Bennett's Cardiac Arrhythmias: Practical Notes on Interpretation and Treatment, Eighth Edition

330 Pages·2012·8.92 MB·English

by  David H. Bennett(auth.)

Bennett’ s Cardiac Arrhythmias
Bennett_ffirs.indd i 10/17/2012 9:55:54 PM
Bennett’ s Cardiac

Arrhythmias
Practical Notes on
Interpretation and
Treatment
8th Edition
David H. Bennett, MD FRCP
Senior Consultant Cardiologist
University Hospital of South Manchester
Manchester, UK
A John Wiley & Sons, Ltd., Publication
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This edition first published 2013 © 2013 by John Wiley & Sons, Ltd.
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Library of Congress Cataloging-in-Publication Data
Bennett, David H.
Bennett’s cardiac arrhythmias : practical notes on interpretation and treatment / David H. Bennett. – 8th ed.
p.; cm.
Cardiac arrhythmias
Rev. ed. of. Cardiac arrhythmias / David H. Bennett. 7th ed., 2006.
Includes bibliographical references and index.
ISBN 978-0-470-67493-2 (pbk. : alk. paper)
I. Bennett, David H. Cardiac arrhythmias. II. Title. III. Title: Cardiac arrhythmias.
[DNLM: 1. Arrhythmias, Cardiac–diagnosis. 2. Arrhythmias, Cardiac–therapy. WG 330]
616.1′28–dc23
2012021105
A catalogue record for this book is available from the British Library.
Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in
electronic books.
Cover image courtesy of the author
Cover design by Andrew Magee Design Ltd
Set in 9/12pt Palatino by SPi Publishers Services, Pondicherry, India
1 2013
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Contents
Preface, vii Treatment, 49
Systemic embolism, 51
Notes, viii
8 Atrial Tachycardia, 52
1 Sinus Rhythm, 1
ECG characteristics, 52
ECG characteristics, 1
Causes, 54
Sinus bradycardia, 4
Treatment, 55
Sinus tachycardia, 4
Multifocal atrial tachycardia, 55
Sinus arrhythmia, 5
9 Atrioventricular Junctional Re-entrant
2 Ectopic Beats, 6
Tachycardias, 56
Prematurity, 6
Mechanism, 56
Atrial ectopic beats, 8
ECG characteristics, 57
Atrioventricular junctional ectopic beats, 9
Clinical features, 62
Ventricular ectopic beats, 10
Treatment, 63
3 Escape Beats, 15
10 Wolff–Parkinson–White Syndrome, 67
Timing, 15
Pre-excitation, 67
Origins, 16
ECG characteristics, 68
4 Bundle Branch and Fascicular Blocks, 17 Arrhythmias, 69
Right bundle branch block, 17 Treatment, 72
Left bundle branch block, 18
Left anterior and posterior fascicular blocks, 19 11 Ventricular Tachyarrhythmias, 77
Ventricular tachycardia, 77
5 The Supraventricular Tachycardias, 24
Ventricular fibrillation, 78
Main types, 24
Supraventricular versus ventricular tachycardia, 78
Atrial origin versus atrioventricular re-entry, 25
Effects of supraventricular tachycardias, 26 12 Monomorphic Ventricular Tachycardia, 79
ECG characteristics, 79
6 Atrial Fibrillation, 29
Causes, 81
ECG characteristics, 29
Mechanisms of ventricular tachycardias, 81
Causes, 33
Investigations, 83
Prevalence, 34
Treatment, 85
Prognosis, 34
Coronary heart disease, 88
Classification, 34
Hypertrophic cardiomyopathy, 88
Management, 35
Arrhythmogenic right ventricular
Systemic embolism, 35
cardiomyopathy, 89
Rhythm management, 38
Dilated cardiomyopathy, 92
7 Atrial Flutter, 44 Ventricular tachycardias not due to structural heart
Common atrial flutter, 44 disease, 92
Causes, 49 Non-sustained ventricular tachycardia, 97
Prevalence, 49 Accelerated idioventricular rhythm, 97
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Contents
13 Polymorphic Ventricular Tachycardia and 20 Sudden Cardiac Death, 167
Ventricular Fibrillation, 98 Definition, 167
Polymorphic ventricular tachycardia, 98 Causes of arrhythmic sudden death, 168
Torsade de pointes tachycardia, 99 Aborted sudden cardiac death, 169
Hereditary long QT syndromes, 102 Athletic activities, 169
Ventricular fibrillation, 106
21 Cardioversion, 171
14 Tachycardias with Broad Ventricular Complexes, 115 Transthoracic cardioversion, 171
Causes of a broad complex tachycardia, 115 Transvenous cardioversion, 174
Useless guidelines, 116
22 Ambulatory ECG Monitoring, 176
Useful guidelines, 116
Continuous ECG recording, 176
15 Atrioventricular Block, 123 Intermittent ECG recording, 183
Classification, 123
23 Cardiac Pacing, 187
Causes of atrioventricular block, 127
Long-term cardiac pacing, 187
Atrioventricular dissociation, 128
Common indications for long-term pacing, 187
Bilateral bundle branch disease, 128
Pacing modes, 190
Clinical aspects of atrioventricular block, 130
Pacemaker hardware, 200
Treatment, 131
Pacemaker implantation, 202
16 Sick Sinus Syndrome, 132 Pacemaker clinic, 215
Causes, 132 Electromagnetic interference, 215
ECG characteristics, 133 Other precautions, 217
Clinical features, 135 Temporary cardiac pacing, 218
Diagnosis, 135
24 Implantable Cardioverter Defibrillators, 221
Treatment, 136
Defibrillator implantation, 223
17 Neurally Mediated Syncope, 137 Indications for ICD implanation, 224
Malignant vasovagal syndrome, 137 Defibrillator function, 226
Carotid sinus syndrome, 141 Precautions, 233
Postural orthostatic tachycardia syndrome, 141
25 Catheter Ablation, 234
Causes of syncope, 142
Procedure, 234
18 Arrhythmias due to Myocardial Infarction, 143 Wolff–Parkinson–White syndrome, 237
Ventricular fibrillation, 144 Typical atrioventricular nodal re-entrant
Ventricular tachycardia, 146 tachycardia, 241
Reperfusion arrhythmias, 146 Atrial tachycardia, 243
Arrhythmias subsequent to recent myocardial Atrial flutter, 244
infarction, 146 Atrial fibrillation, 244
Long-term significance of ventricular Atrioventricular nodal ablation, 245
arrhythmias, 147 Right ventricular outflow tract tachycardia, 247
Accelerated idioventricular rhythm, 147 Fascicular ventricular tachycardia, 248
Supraventricular tachycardias, 148 Ventricular tachycardia due to structural heart
Sinus and junctional bradycardias, 148 disease, 249
Atrioventricular block, 149 Catheter ablation: what should the patient
expect? 250
19 Antiarrhythmic Drugs, 152
Limitations, 152 26 Arrhythmias for Interpretation, 252
Choice of treatment, 153 Questions, 252
Modes of action, 153 Interpretations and answers, 307
Notes on individual drugs, 154
Index, 317
Antiarrhythmic drugs during pregnancy, 166
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Preface
There are several large textbooks which comprehensively medical students, who themselves will soon be responsi-
cover the field of cardiac arrhythmias with thorough refer- ble for dealing with arrhythmias, to nurses working in
encing of scientific papers. This book does not attempt to coronary and intensive care units, to cardiac technicians/
replicate these texts. The purpose of this eighth edition (the physiologists, whose responsibilities nowadays include a
first edition was published in 1981, and there have been major input into arrhythmia management, and to physi-
translations into five other languages) remains the same as cians who want a brief review of the practical aspects of
that of its predecessors: to provide a concise, up-to-date, cardiac arrhythmias. In recent years there has been a trend
practical guide to the diagnosis, investigation and man- to sub-specialisation in cardiology. Whatever the sub-
agement of the main cardiac arrhythmias, with particular specialty, cardiac arrhythmias will frequently be encoun-
emphasis on the problems commonly faced in practice. tered. An appreciation of the significance and management
In order to be proficient in the interpretation of arrhyth- of cardiac arrhythmias is required of all who treat patients
mias it is necessary to study a range of examples of each with cardiac disease.
rhythm disturbance. For this reason, it has always been a I am most grateful to my technical, medical and nursing
purpose of this book to present a large number of electro- colleagues for their help, and to the staff of my new
cardiograms so that the reader can gain experience in publisher at Wiley-Blackwell for their expertise.
ECG interpretation and can test him- or herself out, and The title of this edition, B ennett ’ s Cardiac Arrhythmias ,
thereby gain confidence, during the reading of the book. was chosen by the publisher to indicate that the author has
In this edition there are many new electrocardiograms, described the major disturbances of heart rhythm, not, at
and the quiz section has been revised and enlarged to least to date, that the author has experienced all of them!
provide a challenge to those who may be familiar with The book is dedicated to my family, Irene, Samantha
previous editions. and Sally.
The book has been written with junior hospital doctors
in mind. They receive little formal training in the manage- David H. Bennett, MD FRCP
ment of cardiac arrhythmias and yet, because prompt Senior Consultant Cardiologist
action is often required, the onus of diagnosis and treat- University Hospital of South Manchester
ment usually falls on them. It should also be of interest to Manchester, UK
vii
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Notes
The electrocardiograms in this book have been recorded recorded simultaneously, may be necessary. For example,
at the conventional paper speed of 25 mm/s, unless other- atrial activity is often the key to diagnosis but may not be
wise indicated. At this speed, each large square represents clearly shown in all ECG leads: it is often best seen in
0.2 s and each small square represents 0.04 s. Heart rate leads II and V1. Frequently, a ‘12-lead ECG’ will provide
(beats/minute) can therefore be calculated by dividing much more information than a rhythm strip.
the number of large squares between two consecutive An ECG recorded during an arrhythmia that is of diag-
complexes into 300, or by dividing the number of small nostic importance should always be safely stored in the
squares between two complexes into 1500. patient ’ s notes. This guideline, which may be very impor-
A single ECG ‘rhythm strip’ may be inadequate for tant to the long-term management of a patient, is often
diagnosis. Scrutiny of several ECG leads, preferably ignored, particularly on intensive and coronary care units!
viii
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1
Sinus Rhythm
The sinus node lies at the junction of the superior vena cava and right atrium.
Atrial activation travels inferiorly from the sinus node to the atrioventricular
(AV) node, resulting in a positive P wave in the inferior ECG leads, II, III and aVF.
If the QRS complex is preceded by a P wave that is not positive in the inferior
leads then the rhythm is other than sinus rhythm. The sinus node impulse is
conducted relatively slowly via the AV node to reach the His–Purkinje system,
which then conducts very rapidly to activate the ventricular myocardium.
Normal sinus rhythm is characterised by a rate of 60–100 beats/min; PR
interval 0.12–0.21 s; QRS duration ≤ 0.10 s; QTc ≤ 0.44 s.
ECG characteristics
The sinus node initiates the electrical impulse that activates atrial and then ventricu-
lar myocardium during each normal heartbeat. Sinus node activity itself does not
register on the electrocardiogram (ECG).
P wave
Atrial activity, the P wave, is usually apparent in most ECG leads (Figure  1.1 ).
However, occasionally the P wave in some leads is not visible or is of low amplitude,
and it may be necessary to inspect all leads of the ECG to establish that there is sinus
rhythm (Figure  1.2 ).
The sinus node lies at the junction of the superior vena cava and right atrium. A trial
activation therefore spreads from the sinus node in an inferior direction (i.e. towards the feet)
to the atrioventricular (AV) junction. The P wave, therefore, is upright in those leads
that are directed to the inferior surface of the heart (i.e. II, III and aVF), and is inverted
in aVR, which faces the superior heart surface (Figure  1.1 ). If a P wave does not have
these characteristics then, even though a P wave precedes each ventricular complex,
the sinus node has not activated the atria and the rhythm is abnormal (Figure  1.3 ).
PR interval
The AV node is the only electrical connection between atria and ventricles : the mitral-
tricuspid valve ring that separates the atria from the ventricles is fibrous and cannot
Bennett’s Cardiac Arrhythmias: Practical Notes on Interpretation and Treatment, Eighth Edition. David H. Bennett.
© 2013 John Wiley & Sons, Ltd. Published 2013 by John Wiley & Sons, Ltd.
1
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Bennett’s Cardiac Arrhythmias
I
a VR
II a VL
III a VF
Figure 1.1 Sinus rhythm. Atrial activity is clearly seen in the limb leads.
Figure 1.2 Sinus rhythm with low-amplitude P waves (leads I, II, III and V1). Atrial activity is only clearly seen in V1.
conduct electrical impulses. The AV node conducts relatively slowly, thereby delay-
ing conduction of the atrial impulse to the ventricles. Conduction through the AV
node does not register on the ECG. The PR interval, which is measured from the onset
of the P wave to the onset of the ventricular complex, indicates the time taken for an
atrial impulse to reach the ventricles. The normal PR interval ranges from 0.12 to
0.21 s. It should shorten during sinus tachycardia.
QRS complex
After traversing the AV node, the activating impulse reaches the bundle of His, which
divides into the right and left bundle branches. The bundle of His, the bundle
branches and their ramifications, the Purkinje fibres, constitute the ‘specialised
intraventricular conducting system’ which facilitates very rapid conduction of the
impulse through the ventricular myocardium. Ventricular activation (i.e. depolarisa-
tion) is represented by the QRS complex, which is normally no greater than 0.10 s in
2
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CHAPTER 1 Sinus Rhythm
I aVR VI
II aVL V2
III aVF V3
Figure 1.3 Junctional not sinus rhythm: a P wave precedes each QRS complex but is superiorly directed: i.e. it is negative
in leads II, III and aVF.
duration. The amplitude of the QRS complex is larger than that of the P wave because
the mass of the ventricles is much greater than that of the atria.
T wave
The T wave is the result of the electrical recovery of ventricular myocardium prior to
the next heartbeat, i.e. repolarisation. Sometimes, a low-amplitude wave can be seen
following the T wave, termed a U wave. It is thought to result from repolarisation of
the Purkinje fibres and is usually seen in leads V2–4.
The QT interval, which is measured from the onset of the QRS complex to the end
of the T wave, represents the duration of ventricular activation plus recovery. The QT
interval normally shortens with increasing heart rate, partly due to the increase in
rate itself and partly due to the increase in sympathetic nervous system activity
related to sinus tachycardia. When measuring the QT interval it is necessary to correct
the measured interval for heart rate. The corrected QT interval (QTc) is calculated by
selecting the ECG lead showing the longest QT interval, and then dividing the square
root of the cycle length into the measured QT interval. For example, a patient with a
ECG characteristics of normal sinus rhythm
P wave
Precedes each QRS complex
Upright in leads III, aVF
Inverted in lead aVR
PR interval
Duration 0.12–0.21 s
QRS complex
Duration ≤ 0.10 s
QTc interval
Duration ≤ 0.42 s (men), ≤ 0.44 s (women)
3
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