic visualization or by repeat ventriculography. Successive inflations
at larger balloon diameters is then performed until either a minimum gradient is
achieved or mitral regurgitation begins to increase. This is called the step-wise
method for commissurotomy.
The procedure may also be accomplished using conventional balloons. Typically
two balloons of 15–20 mm diameter are used together. Two wires must be passed
through the transseptal puncture to accomplish this. The wires are looped in the ven-
tricular apex and sometimes passed into the aorta to provide stability for advancing
the balloons into the mitral orifice. The balloon catheters for this approach are longer
than the Inoue balloon and either the balloon catheter tips or the guide wire may
cause ventricular apical perforation. It is also possible to pass balloons retrograde
from the aorta through the left ventricle and across the initial valve. This approach
avoids transseptal puncture, but requires large bilateral femoral sheaths.
The metal commissurotome is a mechanical metal dilator placed on a catheter
shaft. This can be passed into the mitral valve and opened to split the commissures.
The major advantage of this device is that it is a reusable instrument and is especially
attractive in parts of the world where catheter reuse is the rule rather than the excep-
tion. A disadvantage is the large French size and rigidity of the metal working end
of this device. It can be difficult to position in the mitral valve, and cardiac perfora-
tion is a risk. This device is not available in the United States.
Equipment
14F sheath for R femoral venous access

Transseptal sheath & needle
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PA catheter (Swan-Ganz)
26, 28 and 30 mm Inoue balloon catheters
Data Interpretation
Screening transthoracic echo is the first critical step in patient evaluation. The valve
leaflets and subvalvular apparatus must be examined for patient selection for the
procedure. An echocardiographic scoring system assigning 4 points to each of these
categories (maximum score 16) has been devised as a rough guide to patient selec-
tion. Patients with low score (6–9) have the best long-term results. Patients with
higher scores may be treated, recognizing that results will be less durable. Poor
candidates for surgery may be treated even with severe valve deformity (echo score
10–16) as a palliative procedure. During the procedure results are assessed by
hemodynamic measurement of the transvalvular pressure gradient (Fig. 33.4). The
mean gradient typically decreases from 12–14 to 4–6 mmHg. Results are also
assessed by echo measurement of the mitral valve area. Both left ventriculography
in the cath lab and Doppler echo are used to assess mitral regurgitation before and
after BMV.
Fig. 33.4 Transmitral

pressure gradient before
and after BMV. The left
panel shows a mean
gradient of 16 mmHg
(shaded area), representing
the difference between the
left atrial and left
ventricular pressures. The
valve area was 1.cm2. After
BMV the mean gradient
has decreased to 6 mmHg,
and the valve area has
increased to 2.0 cm2. LA
left atrial pressure, LV left
ventricular pressure
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304 T. Feldman
Complications
Major complications of BMV include worsening mitral regurgitation, which is seen

in at least a minor degree in at least 15 % of patients [11]. Severe mitral regurgitation
necessitating mitral valve replacement during the same hospitalization occurs in
2–4 % of patients. Hospital mortality is typically less then 1 %. TIA or stroke also
occurs in less than 1 % of patients. Transseptal puncture is necessary to accomplish
the procedure using antegrade approaches, and cardiac perforation occurs in one half
percent to one and one-half percent of patients. Atrial septal defect complicating the
transseptal puncture with a significant clinical shunt occurs in less than 2 % of patients.
Clinical Vignettes
Case 1
A 33 year old Asian woman presents in the 5th month of pregnancy with dyspnea at
rest. A murmur is noted, and echo shows mitral stenosis with a transmitral gradient
of 20 mmHg, pliable non-calcified leaflets, and no regurgitation. The valve area is
0.6 cm2. TEE shows no left atrial appendage thrombus.
Once on the catheterization table, right femoral 14 F venous access is obtained.
To minimize x-ray exposure, transthoracic echo is used during the procedure to mon-
itor the valve gradient and regurgitation, rather than using hemodynamic measure-
ments. Transseptal puncture is performed. The atrial septum is dilated and the Inoue
balloon placed in the left atrium, then maneuvered into the left ventricle. The balloon
is inflated partially, pulled back against the stenotic valve, and fully inflated. Echo
shows no mitral regurgitation, but the gradient has only decreased to 12 mmHg and
the valve area is 0.8 cm2. A second inflation using a larger inflation volume (and
therefore a larger inflated diameter) is performed, with resultant mild mitral regurgi-
tation and a valve area of 1.9 cm2. The sheaths are removed and after 6 h bedrest the
patient is ambulated. She is discharged the next morning.
Case 2
A 157 cm tall, 54 year old woman presents with a history of slowly increasing dys-
pnea on exertion. She has a history of rheumatic mitral stenosis, and the valve area
has decreased from 1.6 cm2 2 years ago to 1.2 cm2 on a recent echo exam. The is
mild mitral regurgitation. TEE shows no left atrial thrombus, and coronary angiog-
raphy shows no disease.
Bilateral femoral access is obtained, with left arterial 6 F access for pressure moni-
toring and ventriculography, left 8 F venous access for right heart catheterization and
ERRNVPHGLFRVRUJ
cardiac output measurement, and 14 F right venous for transseptal puncture and pas-
sage of the BMV balloon. After transseptal access, atrial septal dilatation, and passage
of the balloon into the left atrium and then left ventricle a first inflation is performed.
Initial balloon inflation diameter is estimated from patient height using the empiric
formula (height in cm/10)/10 = expected inflation diameter. In this case the expected
inflation diameter is 26 mm, so a first inflation of 24 mm is used. This results in no
change in the LA pressure or mitral gradient. A second balloon inflation to 25 mm has
similar results, but after the 3rd inflation to 26 mm balloon diameter the mean gradient
decreases to 7 mmHg and the valve area increase to 2.1 cm2. Repeat left ventriculog-
raphy shows no change in the mild mitral regurgitation. The sheaths are removed and
the patient ambulated after 6 h, She is discharged the next morning.
References
1. Sakata Y, Sayed Z, Salinger MH, Feldman T. Percutaneous balloon aortic valvuloplasty:

antegrade transseptal vs. conventional retrograde transarterial approach. Catheter Cardiovasc
Interv. 2005;64:314–21.
2. Solomon LW, Fusman B, Jolly N, Kim A, Feldman T. Percutaneous suture closure for manage-
ment of large French size arterial puncture in aortic valvuloplasty. J Invasive Cardiol.
2001;13:592–6.
3. Feldman T, Salinger M. Inoue balloon mitral commissurotomy and aortic valvuloplasty. In:
Kern MJ, editor. Interventional cardiac catheterization handbook. 2nd ed. St. Louis: Mosby-
Year Book; 2004. p. 441–80.
4. Kapadia S, Stewart W, Anderson WN, Babaliaros V, Feldman T, Cohen DJ, Douglas PS,
Makkar R, Svensson LG, Webb J, Wong SC, Brown DL, Miller DC, Moses JW, Smith CR,
Leon MB, Tuzcu EM. Outcomes of inoperable symptomatic aortic stenosis patients not under-
going aortic valve replacement: insight into the impact of balloon aortic valvuloplasty from the
PARTNER trial. J Am Coll Cardiol Intv. 2015;8:324–33.
5. Earing MG, Connolly HM, Dearani JA, Ammash NM, Grogan M, Warnes CA. Long-term
follow-up of patients after surgical treatment for isolated pulmonary valve stenosis. Mayo Clin
Proc. 2005;80(7):871–6.
6. Feldman T, Sanborn TA, O’Neill WW. Balloon aortic and pulmonic valvuloplasty. In:
Herrmann HC, editor. Contemporary cardiology: interventional cardiology-percutaneous non-
coronary intervention. Totowa: Humana Press; 2005. p. 29–48.
7. Pedersen WR, Goldenberg IF, Ben-Dor I, Feldman T. Aortic and pulmonic balloon valvulo-
plasty. In: Lasala JM, Rogers JH, editors. Adult structural heart disease: a practical guide for
clinicians, 1st edn. Elsevier, Maryland Heights, MO, USA & Oxford,UK; 2014. p. 50–72.
8. Feldman T, Perlowski A. Chapter 40: Percutaneous balloon mitral commissurotomy, mitral
repair, and pulmonic, tricuspid, and aortic valvuloplasty. In: Kern M, editor. The SCAI inter-
ventional cardiology board review. Philadelphia: Wolters Kluwer Health Lippincott Williams
& Wilkins; 2013. p. 406–16.
9. Feldman T. Hemodynamic results, clinical outcome and complications of Inoue balloon mitral
valvotomy. Cathet Cardiovasc Diagn. 1994;(Supp 2):2–7.
10. Feldman T, Herrmann HC, Inoue K. The technique of percutaneous transvenous mitral
commissurotomy using the Inoue balloon catheter. Cathet Cardiovasc Diagn. 1994;(Supp
2):26–34.
11. Feldman T, Salinger MH. Chapter 16: Percutaneous mitral commissurotomy and balloon aor-
tic valvuloplasty. In: Kern M, editor. Interventional cardiac catheterization handbook. 3rd ed.
Philadelphia: Elsevier Saunders; 2013. p. 340–64.
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Chapter 34
Transcatheter Aortic Valve Replacement
Jason B. Coker, James N. Hadstate, Andrew R. Weintraub,

and Daniel H. Steinberg
Aortic stenosis is the most common valvular pathology in the developed world.
The natural history of aortic stenosis is well established. For patients with severe
aortic stenosis (jet velocity >4 m/s, mean gradient >40 mmHg, valve area
<1 cm2), the cardinal symptoms of cardiac syncope, angina, or exertional dyspnea
portend a very poor prognosis with medical treatment alone. As such, The
American College of Cardiology/American Heart Association guidelines recom-
mend surgical aortic valve replacement for patients with severe, symptomatic
aortic stenosis [1].
Surgical valve replacement has been the standard of care for the overwhelming
majority of patients with symptomatic, severe aortic stenosis. However, many
patients, particularly those of advanced age, have comorbid conditions resulting in
elevated or prohibitive surgical risk. Unfortunately, for patients at prohibitive surgi-
cal risk, medical therapy does little to alter the natural course of disease. The advent
of transcatheter technologies has ushered in a new era in the treatment of valvular
heart disease.
J.B. Coker, MD • J.N. Hadstate, MD

Division of Cardiology, Medical University of South Carolina, Charleston, SC, USA
A.R. Weintraub, MD
Division of Cardiology, Tufts Medical Center, Tufts University School of Medicine,
Boston, MA, USA
D.H. Steinberg, MD (*)
Division of Cardiology, Medical University of South Carolina, Charleston, SC, USA
Division of Cardiology, MUSC, 114 Doughty St, MSC 592, Charleston, SC 29425, USA

DOI 10.1007/978-1-4471-7290-1_34
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308 J.B. Coker et al.
Indications
Appropriate patient evaluation is of paramount importance. The American College

of Cardiology/American Heart Association guidelines recommend the use of a heart
valve team in patients for whom transcatheter aortic valve replacement (TAVR) or
high-risk surgical valve replacement is being considered [1]. A heart valve team
typically consists of an integrated, multidisciplinary group of healthcare profession-
als with expertise in valvular heart disease, cardiac imaging, interventional cardiol-
ogy, cardiac anesthesia, and cardiac surgery [2]. Along with the heart valve team,
there are several objective risk stratification tools currently available to quantify risk
and assist in patient selection for TAVR. The two most commonly used risk tools are
the Society of Thoracic Surgery (STS) and the EuroSCORE.
On the basis of pivotal trials in elevated and extreme risk patients, TAVR is cur-
rently approved for patients deemed at elevated surgical risk as determined by a
heart valve team [1–4]. This determination typically involves either an STS score
predicted mortality of >8 % or 2 or more frailty criteria. Recently published studies
examined current and recent generation transcatheter systems in intermediate risk
patients defined as an STS score predicted mortality of 4–8 % or 1 frailty criterion
with encouraging results [5, 6]. Indications for TAVR in intermediate risk patients
may be expanded in the future. Randomized studies for patients at low risk for sur-
gical valve replacement are currently enrolling.
Contraindications
Absolute contraindications for TAVR implantation are limited to patients who have
less than 1 year life expectancy for reasons other than aortic stenosis. Relative con-
traindications for TAVR implantation are largely anatomic in nature. Inadequate
coronary heights or a narrow sinus of Valsalva may be considered relative contrain-
dications as the implantation of the TAVR can push that native valve leaflets back-
wards and potentially obstruct coronary arteries with a low take-off. This can be
overcome by protecting coronary arteries with wires and undeployed coronary
stents that can then be deployed if there is evidence of coronary obstruction.
Equipment
In the United States, two transcatheter technologies are currently available for com-
mercial use, the balloon expandable Sapien S3 Valve (Edwards Life Sciences, Irvine
CA) (Fig. 34.1) and the self-expanding CoreValve Evolut R (Medtronic, Minneapolis,
MD) (Fig. 34.2). The S3 platform is available in 20, 23, 26 and 29 mm sizes deliv-
ered through a specially- designed 14 French sheath (the 29 mm device requires a
16 French sheath). The Evolut platform is available in 23, 26, 29 and 31 mm sizes
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34 Transcatheter Aortic Valve Replacement 309
Fig. 34.1 (a) Balloon expandable Edwards Sapien three valve (b) Fluoroscopic image of deployed
Edwards Sapien three valve
Fig. 34.2 (a) Medtronic Evolut R CoreValve (b) Fluoroscopic image of deployed medtronic
Evolut R CoreValve
typically delivered via an in-line 14 French sheath (the 31 mm device requires an 18

French sheath). Equipment used in our current practice is summarized in Table 34.1.
Techniques
Current ACC/AHA guidelines recommend the use of a hybrid operating theatre for
implantation of the transcatheter aortic valve, although at some centers, there has
been a transition to procedural performance in appropriately outfitted
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Table 34.1 Procedural equipment

Equipment Comments
Basic Hybrid suite Capable of full catheterization and surgical
essentials needs
Anesthesia setup General or conscious sedation
Surgical setup
Perfusion pump Not necessarily primed, but available
Transvenous pacemaker
Transesophageal As appropriate, not necessary for all cases
echocardiography
PCI equipment Standard guides, wires, stents available
Covered stents Available for vascular complication
Sheaths Standard access equipment May require longer sheaths
Specialty sheath Multiple types available – based on specific
procedure and access site
Catheters JR4, AL1 For crossing valve (others as appropriate)
2 Pigtail catheters For exchange, aortography and hemodynamic
evaluation
Wires 0.035″ angiographic Both 150″ and 260″
0.035″ straight tip For crossing – we prefer hydrophilic wire
0.035″ extra/super stiff Depends on valve type, dedicated pre-curved
wires available
Specialty Valvuloplasty balloon Size chosen by purpose (i.e. priming, sizing,)
Transcatheter valve As appropriate
catheterization laboratories. Current guidelines also mandate that both an interven-

tional cardiologist and cardiothoracic surgeon be present for the procedure [1].
The preoperative evaluation is summarized in Fig. 34.3, and it is essentially con-
gruent with a surgical evaluation with the addition of Multidetector Computed
Tomography (MDCT). This modality is of particular importance for TAVR as it
enables one to choose the appropriate device size based on aortic annular area/
perimeter, evaluate left ventricular outflow tract and valvular calcification, assess
coronary heights, sinus width, sinotubular junction diameters/calcification, angio-
graphic views and potential access routes (Fig. 34.4). While many of these variables
can be assessed through alternative modalities, MDCT is a singular, detailed and
three-dimensional modality with dedicated software systems allowing for reliable
and reproducible analyses and pre-TAVR planning.
Regarding access, the transfemoral route is generally favored for patients with
suitable iliofemoral anatomy to accommodate currently available devices, and
approximately 80 % of procedures are now performed via transfemoral access. For
patients with iliofemoral disease precluding device delivery, alternative access
routes are possible. These alternative sites include open iliac (via conduit), subcla-
vian, direct aortic or transapical. Additionally, direct carotid or transcaval access
(with crossover from the inferior vena cava to the aorta) may be of utility in appro-
priately selected patients.
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• History and Physical

• 2D Echocardiogram
Initial
• Assess comorbid conditions
Assessment • Surgical consultation
• Establish indications for treatment
• TEE if needed
• Catheterization (coronary angiography as indicated, hemodynamics as appropriate)
• MDCT
Ancillary Studies • Pulmonary function tests
• Carotid Studies
• Laboratory studies
• Decision to treat patient

Multidisciplinary • Modality (surgical or transcatheter)
Discussion • Device selection/size
• Anticipated issues/concerns
• Assessment of success
and complications
Procedure
• Post-procedure
monitoring
Fig. 34.3 Procedural evaluation
Fig. 34.4 MDCT assessment. (a) Annulus measurement. (b) Coronal angle at level of annulus. (c)
Sagittal angle at level of annulus. (d) Left coronary height. (e) Right coronary height. (f) Sinus of
Valsava measurements. (g) Right iliofemoral minimums. (h) Iliofemoral scout. (i) Left iliofemoral
minimums
Typical procedural steps for each device are outlined here and described in the
clinical vignettes below. Regardless of the planned primary access site, additional
arterial access is obtained for annular assessment and venous access is obtained for
delivery of a transvenous temporary pacemaker. A pigtail catheter is advanced to the
aortic root and aortography is then performed to identify the annular plane. The
aortic valve is crossed with a straight wire using a JR4 or AL1 coronary catheter,
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and a second pigtail is exchanged for measurement of simultaneous left ventricle-

aortic pressure gradient. A stiff 0.035″ wire is then advanced into the left ventricle.
Priming valvuloplasty is typically preformed under conditions of rapid pacing.
Following priming valvuloplasty, the valve is placed across the aortic valve with
appropriate position confirmed by aortography prior to valve deployment.
The valves are deployed via respective techniques (described in the vignettes
below). Hemodynamic assessment is performed with simultaneous left ventricle-
aortic pressure measurements to assess post implantation gradient and aortic insuf-
ficiency. Positioning and aortic insufficiency is also assessed through aortography
and echocardiography as indicated. Post dilation is performed as needed, usually to
address perivalvular regurgitation. Access site management/closure is performed
based on the chosen access site. In patients undergoing balloon expandable valve
implantation, the pacing wire can be removed if there is no evidence of conduction
disturbance, while for those receiving a self-expanding valve, the temporary pacing
wire should remain in place up to 48 h prior to removal given the enhanced risk of
conduction disturbances with these devices.
Data Interpretation
After valve implantation the operator must assess multiple factors before the proce-
dure is considered successful. Immediate attention is given to the acute hemody-
namics and recovery of systemic pressures. The ECG is examined for conduction
disturbances and/or ST changes suggestive of coronary occlusion. Once stable, the
post implantation pressure gradient is directly measured via catheters in the left
ventricle and aortic root followed by an assessment of aortic insufficiency and coro-
nary patency by aortic root angiography. A transvalvular gradient of <10 mmHg is
expected in the majority of cases, and an increased gradient should lead to re-
evaluation of the valve for complete expansion.
While trace to mild residual aortic insufficiency is generally acceptable, greater
than moderate aortic regurgitation after implantation has been shown to predict long
term mortality throughout TAVR trials. Aortic insufficiency is visually assessed by
aortography and clinically assessed via assessment of diastolic pressure separation.
More than mild-moderate AI should lead to re-evaluation of valve expansion and
deployment location for potential remedies such as post dilation or implantation of
a second valve.
Complications
For purposes of data collection and consistency, complications have been precisely
defined by the Academic Research Consortium and are reported in the Transcatheter
Valve Technologies registry (a requirement for reimbursement in the United States)
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[7]. Procedural success is defined as successful vascular access and appropriate

placement of a single valve with less than moderate aortic insufficiency. With
increased global experience and device iteration, procedural success approaches
95–100 %, and overall complication rates continue to improve with intraprocedural
mortality generally less than 1 % and in-hospital mortality less than 5 %. Major
acute complications include annular rupture, ventricular perforation, acute aortic
insufficiency, coronary obstruction, complete heart block and vascular compromise.
These complications often manifest with acute hemodynamic, electrocardiographic
or echocardiographic changes. Treatment depends on the cause and temporizing
resuscitative measures are often employed while the underlying issue is addressed.
In the post-operative period, the more important complications following TAVR
include clinically evident stroke in about 3–5 % of cases and conduction distur-
bances requiring permanent pacemaker implantation in up to 20 % of cases depend-
ing on the particular valve used. Conduction abnormalities following TAVR are
related to the close proximity of the aortic annulus and specialized conduction tis-
sue, and these are more common with self-expanding valves compared to balloon
expandable devices. Rates of complete heart block also appear dependent on the
depth of implantation relative to the annulus [7].
Clinical Vignette 1
Case #1
A 79 year old male with hypertension, hyperlipidemia, diabetes on oral medica-

tions, moderate lung disease, chronic renal insufficiency, coronary artery disease
with prior CABG, chronic diastolic heart failure and severe aortic stenosis pre-
sented for evaluation. Symptoms were consistent with New York Heart Association
Class 3, and after multidisciplinary evaluation, he was considered at elevated risk
for surgical AVR with an STS predicted risk of mortality of 8.4 %. Physical exam
was consistent with severe aortic stenosis. Echocardiogram demonstrated an ejec-
tion fraction of 60 %, annular diameter 21 mm, aortic valve area of 0.8 cm2, peak
velocity 4.2 m/s and mean gradient 43 mmHg with trace aortic insufficiency.
Coronary artery angiography demonstrated multivessel coronary disease with pat-
ent grafts. CTA of the chest, abdomen and pelvis revealed a trileaflet aortic valve, a
calcium score 6348, annular area 470 mm2, annular-coronary heights greater than
10 mm bilaterally, and iliofemoral minimal diameters of 6.6 mm at the left common
femoral artery, and 6.2 mm at the right common femoral artery.
Percutaneous access was obtained on the right common femoral artery.
Contralateral arterial and venous access was obtained percutaneously. The right
common femoral artery was “preclosed” with 2 suture devices, and using standard
techniques, a 14 French hemostatic sheath was secured in place. The aortic valve
was crossed with a 0.038″ straight-tipped Glidewire and a JR4 catheter. A 0.035″
extra stiff wire was advanced into the ventricle. A priming valvuloplasty was per-
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formed with a 23 mm × 4 cm balloon under rapid pacing. With rapid pacing and
under both fluoroscopic and aortographic guidance, the valve was deployed. After
full deployment, rapid pacing was ceased. Valve positioning and aortic insufficiency
was assessed by aortography and hemodynamics. All equipment was removed, and
percutaneous closure commenced. Completion angiography was performed with no
complications noted.
The patient improved post procedure and was discharged 48 h post TAVR
implant. Predischarge echocardiography demonstrated normal LV systolic function
with a mean gradient across the aortic prosthetic valve of 16 mmHg with trace para-
valvular regurgitation.
Case #2
A 77 year old frail female with hypertension, hyperlipidemia, diabetes on oral

medications, mild lung disease, chronic renal insufficiency, chronic diastolic heart
failure and severe aortic stenosis presented for evaluation. Symptoms were consis-
tent with New York Heart Association Class 3 congestive heart failure, and after
multidisciplinary evaluation, she was considered at elevated risk for surgical AVR
with an STS predicted risk of mortality of 9.3 %. Physical exam was consistent with
severe aortic stenosis. Echocardiogram demonstrated an ejection fraction of 50 %,
annular diameter 20 mm, aortic valve area of 0.7 cm2, peak velocity 4.0 m/s and
mean gradient 40 mmHg with mild aortic insufficiency. Coronary artery angiogra-
phy demonstrated insignificant coronary disease. CTA of the chest, abdomen and
pelvis revealed a trileaflet aortic valve, a calcium score 1555, aortic annular area
380 mm2 and perimeter 68.7 mm, annular-coronary heights greater than 10 mm
bilaterally, and iliofemoral minimums of 6.4 mm at the left common femoral artery,
and 6.2 mm at the right common femoral artery.
Percutaneous access was obtained on the right common femoral artery.
Contralateral arterial and venous access was obtained percutaneously. A 6 F sheath
was inserted in the contralateral femoral artery, and a 5 French pigtail catheter was
placed via through the sheath in the ascending aorta. A transvenous pacemaker wire
was placed via the right internal jugular vein. Pacing thresholds were optimized,
and proper alignment of the aortic cusps was determined via aortography. The right
common femoral artery was “preclosed” with two suture devices, and a 14 F hemo-
static sheath was secured in place via standard techniques. Anticoagulation was
initiated with unfractionated heparin. The aortic valve was crossed with a 0.038″
straight-tipped Glidewire and a JR4 catheter. A soft 0.035″ exchange length wire
was advanced into the ventricle via the JR4, and a 6 F pigtail catheter was exchanged
over the wire. Simultaneous pressures were recorded. A 0.035″ super stiff exchange
length wire was advanced into the ventricle.
Under conditions of rapid pacing, a priming valvuloplasty was performed with a
20 mm × 4 cm balloon, which was then removed. The sheath was exchanged over
the super stiff wire for the in-line 14 F system. A 26 mm self-expanding CoreValve
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Evolut R was loaded onto the delivery catheter and advanced over the exchange
wire into position across the aortic valve. Under fluoroscopic, aortographic and
echocardiographic guidance, the valve was positioned precisely across the aortic
valve, and deployment commenced. Once annular contact was achieved, acceler-
ated pacing was started, and the valve was unsheathed further. After 2/3 deploy-
ment, pacing was ceased. Valve positioning and aortic insufficiency was assessed by
echocardiography and aortography. The valve was fully deployed and detached, the
delivery catheter was removed, and the pigtail catheter was advanced over the
exchange wire for hemodynamic, echocardiographic and aortographic assessment.
The pigtail was then removed.
The second pigtail catheter was placed into the descending aorta, and pacemaker
wire was kept in place. The delivery sheath was retracted, and percutaneous closure
commenced. A completion angiogram was performed. No complications were
noted, and all other equipment was removed.
The patient improved post procedure and was discharged 72 h post TAVR
implant. Predischarge echocardiogram demonstrated normal LV systolic function
with a mean gradient across the aortic prosthetic valve of 10 mmHg with trace para-
valvular regurgitation.
References
1. Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC guideline for the management of
patients with valvular heart disease: executive summary: a report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol.
2014;63(22):2438–88.
2. Leon MB, Smith CR, Mack M, et al. Transcatheter aortic-valve implantation for aortic stenosis
in patients who cannot undergo surgery. N Engl J Med. 2010;363(17):1597–607.
3. Smith CR, Leon MB, Mack MJ, et al. Transcatheter versus surgical aortic-valve replacement in
high-risk patients. N Engl J Med. 2011;364(23):2187–98.
4. Adams DH, Popma JJ, Reardon MJ, et al. Transcatheter aortic-valve replacement with a self-
expanding prosthesis. N Engl J Med. 2014;370(19):1790–8.
5. Leon MB, Smith CR, Mack MJ, et al. Transcatheter or surgical aortic-valve replacement in
intermediate-risk patients. N Engl J Med. 2016;374(17):1609–20.
6. Thourani VH, Kodali S, Makkar RR, et al. Transcatheter aortic valve replacement versus surgi-
cal valve replacement in intermediate-risk patients: a propensity score analysis. Lancet.
2016;387(10034):2218–25.
7. Kappetein AP, Head SJ, Genereux P, et al. Updated standardized endpoint definitions for trans-
catheter aortic valve implantation: the Valve Academic Research Consortium-2 consensus
document. J Am Coll Cardiol. 2012;60(15):1438–54.
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Chapter 35
Endomyocardial Biopsy
Johny Kuttab and Carey Kimmelstiel
Endomyocardial biopsy is an invasive procedure performed by interventional cardi-

ologists. The procedure is widely used to screen and survey transplanted hearts for
signs of cellular or humoral rejection allowing for titration of immunosuppressive
therapy. Although this remains the strongest indication for the procedure [1–3], its
clinical utility could be expanded to the diagnosis of other myocardial processes.
Indications
In general, the use of EMB is recommended in clinical scenarios in which the diag-
nostic yield of the procedure outweighs the procedural risk.
The following are indications for EMB [3]:
1. Surveillance for cardiac allograft rejection remains the most important indica-
tion for EMB.
2. Fulminant heart failure with hemodynamic compromise. The prototype for this
group of patients is lymphocytic myocardidites, eosinophilic myocarditis or
giant cell myocarditis.
3. New-onset heart failure associated with high degree atrioventricular (AV) block
or ventricular arrhythmias. These clinical manifestations could be suggestive of
giant cell myocarditis in which case tissue diagnosis is important for treatment
and prognosis.
J. Kuttab, MD (*)
C. Kimmelstiel, MD

DOI 10.1007/978-1-4471-7290-1_35
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318 J. Kuttab and C. Kimmelstiel
4. Chronic heart failure with high degree AV block or ventricular arrhythmias

which could be suggestive of cardiac sarcoidosis.
5. Unexplained restrictive cardiomyopathy. Cardiac amyloidosis and hemochroma-
tosis are diagnoses that fall within this group of infiltrative cardiomyopathies.
6. Hypereosinophilic syndrome and endomyocardial firboelastosis.
7. The workup of cardiac tumors.
8. The monitoring of anthracycline cardiotoxicity.
9. Unexplained cardiomyopathy in children.
10. The diagnosis of arrhythmogenic right ventricular cardiomyopathy when other
noninvasive or invasive modalities are inconclusive.
Contraindications
There are no absolute contraindications for EBM. Relative contraindications

include [3]:
1. Coagulopathy.
2. Hemodynamic compromise or active heart failure precluding patient positioning
and sedation.
3. Pericardial effusion or tamponade.
Equipment
1. Central venous access kit and sheath: Sheath size depends on the type of biop-
tome used.
2. Bioptome: There are various types of bioptomes. In general, two types of biop-
tomes – those with a floppy shaft which requires the use of a long sheath for
delivery and the more commonly used stiff shaft which is manipulated into the
region being biopsied (usually the right ventricle) after being introduced, via a
short sheath, located within a central vein.
3. Ultrasound (echocardiography) machine: Most EMBs are performed using fluo-
roscopic imaging for bioptome positioning. Occasionally, when a specific region
of the heart requires biopsy, echocardiography may be necessary to guide the
bioptome to that area of the heart. In addition, echocardiography is frequently
used to guide EMB in those instances where the risk of right ventricular perfora-
tion is elevated. Examples of this clinical scenario include patients with fulmi-
nant myocarditis eg. giant cell myocarditis where the combination of the
thin-walled right ventricle and a closed pericardium lead to a heightened risk of
myocardial perforation and subsequent cardiac tamponade. In such cases, echo-
cardiography is frequently used to ensure that the bioptome is pointed toward the
interventricular septum as opposed to the right ventricular free wall (Fig. 35.1).
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35 Endomyocardial Biopsy 319
Fig. 35.1 Panel (a) Fluoroscopic view (top) of bioptome (arrow) in an incorrect position.
Echocardiography (bottom) documents that the tip of the bioptome (arrow) is positioned against
the right ventricular free wall, near the apex – a position putting the patient at risk for perfora-
tion if biopsied there. Panel (b) Fluoroscopy shows that the bioptome (arrow) has been reposi-
tioned to a more appropriate location, pointing superior and posterior (top). Echocardiography
(bottom) documents that the bioptome (arrow) is pointing towards the interventricular
septum (star)
Technique
There are three commonly utilized access sites for EMB. The most commonly
used route is the right internal jugular vein. In this technique, the patient is
prepped and draped in a sterile fashion. Ultrasonography, although not absolutely
necessary, is commonly utilized for obtaining access to the vein. The venous
sheath is then inserted over a wire. Once the sheath is flushed, the bioptome is
inserted through the venous sheath under fluoroscopic guidance and advanced
superiorly and posteriorly towards the interventricular septum. Once positioning
is verified, the bioptome jaws are opened (Fig. 35.2), advanced towards the sep-
tum, and closed. The bioptome is pulled back gently at this time. Once the biop-
tome is free, it is pulled out of the venous sheath and the biopsied tissue is
removed from the forceps and the procedure is repeated over again. Occasionally,
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Fig. 35.2 (a) A bioptome, in the closed position, which has coursed from the right internal jugular
vein through the right atrium, into the right ventricle. (b) The bioptome is in the open position as
the interventricular septum is biopsied. (c) Three biopsies of myocardial tissue obtained during the
procedure
echocardiographic guidance may be utilized to assist in bioptome positioning

while performing EMB.
Other commonly used access sites include the subclavian/axillary vein and the
femoral venous approach. When the femoral vein is used, a longer bioptome is used
(105 cm) which is introduced through a long 7F venous sheath. Internal jugular and
subclavian approaches utilize the standard 50 cm bioptome introduced through a
standard 7F 11 cm long venous sheath.
In rare instances, the femoral arteries could be utilized for EMB of the left
ventricle.
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Data Interpretation
Storage of the sample is dictated by the clinical question to be answered. A mini-

mum of 5 right ventricular samples should be obtained if possible. Standard histo-
logical preparation using paraffin embedding, sectioning and staining can be used in
the diagnosis of allograft rejection, myocarditis or amyloidosis. Polymerase chain
reaction for the detection of viruses can be performed on paraffin-embedded tissue
although the sensitivity is higher when performed on liquid nitrogen frozen tissue.
Complications
The rate of complications during an EMB depends on multiple factors. It is reported

to be <6 % in most case series. The following are possible complications [1–3]:
1. Access site hematoma.
2. Supraventricular and ventricular arrhythmias
3. Transient right bundle branch block.
4. Tricuspid regurgitation.
5. Air embolism
6. Occult pulmonary embolism
7. Vein thrombosis.
8. Pneumothorax.
9. Bleeding.
10. Right ventricular perforation.
11. Pericardial effusion with tamponade physiology.
12. Death.
Clinical Vignettes
Case 1
A 58 year old female patient, presented to the Advanced Heart Failure and
Transplant clinic with progressively worsening dyspnea on exertion, lower extrem-
ity edema, orthopnea, paroxysmal nocturnal dyspnea and cough. She was initially
treated at a community hospital for possible flu, however she experienced a pro-
gressive clinical decline. Her initial echocardiographic assessment revealed an
ejection fraction of 30 %, with left ventricular hypertrophy, bi-atrial enlargement,
and Doppler parameters consistent with stage III diastolic dysfunction. On initial
assessment, she was found to have elevated levels of serum free light chains. A car-
diac MRI was pursued at that time and was significant for multifocal thickening of
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Fig. 35.3 Left – Endomyocardial biopsy from the patient in Case 1. Amyloid deposits appear as
light-pink hyaline extracellular deposits displacing cardiac myocytes. Right – Congo red staining
of the biopsy sample shows apple-green birefringence of the amyloid deposits
the myocardium with sparing of the anterior wall, multifocal delayed transmural
hyperenhancement with relative sparing of the anterior wall, and diffusely decreased
T1 signal, findings consistent with amyloidosis. Shortly after, she underwent a fat
pad biopsy to look for evidence of systemic amyloid. Unfortunately this was non-
diagnostic. An endomyocardial biopsy was ultimately done. Histological findings
(Fig. 35.3) were diagnostic for cardiac amyloidosis.
Case 2
A 57 year old man with a history of familial hypercholesterolemia, complicated by

coronary artery disease requiring multiple coronary artery bypass surgery devel-
oped worsening heart failure secondary to ischemic cardiomyopathy despite opti-
mal heart failure medications, necessitating an orthotopic heart transplantation.
His immediate post-transplant course was uneventful. Six months following trans-
plant, he presented with new onset cardiogenic shock, a newly depressed ejection
fraction and refractory ventricular tachycardia. He underwent a right heart cathe-
terization with an endomyocardial biopsy which was significant for high grade cel-
lular rejection. Based on the biopsy results, he underwent treatment with
thymoglobulin and high dose intravenous steroids with stabilization of his clinical
status.
References
1. Yilmaz A, Kindermann I, Kindermann M, et al. Comparative evaluation of left and right ven-
tricular endomyocardial biopsy: differences in complication rate and diagnostic performance.
Circulation. 2010;122:900.
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2. Cooper LT, Baughman KL, Feldman AM, et al. The role of endomyocardial biopsy in the
management of cardiovascular disease: a scientific statement from the American Heart
Association, the American College of Cardiology, and the European Society of Cardiology.
Circulation. 2007;116:2216.
3. From AM, Maleszewski JJ, Rihal CS. Current status of endomyocardial biopsy. Mayo clinic
proceedings. Mayo Clin Proc. 2011;86(11):1095–102.
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Chapter 36
Circulatory Support Devices
Navin K. Kapur and Michele Esposito
Introduction
The role of percutaneously-delivered mechanical circulatory support (pMCS)

devices in the cardiac catheterization lab has been expanding over the last decade.
Current pMCS options include the intra-aortic balloon pump (IABP), Impella axial
flow catheter, TandemHeart centrifugal pump, and veno-arterial extracorporeal
membrane oxygenation (VA-ECMO). The overall goals of pMCS systems are to:
(1) increase vital organ perfusion, (2) augment coronary blood flow, and (3) reduce
ventricular volume and filling pressures, thereby reducing wall stress, stroke work,
and myocardial oxygen consumption. Clinical scenarios where these devices are
commonly used include: advanced heart failure, cardiogenic shock, mechanical
complications after AMI, high risk coronary and non-coronary intervention, and
high-risk electrophysiologic ablations.
Intra-aortic Balloon Counterpulsation
The hemodynamic effects of IABP counterpulsation work to improve the myocar-

dial supply and demand balance. Rapid expansion of the balloon in early diastole
augments diastolic pressure and can increase coronary perfusion pressure. Rapid
deflation at end-diastole decreases left ventricular (LV) afterload by driving aortic
N.K. Kapur, MD (*)

Acute Circulatory Support Program, Interventional Research Laboratories, Cardiac Biology
Research Center, Tufts Medical Center, Boston, MA, USA
Department of Medicine, Tufts University School of Medicine, Boston, MA, USA
M. Esposito, MD
Acute Circulatory Support Program, Tufts Medical Center, Boston, MA, USA

DOI 10.1007/978-1-4471-7290-1_36
ERRNVPHGLFRVRUJ
326 N.K. Kapur and M. Esposito
Effect:
-Increased myocardial
perfusion
mm
Hg
120 C
D F
100
E
80
A
A. One Complete Cardiac Cycle Effects:

B. Unassisted Aortic End Diastolic Pressure -Decreased afterload
C. Unassisted Systolic Pressure
D. Diastolic Augmentation
-Decreased myocardial
E. Assisted Aortic End Diastolic Pressure oxygen consumption
F. Reduced Systolic Pressure -Increased cardiac output
Fig. 36.1 The IABP improves the myocardial supply and demand balance by increasing myocar-
dial perfusion during diastole and decreasing resistance to left ventricular ejection during systole
(with permission from Datascope)
Table 36.1 Hemodynamic effects of the IABP

Systolic BP Diastolic BP MAP HR CO PCWP
↓ ↑ No change or ↑ ↓ ↑ ↓
volume forward and reducing aortic pressure during systole (Fig. 36.1). Expected
effects on the hemodynamic profile of patients with cardiogenic shock include an
increase in the diastolic pressure; a decrease in the systolic pressure; an overall
maintenance or slight improvement in the mean arterial pressure; a reduction in the
heart rate; an elevation in the cardiac output; and a decrease in the pulmonary capil-
lary wedge pressure (Table 36.1) [1].
Indications
Hemodynamic Compromise
Indications for IABP placement include patients with acute myocardial infarction
(MI) and cardiogenic shock secondary to continued ischemia or myocardial stun-
ning. Without revascularization, survival rates in patients with cardiogenic shock
ERRNVPHGLFRVRUJ
36 Circulatory Support Devices 327
supported with IABP and medical therapy are quite poor. The IABP provides tem-
porary hemodynamic stabilization until definitive revascularization can be per-
formed. The IABP might also be used to support patients with shock due to
mechanical complications of MI—e.g. ventricular septal rupture – until corrective
surgery can be performed. Additionally, it has been shown to be an effective tempo-
rary therapeutic option in patients with shock due to non-ischemic reversible causes,
such as myocarditis or drug toxicity. IABP support is often used in patients who are
difficult to wean off bypass after cardiac surgery due to severe LV dysfunction or
secondary to myocardial stunning from prolonged cardioplegia. Patients with
refractory heart failure and those with end-stage cardiomyopathy awaiting cardiac
transplantation--i.e., “bridge to transplantation” -- might also gain benefit from
IABP support. Furthermore, the IABP can contribute to the management of patients
with medically intractable ventricular arrhythmias, including ventricular tachycar-
dia and ventricular fibrillation [1, 2].
Absence of Hemodynamic Compromise
The IABP is often used to alleviate medically refractory unstable angina in patients
awaiting definitive revascularization -- e.g., a patient with severe triple vessel coro-
nary artery disease awaiting bypass surgery. Prophylactic placement is employed in
patients with severe left main coronary obstruction or decompensated aortic steno-
sis awaiting surgery. The IABP might also be placed to mitigate continued ischemia
following complex/complicated percutaneous coronary intervention (PCI) or to
support patients with failed PCI. In addition, the prophylactic placement of IABP is
occasionally employed during high-risk PCI [1]
Contraindications
Major contraindications to IABP placement include significant aortic regurgitation,

abdominal or thoracic aortic aneurysm, aortic dissection, severe peripheral vascular
disease (aorto-iliac or femoral artery disease), severe bleeding diathesis, and uncon-
trolled septicemia.
Equipment
The intra-aortic balloon pump consists of a polyurethane balloon, which surrounds a

double lumen catheter that is mounted onto a flexible shaft and connected to a con-
sole. It is inflated by a helium gas control system, which is housed within the
console.
ERRNVPHGLFRVRUJ
Technique
Insertion
After the leg is shaved and prepped with anti-septic solution, the femoral artery is
accessed and J-tipped guide wire is passed through a needle to the aortic arch. After
an introducer sheath is inserted, the balloon is advanced over the guide wire with the
radiopaque tip positioned in the descending aorta just distal to the origin of the left
subclavian artery (generally at the level of the carina). When available, fluoroscopic
guidance should always be employed for IABP placement. If fluoroscopic guidance
is not available, the distance from the angle of Louis (or between the second and
third intercostal spaces) to the umbilicus and then obliquely over to the femoral
insertion site can be measured to determine the approximate distance the balloon
should be advanced. After positioning of the IABP is confirmed, the helium gas line
extending from the console is connected. Balloon counterpulsation is then initiated
at 1:2 setting (balloon inflation with every other beat) and fluoroscopy again is used
to confirm uniform expansion. Sheathless insertion is sometimes performed in
patients with peripheral vascular disease in an attempt to reduce the incidence of
lower limb ischemia. However, sheathless insertion does not allow for repositioning
once the balloon is placed, and is associated with higher rates of infection [1].
Inflation and deflation of the balloon are usually timed and triggered by the sur-
face electrocardiogram. Triggering can also be initiated by the arterial pressure
waveform or set to a fixed asynchronous cycle for patients with significant arrhyth-
mias—e.g., ventricular fibrillation – or patients on bypass. Pacing spikes should be
used to trigger the balloon in patients with 100 % paced rhythms. Adjustments to
timing are performed with initial pump triggering set at 1:2, thereby allowing com-
parison of the arterial tracing with and without counterpulsation (Fig. 36.2). Timing
of inflation is delayed after the R wave on the surface ECG such as to begin on the
downslope of the systolic pressure waveform, just before the dicrotic notch (when
the aortic valve closes). Deflation should be timed just before the opening of the
aortic valve to allow for the maximum reduction in aortic systolic pressure com-
pared with an unassisted beat. After timing of inflation and deflation is adjusted, the
balloon counterpulsation is then set at 1:1 (Fig. 36.3) [1].
Management of the Patient During Counterpulsation
When the patient is returned to the appropriate unit, a chest x-ray should be imme-
diately obtained to again verify balloon position and check for any possible migra-
tion during transfer. To prevent thrombus formation, the patient is heparinized, the
activated partial thromboplastin time being carefully maintained at 50–70 s. The
patient must be kept at bedrest and the head of the bed should not be elevated more
than 30°. Daily chest x-ray should be obtained to evaluate balloon position and
ERRNVPHGLFRVRUJ
Diastolic
Augmentation
mmHg
160 Unassisted
Systole Assisted
Systole
140
120
100
80
Unassisted Aortic
60 End-Diastolic
Pressure Assisted Aortic
End-Diastolic
Pressure
Fig. 36.2 Adjustment to timing is performed with the IABP set at 1:2 to allow comparison of the
arterial tracing with and without counterpulsion. Timing of inflation is delayed after the R wave on
the surface ECG such as to begin, just before the dicrotic notch on the aortic pressure waveform.
Deflation is timed to allow for the maximum reduction in aortic systolic pressure compared with
an unassisted beat
migration. During counterpulsation, evaluation of circulation should take place on

every nursing shift (or at least Q8h). Daily monitoring for evidence of sepsis, bleed-
ing, hemolysis, and embolus should also be performed [1].
Weaning from Counterpulsation
Before the IABP is removed, the patient is progressively weaned from its support.
Under close hemodynamic supervision the counterpulsation mode is decreased step-
wise from 1:1 to 1:2, and then to 1:3. The patient should be monitored for 2–3 h at
each downgraded level to ensure tolerance to reduced support. When safety of with-
drawal is established, the balloon is set back to 1:1 and the heparin drip is discontin-
ued for at least 4 h. The activated clotting time is checked until it falls below 160 s.
The balloon and sheath are then removed as a single unit to prevent any tearing of
the balloon membrane. Manual pressure is then applied proximal to the insertion site
for 30–60 min until hemostasis is achieved. After removal the patient is kept at strict
bed rest avoiding hip flexion on the affected side for the next 6–12 h [1].
ERRNVPHGLFRVRUJ
Fig. 36.3 IABP set at 1:1

mmHg
160
140
120
100
80
60
Complications
Vascular complications remain the major risk associated with IABP placement.
Among the significant vascular complications, the most common are limb ischemia,
vascular laceration, and major hemorrhage. Other vascular complications include
arterial dissection, pseudo-aneurysm formation, cholesterol embolization, and cere-
brovascular accident (CVA). Risk of CVA increases if the IABP has been placed too
high or has migrated proximally. Vigorous flushing of the central lumen should also
be avoided, as it can result in dislodgement of thrombus. Overall, major complica-
tions (severe bleeding, major limb ischemia, balloon leak, or in-hospital mortality
related to IABP) associated with IABP placement are relatively rare with an inci-
dence of 2.6 % in the Benchmark Counterpulsation Outcomes Registry [1, 3].
Non-vascular complications include groin infection, sepsis (especially when
counterpulsation is carried out for longer than a week), hemolysis, thrombocytopenia,
and balloon rupture. Although rare, balloon rupture should be considered when
blood is detected in the gas drive-line or if augmentation failure develops.
Clinical Vignettes
Case 1
A 65 year old woman with history of heavy tobacco use, HTN, and hypercholesterol-
emia presents to a community hospital emergency department (ED) with history of 3
days of intermittent chest pain and worsening shortness of breath. On arrival to the
ED she is noted to be in respiratory distress secondary to pulmonary edema and is
urgently intubated. ECG is consistent with inferior ST elevation myocardial infarc-
tion. Due to hypotension dopamine is initiated and she is taken emergently to the
catheterization laboratory (cath lab). Coronary angiogram reveals three-vessel cor-
onary artery disease with acute right coronary artery occlusion. Right heart
ERRNVPHGLFRVRUJ
catheterization is performed and reveals right atrial (RA) pressure 12 mmHg, pulmo-
nary artery (PA) pressure 64/29 (43) mmHg, and pulmonary capillary wedge pres-
sure (PCWP) 33 mmHg with large V waves noted on the PCWP tracing (Fig. 36.4)
consistent with heart failure and severe mitral regurgitation. Transesophageal echo-
cardiogram performed in the catheterization lab reveals papillary muscle rupture
with severe new onset mitral regurgitation—a mechanical complication of acute
myocardial infarction that can result in heart failure and cardiogenic shock.
An intraarotic balloon pump is placed to stabilize the patient for transfer to a
tertiary care center for coronary bypass surgery and mitral valve replacement.
Case 2
A 77 year old male with history of diabetes and hypertension is admitted with unsta-
ble angina. Cardiac catheterization reveals triple vessel coronary artery disease
with 80 % left main coronary artery stenosis, 90 % mid left anterior descending ste-
nosis, 85 % proximal left circumflex stenosis, and 70 % mid right coronary stensosis.
The patient is evaluated by cardiothoracic surgery and planned for CABG surgery in
the morning. Chest pain free and hemodynamically stable, he is transferred to the
coronary care unit for monitoring until surgery. Despite medical therapy with beta
blockers, nitrates, and heparin the patient develops recurrent chest pain with isch-
emic ECG changes. He is returned to the cath lab for IABP placement.
Case 3
A 59 year old male with history of severe ischemic cardiomyopathy (known ejection
fraction of 15 %) is admitted with non-ST elevation myocardial infarction. He is
taken emergently to the cardiac cath lab due to hypotension and persistent chest
mmHg
v v v
v
50
40 a a a
a
Fig. 36.4 PCWP profile in 30
a patient with cardiogenic
shock showing large V
waves suggestive of severe 20
mitral regurgitation.
Echocardiogram revealed 10
papillary muscle rupture
complicating acute inferior
myocardial infarction 0
ERRNVPHGLFRVRUJ
pain. Cardiac catheterization reveals severe three-vessel coronary artery disease.

Right heart catheterization reveals RA 8 mmHg, PA 49/24 (34) mmHg, PCWP
24 mmHg, and cardiac index of 1.14 L/min/M2 consistent with cardiogenic shock.
The severe nature of his three-vessel coronary artery disease precludes percutane-
ous coronary intervention or bypass surgery.
IABP is placed and the patient is referred to the heart failure service for evalua-
tion of heart transplantation. If the patient was not felt by the cardiology team to be
a suitable candidate for heart transplantation (eg. due to old age or significant other
medical comorbidities) placement of IABP would not be appropriate.
Continuous Flow Support Devices
The pMCS systems have grown from counterpulsation balloon systems to centrifu-
gally driven circuits, or catheter-mounted axial-flow pumps. Both surgical LVADs
and pMCS systems are subject to changes in preload and afterload. Inadequate LV
preload due to volume depletion, poor right ventricular function, hypotension, pulmo-
nary obstruction, or valvular disease will reduce flow generation. Similarly, increased
afterload due to hypertension, elevated systemic vascular resistance or valvular dis-
ease will reduce device flow. For these reasons, careful hemodynamic interrogation
before, during, and after initiation of pMCS is essential for optimal device function.
Percutaneous circulatory support devices can be categorized by the type of pump
used as either pulsatile or continuous blood flow devices. Each device impacts native
ventricular function in a unique way and requires adequate preload for optimal use.
Both the Impella (Abiomed Inc) and TandemHeart (CardiacAssist Inc) devices
are rotodynamic pumps that generate continuous, minimally pulsatile blood flow
when functioning optimally (Fig. 36.5) [4, 5]. The Impella devices are catheter-
mounted axial-flow pumps that are placed into the left ventricle in retrograde fash-
ion across the aortic valve. The pump transfers kinetic energy from a circulating
impeller to the blood stream, which results in continuous blood flow from the left
ventricle to ascending aorta. The Impella 2.5 LP and CP devices can be deployed
without the need for surgery, while the Impella 5.0 device requires surgical vascular
access [4, 5]. At present, there is growing experience with the CP device in the
United States. In contrast, the TandemHeart device is an extra-corporeal centrifugal
flow pump that reduces left ventricular preload by transferring oxygenated blood
from the left atrium to the descending aorta via two cannulas: a trans-septal inflow
cannula in the left atrium and an arterial outflow cannula in the femoral artery. The
net effect of these devices is to reduce native left ventricular volume and pressure,
while increasing mean arterial pressure without greatly influencing ventricular
afterload [6]. Advantages of the Impella 2.5 and CP devices is ease of insertion via
a single arterial access, while an advantage of the TandemHeart device is the mag-
nitude of support provided without the need for surgical vascular access. No studies
comparing these continuous flow devices head-to-head exist.
Other centrifugal pumps include the Centrimag, Rotaflow, and Biomedicus
pumps, which are more commonly implanted surgically or used to provide flow for
ERRNVPHGLFRVRUJ
AORTA
Pressure
RA
RV LV
Volume
b
Ao
RA LA
Pressure
RV LV
Blood
pump
Volume
c Ao
RA LA
Pressure
RV LV
Blood
pump
Oxygenator
Volume
Fig. 36.5 Percutaneous non-durable mechanical circulatory support systems. (a) The Impella
axial flow catheters are deployed in retrograde fashion across the aortic valve and directly displace
blood from the LV into the proximal aorta. Immediate effects of the Impella activation include
reduced left ventricular pressures and volume as shown by pressure-volume (PV) loops. (b) The
TandemHeart centrifugal flow pump displaces oxygenated blood from the left atrium (LA) to a
femoral artery, thereby reducing left ventricular preload. The net effect of immediate TandemHeart
activation is a reduction in total LV volume and native left ventricular stroke volume (width of the
PV loop). (c) Venoarterial extracorporeal membrane oxygenation (VA-ECMO) displaces venous
blood from the right atrium (RA) through an extracorporeal centrifugal pump and oxygenator, then
returns oxygenated blood into the femora artery. The immediate effect of VA-ECMO without a left
ventricular decompression mechanism is an increase in left ventricular pressure and a reduction in
left ventricular stroke volume
ERRNVPHGLFRVRUJ
a
Ea1
c VA-ECMO
with an
LV vent
Ea2 VA-ECMO
without
an LV vent
Pressure
b
Volume
Fig. 36.6 Hemodynamic profile of veno-arterial extracorporeal membrane oxygenation

(VA-ECMO) with and without left ventricular venting. (a) A double-lumen pigtail catheter during
activation of VA-ECMO shows increased LV systolic pressure and reduced aortic pulse pressure.
(b) Initiation of an IABP with VA-ECMO shows reduced LV systolic pressure (venting) and ele-
vated aortic diastolic pressure. (c) Venting of the LV with either an IABP, Impella device or trans-
septal left atrial cannula during VA-ECMO support, reduces LV end-systolic pressure and
end-diastolic volume
veno-arterial extra-corporeal membrane oxygenation (VA-ECMO). VA-ECMO is

more commonly used to enhance systemic oxygenation during cardio-respiratory
collapse or biventricular failure. The major effect of VA-ECMO is to displace blood
volume from the venous to the arterial circulation (Fig. 36.5) [6, 7]. As a result, a
reduction in both right and left ventricular volumes can be observed with a con-
comitant increase in mean arterial pressure and both LV systolic and diastolic pres-
sures. This increase in LV afterload or wall stress occurs in contrast to the Impella
or TandemHeart devices since there is no direct venting of the left ventricle with
VA-ECMO (Fig. 36.6). For this reason, operators have combined VA-ECMO with
either an IABP, Impella device, or a trans-septal left atrial cannula to negate the
effect of increased left ventricular afterload during VA-ECMO support [7, 8].
Advantages of VA-ECMO include the relative ease of insertion, the ability to sup-
port systemic oxygenation or biventricular failure, and the ability to provide cardio-
pulmonary support during ventricular tachycardia or fibrillation.
Indications
Clinical scenarios where these devices are commonly used include: cardiogenic
shock, mechanical complications after AMI, high-risk coronary and non-coronary
intervention, and for high-risk electrophysiologic ablations.
ERRNVPHGLFRVRUJ
Contraindications
Major contraindications to Impella placement include the presence of a left ven-

tricular thrombus, severe aortic valve insufficiency, and severe peripheral vascular
disease. Major contraindications to TandemHeart placement include bleeding dia-
thesis, severe peripheral vascular disease. Major contraindications for VA-ECMO
include severe peripheral vascular disease, coagulopathy, and severe aortic valve
insufficiency.
Equipment
The TandemHeart consists of a 21-Fr inlet cannula placed into the femoral vein and
through the right atrium into the left atrium through a trans-septal puncture, an exter-
nal impeller, and a 15-Fr outflow cannula placed into the femoral artery. The Impella
consists of a catheter-mounted microaxial flow pump and a pigtail catheter that is
inserted into the left ventricle, with the inlet and outlet areas on either side of the
aortic valve. VA-ECMO employs a venous inflow cannula and an arterial outflow
cannula. Both are attached to an extracorporeal centrifugal pump and oxygenator.
Technique
To deploy the Impella device, femoral artery access is first obtained and a guidewire
is advanced into the apex of the left ventricle. The placement guidewire is then
inserted into the lumen at the tip of the pigtail, until the catheter is successfully
backloaded onto the guidewire. The catheter is then advanced under fluoroscopic
guidance over the guidewire across the aortic valve using a fixed wire technique.
The inlet area of the catheter should sit 3.5 cm below the level of the aortic valve.
The guide is then removed, and proper placement is confirmed with fluoroscopy as
well as using pressure waveforms from the Impella console. The TandemHeart
requires a trans-septal puncture to deliver a left atrial inflow cannula and a separate
arterial puncture for an outflow cannula. In contrast, percutaneous VA-ECMO
requires a single venous puncture for delivery of a venous inflow cannula into the
superior vena cava and an arterial puncture for an outflow cannula.
Complications
Potential complications of all pMCS devices include clinically significant hemoly-

sis, device malfunction, major bleeding, aortic insufficiency, perforation, hema-
toma, arrhythmias, cerebrovascular accidents, cardiac tamponade, renal failure, or
ERRNVPHGLFRVRUJ
vascular injury. Appropriate placement of the Impella device is crucial for proper
functioning and to avoid the risk of device outflow obstruction. Echocardiography
as well as the utilization of aortic and ventricular pressure waveforms from the
device console should be used to guide placement. Similarly, the TandemHeart left
atrial inflow cannula can displace into the right atrium and requires close monitor-
ing with echocardiography. The major complication associated with VA-ECMO is
left ventricular pressure overload, which requires close monitoring with a pulmo-
nary artery catheter.
References
1. Baim DS, Grossman W. Cardiac catheterization, angiography and intervention. Baltimore:

Williams and Wilkins; 2000.
2. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of
patients with ST-elevation myocardial infarction--executive summary. A report of the American
College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am
Coll Cardiol. 2004;44:671.
3. Ferguson JJ, Cohen M, Freedman RJ, et al. The current practice of intra-aortic balloon coun-
terpulsation: results from the Benchmark registry. J Am Coll Cardiol. 2001;38:1456.
4. Kapur NK, Esposito M. Hemodynamic support with percutaneous devices in patients with
heart failure. Heart Fail Clin. 2015;11:215–30.
5. Kapur NK, Jumean MF. Defining the role for percutaneous mechanical circulatory support
devices for medically refractory heart failure. Curr Heart Fail Rep. 2013;10(2):177–84.
6. Burkhoff D, Sayer G, Doshi D, Uriel N. Hemodynamics of mechanical circulatory support.
J Am Coll Cardiol. 2015;66(23):2663–74.
7. Aghili N, Kang S, Kapur NK. The fundamentals of extra-corporeal membrane oxygenation.
Minerva Cardioangiol. 2015;63(1):75–85.
8. Jumean M, Pham DT, Kapur NK. Percutaneous bi-atrial extracorporeal membrane oxygenation
for acute circulatory support in advanced heart failure. Catheter Cardiovasc Interv.
2015;85(6):1097–9.
ERRNVPHGLFRVRUJ
Index
A Ambulatory electrocardiography (AECG),

Academic College of Radiology (ACR), 107 163, 169
ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/ ACC/AHA guidelines, 165, 167
SCAI/SCMR Appropriate Use clinical studies, 170–172
Criteria for Cardiac Computed complications, 169
Tomography, 97, 99 contraindications, 167
Activated clotting time (ACT), 268, 285 data interpretation, 168–169
Acute coronary syndrome, 238, 245, equipment, 167–168
263, 264 Holter monitoring devices, 163
Acute myocardial infarction (AMI), 6, 46, 64, indications
67, 108, 180, 187, 188, 220, advantages and disadvantages, 165
255–256, 263, 280, 326, 331 antiarrhythmic drug therapy, 165, 166
Acute respiratory distress syndrome, 123 asymptomatic premature ventricular
Adenosine, 53, 56, 57, 59, 71, 252–254, contractions, 167
256, 258, 264 ischemia monitoring, 165, 166
AECG. See Ambulatory electrocardiography pacemaker and ICD function, 165, 166
(AECG) rhythm disturbances, 165, 166
Agaston score, 99 ventricular tachycardia, 167
Age, predicted maximal heart rate long-term implantable loop recorders, 164
(APMHR), 39 noninvasive loop monitors, 164
Air embolism, 129, 191, 289, 321 short-term event monitors, 164
Air-sealed face mask, 46 techniques, 168
Alcohol septal ablation American College of Cardiology/American
clinical studies, 281 Heart Association (ACC/AHA)
complications, 280–281 guidelines, 165, 167, 307–309
contraindications, 275–276 American College of Cardiology (ACC)
data interpretation, 279–280 guidelines, 3
equipment, 276 American College of Emergency Physicians
indications, 275 (ACEP), 141
technique American Heart Association (AHA), 3
echocardiographic view, 277–278 American Society of Anesthesiologists (ASA),
injection, 278 19, 142
left ventricular outflow gradients, 277 American Society of Echocardiography
pre/post-ablation panel, 278, 279 (ASE), 20
Alfentanil, 143 Aminophylline, 56, 58
Allen’s test, 240 Amplatzer® PFO Occluder, 290

DOI 10.1007/978-1-4471-7290-1
ERRNVPHGLFRVRUJ
338 Index
Amplatzer® Septal Occluder (ASO), 284 Atrioventricular (AV) block, 39, 42, 46, 56,
Amplatzer® Sizing balloon, 285 59, 61, 171, 179, 184, 187, 188,
Angiographic catheter, 285 195–198, 227, 253, 317, 318
Anticoagulation, 19, 24, 32, 184, 201, 233, Atrio-ventricular node (AVN), 182
252, 268, 297, 301, 314 Atropine, 56, 58, 66, 152, 183
Antitachycardia pacing (ATP), 211
Aortic stenosis, 9–11, 15, 20, 37, 55, 64, 124,
131, 180, 241, 295, 298, 307, 308, B
313, 314, 327 Balke protocol, 47
Aortic valve area (AVA), 11, 15 Balloon catheters, 265, 267, 269, 273, 276,
Aortic valvuloplasty 278, 296, 299–303
clinical studies, 298–299 Balloon mitral valvotomy (BMV). See Mitral
complications, 298 valvuloplasty
contraindications, 296 Balloon-tipped catheter, 208
data interpretation, 297–298 Balloon valvuloplasty
equipment, 296 aortic valvuloplasty, 295–299
indications, 295 contraindication, 295
techniques, 296–297 mitral valvuloplasty, 301–305
Aortography, 239, 241, 243, 245, 311, 312, pulmonic valvuloplasty, 299–301
314, 315 stenotic lesions treatment, 295
Apical 2 chamber (AP2), 69 β-blocking agents, 281
Apical 4 chamber (AP4), 69 Benzocaines, 21
Arrhythmias, 24, 39, 41, 42, 46, 49, 95, 100, Benzodiazepines, 24, 143–145, 181
164, 167, 169, 171, 175, 176, Beta-blockers, 38, 48, 56, 58, 60, 98, 99, 145,
179–184, 188, 209, 220, 221, 229, 188, 216, 233, 275
230, 232, 239, 271, 290 Bicycle ergometry, 35
Aspirin, 209, 269, 272, 284, 285, 289, 293 Bioabsorbable stents, 268
Atracurium, 149 Bioptome, 318–320
Atrial fibrillation, 17, 24, 42, 56, 98, 128, Bismuth germanate (BGO), 82
131, 145, 164, 165, 167, 169, Biventricular (BiV) pacing. See Cardiac
170, 181, 202, 207, 215, 225, resynchronization therapy (CRT)
233, 299, 301 Blake protocol, 38
Atrial septal defects (ASD), 7, 9–12, 17, 28 Bleeding disorders, 284
Atrial septal defects (ASD), transcatheter Blood pressure (BP), 14, 39, 42, 46, 67, 100,
closure of 102, 121, 138, 139, 142, 153, 154,
complications 176, 177, 202, 216, 233, 234, 254
air embolism, 289 cuff, 37, 65
arrhythmias, 290 monitor, 41, 174, 175
device embolization, 289 recordings, 45, 46
prolapse, 290 Bright blood sequences, 108
right atrial and aortic root perforation, Bruce protocol, 37
290 disadvantages, 38
contraindications, 284 modified, 38
data interpretation, 289 Bubble study, 30, 31, 291, 292
equipment Bupivacaine, 198
Amplatzer® Sizing balloon, 285
ASO, 284
Gore Helex Septal Occluder®, 285 C
indications, 283 Cadmium zinc telluride (CZT) detectors, 72
procedural technique Calcium channel blocker, 38, 99, 188, 233
cine fluoroscopic images, 285, 287 Calcium Score, 99, 100
ICE images, 285, 287–289, 291–293 Cardiac allograft vasculopathy (CAV), 238
TEE images, 285–288 Cardiac catheterization, 332
ERRNVPHGLFRVRUJ
Index 339
Cardiac computed tomography angiography Cardioversion and defibrillation, 211

(CCTA) arrhythmia types and response, 229, 230
CAD assessment, 97 clinical studies, 233–234
clinical studies, 102–103 complications, 233
complications, 101 contraindications, 230
contraindications, 97–99 data interpretation, 232–233
data interpretation, 100–101 equipment, 230–231
equipment, 99 indications, 229–230
indications, 97, 98 monophasic and biphasic waveform, 229
technique, 99–100 technique, 231–232
Cardiac magnetic resonance (CMR) terminating cardiac arrhythmias, 229
clinical studies, 109–111 CCTA. See Cardiac computed tomography
complications, 109 angiography (CCTA)
contraindications, 106–107 Cefazolin, 198, 285
data interpretation, 108–109 Central venous cannulation
equipment, 107 clinical studies, 121
indications complications, 119, 121
acquired myocardial and pericardial contraindications, 116
disease, 106 data interpretation, 118–120
cardiac anatomy and ventricular description, 115
function, 105 equipment, 116
congenital heart disease, 105–106 indications, 115–116
coronary artery disease, 106 technique, 116–118
great vessels assessment, 106 Central venous catheter (CVC), 120
technique, 108 Cerebrovascular accident (CVA), 184, 330
uses, 105 Chest x-ray, 111, 118, 139, 190, 207,
Cardiac resynchronization therapy (CRT), 208, 227, 328
92, 195, 205 cardiomegaly, 137
ACC/AHA guidelines, 206 CVC, 120
clinical studies, 209–210 left side pacemaker, 120
complications, 209 PAC, 119
contraindications, 206 upright, 120
data interpretation, 208 Chronic heart failure, 318
equipment, 206–208 Chronic kidney disease, 98
indications, 206 Claustrophobia, 82, 109
technique, 207–208 Clopidogrel, 269, 284, 285
Cardiac tamponade, 124, 133, 140, 184, 209, CMR. See Cardiac magnetic resonance (CMR)
318, 335 Collimator, 72
Cardiomyopathy, 173, 210, 217 Congenital heart disease, 105–106
hypertrophic, 28, 46, 64, 65, 110, Continuous flow (CW) Doppler, 7
167, 227, 281 Contrast echocardiography (CE), 277–280
ischemic, 81, 121, 130, 209, 322, 331 case studies, 32–33
non-ischemic, 180, 210 complications, 31–32
stress induced, 244 contraindications, 28
Cardiopulmonary exercise testing (CPET) data interpretation, 29–30
complications, 49 equipment, 29
contraindications, 46 indications, 27–28
data interpretation, 47–49 mechanism, 27
equipment, 46 technique, 29
indications, 45 Contrast-induced nephropathy (CIN), 98
patterns, 48, 51 Contrast media, 107
predicted normal parameters for, 48, 50 CoreValve Evolut R, 308, 309, 315
technique, 47 Cornell protocol, 38
ERRNVPHGLFRVRUJ
340 Index
Coronary angiogram, 238, 247, 258–260, 271, Diathermy, 220

279, 285, 330 Digoxin, 37–39, 188
Coronary angiography Dipyridamole, 53, 56–58, 60, 71, 87, 88, 191
clinical studies, 246–247 Dobutamine, 54–56, 58, 71
complications, 245 Double balloon technique, 301
contraindications, 238 Doxorubicin, 91, 92, 96
data interpretation Drug eluting stent (DES), 247, 268, 272, 274
aortography, 243, 245 Dual-chamber pacemaker, 195, 200
coronary anatomy, 242–243 Duke Treadmill Score (DTS), 41
coronary collateral vessels, 243, 244 Dyslipidemia, 67, 68, 157, 160, 176,
imaging techniques, 243 192, 202, 273
left ventriculogram, 243, 244
stenosis determination, 243
TIMI flow assessment, 243 E
equipment, 238–240 Echocardiography, 37, 52, 110, 130, 133, 134,
indications, 237–238 136, 138, 139, 177, 277, 281, 291,
ischemic heart disease evaluation, 237 300, 312, 315, 318, 319, 336
noninvasive tests, 237 clinical application, 3
technique, 239–242 contrast (see Contrast echocardiography
Coronary artery bypass grafting (CABG), (CE))
268, 298, 313, 331 features, 3
Coronary artery disease (CAD), 35, 36, 38, 42, stress (see Stress echocardiography (SE))
63, 64, 68, 71, 77, 78, 81, 83, 87, transesophageal (see Transesophageal
92, 97, 102, 237, 238, 254 echocardiography (TEE))
Coronary blood flow measurements transthoracic (see Transthoracic
angiography, 249–250 echocardiography (TTE))
clinical studies, 258–260 Einthoven, Willem, 157
complications, 256, 258 Elective replacement indicators (ERI), 222
contraindications, 251–252 Electrocardiogram (ECG), 179, 205
coronary Doppler, 250 clinical studies, 160–162
coronary pressure, 250 electrodes, 37
data interpretation equipment and technique, 158
acute myocardial infarction, 255–256 exercise stress test, 64
ischemic thresholds, 254 history, 157
left main coronary artery assessment, indications, 157–158
255, 256 lead placement, 158, 159
multivessel coronary artery disease, patient positioning, 158
254–255 principle, 157
equipment, 252, 253 recordings, 45
indications, 251 Electroconvulsive therapy (ECT), 220
technique Electrophysiology studies (EPS)
coronary flow reserve, 249, 250 clinical studies, 185–186
FFR measurement, 249–250, 252 complications, 184
hyperemic agents, 252–254 contraindications, 180
Coronary flow velocity reserve (CFVR), 252 equipment, 181
Cycle ergometer, 46 indications, 179–180
with NIPS, 179
palpitations and syncope diagnosis, 179
D technique, 181–183
Deep venous thrombosis (DVT), 116 uses, 179
Definity, 28, 29, 31 Endocardial border definition (EBD), 28
Device pocket hematoma, 201 Endomyocardial biopsy (EMB)
Diabetes mellitus, 59, 67, 87, 88, 99, 130, 191, clinical studies, 321–322
246, 313, 314, 331 complications, 321
ERRNVPHGLFRVRUJ
Index 341
contraindications, 318 Fractional flow reserve (FFR),

data interpretation, 321 243, 249–259, 264
equipment, 318–319 Fulminant heart failure, 317
indications, 317
invasive procedure, 317
screen and survey heart G
transplantation, 317 Gagolinium oxyorthosilicate (GSO), 82
technique, 319–320 Galvani, Luigi, 157
use of, 317 Gamma camera, 72, 73, 92
Endomyocardial firboelastosis, 318 Gore Helex Septal Occluder®, 285
Endotracheal intubation Guidewires, 118, 136–138, 200, 250, 252,
for airway protection, 147 265–269, 271, 272, 274, 296, 299,
clinical studies, 153–154 300, 335
complications, 152–153 Guiding catheters, 208, 252, 256, 265–269,
contraindications, 148–149 271, 274
data interpretation, 152
essential equipment, 149–150
indications, 147 H
technique, 150–151 Hemodynamic tailored therapy, 124
Endotracheal tubes, 148, 149, 152, 154 Heparin, 252, 268, 272, 285, 291, 293, 297,
Epinephrine, 183 314, 329, 331
EPS. See Electrophysiology studies (EPS) His-Purkinje block, 179
Equilibrium radionuclide angiography Holter monitors, 163
(ERNA), 91 Human serum albumin (HSA), 92
Etomidate, 143–145, 149, 231 Hypereosinophilic syndrome, 318
EuroSCORE, 308 Hypertension, 3, 14, 15, 32, 42, 43, 45, 46, 56,
Exercise metabolic test, 48 67, 77, 78, 88, 109, 121, 124, 130,
Exercise stress testing 131, 144, 145, 157, 160, 176, 191,
ACC/AHA guidelines, 35 192, 202, 246, 247, 313, 331, 332
CAD Hypertrophic cardiomyopathy, 28, 46, 64, 65,
diagnosis, 35 110, 167, 227
pretest probability of, 36 Hypertrophic obstructive cardiomyopathy
case studies, 42–44 (HOCM), 275, 279, 280
complications, 42 Hypotension, 6, 24, 42, 55, 61, 101, 123, 124,
contraindications, 37 143–145, 152, 173, 175, 176, 230,
data interpretation, 40–42 233, 245, 258, 271, 298, 331, 332
imaging modality, 37
indications, 35–37
patients with valvular heart disease, 37 I
stress testing modality, 53 ICD. See Implantable cardioverter
technique, 38–40 defibrillator (ICD)
types, 35 Impella axial flow catheter, 325
Extra back up (EBU) guiding catheter, 265 Implantable cardioverter defibrillator (ICD),
165, 170, 180, 220
ACC/AHA/HRS guidelines, 212–213
F clinical studies, 216–217
Fentanyl, 143, 145, 150, 231 complications, 216
Fixed-wire angioplasty balloon catheters, 267 contraindications, 213
Flumazenil, 24, 145 data interpretation, 215
Fluoro-2-deoxyglucose F-18 FDG, equipment, 213, 214
82, 83, 85 indications, 211–213
Fluoroscopy, 118, 125, 133, 134, 136, for SCD prevention, 211
181, 189, 198, 239, 240, 288, technique, 213, 215, 216
319, 328, 335 use of, 211
ERRNVPHGLFRVRUJ
342 Index
Implantable devices, 107 Left ventricular outflow tract (LVOT), 11

Inoue balloon technique, 301, 302 Left ventricular (LV) systolic
Intra-aortic balloon pump (IABP), 331, 332 dysfunction, 205
clinical studies, 330–332 Left ventriculography, 241, 243,
complications, 330 244, 303, 305
contraindications, 327 LEMON (Look, Evaluate, Mallampati Class,
equipment, 327 Obstruction/Obesity, Neck
hemodynamic effects, 325, 326 mobility), 148
increased myocardial supply, 325–326 Lidocaine, 143, 150, 198
indications, 326–327 Lithotripsy, 220
technique Local anesthesia, 19, 116, 117, 134, 135, 143,
insertion, 328–330 152, 198, 239
patient management during Lumason, 28
counterpulsation, 328–329 Lutetium oxyorthosilicate (LSO), 82
weaning from counterpulsation, 329
with VA-ECMO, 334
Intracardiac echocardiography (ICE), 285, M
287–289, 291–293 MAC (Monitored anesthesia care), 24
Intra-cardiac electrograms, 220 Macintosh blade, 149
Intravascular ultrasound (IVUS), 243, 249, Magnetic resonance imaging (MRI)
258, 260, 264, 269 equipment, 107, 108
Intravenous lead, 199 Mallampati class I–IV, 19, 148, 149
Ischemic cardiomyopathy, 81, 121, 130, 209, Measurable metabolic equivalent (MET), 45
322, 331 Metal commissurotome, 301, 302
Ischemic heart disease, 35, 106, 167, Midazolam, 143, 145, 149, 231
175, 188, 237 Miller blade, 149
Isoproterenol, 175, 176, 183 Mitral valve area (MVA), 12
Mitral valvuloplasty
clinical studies, 304–305
J complications, 304
Joint Commission on Accreditation of contraindications, 301
Healthcare Organizations in the data interpretation, 303
United States (JCAHO), 141 equipment, 302–303
Junction box, 181 indications, 301
technique, 301–302
Monorail balloon catheters, 267
K Multidetector Computed Tomography
Ketamine, 143, 144, 149, 231 (MDCT), 310, 311
Multiple gated cardiac blood pool imaging
(MUGA) scan, 91
L Myocardial infarction (MI), 28, 31–33, 60, 78,
Laryngoscope, 148–150, 152 153, 196, 238, 245, 251, 255–256,
Left anterior descending (LAD) artery, 102, 264, 271
242, 277, 278, 280, 281 Myocardial necrosis, 233, 278
Left anterior oblique (LAO) projection, 93–94 Myocardial oxygen consumption (MVO2), 34
Left atrial appendage (LAA), 17, 133 Myocardial perfusion imaging (MPI), 54, 57,
Left bundle branch block (LBBB), 37, 39, 206 71, 77, 85
Left circumflex (LCx) artery, 102, 243 Myocardial perfusion imaging
Left ventricular ejection fraction (LVEF), (MPI-SPECT), 3
92, 93, 95
Left ventricular end-diastolic pressure
(LVEDP), 129 N
Left ventricular (LV) function, 91 Naloxone, 24, 145
Left ventricular hypertrophy (LVH), 37, 39, 77 N-13 ammonia, 82, 84, 85
Left ventricular opacification (LVO), 28 Naughton protocol, 37, 38, 47
ERRNVPHGLFRVRUJ
Index 343
Nephrogenic sclerosing fibrosis, 109 indications, 290

Nephrotoxic drugs, 99 prevalence, 290
New-onset heart failure, 317 technique, 291–292
New York Heart Association (NYHA) heart PBV. See Pulmonic balloon valvuloplasty
failure class, 205 (PBV)
Nickel allergy, 284 Percutaneous coronary intervention
Nitrates, 175 (PCI), 327
Nitroglycerin, 56 catheter-based procedures, 263
Nitroprusside, 254 clinical studies, 272–274
Noninvasive loop monitors, 164 complications, 271–272
Non-invasive programmed stimulation contraindications, 264
(NIPS), 179 data interpretation, 271
Non-ischemic cardiomyopathy, 180, 210 equipment
Non-reactive pulmonary vascular disease, 284 access, 265
balloon catheters, 267
guidewires, 265–267
O guiding catheters, 265, 266
Occupational Safety and Health stents, 268
Administration (OSHA) indications, 264
guidelines, 93 technique
One-day rest-stress technetium protocol, 73, 74 bifurcation lesions, 270
Opioids, 24, 143, 145 calcified lesions, 270–271
Optical coherence tomography (OCT), 243 guiding catheter, 268
Optison, 28, 29, 31 intravenous anticoagulation
Orbital atherectomy, 270 regimen, 268
Over-the-wire balloon catheters, 267 saphenous vein graft intervention, 270
Syntax score, 268
uses, 263
P Percutaneously-delivered mechanical
Pacemaker interrogation and circulatory support (pMCS)
programming, 219 goals, 325
clinical studies, 227 IABP
data-interpretation clinical studies, 330–332
battery status, 222 complications, 330
event markers and electrograms, 225 contraindications, 327
intracardiac electrogram, 225–226 equipment, 327
lead impedance, 222 hemodynamic effects, 325, 326
rate-adaptive pacing and mode increased myocardial supply, 325–326
switching, 225 indications, 326–327
sensing and pacing thresholds, 223–224 technique, 328–330
equipment, 220–221 with VA-ECMO, 334
implantation of, 219 impella axial flow catheter, 325
indications, 219–220 advantage, 332
patient positioning, 221 catheter-mounted axial-flow pumps,
technique, 221 332, 333
Parasternal long axis (PLAX), 6–7, 69 complications, 336
Parasternal short axis (PSAX), 6–8, 69 contraindications, 335
Patent ductus arteriosus (PDA), 7 equipment, 335
Patent foramen ovale (PFO), 7, 9–11, 17, 28 indications, 334
transcatheter closure of 2.5 LP and CP devices, 332
clinical studies, 292–293 technique, 335
complications, 292 with VA-ECMO, 334
contraindications, 290 role, 325
data interpretation, 291–292 TandemHeart centrifugal pump, 325
equipment, 290 advantage, 332
ERRNVPHGLFRVRUJ
344 Index
Percutaneously-delivered mechanical Pharmacological stress testing, 107

circulatory support (pMCS) (cont.) clinical studies, 59–61
complications, 336 complications, 58–59
contraindications, 335 contraindications, 55–56
equipment, 335 data interpretation, 58
extra-corporeal centrifugal flow dobutamine stress, 58
pump, 332 equipment, 56
indications, 334 indications, 55
rotodynamic pumps, 332, 333 infusion protocols, 56–57
technique, 335 vasodilator stress (see Vasodilator stress
with VA-ECMO, 334 testing)
VA-ECMO, 325, 332, 334 Photomultiplier tubes (PMT), 72
advantages, 334 Planned intubation, 147
complication, 336 pMCS. See Percutaneously-delivered
contraindications, 335 mechanical circulatory support
effect of, 333, 334 (pMCS)
enhance systemic oxygenation, 334 Pneumothorax, 117–119, 129, 138, 152, 189,
equipment, 335 191, 200, 201, 215, 216, 321
hemodynamic profile, 334 Positron emission tomography (PET), 53
technique, 335 advantages, 81
Percutaneous transvenous mitral clinical studies, 87–89
commissurotomy (PTMC). complications, 87
See Mitral valvuloplasty contraindications, 82
Perflutren Lipid Microspheres, 28 data interpretation, 85–87
Perflutren Protein-Type A Microspheres, 28 equipment, 82–84
Pericardiocentesis indications, 81–82
clinical studies, 138–140 radiotracers, 82–83
complications, 138 vs. SPECT, 81
contraindications, 134 technique, 84–85
data interpretation, 138 Posterior descending artery (PDA), 243
equipment, 134 Pressure half time (PHT), 12
indications, 133 Procedural sedation and analgesia (PSA)
technique clinical studies, 145–146
apical approach, 138 complications, 145
ECG guidance, 136 contraindications, 142
left parasternal approach, 137–138 definition, 141
subxiphoid approach, 135–137 equipment, 142
Peripherally inserted central catheters evaluation, 144
(PICC), 116 indications, 142
Permanent pacemaker medications
clinical studies, 202–203 for adult, 143
complications, 201–202 benzodiazepines, 143, 144
contraindications, 196–197 etomidate, 144
data interpretation, 200–201 ketamine, 144
equipment, 198, 199 midazolam and fentanyl, 143
indications opioids, 143
AV blocks in adults, 196, 197 propofol, 144–145
in chronic bifascicular block, 196, 198 Propofol, 144–145, 149, 231
in neurocardiogenic syncope, 196 Pulmonary artery (PA) catheter, 119, 125, 126,
in sinus node dysfunction, 196 192, 276, 302, 336
SND, 195–196 Pulmonary artery systolic pressure (PASP),
technique, 198, 200 12, 66, 301
Persistent left superior vena cava (PLSVC), Pulmonary capillary wedge pressure (PCWP),
119, 120 123, 124
PET. See Positron emission tomography (PET) Pulmonary edema, 233
ERRNVPHGLFRVRUJ
Index 345
Pulmonic balloon valvuloplasty (PBV) equipment, 125, 126

clinical studies, 300–301 indications, 123–124
complications, 300 technique, 125, 127–128
contraindications, 299 vital physiologic information, 123
data interpretation, 300 Right ventricular ejection fraction (RVEF), 93
equipment, 299–300 Right ventricular (RV), 127, 128, 130, 131,
indications, 299 207, 208
technique, 300 biopsy, 115
circumferential pericardial effusion, 139
free wall motion, 9, 105
Q function, 93, 95, 105
QRS complex, 93, 180, 186, 190, 192, 196, inflow, 7
205, 229, 232 outflow, 8, 21
pressure, 129, 300
Right ventricular systolic pressure
R (RVSP), 7, 30
Radiofrequency ablation, 220 RNA. See Radionuclide angiography (RNA)
Radionuclide angiography (RNA) Rocuronium, 149
clinical studies, 96 Rubidium Rb-82, 82–85, 87
complications, 95
contraindications, 92
data interpretation, 94–95 S
equipment, 92 Saline injection, 30
history, 91 Sapien S3 Valve, 308, 309
indications, 91–92 SE. See Stress echocardiography (SE)
parameters, 91 Seldinger technique, 181
technique, 93–95 Short-term event monitors, 164
Radionuclide cine angiography (RNCA), 91 Silvadene, 233
Radionuclide ventriculography (RVG), 91 Single-chamber pacemaker, 195
Radiopharmaceutical tracers, 72 Single-photon emission computed tomography
Radiotracers, 56, 72–74, 82–84 (SPECT), 53
Ramp protocol, 47 clinical studies, 77–79
Rapid sequence intubation, 147 complications, 77
Recording computer system, 37 contraindications, 71
Regadenoson, 53–58, 60, 61, 71, 254, 255 data interpretation
Remifentanil, 143 artifact, 77
Respiratory exchange ratio (RER), 47 five point model, 76
Resynchronization therapy, 211 ischemic myocardium, 74, 75
Retrograde transarterial technique, 301 myocardial perfusion imaging, 74–76
Right atrial pressure (RAP), 12 17-segment model, 76
Right bundle branch block (RBBB), 37 semiquantitative defect analysis, 76
Right coronary (RCA) artery, 74–76, 78, TID detection, 76–77
102, 242, 244, 246, 247, 253, equipment, 72
272, 273, 299 indications, 71, 72
Right heart catheterization (RHC) technique
clinical studies, 130–131 2D/3D imaging, 73
clinical trials, 123 one-day rest-stress technetium protocol,
complications, 129 73–74
contraindications, 125 pharmacological stress testing, 73
data interpretation radiopharmaceutical protocols, 73
normal hemodynamic values, 129 uses, 71
PCWP, 129 Single-shot, fast spin echo (SS-FSE), 108
PV systolic pressure, 129 Sinoatrial (SA) node, 182
RA pressure, 128 Society of Cardiovascular Computed
RV systolic pressure, 129 Tomography (SCCT), 99–101
ERRNVPHGLFRVRUJ
346 Index
Society of Thoracic Surgery (STS), 308 Temporary transvenous pacing

Sodium iodide crystal (NaI), 72 clinical studies, 191–193
SPECT. See Single-photon emission computed complications, 190–191
tomography (SPECT) contraindications, 188
ST-elevation myocardial infarction data interpretation, 190
(STEMI), 161 equipment, 189
Stents, 265, 268, 270, 308 indications, 187–188
Stress echocardiography (SE), 28, 36 recommendations, 188
clinical studies, 67–69 technique, 189–190
complications, 67 Terminating exercise testing, 39, 40
contraindications, 64–65 3-D mapping systems, 181
data interpretation, 66–67 Thrombolysis in myocardial infarction
ECG exercise stress test, 64 (TIMI), 243
equipment, 65 Tilt table testing (TTT)
indications, 63–64 clinical studies, 176–177
technique complications, 176
Doppler imaging, 66 contraindications, 174
exercise, 66 data interpretation, 175–176
intravenous contrast enhancement, 65 description, 173
pharmacologic stress testing, 66 equipment, 174–175
uses, 63 indications, 173
Stroke volume (SV), 9–11, 47, 91, 105, 175 postural tachycardia syndrome, 173
Strontium-82 generator, 83 technique, 175
Subclavian (SC) venous, 116, 118–121, 125, Topical anesthesia, 198
126, 181, 189, 191, 198, 201, 208 Transcatheter aortic valve replacement
Succinylcholine, 149 (TAVR)
Sudden cardiac death (SCD), 211, 217 ACC/AHA guidelines, 307, 308
Superior vena cava (SVC), 21, 31, 119, 120, clinical studies, 313–315
209, 286, 287, 291 complications, 312–313
Supraventricular arrhythmias (SVT), 182 contraindications, 308
Swan Ganz PA catheter, 125 data interpretation, 312
Systemic vascular resistance (SVR), 124 EuroSCORE score, 308
indications, 308
procedural equipment, 308–310
T standard of care, 307
Takotsubo cardiomyopathy, 67 STS score, 308
TandemHeart centrifugal pump, 325 techniques
advantage, 332 access site management/closure, 312
complications, 336 annular assessment, 311
contraindications, 335 hemodynamic assessment, 312
equipment, 335 MDCT, 310–311
extra-corporeal centrifugal flow pump, 332 preoperative evaluation, 310, 311
indications, 334 priming valvuloplasty, 312
rotodynamic pumps, 332, 333 Transcranial Doppler (TCD), 291, 293
technique, 335 Transesophageal echocardiography (TEE)
with VA-ECMO, 334 ASD anatomy assessment, 285–288
Technetium-99m-pertechnate (Tc-99m), 92 clinical studies, 24–26
diethylenetriaminepentaacetic acid, 93 complications, 21–24
perctechnetate, 93 contraindications, 18
sestamibi, 72 data interpretation
tetrofosmin, 72 aortic images, 21, 23
TEE. See Transesophageal echocardiography mid esophageal images, 20
(TEE) mitral valve prolapse images, 21, 24
ERRNVPHGLFRVRUJ
Index 347
transgastric images, 20–22 V

upper esophageal images, 20, 21 Vancomycin, 198
equipment, 18–19 Vasodilator stress testing
indications, 17–18 adenosine, 53
technical procedure auto-regulation of flow, 53, 54
hands-in or hands-out techniques, 19 contraindications, 55
local anesthesia, 19 coronary flow, 53, 54
patient positioning, 19 dobutamine, 54–55
physical examination, 19 indications, 58
probe manipulation, 20 infusion protocols, 56–57
semi-invasive procedure, 19 patient preparation, 56
vs. TEE, 17 physical examination, 56
Transient ischemic dilation (TID), 73, 76 regadenoson, 53–54
Transthoracic echocardiography (TTE) Vecuronium, 149
clinical studies, 14–15 Veno-arterial extra-corporeal membrane
complications, 14 oxygenation (VA-ECMO), 325,
contraindications, 5–6 332, 334
data interpretation advantages, 334
aortic stenosis evaluation, 11 complication, 336
diastolic dysfunction assessment, contraindications, 335
12–13 effect of, 333, 334
flows rate calculation, 11 enhance systemic oxygenation, 334
mitral stenosis evaluation, 11–12 equipment, 335
RAP estimation, 12 hemodynamic profile, 334
RVSP and PASP estimation, 12 technique, 335
systemic approach, 10–11 Venous stenosis, 202
valvular regurgitation, quantification Venous thromboembolism (DVT/PE), 184
of, 12, 13 Ventilatory anaerobic threshold (VAT), 47
equipment, 6 Ventricular arrhythmias, 6, 119, 129, 179, 180,
indications, 3–5 183, 185, 227, 238, 279–281, 317,
technique 318, 321
A2C view, 8, 9 Ventricular fibrillation (VF), 211, 229,
A3C view, 8–9 230, 232
A4C view, 7–9 Ventricular paced rhythm, 37, 39, 53, 59
Doppler, 6 Ventricular septal defect (VSD), 7, 8, 10–12,
PLAX views, 6–7 28, 106
PSAX views, 7, 8 Ventricular tachycardia (VT), 39, 133, 170,
RV inflow, 7 181, 211, 229, 230, 232
subcostal view, 9–10 Verapamil, 281
suprasternal view, 10
Treadmill ECG stress test, 37
Treadmill ergometer, 35, 46 W
Tricuspid regurgitation (TR), 30 Wall motion abnormalities (WMA), 36
TTE. See Transthoracic echocardiography Ware protocol, 47
(TTE) Wolff-Parkinson-White (WPW) syndrome,
TTT. See Tilt table testing (TTT) 37, 162, 180, 184
U X
Ultrasound, 3, 5, 65, 116–118, 318 Xtra backup (XB) guiding catheter, 265
ERRNVPHGLFRVRUJ

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Cardiology Procedures

ISBN 978-1-4471-7288-8 ISBN 978-1-4471-7290-1 (eBook)

Library of Congress Control Number: 2016955806

© Springer-Verlag London 2017

Printed on acid-free paper

This Springer imprint is published by Springer Nature

Part I Noninvasive Cardiology

12 Cardiac Magnetic Resonance. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105

Part II Critical Care

13 Central Venous Cannulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115

Part III Electrophysiology

18 The Electrocardiogram. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 157

Part IV Interventional Cardiology

28 Coronary Angiography. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237

E. Karnabi, MD, PhD, FASE

© Springer-Verlag London 2017 3

Table 1.1 Appropriate indications for transthoracic echocardiography

Table 1.1 (continued)

Transthoracic echocardiography has no contraindications, as the use of ultrasound

Contrast agents, when used, include the following contraindications:

The necessary equipment for performing an echocardiographic exam includes the

The echocardiographic examination starts by connecting the ECG electrodes and

assessing the extent of pericardial effusion, and respirophasic characteristics of

Physicians with specialized training should perform data interpretation as estab-

Right Ventricle: Chamber dimension, wall thickness and global function.

Table 1.2 Recommendations for classification of AS severity [4]

Table 1.3 Recommendations for classification of MS severity [4]

As mentioned, echocardiography is generally very safe with no complications. The

Sixty-five-year-old male with history of hypertension, hyperlipidemia and heavy

Transesophageal echocardiography (TEE), in comparison to transthoracic echocar-

E. Karnabi, MD, PhD, FASE

© Springer-Verlag London 2017 17

Table 2.1 Indications for transesophageal echocardiography [2, 3]

Absolute contraindications Relative contraindications

Similar to a TTE, the necessary equipment’s are the portable echocardiography

According to the American Society of Echocardiography (ASE), a comprehensive

aortic valve velocity can be obtained in the TG either at 0° deep TG or at 120° TG

methemoglobinemia that presents as central cyanosis, oxygen desaturation, and

Fig. 2.4 TG TEE view of

Sixty-four-year-old female with a history of ovarian cancer, hyperlipidemia has been

Fourty-two-year-old male with a history of polysubstance abuse and intravenous

Cesia Gallegos, Eddy Karnabi, and Robert C. Hendel

Despite the development of improved imaging techniques, contrast echocardiogra-

© Springer-Verlag London 2017 27

The indications for CE with agitated saline use include:

Although generally safe and effective, contrast agents have some

Fig. 3.1 Bubble study

of complications of myocardial infarction such as LV aneurysm, pseudoaneurysm,

1. Stewart MJ. Contrast echocardiography. Heart. 2003;89:342–8.

Exercise testing (ET) is a well-validated procedure for the diagnosis of coronary

E. Karnabi, MD, PhD FASE

© Springer-Verlag London 2017 35

Magnitude of ischemia Stress Angina

Nuclear Systolic dysfunction/WMA

Table 4.1 Indications for 1. Symptoms suggestive of CAD

Table 4.2 Pretest probability of CAD

Contraindications (Table 4.3)

Table 4.3 Contraindications to exercise stress testing [1]

Table 4.4 Bruce protocol