Cardiac arrhythmias : interpretation, diagnosis, and treatment [2nd; ed.] 9781260118216, 1260118215

Table of contents :
Cardiac Arrhythmias Interpretation, Diagnosis and Treatment, Second Edition
Half Title
Title Page
Copyrigh
Dedication
Contents
Preface
PART I Basic Electrocardlographlc Observations and Clinical Electrophysiologic Correlates
Chapter 1 Cardiac Conduction
Chapter 2 Electrocardiographic Consequences of Atrial and Ventricular Ectopy
Chapter 3 Bundle Branch Block
Chapter 4 Apparent Paradoxical Conduction
Chapter 5 Mechanisms of Tachycardia
PART II Arrhythmias
Chapter 6 Supraventricu lar Tachycardia
Chapter 7 Preexcitation Syndromes
Chapter 8 Ventricular Tachycardia
Chapter 9 Atrial Fibrillation
Chapter 10 Bradycardia: Causes of Pauses
PART III Clinical Presentations
Chapter 11 Electrocardiographic Abnormalities in Asymptomatic Individuals
Chapter 12 Narrow QRS Tachycardia
Chapter 13 Wide QRS Tachycardia
Chapter 14 Undiagnosed Syncope, Dizzy Spells, Palpitations
Chapter 15 Sudden Cardiac Arrest/Sudden Cardiac Death
PART IV Methods and Therapy
Chapter 16 Electrophysiologic Testing and Diagnostic Maneuvers
Chapter 17 Catheter Ablation of Supraventricular Tachycardias
Chapter 18 Catheter Ablation of Ventricular Tachyarrhythmias
Chapter 19 Cardiac Implantable Electronic Devices
Index

Citation preview

Cardiac Arrhythmias: Interpretation, Diagnosis, and Treatment Second Edition

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Cardiac Arrhythmias: Interpretation, Diagnosis, and Treatment Second Edition

Eric N. Prystowsky, MD

Director, Cardiac Arrhythmia Service St. Vincent Hospital Indianapolis, Indiana Consulting Professor of Medicine Duke University Medical Center Durham, North Carolina George J. Klein, MD Professor of Medicine Western University London, Ontario, Canada James P. Daubert, MD

Professor of Medicine Director, Cardiac Electrophysiology Duke University Medical Center Durham, North Carolina

New York Chicago San Francisco Athens London Madrid Mexkx> Oty Mlan New Detil Singapore Sydney Toronto

Copyright© 2020 by McGraw Hill LLC. All rights reserved. Except as permitted under the United States Copyright Act of 1976, no part of this publication may be reproduced or distributed in any form or by any means, or stored in a database or retrieval system, without the prior written permission of the publisher. ISBN: 978-1-26-011821-6 MHID: 1-26-011821-5 The material in this eBook also appears in the print version of this title: ISBN: 978-1-26-011820-9, MHID: 1-26-011820-7. eBook conversion by codeMantra Version 1.0 All trademarks are trademarks of their respective owners. Rather than put a trademark symbol after every occurrence of a trademarked name, we use names in an editorial fashion only, and to the benefit of the trademark owner, with no intention of infringement of the trademark. Where such designations appear in this book, they have been printed with initial caps. McGraw-Hill Education eBooks are available at special quantity discounts to use as premiums and sales promotions or for use in cmporate training programs. To contact a representative, please visit the Contact Us page at www.mhprofessional.com. Notice Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required. The authors and the publisher of this work have checked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards accepted at the time of publication. However, in view ofthe possibility of human error or changes in medical sciences, neither the authors nor the publisher nor any other party who has been involved in the preparation or publication ofthis work warrants that the information contained herein is in every respect accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information contained in this work. Readers are encouraged to confirm the information contained herein with other sources. For example and in particular, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this work is accurate and that changes have not been made in the recommended dose or in the contraindications for administration. This recommendation is of particular importance in connection with new or infrequently used drugs. TERMSOFUSE This is a copyrighted work and McGraw-Hill Education and its licensors reserve all rights in and to the work. Use of this work is subject to these terms. Except as permitted under the Copyright Act of 1976 and the right to store and retrieve one copy of the work, you may not decompile, disassemble, reverse engineer, reproduce, modify, create derivative works based upon, transmit, distribute, disseminate, sell, publish or sublicense the work or any part of it without McGraw-Hill Education's prior consent. You may use the work for your own noncommercial and personal use; any other use of the work is strictly prohibited. Your right to use the work may be terminated if you fail to comply with these terms. THE WORK IS PROVIDED "AS IS." McGRAW-HILL EDUCATION AND ITS LICENSORS MAKE NO GUARANTEES OR WARRANTIES AS TO THE ACCURACY, ADEQUACY OR COMPLETENESS OF OR RESULTS TO BE OBTAINED FROM USING THE WORK, INCLUDING ANY INFORMATION THAT CAN BE ACCESSED THROUGH THE WORK VIA HYPERLINK OR OTHERWISE, AND EXPRESSLY DISCLAIM ANY WARRANTY, EXPRESS OR IMPLIED, INCLUDING BUT NOT LIMITED TO IMPLIED WARRANTIES OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. McGraw-Hill Education and its licensors do not warrant or guarantee that the functions contained in the work will meet your requirements or that its operation will be uninterrupted or error free. Neither McGraw-Hill Education nor its licensors shall be liable to you or anyone else for any inaccuracy, error or omission, regardless of cause, in the work or for any damages resulting there:from. McGraw-Hill Education has no responsibility for the content of any information accessed through the work. Under no circumstances shall McGraw-Hill Education and/or its licensors be liable for any indirect, incidental, special, punitive, consequential or similar damages that result from the use of or inability to use the work, even if any of them has been advised of the possibility of such damages. This limitation of liability shall apply to any claim or cause whatsoever whether such claim or cause arises in contract, tort or otherwise.

To my wife Bonnie, my constant source oflove and support for over 50 years. To my sons David and Daniel, whose lives have filled me with pride and joy, and their wives, Malia and Beth, who are the daughters we never had. And for my grandchildren, Dylan, Laila, Amber, and Noah, who always bring boundless joy and sunshine into our lives. And in loving memory of my parents, Drs. Rose and Milton Prystowsky, compassionate physicians who taught me that being a physician is not a gift to be wasted.

-Eric N. Prystowsky, MD

To my wife and best friend, Klara. To my son Ben and daughter-in-law Elissa and their children Adam, Leah, Beth, and Talya, and to my daughter Anna and son-in-law Mark and their children Lucy, Nate, and Sari, who are all my real source of pride and joy. To the memory of my unselfish and giving parents, Paul and Clara.

-George/. Klein, MD

To the memory of my late parents, Dr. James J. Daubert and Irene M. Daubert, recognizing their inspiration for and support of my education. To my wife Amy for her tremendous support and wise counsel throughout my medical career. And to our children, Patrick, Thomas (MD), Mairin, and James. -James P. Daubert, MD

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Contents

PARTI Basic Electrocardlographlc Observations and Clinical Electrophysiologic Correlates-........- ....•..- · 1

1 Cardiac Conduction ..........-................._,_...........-.......- ...........- .......................- ...........- ..............-·-···......................... 3 Eric N. Prystowsky, MD

2 Electrocardiographic Consequences of Atrial and Ventricular Ectopy..........-..........._,_....................-....... 35 Eric N. Prystowsky, MD 3 Bundle Branch Block......... _................. _,_ ..,...,.... _...,..._........... _....................... _........... _..,........... _,_,,, ....................... 57 Eric N. Prystowsky, MD 4 Apparent Parado.xical Conduction ............................................................................................................................83 Eric N. Prystowsky, MD 5 Mechanisms of Tachycardia .............._,_...........-.......-...........-.......................-...........-.............._,_.......................... 95 George J. Klein, MD

PARTll A1Th-ythmfas ..............~··········.....••••••••.....••••••......••••••••.....••••••......·······~··········.....••••••••.....••••••......••••••••.....······" 111

6 Supraventricular Tachycardia ..........._,_...........-.......-...........-.......................-...........-.............._,_....................... 113 George J. Klein, MD 7 Preexcitation Syndromes-................. _,_ ...........-.......-...........-.......................-...........-.............. _,_....................... 139 Eric N. Prystowsky, MD 8 Ventrlcular Tachycardia....................................................................................................................................................... 171

Eric N. Prystowsky, MD 9 Atrial Fibrillation ................................................................................................................................................................................. 213 Eric N. Prystowsky, MD 10 Bradycardia: Causes of Pauses ........._,_...........-.......-...........-.......................-...........-.............._,_....................... 235 George J. Klein, MD

PARTlll Clinical Presentations ......................................................................................................................................... 253

Electrocardiographic Abnormalities in Asymptomatic Individuals...-...........-..........._,_....................-.... 255 George J. Klein, MD 12 Narrow QRS Tachycardia._................._,_..,........-......._..........._......................._..........._..,..........._,_,,..................... 287 George J. Klein, MD 13 Wide QRS Tachycardia ................................................................................................................................................. 301 George J. Klein, MD

11

vii

viii

CONTENTS

14 Undiagnosed Syncope, Dizzy Spells, Palpitations ............................................................................................ 323 George J. Klein, MD 15 Sudden Cardiac Arrest/Sudden Cardiac Death .................................................................................................. 341 James P. Daubert, MD

PART IV Methods and Therapy........................................................................................................................................ 371 16 Electrophysiologic Testing and Diagnostic Maneuvers .................................................................................. 373 Eric N. Prystowsky, MD 17 Catheter Ablation ofSupraventricularTachycardias ........................................................................................ 401 James P. Daubert, MD 18 Catheter Ablation ofVentricularTachyarrhythmias ......................................................................................... 447 James P. Daubert, MD 19 Cardiac Implantable Electronic Devices ............................................................................................................... 479 James P. Daubert, MD

lndex ........................................................................................................................................................................................... 501

Preface Twenty-five years ago, Drs. Pryst.owsky and Klein authored the first edition ofthis textbook. Our purpose was to "write a comprehensive textbook on an integrated approach to cardiac arrhythmias for individuals without a background in clinical electrophysiology.' While we hoped clinical electrophysiologist.s would find our book useful, our intent was to educate the broader field of clinicians, for example, medical students, house staff, primary care physicians, cardiologists, and nurses, on the diagnosis and treatment of patients with cardiac arrhythmias. Thousands of copies of the book were sold, and we hope those readers found it useful. We received much feedback from our colleagues and trainees over the years and discussed with each other some alterations to consider when we wrote a second edition. While othe.r textbooks on cardiac arrhythmias are available, we felt there remained a void in providing our practical application ofelectrophysiological principles and electrocardiographic correlations to the broader community involved in caring for patients as well as the clinical electropbysiologist. This motivated us to pursue a second edition of our book. We welcome our new co-author, Dr. James Daubert, also a Duhtrained electrophysiology fellow. and long-standing friend and colleague. There has been a sea change in the last 25 years to our therapy of cardiac arrhythmias. Surgery to cure arrhythmias is nearly extinct, and new antiarrhythmic drug development has been stagnant At the same time, the.re have been remarkable advances in catheter ablation technology and its application to treat a wide variety of cardiac: arrhythmias, as well as development of newer implantable cardiac electrical devices and indications for their use. The content of our second edition reflects these changes in our field, and we have deleted specific chapters on arrhythmias in acute myocardial infarction, pharmacologic therapy, operative therapy of arrhythmias, and noninvasive methods. Important information on drug therapy and noninvasive methods is covered in other chapters. Further, we have added new chapters on atrial fibrillation, catheter ablation of supraventricular tachycardia, catheter ablation of ventricular tachycardia, and provide a major update in the chapters on sudden cardiac death and device therapy. Many new figures and information have been added to the existing chapters. To allow for easier reading, there is some deliberate overlap of information between various chapters. Key references of c:lassic and up-to-date articles are provided for each chapter. Like the first edition, this book represents our personal approach to patients with cardiac arrhythmias. Nonetheless, it would be unrealistic to expect 3 electrophysiologists to have entirely uniform approaches to diagnosis and therapy. Hence, the primary author's views in individual chapters prevailed when there were minor differences in approach. Each of us reviewed all the chapters and made recommendations for change. In the end, we did not feel there were any substantial differences in our approach to patient care and were comfortable in signing off on the total content

ix

x

PREFACE

The book is divided into 4 parts. Part I is Basic Electrocardiographic Observations and Clinical Electrophysiologic Correlates. There are in-depth discussions of cardiac conduction with major additions on the effects of alterations in autonomic tone, effects of premature atrial and ventricular ectopy on conduction and automaticity, concealed conduction and apparent paradoxical conduction, bundle branch block, and mechanisms of tachycardia Part II focuses on specific arrhythmias. It begins with an in-depth chapter on a clinical classification of supraventricular tachycardia and includes chapters on the preexcitation syndrome (Wolff-Parkinson-White), ventricular tachycardia, atrial fibrillation, and bradycardia. Diagnostic information from patient history, physical examination, and laboratory tests is given, as well as an approach to therapy for each arrhythmia. Part III includes chapters on common clinical presentations of arrhythmias. An approach is given for patients who are asymptomatic but have electrocardiographic abnormalities, and for those who present with a narrow QRS tachycardia, wide QRS tachycardia, syncope, dizziness, palpitations, or who have survived a cardiac arrest. Part IV consists of chapters on diagnostic techniques and therapeutic modalities. Included are methods of electrophysiologic testing and diagnostic pacing maneuvers, catheter ablation of supraventricular tachycardia, catheter ablation of ventricular tachycardia, and device therapy. Acknowledgements: Dr. Prystowsky thanks Mrs. Jane Gilmore, CMI, for her outstanding artwork.

Eric N. Prystowsky, MD George J. Klein, MD James P. Daubert, MD

PART

Basic Electrocardiographic Observations and Clinical Electrophysiologic Correlates Chapter 1 Chapter 2 Chapter 3 Chapter 4 Chapter 5

Cardiac Conduction Electrocardiographic Consequences of Atrial and Ventricular Ectopy Bundle Branch Block Apparent Paradoxical Conduction Mechanisms of Tachycardia

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Cardiac Conduction Eric N. Prystowsky, MD

GENERAL CONCEPTS The normal cardiac: impulse originates in the sinus node, a crescent-shaped structure approximately 9 to 15 mm long that is located at the juncture of the superior vena cava and right atrium (Figure 1-1).1 After the electrical impulse exits the sinus node, it proceeds to activate the right and left atria. Activation of the atria is responsible for the P wave recorded on the electrocardiogram (ECG) (Figure 1-1, orange color). Activation of the normal human atria takes approximately 90 to 100 ms, the right atrium being activated within approximately 65 ms.2 The last area to be activated is the left atrial appendage, although atrial tissue near the left inferior pulmonary vein can also be activated very late. It should be noted that as the spread of atrial activation occurs, some sections of the right and left atria are activated at the same time.2 A controversy has existed for decades concerning the existence of specialized internodal pathways for conduction between the sinoatrial (SA) node and the atrioventricular (AV) node. The essence of this controversy is whether preferential atrial conduction between the SA and AV nodes occurs over specialized pathways or whether the activation wavefront proceeds through nonspecialized or ordinary atrial myocardium.1" Most data strongly suggest that no specialized pathways of conduction exist. The observed preferential conduction of atrial impulses along various anatomical routes can be explained adequately by various factors, such as the complex anatomy of the right atrium, which includes multiple "holes" such as the orifices of the inferior and superior venae cavae and coronary sinus ostium, as well as the orientation of atrial fibers in longitudinal and perpendicular directions, with conduction being faster in the longitudinal direction.' The PR interval in the ECG encompasses activation in the atria, AV node, His-Purldnje system, and ventricles (Figure 1-1). The AV node is a complex structure that includes the compact node and its posterior extensions.5 The AV node was initially considered to be subdivided into 3 functional zones: the AN, N, and NH zones.0 The N zone appears to be the most common area where block occurs in the AV node. However, a more recent microelectrode mapping of the AV node suggests that it includes 6 different cell types.9 Slow conduction through the AV node is multifactorial, in part related to the complex arrangement of nodal cells and connective tissue, reduced electrical cellular coupling, and action potentials that are dependent on the

4

CARDIAC ARRHYTHMIAS: INTERPRETATION, DIAGNOSIS, AND TREATMENT

R

T

Sinus node (pacemaker)

I

( Atrioventricular node (delay)

Purkinje fibers (activation)

FIGURE 1·1 • Schematic of the electrocardiogram and cardiac conduction 5Y$tem. The pink color represents the electrical sy:stem,

orange activation of the atria, and green activation of the ventticles. (See text for details.)

slow inward calcium current.10 The impulses exit from the AV node into the ventricular specialized conduction system that has more rapid conduction properties, which consists of the His bundle, the left and right bundle branches with their subdivisions, and the peripheral network of Purkinje fibers, which terminate into ventricular myocardium. The left bundle branch is often described as having two primary f u.nctional divisions, the anterior and posterior fascicles. However, as early as 1906, Tawara11 identified a third fascicle of the left bundle branch that enters into the left interventricular septum, an observation confirmed by others (Figure 1-2).' In a classic study by Durrer et al.2 on excitation of the human heart, 3 endocardial areas were consistently shown to be excited synchronously 0 to S ms after the

CHAPTER 1 • Cardiac Conduction

S

acd-------

mpa--·

FIGURE 1-2 • Photomiaogr.iph demonstrating the distribution of the left bundle branch in the human heart taken from the original publication ofTawara. (Reproduced wtth permission from Tawara S. Dos Relzteltungssymm des Sougetlerherzens. Jena, Germany: Fischer; 1906J

beginning of the left ventricular cavity potential. giving credence to the concept of a functional trifascicular left bundle branch system. In the absence of bundle branch block. ventricular activation is quire rapid. usually less than 100 ms, and is represented on the electrocardiogram. by the QRS complex (Figure 1-1, green color). Examples of ventricular epicardial activation in normal hearts of patients undergoing swge.ry for ablation ofthe accessorypathwa:yin the Wolff-Parkinson-White syndrome are demonstrated in Figures 1-3 through 1-5. These maps were computer generated during activation of 1 QRS complex. using a 56-electrode array sock. Figure 1-3 shows normal ventricular activation; right bundle branch block and left bundle branch block are noted in Figures 1-4 and 1-5, respectively.

ELECTROPHYSIOLOGIC-ELECTROCARDIOGRAPHIC CORRELATIONS Electrophysiologic studies utilize several multipolar electrode catheters positioned at various locations in the heart (Figure 1-6). These catheters make it possible to record electrical potentials from within the heart and to stimulate various cardiac chambers in the diagnosis and management of cardiac arrhythmias. Whereas the electrocardiographer analyzes the surface electrocardiogram, the clinical electrophysiologist peers through this tracing to analyze its component parts (Figure 1-7). In essence, the more one knows about intracardiac events, the easier it is to analyze the surface electrocardiogram.

6

CARDIAC ARRHYTHMIAS: INTERPRETATION, DIAGNOSIS, AND TREATMENT

ANTERIOR

FIGURE 1·3 • Normal eplcardlal ventTlcular activation. The format for Rgures 1·3, 1-4, and 1·S Is the same. At the time of surgery, a 56-electrode array sock was positioned on the epicardlal surface of the heart; during 1 QRS compleX', ventrlcular activation was obtained at all sites. Each site Is noted by a letter and number that designate the electrode position and, undemeath, the local activation time. using the initiation of the surface QRS complex as time 0. The left anterior descending (LAO) coronary artery is schematically represented in the anterior view and the posterior descending {PDA) coronary artery is represented similarly in the posterior view. These are approximate posltlOI\$ as noted during surgery. In thb figure, note the rapid ac:ttvatlon of the entire right and left venuldes. The last area activated Is the base of the right ventrlc!e, and activation time Is complete within 78 ms. The right ventricle In the anterior view Is to the left of the LAO and In the posterior view to the right of the PDA. This method of dlsplayf ng the heart assumes that the posterior aux of the heart Is dMded and the ventricles are then laid out flat The base of the heart with the atria removed is at the top of the figure and the apex (electrodes A1 through AS) is at the bottom. It is not that critical to analyze each point but rather to realize that the entire epicardial surface of the ventricle is activated relatively quickly.

PR Interval Figure 1-8 demonstrates int.racardiac electrophysiologic events.1'·u The top tracing is surface ECG lead V1; simultaneous intra.cardiac recordings are from 1 catheter in the high right atrium (HRA) and from another positioned across the tricuspid valve to record electrical signals coming from the AV junction near the His bundle electrogram (HBE). This was a quadripolar catheter, and the proximal 2 electrodes (HBE PROX) are closer to the atrial side ofthis juncture, recording a large atrial (A) depolarization along with a His bundle deflection (H) and a ventricular (V) electrogram that represents activation of the high ventricular septum. The distal bipolar electrode pair (HBE DIST) is situated more into the ventricle, and this enabled the recording of a right bundle branch (RB) potential. The PA interval, a measure of atrial conduction, is taken from the onset of the surface P wave to local atrial activation in the His bundle electrogram. In our opinion, this interval is of minimal value, since it only records atrial activation through a part of the right atriwn. More important measurements are the atrio-His (AH) .interval, which is an approximation of AV nodal conduction time, and the His-ventricle (HV) interval, which reflects conduction through the HisPurkinje system. Measurement of the AH interval is taken from the first rapid deflection in the

CHAPTER 1 • Cardiac Conduction

7

ANTERIOR FIGURE 1·4 • Eplcardlal ventricular activation during right bundle branch block. (See Figure 1-3 f'or details of mapping methods.) Note that the left ventricle, represented by electrodes 8 through D, is activated in a nonnal fashion and relatively quickly. However, ttie right ventrfde, represented by electrodes Ettirough G, Is ac:ttva'ted late, as would be expected In right bundle branch block. Point F, Is activated 115 ms after the Initiation of the surface QRS complex. Compare this acttvatlon with that noted In Figure 1-3.

ANTERIOR

FIGURE 1·5 • Eplcardlal ventrlcular activation In left bundle branch block. (See Figure 1-3 for dmlls of mapping.) In contrast to Agure 1-4, the earilest activated sites In this patient are on the right ventricle and the latter activated points on the left ventricle, as expected with left bundle branch block. Right ventricular points are prlmarily noted by G and E, which are left of the LAD In the antEt'lor view and right of ttie PDA In the posterior view. Note that the last area to be activated Is on the left ventricle at 02 (117 ms}, In contrast to the last area activated during right bundle branch block. which is on the right ventricular epicaRlial surface {see Figure 1-4).

8

CARDIAC ARRHYTHMIAS: INTERPRETATION, DIAGNOSIS, AND TREATMENT

FIGURE 1-t • Radlograph of endocardlal atheter placement. (Key: RA= rtght atrium; CS= coronary sinus; RV= rlghtventrlde; H =His bundle area.)

~~ AH

d

V

~

===

i:::_ -_~

FIGURE 1·7 • A cllnlal electrophyslologlst's view of the electroCllrdlogram.

p

R

CHAPTER 1 • Cardiac Conduction

9

FIGURE 1-8 • lntracardlac electrophyslologlc conduction Intervals during the PR Interval. {See text for detalls.) {Key: HRA =high right atrium; HBE {Prox) =proximal His bundle electrode pair; HBE (Dlst) = dlstal His bundle electrode pair; A= atria~ H =His; V =ventricle; RB= right bundle.)

atrial electrogram on the His bwidle 1racing to the onset of the His bundle defledion.14 The first rapid deflection represents local atrial activation in the vicinity of the AV node, but the earliest ident:illable His bundle activity is chosen because the measurement ofinterest is conduction time through the AV node-not conduction time to a speciflc local area in the His bundle. In other words, when the His bundle act:iv:ity is seen. conduction through the AV node is confirmed. In contrast. the HV interval is measured from the earliest identifiable His deflection to the earliest onset of ventricular acti:v.ity recorded from either an .intra.cardiac electrogram or any surface QRS complex. For this measurement the desired conduction time is from the earliest evidence of acti:v.ity in the His bwidle to any point conmming ventricular activity, regardless of the area from which this activity is generated. We consider an AH interval between 60 and 120 ms and an HV interval between 35 and 55 ms recorded during sinus rhythm as normal for our laboratories. .Abnormalities of AV conduction are discussed in more detail in Chapters 3 and 10, but some examples are offered here to illustrate the usefulness of intracardiac recordings in defining the location of conduction disturbances. In Figure 1-9, first-degree AV block (since no atrial activation is actually "blocked" from conducting to the ventricles. we prefer the term first-degree conduction delay) is demonstrated by a PR interval of 220 ms (0.22 s) and conduction of every P wave. The QRS duration is 90 ms. which is normal. The cause offirst-degree conduction delay is noted in the His bundle electrogram. The AH interval measured 155 ms. which is markedly prolonged. However, in Figure 1-10, the prolonged PR interval in a patient with first-degree AV conduction delay and left bundle branch block is due to a severe conduction abnormality in the His-Purkinje system. as demonstrated by an HV interval of 165 ms. This latter situation represents a more aitical cardiac conduction disturbance, as discussed in more detail in Chapter 10. A third example of first-degree AV conduction delay is shown in Figure 1-11. This patient

10

CARDIAC ARRHYTHMIAS: INTERPRETATION, DIAGNOSIS, AND TREATMENT

RV--t FIGURE 1.. • First-degree AV block due to abnormal conduction in the AV node. (Key: RV= right ventricle. See Figure 1-8 for other abbrevlrtlons. TI me llnes: each major dfvlslon =50 ms.}

has a PR interval of 210 ms and left bundle branch block. However, the HV interval is only moderately prolonged to 65 ms, but a combination of all conduction times still yields an ECG pattern of first-degree AV conduction delay. Finally. first-degree AV conduction delay can be due to conduction abnormalities in both the AV node and His-Purkinje system (Figure 1-12). ThePRintervalrecm:dedduringsinusrhythm.usuallydemonst:ra:resminimalvariabilit.yunlessmarlced changes in autonomic tone occur (see "Autonomic Nervous System Effects;' later in chaprer). Thus, the appearance of 2 distinctly different stable PR intErvals during electrocardiographic recording

I 11 i i 1 1 1 1111 1

PR2SO

Ill

HRA

/i 0

A H

~1 ~m11-----1-"'---" 70

165

FIGURE 1·10 • First-degree AV block and left bundle branch block with a markedly prolonged HV interval. (See text for details.)

CHAPTER 1 • Cardiac Conduction

111 11111 1111 111111 II 1 11 1111111 111 11 111 I 11 111 11 1111111111

11-......__, .__ _ _ ___,_ _, .__ _ ____,,_ _

III

---"V-------"V------~

~

HRA--4

AH85

HB£--')h-il·---A HV0i4i~ 1

FIGURE 1·11 • First-degree AV block with left bundle branch blockand minimal intracardi;ac conduction abnonnalities.

II

Ill

v v

v

v v

v

aVF V1

v, HRA A

H v

AH 130 HV95

HBE

FIGURE 1·12 • First-degree AV block with combined AV nodal and Hls-PurklnJe conduction abnormalltles.

11

12

CARDIAC ARRHYTHMIAS: INTERPRETATION, DIAGNOSIS, AND TREATMENT

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f+ .

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, ...,

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j1 rL J , I' Jlr'rt L.t1~:. . L-'-' LL.l_j_ ....J...JL :

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FIGURE 1·13 • Two separate and stable PR intervals. This patient had stable PR intervals that were either normal {A) or long (8). (Reproduced with permission from KelleyWN,ed. Ttxtbookoflntemaf Medfdnt. Phlladefphla, PA: Lippincott 1989.)

strongly suggests the existence of 2 functionally separate anterograde conduction pa1hways. both preswnably in the AV node (Figure 1-13). The PR interval in panel A is 180 ms and in panel B 400 ms. This patient had dual AV nodal physiology; as illustrated in Figure l-l4.1s.19 In this figure, the first 3 PR intervals represent AV nodal conduction over the slowly conducting pathway, and the 1111 l llllrl1n1111 r11n II I 1111 l IIii ii iii i 11 iii Ii ii i I iiii i If ii IIii I itmrffm'l'll I I II 11m'ffTTTlfm

v1 -

-

HRA -J\--------.1\oo------..Jfpa--~

AH290

S2

AH80

~

Rv-t----it----t'

1~t---H~H~ t r t-

FIGURE 1·14 • Dual AV nodal physiology demonstrated at electrophysiologic study. (See text for details.} {Reproduced with permission fA>m PrystewSky EN, Page RL Elearophysiologyofthe Sino-Atriof ondAtriovetlttkuforNodes. New York. NY: Alan R. US$; 1988.)

CHAPTER 1 • Cardiac Conduction

i+-t--+~----t-1~ 1

2

3

13

i

FIGURE 1·15 • Schematic ofWenckebach AV nodal block during incremental atTial pacing.

AH .interval is 290 ms. A premature atrial stimulus (S1) -was inttoduced into the high right atrium and blocbd in the AV node (no His depolarization after atrial premature compla). .Attioventricular nodal c.onducti.on resumed over the fast conducting pathway. as shown in the last 3 complexes on this tracing and demonstrated by a normal PR.interval and an AH conduction time of80 ms. Attfoventrlcular nodal block Incremental atrial pacing is used to evaluate AV nodal function in the electrophysiology laboratory. Amal pacing is started at a rate slightly faster than the spontaneous sinU8 rate and is progres-

sively increased until AV nodal block occurs. The AH interval increases with faster-paced rates as shown schematically in Figure 1-15. This is an example of 3:2 Wenckebach block. Complex 1 is the baseline interval and conducts with relatively minimal AV nodal delay; complex 2 shows a substantial increase in the AH int.erval; and complex 3 fails to conduct to the His bundle. Records from a patient are demonstrated in Figure 1-16. Not.e in ECG lead II a progressive increase in the PR int.erval for the first 3 paced beats, followed by a P wave without conduction to the ven1Jicle; conduction resumes with the last paced beat, and the PR interval is shorter than the PR int.erval of the last conducted beat prior to block. The first PR increment is the largest of the sequence (30 vs 10 ms). consistent with Wenckebach behavior. This pattern of conduction abnormality is referred to as Wenckebach. or Mobitz type I serond-degree, AV block. The changes in PR interval in this example occur within the AV node, as demonstrated by the progressive increase in the AH interval from 70 to 110 ms without change in the HV interval. Not.e that in the fourth paced beat the a1Jial depolarization in the HBE tracing is not followed by a His bundle deflection, confirming bloclc: within the AV node. Conduction resumes with an AH interval of 70 ms. In very unusual instances it is difficult to detect a measurable increase in the PR interval prior to block. An example of this is noted in Figure 1-17. This patient had spontaneous episodes while awake of nonconducted Pwaves with minimal or no prior PR prolongation. Figure 1-17Awas recorded upon electroph}'5iologic study at a routine ECG paper speed of25 mm/s. There is only

14

CARDIAC ARRHYTHMIAS: INTERPRETATION, DIAGNOSIS, AND TREATMENT

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a minimal change in the PR interval measurable in this example. Analysis of the intracardiac electrograms reveals conduction block in the AV node. with a mere 10 to 15 ms increase in the AH interval prior to the nonconducted P wave (Figure l-17B). This recording was done at a 100-mm/s paper speed. where more precise measurements can be obtained. The normal 25mm/s

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CHAPTER 1 • Cardiac Conduction

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QRS complex strongly suggests that block will be in the AV node or His bundle, not below the His bundle. However, one should suspect block with.in the His bundle in cases ofWenc:ktbach or 2:1 block with baseline normal PR and QRS intervals with minimal changes in PR interval before block (Flgute l-18A). Note in this example of 2:1 block the normal PR and QRS intervals on the conducted complexes, and the intrac:ardiac: electrograms showing a split His potential with block after the first His deflection, or intraHis block (Figure l-18B.C). On occasion, a Wenckebach conduction pattern can occur in the His-Purkin.je system (F1gu.re 1-19). At electrophysiologic study during inc.remental atrial pacing, there was a progressive increase in the PR interval, as noted in ECG lead II. Analysis of conduction times in the His bundle elec:trogram shows a progressive inc.rease in the HV interval from 130 to 165 ms prior to a nonconducted P wave. The AH interval.remained constant. Note that the fifth paced atrial complex. demonstrates activation of the His bundle but no conduction beyond this point. Thus, conduction block is infra-His, which represents a severe form ofconduction disturbance. Note that the patient has a right bundle branch block pattern. Even with a bundle branch block pattern, a Wenckebach conduction sequence most commonly implies conduction delay and block in the AV node. Testing of the AV nodal conduction system with incremental atrial pacing in the el.ectrophysiology laboratory yields a wide range ofatrial paced cycle lengths at which Wenckebach AV nodal block

occurs. In the resting state during electrophysiologic testing, we consider AV nodal conduction to be normal if 1:1 conduction is present to a right atrial paced cycle length ofless than 505 ms.20 Of particular interest is that even though Wenckebach block may occur at a wide range of cycle lengths, the AV nodal function curve is physiologically similar for all patients. This is demonstrated in Figure 1-20, which shows the lengthening of the AH interval, noted on the ordinate,

16

CARDIAC ARRHYTHMIAS: INTERPRETATION, DIAGNOSIS, AND TREATMENT

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CHAPTER 1 • Cardiac Conduction

17

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as a function of shortening of the atrial pacing cycle length (increased heart rate), noted on the abscissa.21 Each line represents a group of patients with Wenckebach block occurring at different cycle lengths. For example, the curve on the far right includes patients in whom Wenclcebach block occurs at cycle lengths greater than 500 ms. whereas the curve on the far left represents patients in whom Wenclcebach o«:urs at paced cycle lengths less than 300 ms. Each curve is divided into separate segments, with the most distal segment represented by A. Analysis of these data showed that the curves were progressively shi&d to the left as shorter atrial paced cycle lengths were required to yield Wenclcebach block. but the slopes of each part of the curves were similar for all curves. In essence, only minimal to moderate prolongation of the AH interval o«:urs until the Wenclcebach cycle length is approached. As a corollary, drugs that demonstrate negative dromotroplc effects,

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Mechanisms The mechanism ofatrial flutter, long debated.'·17 was elucidated in the era ofoperative arrhythmia ablation18 followed by the era ofcatheter ablation.19 The ECG pattern oftypical flutter is associated with a macro reentrant right atrial circuit that conforms to classic reent.rr°'21 with an excitable gap

FIGURE 6-10 • Twelve-lead ECG oftypic;il atrial fluttet'. (See text for details.)

122

CARDIAC ARRHYTHMIAS: INTERPRETATION, DIAGNOSIS, AND TREATMENT

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(Figure 6-11). The excitable gap can be demonstrated using single atrial extrastimuli or entrainment by incremental atrial pacing (Figure 6-11). Mapping of the circuit demonstrates a low-tohigh sequence up the anterior and septal walls, with a high-to-low sequence down the lateral and posterior walls (Figure 6-12). A corridor ofblock characterized by "double spike" potentials can be demonstrated during endocardial mapping during flutter and largely corresponds to the crista terminalis as a line of block.22 A relative slow conduction zone of the circuit is in the region of the isthmus between the inferior vena cava orifice and the inferior tricuspid ring, with the impulse emerging from this zone near the orifice of the coronary sinus. The tricuspid caval isthmus (TCI) is the narrowest part of the circuit and serves as a convenient target for catheter ablation. Atrial flutter that is electrocardiographically atypical has eclectic mechanisms that depend on context (post AF ablation, associated with congenital heart disease, etc.), but the most common remains RA macro reentry as per Figure 6-11 with the circuit reversed, i.e., clockwise. The target of ablation remains the narrowest part of the circuit as per typical flutter, the TCI.

Clinical Presentation Atrial flutter is observed in patients of any age with common risk factors similar to those for atrial fibrillation, namely organic heart disease, hypertension, obesity, diabetes, alcohol, and others. The clinical setting overlaps considerably with that of atrial fibrillation with both arrhythmias observed in the same individual relatively frequently. Atrial flutter may be paroxysmal

CHAPTER 6 • Supraventricular Tachycardia

123

(self-terminating) or persistent. TCI-dependent flutter terminates in less than a few minutes very infrequently, and other mechanisms should be sought if that occurs. It usually presents as palpitations but can present with syncope, hypotension, and even cardiac arrest in individuals capable of one-to-one AV conduction during flutter. Importantly, asymptomatic or minimally symptomatic patients may present with effort intolerance, dyspnea, or congestive heart failure.

Acute Therapy23 The "traditional" strategy in managing any atrial arrhythmia is control of the ventricular rate using AV node blocking drugs. Subsequent consideration is then made to reversion to sinus rhythm using membrane-active agents, such as propafenone with cardioversion considered if the former is not adequate or hemodynamic compromise occurs. This "classic" approach is frequently difficult to apply in atrial flutter. Control of the ventricular rate is difficult to achieve and abrupt transitions from too fast to too slow can occur. Membrane-active drugs, especially the le agents propafenone and Flecainide, are very effective at prolonging the flutter cycle length but less effective at terminating flutter with the drug ibutilide24 more successful at conversion at the cost of a small risk of proarrhythmia. For these reasons, it is appropriate to consider cardioversion as an early strategy. Atrial pacing techniques may be useful if an implanted device has such capability or an atrial lead is present for another reason such as after cardiac surgery. Atrial pacing by the esophageal route is preferred by some, although it can be painful and not widely used. An abrupt change in flutter-wave morphology indicates termination of flutter with incremental atrial pacing (Figure 6-12). The critical rate required to terminate type 1 flutter is usually between 115% and 125% of the flutter rate. Attempts at pace termination of atrial flutter may result in induction of atrial fibrillation, which is frequently self-terminating in the patient without a history of atrial fibrillation.

Chronic Management Pharmacologic prophylactic therapy for atrial flutter is empirical with efficacy determined by trial and error. Dual therapy with both an AV node blocking drug and a membrane-active drug is recommended except for drugs such as sotalol and amiodarone, which have both properties. The use of membrane-active drugs alone may slow the atrial rate sufficiently to allow oneto-one AV conduction in some patients and are thus potentially "proarrhythmic" when used alone (Figure 6-13). Thus, a drug to prolong AV node refractoriness such as a beta blocker, verapamil, or Cardizem is usually recommended to accompany membrane-active drugs such as propafenone. It is fair to say that chronic pharmacological management of atrial flutter has largely been supplanted by catheter ablation (Chapter 17).25.211

AV NODE REENTRY Gordon Moe and coworkers27 originally demonstrated AV node reentry in the dog and introduced the concept of dual pathways in the AV junctional region as the substrate for this arrhythmia. This concept was supported in human studies by Kistin,28 who observed 2 populations of PR intervals in selected patients during electrocardiographic recording, with short PR intervals postulated to be over the "fast pathway" and long PR intervals postulated to be over the "slow pathway." Schuilenburg and Durrer29 first demonstrated dual-pathway curves in humans utilizing the extrastimulus technique, relating inter atrial interval (A1-A2) to prematurity of a

124

CARDIAC ARRHYTHMIAS: INTERPRETATION, DIAGNOSIS, AND TREATMENT

ventricular extrastimulus. Finally, Rosen,:ro Denes,'1 Wu,32 and others proposed the connection between paroxysmal supraventricular tach.ycardia in humans and dual-pathway physiology demonstrated by the extrastimulus tec.hnique.

Clinical Presentation and Electrocardiographic Recognition AV node reentry accounts for the majority of cases of paroxysmal supraventricular tachycardia referred to an electrophysiology laboratory.» It can occur in any age group but most frequently presents in young to middle-aged adults, being slightly more prevalent in women than in men. After presentation, further episodes will vary in frequency and duration but will usually persist for years. Once tachycardia has established a pattern, recunence is the rule. There are generally no precipitating factors, although some patients will report a consistent relationship to exercise, posture, or gastrointestinal symptoms with initiation of tachycardia. The onset is typically

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PanelA FIGURE 6-12 • Entrainment during atrial flutter. Panel A illustrates atrial pacing at progressively more rapid rates, with acceleration of the flumr cycle length to me paced rate. A Is the control strip and the paced rate Is progresslvely Increased frcm strip Bto strip D. The pacing has not altefed the flutter-wave morphology, and the arrhythmia resumes at Its fonnef rate after cessation of pacing In each strip. Panel B Illustrates the effect offurther aa:eleratlon of the padng rate. At the first astmsk In stl'lp A. there Is a sudden change In the flutter-wave mOfphology, signifying the transition from entrainment of me drcult to cessation of reentry. Sinus rhythm ensues after discontinuation of peeing In strip Bend continues In slTip C. S denotes stimulus artefact. (Reproduced with pennlsslon from Wildo AL. Carlson MO, Biblo LA. Henthom RW. The role c:K transient entrainment in atrial fluttet'. In: Touboul P, waldo AL eds. AtriofAtrllytflmios: C.Urrerit Concept$ and Management. St Lcuis. MO: Mosby Year Book; 1990:21 o. Copyright c Elsevier.)

CHAPTER 6 • Supraventrlcular Tachycardia

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PanelA FIGURE 6-U • Propafenone In at?tal flutter. The records are fn:lm a patient treated wtth prapafertone as monotherapy for praphyla)ds of atrial flutcer. The patient retumed wtth wide QRS tachycardia necessttaUng cardlove1'$1on. Electrophyslologlcal tesUng In 1tie absence of drug n!ll'l!lled Inducible atrial flutter (Panel A) at an atrial cycle length of 220 ms. The adcllUon of pmpafenone (Panel B) 140 mg Intravenously resulted In pralongatton ofthe flutter cycle length ccruidenlbly, to 320 ms. At this point. upright ttlt {Panll C) resulted. In aslfght shortl!nlng of cydelength to 285 ms with the occurrence of 1:1 AV conduction wlthaberrancy and reproductfonof thepattl!fTB dtnk:ill tadlyca!dla. One-to-one AV-node conduction during tllt was related to tllt-indU