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The ECG In Practice For Elsevier Content Strategist: Laurence Hunter Content Development Specialist: Helen Leng Project Manager: Louisa Talbott Designer/Design Direction: Helius and Mark Rogers Illustration Manager: Jennifer Rose Illustrators: Helius and Gecko Ltd 1 The ECG In Practice SIXTH EDITION John R. Hampton DM MA DPhil FRCP FFPM FESC Emeritus Professor of Cardiology, University of Nottingham, UK With contributions by David Adlam BA BM BCh DPhil MRCP Senior Lecturer in Acute and Interventional Cardiology and Honorary Consultant Cardiologist, University of Leicester, UK EDINBURGH LONDON NEW YORK OXFORD PHILADELPHIA ST LOUIS SYDNEY TORONTO 2013 Notices Knowledge and best practice in this ﬁeld are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. © 2013 Elsevier Ltd. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the publisher (other than as may be noted herein). First edition 1986 Second edition 1992 Third edition 1997 Fourth edition 2003 Fifth edition 2008 Sixth edition 2013 ISBN 978-0-7020-4643-8 International ISBN 978-0-7020-4644-5 e-book ISBN 978-0-7020-5244-6 British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Practitioners and researchers must always rely on their own experience and knowledge in evaluating and us; ing any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identiﬁed, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Library of Congress Cataloging in Publication Data A catalog record for this book is available from the Library of Congress Printed in China www.cambodiamed.blogspot.com | Best Medical Books | Chy Yong 1 Preface WHAT TO EXPECT OF THIS BOOK I assume that the reader of this book will have the level of knowledge of the ECG that is contained in The ECG Made Easy, to which this is a companion volume. The ECG is indeed easy in principle, but the variations in pattern seen both in normal people and in patients with cardiac and other problems can make the ECG seem more complex than it really is. This book concentrates on these variations, and contains several examples of each abnormality. It is intended for anyone who understands the basics, but now wants to use the ECG to its maximum potential as a clinical tool. The ECG is not an end in itself, but is an extension of the history and physical examination. Patients do not visit the doctor wanting an ECG, but come either for a health check or because they have symptoms. Therefore, this book is organized according to clinical situations, and the chapters cover the ECG in healthy subjects and in patients with palpitations, syncope, chest pain, breathlessness or non-cardiac conditions. To emphasize that the ECG is part of the general assessment of a patient, each chapter begins with a brief section on history and examination and ends with a short account of what might be done once the ECG has been interpreted. This sixth edition continues the philosophy of its predecessors in that the patient is considered more important than the ECG. However, the ECG is a vital part of diagnosis and, increasingly, dictates treatment. Electrical devices of various sorts are standard treatment in cardiology, and patients with such devices are now commonly seen in patients who present with non-cardiological problems. Those who are not specialists in cardiology need to understand them. Therefore there is a series of changes in the text compared with previous editions, and the sections on pacemakers, defibrillators and electrophysiology have been integrated into the relevant chapters. WHAT TO EXPECT OF THE ECG The ECG has its limitations. Remember that it provides a picture of the electrical activity of the heart, but gives only an indirect indication of the heart’s structure and function. It is, however, invaluable for assessing patients whose symptoms may be due to electrical v Preface malfunction in the heart, including patients with conduction problems and those with arrhythmias. In healthy people, finding an apparently normal ECG may be reassuring. Unfortunately the ECG can be totally normal in patients with severe coronary disease. Conversely the range of normality is such that a healthy subject may quite wrongly be labelled as having heart disease on the basis of the ECG. Some ECG patterns that are undoubtedly abnormal (for example, right bundle branch block) are seen in perfectly healthy people. It is a good working principle that it is the individual’s clinical state that matters, not the ECG. When a patient complains of palpitations or syncope, the diagnosis of a cardiac cause is only certain if an ECG is recorded at the time of symptoms – but even when the patient is symptom-free, the ECG may provide a clue for the prepared mind. In patients with chest pain the ECG may indicate the diagnosis, and treatment can be based upon it, but it is essential to remember that the ECG may remain normal for a few hours after the onset of a myocardial infarction. In breathless patients a totally normal ECG probably rules out heart failure, but it is not a good way of diagnosing lung disease or pulmonary embolism. Finally, it must be remembered that the ECG can be vi quite abnormal in a patient with a variety of noncardiac conditions, and one must not jump to the conclusion that an abnormal ECG indicates cardiac pathology. ACKNOWLEDGEMENTS In this sixth edition of The ECG in Practice I have been helped by many people. In particular, I am grateful to David Adlam for providing many illustrations, and for contributing the sections on devices and electrophysiology, which takes the book beyond the routine ECG into the realm of sophisticated diagnosis and electrical treatments – which are nevertheless based on an understanding of the ECG. I am also extremely grateful to my copy-editor, Alison Gale, for her enormous attention to detail that led to many improvements in the text. I am also grateful to Laurence Hunter and his team at Elsevier for their encouragement and patience. As before, I am grateful to many friends and colleagues who have helped me to find the wide range of examples of normal and abnormal ECGs that form the backbone of the book. John Hampton Nottingham, 2013 1 Contents 12-lead ECGs 1. The ECG in healthy people 2. The ECG in patients with palpitations and syncope: between attacks viii 1 58 3. The ECG when the patient has a tachycardia 101 4. The ECG when the patient has a bradycardia 169 5. The ECG in patients with chest pain 208 6. The ECG in patients with breathlessness 287 7. The effect of other conditions on the ECG 316 8. Conclusions: four steps to making the most of the ECG 346 Index 350 vii 12-lead ECGs viii AAI pacing 196 Accelerated idionodal rhythm 48 Accelerated idioventricular rhythm 28 Anorexia nervosa 342 Aortic stenosis, severe, left ventricular hypertrophy with 298 Aortic stenosis and left bundle branch block 296 Atrial ﬁbrillation 124, 178 Atrial ﬁbrillation, uncontrolled 290 Atrial ﬁbrillation and anterior ischaemia 244 Atrial ﬁbrillation and coupled ventricular extrasystoles 290 Atrial ﬁbrillation and digoxin effect at rest 280 Atrial ﬁbrillation and digoxin effect on exercise 280 Atrial ﬁbrillation and inferior infarction 140 Atrial ﬁbrillation and left bundle branch block 128, 130 Atrial ﬁbrillation and right bundle branch block 134 Atrial ﬁbrillation and Wolff–Parkinson-White syndrome 148 Atrial ﬂutter and 1:1 conduction 120 Atrial ﬂutter and 2:1 block 118 Atrial ﬂutter and 4:1 block 120 Atrial ﬂutter and intermittent VVI pacing 194 Atrial ﬂutter and variable block 176 Atrial ﬂutter in hypothermia 318 Atrial septal defect and right bundle branch block 326 Atrial tachycardia 110, 116 Atrioventricular nodal re-entry tachycardia (AVNRT) 122 Atrioventricular nodal re-entry tachycardia (AVNRT) and anterior ischaemia 244 Bifascicular block 90 Biventricular pacing 314 Broad complex tachycardia of uncertain origin 136, 138 Brugada syndrome 80 Chronic lung disease 310 Complete heart block 180 12-lead ECGs Complete heart block and Stokes–Adams attack 182 Congenital long QT syndrome 76 DDD pacing, atrial tracking 200 DDD pacing, atrial and ventricular pacing 198 DDD pacing, intermittent 200 Dextrocardia 10 Dextrocardia, leads reversed 10 Digoxin effect 334 Digoxin effect and ischaemia 262 Digoxin toxicity 336 Ebstein’s anomaly, right atrial hypertrophy and right bundle branch block 324 Ectopic atrial rhythm 8 Electrical alternans 328 Exercise, digoxin effect, atrial ﬁbrillation 280 Exercise-induced ischaemia 272 Exercise-induced ST segment depression 278 Exercise-induced ST segment elevation 274 Exercise testing, normal ECG 272, 278 Fallot’s tetralogy, right ventricular hypertrophy in 324 Fascicular tachycardia 136 First degree block 84 First degree block and left bundle branch block 88 First degree block and right bundle branch block 90, 174, 182 Friedreich’s ataxia 344 Hyperkalaemia 330 Hyperkalaemia, corrected 332 Hypertrophic cardiomyopathy 68, 300 Hypokalaemia 334 Hypothermia 318 Hypothermia, atrial ﬂutter 318 Hypothermia, re-warming after 320 Intermittent VVI pacing 192 Ischaemia, anterior 242 Ischaemia, anterior and atrial ﬁbrillation 244 Ischaemia, anterior and AV nodal re-entry tachycardia 244 Ischaemia, anterior and inferior infarction and right bundle branch block 238 Ischaemia, anterior and possible old inferior infarction 240 Ischaemia, anterior and right bundle branch block 238 Ischaemia, anterolateral 242 Ischaemia, digoxin effect and 262 Ischaemia, exercise-induced 272 Ischaemia, ?left ventricular hypertrophy 300 Ischaemia, probable 298 Junctional tachycardia with right bundle branch block 136 Left anterior hemiblock 88, 302 Left atrial hypertrophy 70 Left atrial hypertrophy and left ventricular hypertrophy 292 Left axis deviation 86 Left bundle branch block 66, 234 Left bundle branch block and aortic stenosis 296 Left bundle branch block and ?right ventricular overload 234 Left posterior hemiblock 92 Left ventricular hypertrophy 64, 252, 260, 294, ix 12-lead ECGs 296, 322 Left ventricular hypertrophy and ?ischaemia 300 Left ventricular hypertrophy and left atrial hypertrophy 292 Left ventricular hypertrophy and severe aortic stenosis 298 Lithium treatment 340 Long QT syndrome, congenital 76 Long QT syndrome, drug toxicity 146 Lown–Ganong–Levine syndrome 74 x Malignant pericardial effusion 328 Mediastinal shift 22 Mitral stenosis and pulmonary hypertension 292 Myocardial infarction, acute anterior and old inferior 232 Myocardial infarction, acute anterolateral, with left axis deviation 222 Myocardial infarction, acute inferior 214 Myocardial infarction, acute inferior and anterior ischaemia 230 Myocardial infarction, acute inferior (STEMI) and anterior NSTEMI 232 Myocardial infarction, acute inferior and old anterior 230 Myocardial infarction, acute inferior and RBBB 236 Myocardial infarction, acute lateral 220 Myocardial infarction, anterior 218 Myocardial infarction, anterior, ?age 274 Myocardial infarction, anterior NSTEMI 240 Myocardial infarction, anterolateral, ?age 224 Myocardial infarction, evolving inferior 216 Myocardial infarction, inferior and atrial ﬁbrillation 140 Myocardial infarction, inferior and right bundle branch block 236 Myocardial infarction, inferior and right bundle branch block and ?anterior ischaemia 238 Myocardial infarction, inferior and right ventricular infarction 228 Myocardial infarction, inferior and ventricular tachycardia 140 Myocardial infarction, lateral (after 3 days) 222 Myocardial infarction, old anterior 224 Myocardial infarction, old anterolateral NSTEMI 260 Myocardial infarction, old inferior (possible) and anterior ischaemia 240 Myocardial infarction, old posterior 254 Myocardial infarction, posterior 226 Myocardial infarction, posterior infarct with normal QT interval 78 Normal ECG 8, 12, 272, 278 Normal ECG, accelerated idionodal rhythm 48 Normal ECG, black people 42 Normal ECG, child 52 Normal ECG, ectopic atrial rhythm 8 Normal ECG, exercise testing 272, 278 Normal ECG, high take-off ST segment 32 Normal ECG, junctional escape beat 4 Normal ECG, left axis deviation 50 Normal ECG, ‘leftward’ limit of normality 16 Normal ECG, notched (biﬁd) P wave 12 Normal ECG, notched S wave (V2) 26 Normal ECG, P wave, biﬁd (notched) 12 Normal ECG, P wave inversion 8, 40 Normal ECG, P wave inversion (lead VR, VL) 40 Normal ECG, partial right bundle branch block pattern 34 Normal ECG, PR interval variation 48 Normal ECG, pre-exercise 282 12-lead ECGs Normal ECG, R wave, tall (voltage criteria and) 294 Normal ECG, R wave dominance (lead II) 14 Normal ECG, R wave dominance (V1) 22, 308 Normal ECG, R wave dominance (V3) 20 Normal ECG, R wave dominance (V4) 18 Normal ECG, R wave dominance (V5) 20, 24 Normal ECG, R wave dominance (V6) 18 Normal ECG, R wave size 14 Normal ECG, right axis deviation 16 Normal ECG, ‘rightward’ limit of normality 14 Normal ECG, R–R interval variation 2 Normal ECG, RSR1 pattern 26 Normal ECG, RSR1S1 pattern 26 Normal ECG, S wave dominance (lead I) 16 Normal ECG, S wave dominance (lead III) 16 Normal ECG, S wave dominance (V1) 18 Normal ECG, S wave dominance (V2) 20, 24 Normal ECG, S wave dominance (V3) 18 Normal ECG, S wave dominance (V4) 20 Normal ECG, septal Q wave 28, 50 Normal ECG, small Q wave 30, 38 Normal ECG, ST segment, isoelectric and sloping upward 30 Normal ECG, ST segment depression 34 Normal ECG, ST segment depression (nonspeciﬁc) 36 Normal ECG, ST segment elevation 32 Normal ECG, T wave, biphasic 34, 40, 52 Normal ECG, T wave, peaked 332 Normal ECG, T wave, tall peaked 44 Normal ECG, T wave ﬂattening 44 Normal ECG, T wave inversion (lead III) 38 Normal ECG, T wave inversion (lead V1) 38 Normal ECG, T wave inversion (lead V2) 40 Normal ECG, T wave inversion (lead V3) 42 Normal ECG, T wave inversion (lead VR) 36 Normal ECG, T wave inversion (lead VR, V1–V2) 40 Normal ECG, T wave inversion (lead VR, VL) 40, 42 Normal ECG, T wave inversion in black people 42 Normal ECG, U wave, prominent/large 46, 50 Pericardial effusion, malignant 328 Pericarditis 250 Pre-exercise normal ECG 282 Prolonged QT interval due to amiodarone 78, 338 Pseudonormalization 276 Pulmonary embolus 246, 248, 250, 310 Pulmonary hypertension and mitral stenosis 292 Pulmonary stenosis 322 Re-warming after hypothermia 320 Right atrial hypertrophy 304 Right atrial hypertrophy and right bundle branch block, in Ebstein’s anomaly 324 Right atrial hypertrophy and right ventricular hypertrophy 304 Right bundle branch block and acute inferior infarction 236 Right bundle branch block and anterior infarction 236 Right bundle branch block and anterior ischaemia 238 Right bundle branch block and atrial septal defect 326 Right bundle branch block and inferior infarction, ?anterior ischaemia 238 Right bundle branch block and right atrial hypertrophy, in Ebstein’s anomaly 324 Right ventricular hypertrophy 66, 308 Right ventricular hypertrophy, marked 306 Right ventricular hypertrophy in Fallot’s tetralogy 324 xi 12-lead ECGs Right ventricular hypertrophy and right atrial hypertrophy 304 Right ventricular outﬂow tract ventricular tachycardia (RVOT-VT) 104, 144 RSR1 pattern 26, 80 RSR1S1 pattern 26 Second degree block (2:1) 86, 180 Second degree block (Wenckebach) 84 Second degree block and left anterior hemiblock 94 Second degree block and left anterior hemiblock and right bundle branch block 94 Sick sinus syndrome 172 Sinus arrhythmia 2, 112 Sinus bradycardia 4, 170, 172 Sinus rhythm, after cardioversion 118, 122, 138 Sinus rhythm, in Wolff–Parkinson-White syndrome type A 108 Sinus rhythm and left bundle branch block 128 Sinus rhythm and normal conduction, post-cardioversion 138 Sinus tachycardia 4, 112 ST segment, nonspeciﬁc changes 210 ST segment depression, exercise-induced 278 ST segment elevation, exercise-induced 274 Subarachnoid haemorrhage 344 Supraventricular extrasystole 6, 114 xii Supraventricular tachycardia 106 T wave, nonspeciﬁc changes 210 T wave, nonspeciﬁc ﬂattening 262 T wave, unexplained abnormality 258 Thyrotoxicosis 326 Trauma 342 Trifascicular block 92 Ventricular extrasystole 6, 114 Ventricular extrasystoles, coupled and atrial ﬁbrillation 290 Ventricular ﬁbrillation 162 Ventricular tachycardia 132, 134 Ventricular tachycardia, fusion and capture beats 142 Ventricular tachycardia and inferior infarction 140 VVI pacing, bipolar 190 VVI pacing, intermittent 192 VVI pacing, unipolar 192 VVI pacing in complete block 194 Wolff–Parkinson-White syndrome and atrial ﬁbrillation 148 Wolff–Parkinson-White syndrome type A 70, 72, 148, 256, 302 Wolff–Parkinson-White syndrome type B 74, 258 The ECG in healthy people 1 The ‘normal’ ECG 2 What to do 54 The normal cardiac rhythm 2 The range of normality 54 The heart rate 2 Extrasystoles 7 The prognosis of patients with an abnormal ECG 54 The P wave 7 Further investigations 56 Treatment of asymptomatic ECG abnormalities 56 The PR interval 13 The QRS complex 15 The ST segment 31 The T wave 37 The QT interval 48 The ECG in athletes 48 The ECG in pregnancy 52 The ECG in children 52 Frequency of ECG abnormalities in healthy people 54 For the purposes of this chapter, we shall assume that the subject from whom the ECG was recorded is asymptomatic, and that physical examination has revealed no abnormalities. We need to consider the range of normality of the ECG, but of course we cannot escape from the fact that not all disease causes symptoms or abnormal signs, and a subject who appears healthy may not be so and may therefore have an abnormal ECG. In particular, individuals who present for screening may well have symptoms about which they have not consulted a doctor, so it cannot 1 The ECG in healthy people be assumed that an ECG obtained through a screening programme has come from a healthy subject. The range of normality in the ECG is therefore debatable. We first have to consider the variations in the ECG that we can expect to find in completely healthy people, and then we can think about the significance of ECGs that are undoubtedly ‘abnormal’. rate is increased) during inspiration, and this is called sinus arrhythmia (Fig. 1.1). When sinus arrhythmia is marked, it may mimic an atrial arrhythmia. However, in sinus arrhythmia each P–QRS–T complex is normal, and it is only the interval between them that changes. Sinus arrhythmia becomes less marked with increasing age of the subject, and is lost in conditions such as diabetic autonomic neuropathy due to impairment of the vagus nerve function. THE ‘NORMAL’ ECG THE NORMAL CARDIAC RHYTHM THE HEART RATE Sinus rhythm is the only normal sustained rhythm. In young people the R–R interval is reduced (i.e. the heart Fig. 1.1 I VR V1 V4 II VL V2 V5 III VF V3 V6 II 2 There is no such thing as a normal heart rate, and the terms ‘tachycardia’ and ‘bradycardia’ should be used The heart rate with care. There is no point at which a high heart rate in sinus rhythm has to be called ‘sinus tachycardia’ and there is no upper limit for ‘sinus bradycardia’. Nevertheless, unexpectedly fast or slow rates do need an explanation. SINUS TACHYCARDIA The ECG in Figure 1.2 was recorded from a young woman who complained of a fast heart rate. She had no other symptoms, but was anxious. There were no other abnormalities on examination, and her blood count and thyroid function tests were normal. Box 1.1 shows possible causes of sinus rhythm with a fast heart rate. 1 Box 1.1 Possible causes of sinus rhythm with a fast heart rate • Pain, fright, exercise • Hypovolaemia • Myocardial infarction • Heart failure • Pulmonary embolism • Obesity • Lack of physical ﬁtness • Pregnancy • Thyrotoxicosis • Anaemia • Beri-beri • CO retention • Autonomic neuropathy • Drugs: 2 – – – – sympathomimetics salbutamol (including by inhalation) caffeine atropine Sinus arrhythmia Note • Marked variation in R–R interval • Constant PR interval • Constant shape of P wave and QRS complex 3 The ECG in healthy people Fig. 1.2 Fig. 1.3 I VR V1 V4 II VL V2 V5 III VF V3 V6 I VR V1 V4 II VL V2 V5 III VF V3 V6 II 4 The heart rate Sinus tachycardia Note • Normal P–QRS–T waves • R–R interval 500 ms • Heart rate 120/min 1 SINUS BRADYCARDIA The ECG in Figure 1.3 was recorded from a young professional footballer. His heart rate was 44/min, and at one point the sinus rate became so slow that a junctional escape beat appeared. The possible causes of sinus rhythm with a slow heart rate are summarized in Box 1.2. Box 1.2 Possible causes of sinus rhythm with a slow heart rate Sinus bradycardia Note Sinus rhythm Rate 44/min One junctional escape beat • • • • Physical ﬁtness • Vasovagal attacks • Sick sinus syndrome • Acute myocardial infarction, especially inferior • Hypothyroidism • Hypothermia • Obstructive jaundice • Raised intracranial pressure • Drugs: – beta-blockers (including eye drops for glaucoma) – verapamil – digoxin Junctional escape beat 5 The ECG in healthy people Fig. 1.4 I VR V1 V4 II VL V2 V5 III VF V3 V6 I VR V1 V4 II VL V2 V5 III VF V3 V6 II Fig. 1.5 II 6 The P wave Supraventricular extrasystole Note • In supraventricular extrasystoles the QRS complex and • the T wave are the same as in the sinus beat The fourth beat has an abnormal P wave and therefore an atrial origin Early abnormal P wave 1 EXTRASYSTOLES Supraventricular extrasystoles, either atrial or junctional (AV nodal), occur commonly in normal people and are of no significance. Atrial extrasystoles (Fig. 1.4) have an abnormal P wave; in junctional extrasystoles either there is no P wave or the P wave may follow the QRS complex. Ventricular extrasystoles are also commonly seen in normal ECGs (Fig. 1.5). In healthy people, normal sinus rhythm may be replaced by what are, in effect, repeated atrial extrasystoles. This is sometimes called an ‘ectopic atrial rhythm’ and it is of no particular significance (Fig. 1.6). THE P WAVE Ventricular extrasystole Note Sinus rhythm, with one ventricular extrasystole Extrasystole has a wide and abnormal QRS complex and an abnormal T wave • • Ventricular extrasystole In sinus rhythm, the P wave is normally upright in all leads except VR. When the QRS complex is predominantly downward in lead VL, the P wave may also be inverted (Fig. 1.7). In patients with dextrocardia the P wave is inverted in lead I (Fig. 1.8). In practice this is more often seen if the limb leads have been wrongly attached, but dextrocardia can be recognized if leads V5 and V6, which normally ‘look at’ the left ventricle, show a predominantly downward QRS complex. If the ECG of a patient with dextrocardia is repeated with the limb leads reversed, and the chest leads are placed on the right side of the chest instead of the left, in corresponding positions, the ECG becomes like that of a normal patient (Fig. 1.9). A notched or bifid P wave is the hallmark of left atrial hypertrophy, and peaked P waves indicate right atrial hypertrophy – but bifid or peaked P waves can also be seen with normal hearts (Fig. 1.10). 7 The ECG in healthy people Fig. 1.6 I VR V1 V4 II VL V2 V5 III VF V3 V6 II Fig. 1.7 8 I VR V1 V4 II VL V2 V5 III VF V3 V6 The P wave 1 Normal variant: ectopic atrial rhythm Note Sinus rhythm Inverted P wave in leads II–III, VF, V4–V6 Constant PR interval • • • Inverted P waves in lead II Normal ECG Note • In both leads VR and VL the P wave is inverted, and the QRS complex is predominantly downward Inverted P wave in lead VL 9 The ECG in healthy people Fig. 1.8 Fig. 1.9 10 I VR V1 V4 II VL V2 V5 III VF V3 V6 I VR V1 V4 II VL V2 V5 III VF V3 V6 The P wave 1 Dextrocardia Note Inverted P wave in lead I No left ventricular complexes seen in leads V5–V6 • • Inverted P wave and dominant S wave in lead I Persistent S wave in lead V6 Dextrocardia, leads reversed Note Same patient as in Figure 1.8 P wave in lead I upright QRS complex upright in lead I Typical left ventricular complex in lead V6 • • • • Upright P wave and QRS complex in lead I Normal QRS complex in lead V6 11 The ECG in healthy people Fig. 1.10 I VR V1 V4 II VL V2 V5 III VF V3 V6 II Fig. 1.11 12 I VR V1 V4 II VL V2 V5 III VF V3 V6 The PR interval 1 Normal ECG Note Sinus rhythm Biﬁd P waves, best seen in leads V2–V4 Peaked T waves and U waves, best seen in leads V2–V3 – normal variants • • • Biﬁd P wave in lead V3 THE PR INTERVAL Normal ECG Note • PR interval 170 ms • PR interval constant in all leads • Notched P wave in lead V is often normal 5 PR interval 170 ms In sinus rhythm, the PR interval is constant and its normal range is 120–200 ms (3–5 small squares of ECG paper) (Fig. 1.11). In atrial extrasystoles, or ectopic atrial rhythms, the PR interval may be short, and a PR interval of less than 120 ms suggests pre-excitation. A PR interval of longer than 220 ms may be due to first degree block, but the ECGs of healthy individuals, especially athletes, may have PR intervals of slightly longer than 220 ms – which can be ignored in the absence of any other indication of heart disease. PR interval ‘abnormalities’ will be discussed further in the context of normal people in Chapter 2. 13 The ECG in healthy people Fig. 1.12 I VR V1 V4 II VL V2 V5 III VF V3 V6 Fig. 1.13 14 I VR V1 V4 II VL V2 V5 III VF V3 V6 The QRS complex Normal ECG Note • QRS complex upright in leads I–III • R wave tallest in lead II Normal ECG Note • This record shows the ‘rightward’ limit of normality of the cardiac axis • R and S waves equal in lead I 1 THE QRS COMPLEX THE CARDIAC AXIS There is a fairly wide range of normality in the direction of the cardiac axis. In most people the QRS complex is tallest in lead II, but in leads I and III the QRS complex is also predominantly upright (i.e. the R wave is greater than the S wave) (Fig. 1.12). The cardiac axis is still perfectly normal when the R wave and S wave are equal in lead I: this is common in tall people (Fig. 1.13). When the S wave is greater than the R wave in lead I, right axis deviation is present. However, this is very common in perfectly normal people. The ECG in Figure 1.14 is from a professional footballer. It is common for the S wave to be greater than the R wave in lead III, and the cardiac axis can still be considered normal when the S wave equals the R wave in lead II (Fig. 1.15). These patterns are common in fat people and during pregnancy. When the depth of the S wave exceeds the height of the R wave in lead II, left axis deviation is present (see Figs 2.25 and 2.26). 15 The ECG in healthy people Fig. 1.14 Fig. 1.15 16 I VR V1 V4 II VL V2 V5 III VF V3 V6 I VR V1 V4 II VL V2 V5 III VF V3 V6 The QRS complex 1 ?Normal ECG Note Right axis deviation: S wave greater than R wave in lead I Upright QRS complexes in leads II–III • • Dominant S wave in lead I Normal ECG Note • This shows the ‘leftward’ limit of normality of the cardiac axis • S wave equals R wave in lead II • S wave greater than R wave in lead III S wave = R wave in lead II S wave > R wave in lead III 17 The ECG in healthy people Fig. 1.16 Fig. 1.17 18 I VR V1 V4 II VL V2 V5 III VF V3 V6 I VR V1 V4 II VL V2 V5 III VF V3 V6 The QRS complex 1 Normal ECG Note • Lead V • 1 shows a predominantly downward complex, with the S wave greater than the R wave Lead V6 shows an upright complex, with a dominant R wave and a tiny S wave S wave > R wave in lead V1 Dominant R wave in lead V6 THE SIZE OF R AND S WAVES IN THE CHEST LEADS Normal ECG Note • In lead V there is a dominant S wave • In lead V there is a dominant R wave • The transition point is between leads V 3 4 3 and V4 In lead V1 there should be a small R wave and a deep S wave, and the balance between the two should change progressively from V1 to V6. In lead V6 there should be a tall R wave and no S wave (Fig. 1.16). Typically the ‘transition point’, when the R and S waves are equal, is seen in lead V3 or V4 but there is quite a lot of variation. Figure 1.17 shows an ECG in which the transition point is somewhere between leads V3 and V4. 19 The ECG in healthy people Fig. 1.18 Fig. 1.19 20 I VR V1 V4 II VL V2 V5 III VF V3 V6 I VR V1 V4 II VL V2 V5 III VF V3 V6 The QRS complex Normal ECG Note • Dominant S wave in lead V • R wave just bigger than S wave in lead V 4 5 Normal ECG Note • Dominant S wave in lead V • Dominant R wave in lead V • The transition point is between leads V 2 1 Figure 1.18 shows an ECG with a transition point between leads V4 and V5, and Figure 1.19 shows an ECG with a transition point between leads V2 and V3. The transition point is typically seen in lead V5 or even V6 in patients with chronic lung disease (see Ch. 6), and this is called ‘clockwise rotation’. In extreme cases, the chest lead needs to be placed in the posterior axillary line, or even further round to the back (leads V7–V9) before the transition point is demonstrated. A similar ECG pattern may be seen in patients with an abnormal chest shape, particularly when depression of the sternum shifts the mediastinum to the left, although in this case the term ‘clockwise rotation’ is not used. The patient from whom the ECG in Figure 1.20 was recorded had mediastinal shift. Occasionally the ECG of a totally normal subject will show a ‘dominant’ R wave (i.e. the height of the R wave exceeds the depth of the S wave) in lead V1. There will thus, effectively, be no transition point, and this is called ‘counterclockwise rotation’. The ECG in Figure 1.21 was recorded from a healthy footballer with a normal heart. However, a dominant R wave in lead V1 is usually due to either right ventricular hypertrophy (see Ch. 6) or a true posterior infarction (see Ch. 5). 3 2 and V3 21 The ECG in healthy people Fig. 1.20 Fig. 1.21 22 I VR V1 V4 II VL V2 V5 III VF V3 V6 I VR V1 V4 II VL V2 V5 III VF V3 V6 The QRS complex V7 1 Mediastinal shift Note ‘Abnormal’ ECG, but a normal heart Shift of the mediastinum means that the transition point is under lead V6 Ventricular complexes are shown in leads round the left side of the chest, in positions V7–V9 • • • V8 V9 Normal ECG Note • Dominant R waves in lead V 1 Dominant R wave in lead V1 23 The ECG in healthy people Fig. 1.22 Fig. 1.23 I VR V1 II VL V2 V5 III VF V3 V6 I VR V1 II VL V2 V4 V4 V5 III VF V3 V6 24 The QRS complex Normal ECG Note • S wave in lead V 2 is 36 mm Although the balance between the height of the R wave and the depth of the S wave is significant for the identification of cardiac axis deviation, or right ventricular hypertrophy, the absolute height of the R wave provides little useful information. Provided that the ECG is properly calibrated (1 mV causes 1 cm of vertical deflection on the ECG), the limits for the sizes of the R and S waves in normal subjects are usually said to be: • • • S wave > 25 mm in lead V2 Normal ECG Note R wave in lead V5 is 42 mm • R wave > 25 mm in lead V5 1 25 mm for the R wave in lead V5 or V6 25 mm for the S wave in lead V1 or V2 Sum of R wave in lead V5 or V6 plus S wave in lead V1 or V2 should be less than 35 mm. However, R waves taller than 25 mm are commonly seen in leads V5–V6 in fit and thin young people, and are perfectly normal. Thus, these ‘limits’ are not helpful. The ECGs in Figures 1.22 and 1.23 were both recorded from fit young men with normal hearts. THE WIDTH OF THE QRS COMPLEX The QRS complex should be less than 120 ms in duration (i.e. less than 3 small squares) in all leads. If it is longer than this, then either the ventricles have been depolarized from a ventricular rather than a supraventricular focus (i.e. a ventricular rhythm is present), or there is an abnormality of conduction within the ventricles. The latter is most commonly due to bundle branch block. An RSR1 pattern, resembling that of right bundle branch block but with a narrow QRS complex, is sometimes called ‘partial right bundle branch block’ and is a normal variant (Fig. 1.24). An RSR1S1 pattern is also a normal variant (Fig. 1.25), and is sometimes called a ‘splintered’ complex. 25 The ECG in healthy people Fig. 1.24 Fig. 1.25 26 I VR II VL III VF V4 V1 V2 V3 V5 V6 I VR V1 V4 II VL V2 V5 III VF V3 V6 The QRS complex 1 Normal ECG Note • RSR pattern in lead V • QRS complex duration 100 ms • Partial right bundle branch block pattern 1 2 RSR1 pattern and QRS complex 100 ms in lead V1 Normal ECG Note • RSR S pattern in lead V • Notched S wave in lead V • QRS complex duration 100 ms • Partial right bundle branch block pattern 1 1 1 2 RSR1S1 pattern in lead V1 Notched S wave in lead V2 27 The ECG in healthy people Fig 1.26 I VR V1 V4 II VL V2 V5 III VF V3 V6 II Fig. 1.27 28 I VR V1 II VL V2 III VF V3 V4 V5 V6 The QRS complex Accelerated idioventricular rhythm Note • Sinus rhythm • First and last beats are ventricular extrasystoles • The ﬁfth beat starts a run of ventricular rhythm at about 80/min 1 In perfectly normal hearts the normal rhythm may be replaced by an accelerated idioventricular rhythm, which looks like a run of regular ventricular extrasystoles, with wide QRS complexes (Fig. 1.26). Q WAVES The normal depolarization of the interventricular septum from left to right causes a small ‘septal’ Q wave in any of leads II, VL or V5–V6. Septal Q waves are usually less than 3 mm deep and less than 1 mm across (Fig. 1.27). A small Q wave is also common in lead III in normal people, in which case it is always narrow but can be more than 3 mm deep. Occasionally there will be a similar Q wave in lead VF (Fig. 1.28). These ‘normal’ Q waves become much less deep, and may disappear altogether, on deep inspiration (see Fig. 1.36). Idioventricular rhythm in lead II Normal ECG Note • Septal Q waves in leads I, II, V –V 4 6 Septal Q wave in lead V5 29 The ECG in healthy people Fig. 1.28 I VR II VL III VF V4 V1 V2 V5 V3 V6 Fig. 1.29 30 I VR V1 V4 II VL V2 V5 III VF V3 V6 The ST segment 1 THE ST SEGMENT Normal ECG Note • Narrow but quite deep Q wave in lead III • Smaller Q wave in lead VF Narrow Q wave in lead III Normal ECG The ST segment (the part of the ECG between the S wave and the T wave) should be horizontal and ‘isoelectric’, which means that it should be at the same level as the baseline of the record between the end of the T wave and the next P wave. However, in the chest leads the ST segment often slopes upwards and is not easy to define (Fig. 1.29). An elevation of the ST segment is the hallmark of an acute myocardial infarction (see Ch. 5), and depression of the ST segment can indicate ischaemia or the effect of digoxin. However, it is perfectly normal for the ST segment to be elevated following an S wave in leads V2–V5. This is sometimes called a ‘high take-off ST segment’. The ECGs in Figures 1.30 and 1.31 were recorded from perfectly healthy young men. The ST segment is apparently raised when there is ‘early repolarization’, which causes the ST segment to be arched, and is usually only seen in the anterior leads, not the limb leads (see Fig. 1.39). Note • ST segment is isoelectric but slopes upwards in leads V2–V5 Upward-sloping ST segment in lead V4 31 The ECG in healthy people Fig. 1.30 Fig. 1.31 32 I VR V1 V4 II VL V2 V5 III VF V3 V6 I VR V1 V4 II VL V2 V5 III VF V3 V6 The ST segment 1 Normal ECG Note • In lead V 4 there is an S wave followed by a raised ST segment. This is a ‘high take-off’ ST segment High take-off ST segment in lead V4 Normal ECG Note • Marked ST segment elevation in lead V 3 follows an S wave High take-off ST segment in lead V3 33 The ECG in healthy people Box 1.3 shows the possible causes of ST segment elevation, other than myocardial infarction. ST segment depression is measured relative to the baseline (between the T and P waves), 60–80 ms after the ‘J’ point, which is the point of inflection at the junction of the S wave and the ST segment. Minor depression of the ST segment is not uncommon in normal people, and is then called ‘nonspecific’; the Fig. 1.32 I VR V1 V4 II VL V2 V5 VF V3 V6 III 34 advantage of using this word is that it leaves the way open for a later change of diagnosis. ST segment depression in lead III but not VF is likely to be nonspecific (Fig. 1.32). Nonspecific ST segment depression should not be more than 2 mm (Fig. 1.33), and the segment often slopes upwards. Horizontal ST segment depression of more than 2 mm indicates ischaemia (see Ch. 5). The ST segment 1 Box 1.3 Causes of ST segment elevation other than myocardial infarction • Normal variants (high take-off and early repolarization) • Left bundle branch block • Acute pericarditis and myocarditis • Hyperkalaemia • Brugada syndrome • Arrhythmogenic right ventricular cardiomyopathy • Pulmonary embolism Normal ECG Note • ST segment depression in lead III but not VF • Biphasic T wave (i.e. initially inverted but then upright) in lead III but not VF • Partial right bundle branch block pattern ST segment depression and biphasic T wave in lead III 35 The ECG in healthy people Fig. 1.33 I VR V1 II VL V2 VF V3 III Fig. 1.34 36 V4 V5 V6 I VR V1 V4 II VL V2 V5 III VF V3 V6 The T wave 1 Possibly normal ECG Note ST segment depression of 1 mm in leads V3–V6 In a patient with chest pain this would raise suspicions of ischaemia but, particularly in women, such changes can be nonspeciﬁc • • Nonspeciﬁc ST segment depression in lead V5 Normal ECG Note • T wave is inverted in lead VR but is upright in all other leads THE T WAVE In a normal ECG the T wave is always inverted in lead VR, and often in lead V1, but is usually upright in all the other leads (Fig. 1.34). The T wave is also often inverted in lead III but not VF. However, its inversion in lead III may be reversed on deep inspiration (Figs 1.35 and 1.36). Inverted T wave in lead VR 37 The ECG in healthy people Fig. 1.35 I VR II VL VF III V4 V1 V5 V2 V6 V3 Fig. 1.36 Normal ECG during inspiration Inspiration Note III • ECG recorded from same patient as in Figure 1.35, but during deep inspiration • Q wave in lead III disappears • T wave becomes upright 38 The T wave 1 Normal ECG Note • Small Q wave in lead III but not VF • Inverted T wave in lead III but upright T wave in VF • Inverted T wave in lead V 1 Q wave and inverted T wave in lead III T wave inversion in lead VL as well as in VR can be normal, particularly if the P wave in lead VL is inverted. The ECG in Figure 1.37 was recorded from a completely healthy young woman. T wave inversion in leads V2–V3 as well as in V1 occurs in pulmonary embolism and in right ventricular hypertrophy (see Chs 5 and 6) but it can be a normal variant. This is particularly true in black people. The ECG in Figure 1.38 was recorded from a healthy young white man, and that shown in Figure 1.39 from a young black professional footballer. The ECG in Figure 1.40 was recorded from a middle-aged black woman with rather nonspecific chest pain, whose coronary arteries and left ventricle were shown to be entirely normal on catheterization. Box 1.4 summarizes the situations in which T wave inversion is seen. Inverted T wave in lead V1 Box 1.4 Causes of T wave inversion • Normal in leads VR, V –V and V , in black people • Normal in lead III when the T wave in lead VF is upright • Ventricular extrasystoles and other ventricular rhythms • Bundle branch block (right or left) • Myocardial infarction • Right or left ventricular hypertrophy • The Wolff–Parkinson–White syndrome 1 2 3 39 The ECG in healthy people Fig. 1.37 Fig. 1.38 40 I VR V1 V4 II VL V2 V5 III VF V3 V6 V1 V4 I VR II VL III VF V2 V3 V5 V6 The T wave 1 Normal ECG Note • Inverted T waves in leads VR, VL • Inverted P waves in leads VR, VL Inverted P and T waves in lead VL Normal ECG Note • T wave inversion in leads VR, V –V • Biphasic T wave in lead V 1 2 3 Inverted T wave in lead V2 41 The ECG in healthy people Fig. 1.39 Fig. 1.40 42 I VR V1 V4 II VL V2 V5 III VF V3 V6 I VR V1 V4 II VL V2 V5 III VF V3 V6 The T wave 1 Normal ECG, from a black man Note T wave inversion in leads VR, V1–V3 Early repolarization in leads V2–V3 • • Inverted T wave in lead V3 Normal ECG, from a black woman Note • Sinus rhythm • T wave inversion in lead VL and all chest leads • Presumably a normal variant: coronary angiography and echocardiography were normal 43 The ECG in healthy people Fig. 1.41 Fig. 1.42 44 I VR V1 V4 II VL V2 V5 III VF V3 V6 I VR V1 V4 II VL V2 V5 III VF V3 V6 The T wave 1 Possibly normal ECG Note Sinus rhythm Normal axis Normal QRS complexes T wave ﬂattening in all chest leads T wave inversion in leads III, VF In an asymptomatic patient, these changes are not necessarily signiﬁcant • • • • • • Flattened T wave in lead V3 Normal ECG Note • Sinus rhythm • Normal axis • Normal QRS complexes • Very tall and peaked T wave Tall peaked T wave in lead V3 Generalized flattening of the T waves with a normal QT interval is best described as ‘nonspecific’. In a patient without symptoms and whose heart is clinically normal, the finding has little prognostic significance. This was the case with the patient whose ECG is shown in Figure 1.41. In patients with symptoms suggestive of cardiovascular disease, however, such an ECG would require further investigation. Peaked T waves are one of the features of hyperkalaemia, but they can also be very prominent in healthy people (Fig. 1.42). Tall and peaked T waves are sometimes seen in the early stages of a myocardial infarction, when they are described as ‘hyperacute’. They are, however, an extremely unreliable sign of infarction. The T wave is the most variable part of the ECG. It may become inverted in some leads simply by hyperventilation associated with anxiety. 45 The ECG in healthy people Fig. 1.43 Fig 1.44 I VR V1 V4 II VL V2 V5 III VF I VR V1 V4 II VL V2 V5 III VF V3 II 46 V6 V3 V6 The T wave Normal ECG Note • Prominent U waves following normal T waves in leads V2–V4 1 An extra hump on the end of the T wave, a ‘U’ wave, is characteristic of hypokalaemia. However, U waves are commonly seen in the anterior chest leads of normal ECGs (Fig. 1.43), where they can be remarkably prominent (Fig. 1.44). It is thought that they represent repolarization of the papillary muscles. A U wave is probably only important if it follows a flat T wave. U wave in lead V3 Normal ECG Note • Very large U waves following normal T waves in leads V1–V4 Very large U wave in lead V3 47 The ECG in healthy people THE QT INTERVAL The QT interval (from the Q wave to the end of the T wave) varies with the heart rate, gender and time of day. There are several different ways of correcting the QT interval for heart rate, but the simplest is Bazett’s formula. In this, the corrected QT interval (QT c) is calculated by: QTc = THE ECG IN ATHLETES QT (R − R interval) An alternative is Fridericia’s correction, in which QT c is the QT interval divided by the cube root of the R–R Fig. 1.45 Any of the normal variations discussed above can be found in athletes. There can be changes in rhythm and/or ECG pattern, and the ECGs of athletes may I VR V1 V4 II VL V2 V5 III VF V3 V6 II 48 interval. It is uncertain which of the corrections is clinically more important. The upper limit of the normal QT c interval is longer in women than in men, and increases with age. Its precise limit is uncertain, but is usually taken (following Bazett’s correction) as 450 ms for adult men and 470 ms for adult women. The ECG in athletes also show some features that might be considered abnormal in non-athletic subjects, but are normal in athletes (see Box 1.5). Figure 1.45 shows the short and varying PR interval of an ‘accelerated idionodal rhythm’ (also known as a ‘wandering atrial pacemaker’). Here the sinus node rate has slowed, and the heart rate is controlled by the AV node, which is discharging faster than the SA node. The ECGs in Figures 1.45, 1.46 and 1.47 were all recorded during the screening examinations of healthy young footballers. 1 Box 1.5 Possible ECG features of healthy athletes Variations in rhythm Sinus bradycardia Marked sinus arrhythmia Junctional rhythm ‘Wandering’ atrial pacemaker First degree block Wenckebach phenomenon Second degree block • • • • • • • Variations in ECG pattern • Tall P waves • Prominent septal Q waves • Tall R waves and deep S waves • Counterclockwise rotation • Slight ST segment elevation • Tall symmetrical T waves • T wave inversion, especially in lateral leads • Biphasic T waves • Prominent U waves Normal ECG with accelerated idionodal rhythm Note • SA node stimulates the atria at a constant rate of 50/min • Ventricular rate is slightly faster than the atrial rate • Narrow QRS complexes, originating in the AV node • QRS complexes appear to ‘overtake’ the P waves, which are not suppressed – causing an apparent variation in the PR interval Variation of PR interval 49 The ECG in healthy people Fig. 1.46 Fig. 1.47 50 I VR II VL III VF V4 V1 V5 V2 V6 V3 I VR V1 V4 II VL V2 V5 III VF V3 V6 The ECG in athletes 1 Normal ECG Note • Heart rate 53/min • Sinus rhythm • Prominent U waves in leads V –V • Inverted T waves in lead VL 2 5 U wave in lead V3 Normal ECG Note • Sinus rhythm • Left axis deviation • Septal Q waves in leads V –V 5 6 51 The ECG in healthy people Fig. 1.48 I VR V1 V4R II VL V2 V5 III VF V3 V6 THE ECG IN PREGNANCY Minor changes in the ECG are commonly seen in pregnancy (see Box 1.6). Ventricular extrasystoles are almost universal. THE ECG IN CHILDREN 52 The normal heart rate in the first year of life is 140–160/min, falling slowly to about 80/min by puberty. Sinus arrhythmia is usually quite marked in children. At birth, the muscle of the right ventricle is as thick as that of the left ventricle. The ECG of a normal child in the first year of life has a pattern that would indicate right ventricular hypertrophy in an adult. The ECG in Figure 1.48 was recorded from a normal 1-month-old child. Box 1.6 Possible ECG features in pregnancy • Sinus tachycardia • Supraventricular and ventricular extrasystoles • Nonspeciﬁc ST segment/T wave changes The changes suggestive of right ventricular hypertrophy disappear during the first few years of life. All the features other than the inverted T waves in leads V1 and V2 should have disappeared by the age of 2 years, and the adult ECG pattern should have developed by the age of 10 years. In general, if the infant ECG pattern persists beyond the age of 2 years, then right ventricular hypertrophy is indeed present. If the normal adult pattern is present in the first year of life, then left ventricular hypertrophy is present. The ECG changes associated with childhood are summarized in Box 1.7. The ECG in children 1 Normal ECG, from a child 1 month old Note Heart rate 170/min Sinus rhythm Normal axis Dominant R waves in lead V1 Inverted T waves in leads V1–V2 Biphasic T waves in lead V3 Lead V4R (a position on the chest equivalent to V4, but on the right side) has been recorded instead of V4 • • • • • • • Box 1.7 The ECG in normal children At birth • Sinus tachycardia • Right axis deviation • Dominant R waves in lead V • Deep S waves in lead V • T waves inverted in leads V –V At 2 years of age Normal axis S waves greater than R waves in lead V1 T waves inverted in leads V1–V2 • • • 1 6 1 4 At 1 year of age Sinus tachycardia Right axis deviation Dominant R waves in lead V1 T waves inverted in leads V1–V2 • • • • At 5 years of age Normal QRS complexes T waves still inverted in leads V1–V2 • • At 10 years of age Adult pattern • 53 The ECG in healthy people FREQUENCY OF ECG ABNORMALITIES IN HEALTHY PEOPLE The ECG findings we have discussed so far can all be considered to be within the normal range. Certain findings are undoubtedly abnormal as far as the ECG is concerned, yet do occur in apparently healthy people. The frequency with which abnormalities are detected depends on the population studied: most abnormalities are found least often in healthy young people recruited to the armed services, and become progressively more common in populations of increasing age. An exception to this rule is that frequent ventricular extrasystoles are very common in pregnancy. The frequency of right and left bundle branch block has been found to be 0.3% and 0.1% respectively in populations of young recruits to the services, but in older working populations these abnormalities have been detected in 2% and 0.7% respectively of apparently healthy people. WHAT TO DO When an apparently healthy subject has an ECG record that appears abnormal, the most important thing is not to cause unnecessary alarm. There are four questions to ask: 54 1. Does the ECG really come from that individual? If so, is he or she really asymptomatic and are the findings of the physical examination really normal? 2. Is the ECG really abnormal or is it within the normal range? 3. If the ECG is indeed abnormal, what are the implications for the patient? 4. What further investigations are needed? THE RANGE OF NORMALITY Normal variations in the P waves, QRS complexes and T waves have been described in detail. T wave changes usually give the most trouble in terms of ECG interpretation, because changes in repolarization occur in many different circumstances, and in any individual, and variations in T wave morphology can occur from day to day. Box 1.8 lists some of the ECG patterns that can be accepted as normal in healthy patients, and some that must be regarded with suspicion. THE PROGNOSIS OF PATIENTS WITH AN ABNORMAL ECG In general, the prognosis is related to the patient’s clinical history and to the findings on physical examination, rather than to the ECG. An abnormal ECG is much more significant in a patient with symptoms and signs of heart disease than it is in a truly healthy subject. In the absence of any other evidence of heart disease, the prognosis of an individual with one of the more common ECG abnormalities is as follows. CONDUCTION DEFECTS First degree block (especially when the PR interval is only slightly prolonged) has little effect on prognosis. Second and third degree block indicate heart disease and the prognosis is worse, though the congenital form of complete block is less serious than the acquired form in adults. Left anterior hemiblock has a good prognosis, as does right bundle branch block (RBBB). The presence of left bundle branch block (LBBB) in the absence of other manifestations of cardiac disease is associated The prognosis of patients with an abnormal ECG 1 Box 1.8 Variations in the normal ECG in adults Rhythm Marked sinus arrhythmia, with escape beats Lack of sinus arrhythmia (normal with increasing age) Supraventricular extrasystoles Ventricular extrasystoles • • • • P wave • Normally inverted in lead VR • May be inverted in lead VL Cardiac axis • Minor right axis deviation in tall people QRS complexes in the chest leads Slight dominance of R wave in lead V1, provided there is no other evidence of right ventricular hypertrophy or posterior infarction The R wave in the lateral chest leads may exceed 25 mm in thin ﬁt young people Partial right bundle branch block (RSR1 pattern, with QRS complexes less than 120 ms) Septal Q waves in leads III, VL, V5–V6 • ST segment Raised in anterior leads following an S wave (high take-off ST segment) Depressed in pregnancy Nonspeciﬁc upward-sloping depression • • • T wave • Inverted in lead VR and often in V • Inverted in leads V –V , or even V in black people • May invert with hyperventilation • Peaked, especially if the T waves are tall 1 2 3 4 U wave Normal in anterior leads when the T wave is not ﬂattened • • • • with about a 30% increase in the risk of death compared with that of individuals with a normal ECG. The risk of death doubles if a subject known to have a normal ECG suddenly develops LBBB, even if there are no symptoms – the ECG change presumably indicates progressive cardiac disease, probably most often ischaemia. Bifascicular block seldom progresses to complete block, but is always an indication of underlying heart disease – the prognosis is therefore relatively poor compared to that of patients with LBBB alone. ARRHYTHMIAS Supraventricular extrasystoles are of no importance whatsoever. Ventricular extrasystoles are almost universal, but when frequent or multiform they indicate populations with a statistically increased risk of death, presumably because in some people they indicate subclinical heart disease. The increased risk to an individual is, however, insignificant and there is no evidence that treating ventricular extrasystoles prolongs survival. Atrial fibrillation is frequently the result of rheumatic or ischaemic heart disease or cardiomyopathy, and the prognosis is then relatively poor. In about one third of individuals with atrial fibrillation no cardiac disease can be demonstrated. However, even in these people the risk of death is increased by three or four times, and the risk of stroke is increased perhaps tenfold, compared with people of the same age whose hearts are in sinus rhythm. 55 The ECG in healthy people FURTHER INVESTIGATIONS Complex and expensive investigations are seldom justified in asymptomatic patients whose hearts are clinically normal, but who have been found to have an abnormal ECG. An echocardiogram should be recorded in all patients with bundle branch block, to assess the size and function of the individual heart chambers. Patients with LBBB may have a dilated cardiomyopathy, and the echocardiogram will then show a dilated left ventricle which contracts poorly. Alternatively they may have ischaemia, and the echocardiogram will show some segments of the left ventricle failing to contract or contracting poorly. Patients with LBBB may also have unsuspected aortic stenosis. Patients with RBBB may have an atrial septal defect or pulmonary hypertension, but quite frequently the echocardiogram shows no abnormality. Echocardiography may be helpful in establishing the cause of T wave inversion, which might be due to ischaemia, ventricular hypertrophy or cardiomyopathy. Patients with frequent ventricular extrasystoles seldom need detailed investigation, but if there is any question of underlying heart disease an echocardiogram may help to exclude the possibility of a cardiomyopathy. It is also worth checking their blood haemoglobin level. In patients with atrial fibrillation, an echocardiogram is useful for defining or excluding structural 56 abnormalities, and for studying left ventricular function. An echocardiogram is indicated if there is anything that might suggest rheumatic heart disease. Since atrial fibrillation can be the only manifestation of thyrotoxicosis, thyroid function must be checked. Atrial fibrillation may also be the result of alcoholism, and this may be denied by the patient, so it may be fair to check liver function. Table 1.1 shows investigations that should be considered in the case of various cardiac rhythms and indicates which underlying diseases may be present. TREATMENT OF ASYMPTOMATIC ECG ABNORMALITIES It is always the patient who should be treated, not the ECG. The prognosis of patients with complete heart block is improved by permanent pacing, but that of patients with other degrees of block is not. Ventricular extrasystoles should not be treated because of the risk of the pro-arrhythmic effects of antiarrhythmic drugs. Atrial fibrillation need not be treated if the ventricular rate is reasonable, but anticoagulation must be considered in all cases. In the case of patients with valve disease and atrial fibrillation, however, anticoagulant treatment is essential. Treatment of asymptomatic ECG abnormalities 1 Table 1.1 Investigations in apparently healthy people with an abnormal ECG ECG appearance Diagnosis to be excluded Possible investigations Sinus tachycardia Thyrotoxicosis Anaemia Changes in heart size Heart failure Systolic dysfunction Thyroid function Haemoglobin } Echocardiogram Sinus bradycardia Myxoedema Thyroid function Frequent ventricular extrasystoles Left ventricular dysfunction Anaemia Echocardiogram Haemoglobin Right bundle branch block Heart size Lung disease Atrial septal defect Echocardiogram Left bundle branch block Heart size Aortic stenosis Cardiomyopathy Ischaemia Echocardiogram T wave abnormalities High or low potassium or calcium Ventricular systolic dysfunction Hypertrophic cardiomyopathy Ischaemia Electrolytes Atrial ﬁbrillation Thyrotoxicosis Alcoholism Valve disease, ventricular and left atrial dimensions Myxoma } Echocardiogram Exercise test Myocardial perfusion scan Thyroid function Liver function } Echocardiogram 57 2 58 The ECG in patients with palpitations and syncope: between attacks The clinical history and physical examination 59 Palpitations 59 Dizziness and syncope 60 Physical examination 64 The ECG 64 Syncope due to cardiac disease other than arrhythmias 64 Patients with possible tachycardias 69 Patients with possible bradycardias 82 Ambulatory ECG recording 96 The ECG is of paramount importance for the diagnosis of arrhythmias. Many arrhythmias are not noticed by the patient, but often they cause symptoms. These symptoms are often transient, and the patient may be completely well at the time he or she consults a doctor. Obtaining an ECG during a symptomatic episode is then the only certain way of making a diagnosis, but as always the history and physical examination are also extremely important. The main purpose of the history and examination is to help decide whether a patient’s symptoms could be the result of an arrhythmia, and whether the patient has a cardiac or other disease that may cause an arrhythmia. Palpitations THE CLINICAL HISTORY AND PHYSICAL EXAMINATION • PALPITATIONS ‘Palpitations’ mean different things to different patients, but a general definition would be ‘an awareness of the heartbeat’. Arrhythmias, fast or slow, can cause poor organ perfusion and so lead to syncope (a word used to describe all sorts of collapse), breathlessness and angina. Some rhythms can be identified from a patient’s description, such as: • A patient recognizes sinus tachycardia because it feels like the palpitations that he or she associates with anxiety or exercise. • 2 Extrasystoles are described as the heart ‘jumping’ or ‘missing a beat’. It is not possible to distinguish between supraventricular and ventricular extrasystoles from a patient’s description, although they can be differentiated from an ECG. A paroxysmal tachycardia begins suddenly and sometimes stops suddenly. The heart rate is often ‘too fast to count’. Severe attacks are associated with dizziness, breathlessness and chest pain. Table 2.1 compares the symptoms associated with sinus tachycardia and a paroxysmal tachycardia, and shows how a diagnosis can be made from the history. Note that a heart rate between 140/min and 160/min may be associated with either sinus or paroxysmal tachycardia. Table 2.1 Diagnosis of sinus tachycardia or paroxysmal tachycardia from a patient’s symptoms Symptoms Sinus tachycardia Paroxysmal tachycardia Timing of initial attack Attacks probably began recently Attacks probably began in teens or early adult life Associations of attack Exercise, anxiety Usually no associations, but occasionally exercise-induced Rate of start of palpitations Slow build-up Sudden onset Rate of end of palpitations ’Die away’ Classically sudden, but often ‘die away’ Heart rate <140/min >160/min Associated symptoms Paraesthesia due to hyperventilation Chest pain Breathlessness Dizziness Syncope Ways of terminating attacks Relaxation Breath holding Valsalva’s manoeuvre 59 The ECG in patients with palpitations and syncope: between attacks DIZZINESS AND SYNCOPE These symptoms may have a cardiovascular or a neurological cause. Remember that cerebral hypoxia, however caused, may lead to a seizure, and that can make the differentiation between cardiac and neurological syncope very difficult. Syncope is defined as ‘a transient loss of consciousness characterized by unresponsiveness and loss of postural tone, with spontaneous recovery and not requiring specific resuscitative intervention’. Figure 2.1 shows an EEG that was being recorded in a 46-year-old woman with episodes of limb shaking, suspected of being generalized tonic–clonic seizures. She lost awareness during events, and had violent limb shaking for several seconds as she came round. She felt nauseated, but was rapidly reorientated. By chance, she had one of her ‘attacks’ while her EEG was being recorded, and from the ECG being routinely recorded in parallel, it became clear that the problem was not seizures, but periods of asystole – in this case lasting about 15 s. The numbered arrows in Figure 2.1 mark significant features. The recording begins with a routine period of hyperventilation, with the EEG showing an 60 eye blink in the anterior leads and the ECG showing sinus rhythm. There are then (at arrow 1 on the record) one (or possibly two) ventricular extrasystoles, followed by a narrow complex beat (probably sinus) and another ventricular extrasystole, with a different configuration from the previous ones. Asystole follows, and after 7–8 s (at arrow 2) there is global EEG slowing, and the patient became unresponsive. After 4 s (at arrow 3), there is global attenuation (reduction in signals) in the EEG and after another 3 s, there is an escape beat whose morphology suggests a ventricular origin. This is followed by a beat with a narrow QRS complex and possibly an inverted T wave, and then there is gross artefact due to the ECG lead being checked. During that period, sinus rhythm was restored. There was then (at arrow 4) global EEG slowing for 5 s, followed by (at arrow 5) violent limb thrashing for about 12 s as the patient regained consciousness – these movements were not clonic, and were thought to represent anxiety or fear. Normal EEG and ECG activity were then resumed (at arrow 6). Some causes of syncope are summarized in Box 2.1. Table 2.2 shows some clinical features of syncope, and possible causes. Dizziness and syncope Box 2.1 Cardiovascular causes of syncope Obstructed blood ﬂow in heart or lungs • Aortic stenosis • Pulmonary embolus • Pulmonary hypertension • Hypertrophic cardiomyopathy • Pericardial tamponade • Atrial myxoma Arrhythmias • Tachycardias: patient is usually aware of a fast heartbeat before becoming dizzy • Bradycardias: slow heart rates are often not appreciated. A classical cause of syncope is a Stokes–Adams attack, due to a very slow ventricular rate in patients with complete heart block. A Stokes–Adams attack can be recognized because the patient is initially pale but ﬂushes red on recovery Postural hypotension, occurring immediately on standing Seen with: Loss of blood volume Autonomic nervous system disease (e.g. diabetes, Shy–Drager syndrome, amyloid neuropathy) Patients being treated with antihypertensive drugs • • • Neurally-mediated reﬂex syncopal syndromes Vasovagal (neurocardiogenic) (simple faints) Situational (e.g. after coughing, sneezing, gastrointestinal stimulation of various sorts, post-micturition) Carotid sinus hypersensitivity • • • 2 Table 2.2 Diagnosis of causes of syncope Symptoms and signs Possible diagnosis Family history of sudden death Long QT syndrome, Brugada syndrome, hypertrophic cardiomyopathy Caused by unpleasant stimuli, prolonged standing, hot places (situational syncope) Vasovagal syncope Occurs within seconds or minutes of standing Orthostatic hypotension Temporal relation to medication Orthostatic hypotension Occurs during exertion Obstruction to blood ﬂow (e.g. aortic stenosis, pulmonary hypertension) Occurs with head rotation or pressure on neck Carotid sinus hypersensitivity Confusion for more than 5 min afterwards Seizure Tonic–clonic movements, automatism Seizure Frequent attacks, usually unobserved, with somatic symptoms Psychiatric illness Symptoms or signs suggesting cardiac disease Cardiac disease 61 The ECG in patients with palpitations and syncope: between attacks Fig. 2.1 EEG recorded during a syncopal attack 1 2 Fp2 F8 F8 T4 T4 T6 T6 O2 Fp1 F7 F7 T3 T3 T5 T5 O1 Fp2 F4 F4 C4 C4 P4 P4 O2 Fp1 F3 F3 C3 C3 P3 P3 O1 ECG lead I (a) 62 (b) 3 Dizziness and syncope 2 Courtesy of Dr A. Michell, Addenbrooke’s Hospital, Cambridge 4 5 6 Note EEG and ECG lead I (lower trace) Paper speed ﬁve times normal ECG speed (a) Sinus rhythm at about 70/min, ventricular extrasystoles interrupted by one narrow complex beat, then asystole (b) Asystole followed by an escape beat, a narrow complex beat, and gross artefact (c) Sinus rhythm restored, with a period of limb thrashing before resumption of a normal record • • • • (c) • 63 The ECG in patients with palpitations and syncope: between attacks continuously, in the hope that an episode of the arrhythmia will be detected. PHYSICAL EXAMINATION If the patient has no symptoms at the time of the examination, look for: • • • • Evidence of any heart disease that might cause an arrhythmia Evidence of non-cardiac disease that might cause an arrhythmia Evidence of cardiovascular disease that might cause syncope without an arrhythmia Evidence (from the history or examination) of neurological disease. It is only possible to make a confident diagnosis that an arrhythmia is the cause of palpitations or syncope if an ECG recording of the arrhythmia can be obtained at the time of the patient’s symptoms. If the patient is asymptomatic at the time of examination, it may be worth arranging for an ECG to be recorded during an attack of palpitations, or to be recorded THE ECG Even when the patient is asymptomatic, the resting ECG can be very helpful, as summarized in Table 2.3. SYNCOPE DUE TO CARDIAC DISEASE OTHER THAN ARRHYTHMIAS The ECG may indicate that syncopal attacks have a cardiovascular cause other than an arrhythmia. ECG evidence of left ventricular hypertrophy or of left bundle branch block may suggest that syncope is due to aortic stenosis. The ECGs in Figures 2.2 and 2.3 were recorded from patients who had syncopal attacks on exercise due to severe aortic stenosis. Fig. 2.2 64 I VR V1 V4 II VL V2 V5 III VF V3 V6 Syncope due to cardiac disease other than arrhythmias 2 Table 2.3 ECG features between attacks of palpitations or syncope ECG appearance Possible cause of symptoms ECG completely normal Symptoms may not be due to a primary arrhythmia – consider anxiety, epilepsy, atrial myxoma or carotid sinus hypersensitivity ECGs that suggest cardiac disease Left ventricular hypertrophy or left bundle branch block – aortic stenosis Right ventricular hypertrophy – pulmonary hypertension Anterior T wave inversion – hypertrophic cardiomyopathy ECGs that suggest intermittent tachyarrhythmia Left atrial hypertrophy – mitral stenosis, so possibly atrial ﬁbrillation Pre-excitation syndromes Long QT syndrome Flat T waves suggest hypokalaemia Digoxin effect – ?digoxin toxicity ECGs that suggest intermittent bradyarrhythmia Second degree block First degree block plus bundle branch block Digoxin effect Left ventricular hypertrophy Note Sinus rhythm Biﬁd P waves suggest left atrial hypertrophy (best seen in leads V4–V5) Normal axis Tall R waves and deep S waves T waves inverted in leads I, VL, V5–V6 • • • • • Tall R wave, inverted T wave in lead V5 65 The ECG in patients with palpitations and syncope: between attacks Fig. 2.3 I VR II VL V1 V2 V4 V5 V3 III Fig. 2.4 66 V6 VF I VR V1 V4 II VL V2 V5 III VF V3 V6 Syncope due to cardiac disease other than arrhythmias Left bundle branch block Note • Sinus rhythm • Slight PR interval prolongation (212 ms) • Broad QRS complexes • ‘M’ pattern in lateral leads • T wave inversion in leads I, VL, V –V 5 6 M pattern of left bundle branch block in lead VL 2 ECG evidence of right ventricular hypertrophy suggests thromboembolic pulmonary hypertension. The ECG in Figure 2.4 is that of a middle-aged woman with dizziness on exertion, due to multiple pulmonary emboli. Syncope due to hypertrophic cardiomyopathy (Fig. 2.5) may be associated with a characteristic ECG (Fig. 2.6) that resembles that of patients with an anterior non-ST segment elevation myocardial infarction (NSTEMI) (compare with Fig. 5.23, p. 240). With hypertrophic cardiomyopathy, the T wave inversion is usually more pronounced than with an NSTEMI, but differentiation really depends on the clinical picture, not on the ECG appearance. Hypertrophic cardiomyopathy can cause syncope due to obstruction to outflow from the left ventricle, or can cause symptomatic arrhythmias. Right ventricular hypertrophy Note Sinus rhythm Right axis deviation Dominant R waves in lead V1 Inverted T waves in leads V1–V4 • • • • Dominant R wave in lead V1 67 The ECG in patients with palpitations and syncope: between attacks Fig 2.5 MR image of a heart with hypertrophic cardiomyopathy RV Septum RA LV LV Free wall Note RA – right atrium RV – right ventricular cavity Septum – interventricular septum LV – left ventricular cavity LA – left atrium LV free wall – left ventricular myocardium • • • • • • LA Fig. 2.6 68 I VR V1 V4 II VL V2 V5 III VF V3 V6 Patients with possible tachycardias PATIENTS WITH POSSIBLE TACHYCARDIAS MITRAL STENOSIS Mitral stenosis leads to atrial fibrillation, but when the heart is still in sinus rhythm the presence of the characteristics of left atrial hypertrophy on the ECG may give a clue that paroxysmal atrial fibrillation is occurring (Fig. 2.7). PRE-EXCITATION SYNDROMES Normal conduction between the atria and ventricles involves the uniform spread of the depolarization wave front in a constant direction, down the bundle of His. In the pre-excitation syndromes, an abnormal additional pathway, or multiple pathways, connect the atria and ventricles. These accessory pathways bypass the AV node, where normal conduction is delayed, and Hypertrophic cardiomyopathy Note • Sinus rhythm • Marked T wave inversion in leads V –V 3 6 2 therefore conduct more rapidly than the normal pathway. The anatomical combination of the normal AV node–His bundle pathway and the accessory pathway creates a potential circuit around which excitation may spread, causing a ‘re-entry’ tachycardia (Ch. 3, p. 105). The Wolff–Parkinson–White syndrome In the Wolff–Parkinson–White (WPW) syndrome, an accessory pathway (the ‘bundle of Kent’) connects either the left atrium and left ventricle, or the right atrium and right ventricle. Conduction may at times occur only through the normal His bundle pathway, so the QRS complexes will be normal and narrow; the accessory pathway is then said to be concealed. At other times, conduction may occur through both pathways simultaneously, but the heart will remain in sinus rhythm if conduction occurs in a forward direction via both the AV node–His bundle pathway and the accessory pathway. The faster conduction down the accessory pathway causes part of the ventricle to depolarize early, resulting in a short PR interval and a slurred upstroke to the QRS complex (delta wave), causing a wide QRS complex. With a left-sided accessory pathway, the ECG shows a dominant R wave in lead V1. This is called the ‘type A’ pattern (Fig. 2.8). This pattern can easily be mistaken for right ventricular hypertrophy, the differentiation being made by the presence or absence of a short PR interval. Inverted T wave in lead V4 69 The ECG in patients with palpitations and syncope: between attacks Fig. 2.7 I II III Fig. 2.8 70 VR V1 V4 VL V2 V5 VF V3 V6 I VR V1 V4 II VL V2 V5 III VF V3 V6 Patients with possible tachycardias 2 Left atrial hypertrophy Note Sinus rhythm Biﬁd P waves, most clearly seen in leads I, II, V3–V5 • • Biﬁd P wave in lead II The Wolff–Parkinson–White syndrome, type A Note • Sinus rhythm • Short PR interval • Broad QRS complexes • Dominant R wave in lead V • Slurred upstroke to QRS complexes – the delta wave • Inverted T waves in leads II, III, VF, V –V 1 1 4 Delta wave in lead III 71 The ECG in patients with palpitations and syncope: between attacks Fig. 2.9 I VR V1 V4 II VL V2 V5 III VF V3 V6 The ECG in Figure 2.9 is from a young man who complained of symptoms that sounded like paroxysmal tachycardia. His ECG shows the WPW syndrome type A, but it would be quite easy to miss the short PR interval unless the whole of the 12-lead trace were carefully inspected. The short PR interval and delta waves are most obvious in leads V4 and V5. When the accessory pathway is on the right side of the heart, there is no dominant R wave in lead V1, and this is called the ‘type B’ pattern (Fig. 2.10). ECGs indicating pre-excitation of the WPW type are found in approximately 1 in every 3000 healthy young people. Only half of these ever have an episode 72 of tachycardia, and many have only very occasional attacks. The ECG features associated with the WPW syndrome are summarized in Box 2.2. The Lown–Ganong–Levine syndrome Where an accessory pathway connects the atria to the bundle of His rather than to the right or left ventricle, there will be a short PR interval but the QRS complex will be normal. This is called the Lown–Ganong–Levine (LGL) syndrome (Fig. 2.11). This syndrome must be differentiated from accelerated idionodal rhythm, where the PR interval varies (see p. 49 and Fig. 1.45). Patients with possible tachycardias 2 The Wolff–Parkinson–White syndrome, type A Note • Sinus rhythm • Short PR interval, especially obvious in leads V –V • Slurred upstroke to QRS complexes, obvious in leads 3 5 V3–V5 but not obvious in the limb leads • Dominant R wave in lead V • No T wave inversion in the anterior leads (cf. Fig. 2.8) 1 Delta wave in lead V5 Box 2.2 The Wolff–Parkinson–White syndrome: ECG features • Short PR interval • Wide QRS complexes with delta wave with normal terminal segment • ST segment/T wave changes • Left-sided pathway (type A): dominant R waves in leads V –V • Right-sided pathway (type B): dominant S wave in lead V , and sometimes, anterior T wave inversion • Arrhythmias (narrow or wide complex) • Arrhythmia with wide, irregular complex suggests the 1 6 1 WPW syndrome with atrial ﬁbrillation 73 The ECG in patients with palpitations and syncope: between attacks Fig. 2.10 I VR V1 V4 II VL V2 V5 VF V3 V6 III Fig. 2.11 74 I VR V1 V4 II VL V2 V5 III VF V3 V6 Patients with possible tachycardias 2 The Wolff–Parkinson–White syndrome, type B Note Sinus rhythm Short PR interval Broad QRS complexes with delta waves No dominant R waves in lead V1 (cf. Figs 2.8 and 2.9) T wave inversion in leads III, VF, V3 • • • • • Short PR interval; broad QRS complex in lead III The Lown–Ganong–Levine syndrome Note Sinus rhythm Short PR interval Normal QRS complexes and P waves • • • Short PR interval in lead II 75 The ECG in patients with palpitations and syncope: between attacks THE LONG QT SYNDROME Delayed repolarization occurs for a variety of reasons (Box 2.3), and causes a long QT interval. A prolonged QT interval is associated with paroxysmal ventricular tachycardia, and therefore can be the cause of episodes of collapse or even sudden death. The ventricular tachycardia associated with a prolonged QT interval usually involves a continual change from upright to downward QRS complexes. This is called ‘torsade de pointes’ (Fig. 2.12), and it usually occurs at times of increased sympathetic nervous system activity. Several genetic abnormalities have been described that lead to familial prolongation of the QT interval. The ECG in Figure 2.13 is from a 10-year-old girl who suffered from ‘fainting’ attacks. Her sister had died suddenly; three other siblings and both parents had normal ECGs. Fig. 2.12 Torsade de pointes ventricular tachycardia Note • Broad complex tachycardia at 300/min • Continually changing shape of QRS complexes Fig. 2.13 76 I VR V1 V4 II VL V2 V5 III VF V3 V6 Patients with possible tachycardias Box 2.3 Possible causes of a prolonged QT interval Congenital Jervell–Lange–Nielson syndrome Romano–Ward syndrome • • Antiarrhythmic drugs • Quinidine (of historical interest only) • Procainamide • Disopyramide • Amiodarone • Sotalol Other drugs • Tricyclic antidepressants • Erythromycin Plasma electrolyte abnormality • Low potassium • Low magnesium • Low calcium 2 The most common cause of QT prolongation is drug therapy. The ECG in Figure 2.14 is from a patient who had a posterior myocardial infarction (see Ch. 5). He was treated with amiodarone because of recurrent ventricular tachycardias, and developed a prolonged QT interval. Figure 2.15 shows his record 4 months later: the prolonged QT interval reverted to normal when the amiodarone treatment was stopped. Episodes of symptomatic ventricular tachycardia occur in about 8% of affected subjects each year, and the annual death rate due to arrhythmias is about 1% of patients with a long QT syndrome. The precise relationship between QT c interval prolongation and the risk of sudden death is unknown; neither is it clear whether prolongation of the QT or QT c interval is more significant. There is no absolute threshold of risk. However, torsade de pointes ventricular tachycardia seems rare when the QT or QT c interval is less than 500 ms. Congenital long QT syndrome Note Sinus rhythm Normal axis QT interval 520 ms Marked T wave inversion in leads V2–V4 • • • • Long QT interval and inverted T wave in lead V3 77 The ECG in patients with palpitations and syncope: between attacks Fig. 2.14 Fig. 2.15 I VR II VL III VF I VR II VL III VF V4 V1 V2 V5 V6 V3 V4 V1 V2 78 V5 V3 V6 Patients with possible tachycardias 2 Prolonged QT interval due to amiodarone Note • Sinus rhythm • Normal axis • Dominant R waves in lead V due to posterior infarction • QT interval 800 ms • Bizarre T wave shape in anterior leads 1 Long QT interval and bizarre T wave in lead V2 Posterior infarct with normal QT interval Note Same patient as in Figure 2.14 Sinus rhythm Normal axis Dominant R waves in lead V1 Ischaemic ST segment depression Normal QT interval • • • • • • ST segment depression in lead V2 79 The ECG in patients with palpitations and syncope: between attacks Fig. 2.16 Fig. 2.17 80 I VR II VL III VF V4 V1 V2 V3 V5 V6 I VR V1 V4 II VL V2 V5 III VF V3 V6 Patients with possible tachycardias 2 Brugada syndrome Note • Sinus rhythm • Normal axis • Normal QRS complex duration • RSR pattern in leads V –V • No wide S wave in lead V • Raised, downward-sloping ST segment in leads V –V 1 1 2 6 1 2 RSR1 pattern and raised ST segment in lead V2 Brugada syndrome Note Same patient as in Figure 2.16 Normal ECG • • Normal appearance in lead V2 THE BRUGADA SYNDROME Sudden collapse due to ventricular tachycardia and fibrillation occurs in a congenital disorder of sodium ion transport called the Brugada syndrome. Between attacks, the ECG superficially resembles that associated with right bundle branch block (RBBB), with an RSR1 pattern in leads V1 and V2 (Fig. 2.16). However, the ST segment in these leads is raised, and there is no wide S wave in lead V6 as there is in RBBB. The changes are seen in the right ventricular leads because the abnormal sodium channels are predominantly found in the right ventricle. The ECG abnormality can be transient – the ECG in Figure 2.17 was taken a day later from the same patient as in Figure 2.16. 81 The ECG in patients with palpitations and syncope: between attacks PATIENTS WITH POSSIBLE BRADYCARDIAS When a patient is asymptomatic, an intermittent bradycardia can be suspected if the ECG shows any evidence of an escape rhythm or a conduction defect. However, it must be remembered that conduction defects and escape rhythms are quite common in healthy people, and their presence may be coincidental. ESCAPE RHYTHMS Myocardial cells are only depolarized when they are stimulated, but the cells of the SA node, those around the AV node (the ‘junctional’ cells) and those of the conducting pathways all possess the property of spontaneous depolarization or ‘automaticity’. The automaticity of any part of the heart is suppressed by the arrival of a depolarization wave, and so the heart rate is controlled by the region with the highest automatic depolarization frequency. Normally the SA node controls the heart rate because it has thehighest frequency of discharge, but if for any reason this fails, the region with the next highest intrinsic depolarization frequency will emerge as the pacemaker and set up an ‘escape’ rhythm. The atria and the junctional region have automatic Fig. 2.18 Junctional escape beat Note • After two sinus beats there is no P wave • After an interval there is a narrow QRS complex, with • • the same conﬁguration as that of the sinus beats but without a preceding P wave This is a junctional beat (arrowed) Sinus rhythm then reappears Fig. 2.19 Junctional (escape) rhythm P Note • Two sinus beats are followed by an interval with no P waves • A junctional rhythm then emerges (with QRS complexes the same as in sinus rhythm) • A P wave (arrowed) can be seen as a hump on the T wave of the junctional beats: the atria have been depolarized retrogradely 82 Patients with possible bradycardias depolarization frequencies of about 50/min, compared with the normal SA node frequency of 60–70/min. If both the SA node and the junctional region fail to depolarize, or if conduction to the ventricles fails, a ventricular focus may emerge, with a rate of 30–40/min; this is classically seen in complete heart block. Escape beats may be single or may form sustained rhythms. They have the same ECG appearance as the corresponding extrasystoles, but appear late rather than early (Fig. 2.18). In sustained junctional escape rhythms, atrial activation may be seen as a P wave following the QRS 2 complex (Fig. 2.19). This occurs if depolarization spreads in the opposite direction from normal, from the AV node to the atria, and is called ‘retrograde’ conduction. Figure 2.20 also shows a junctional escape rhythm. Figure 2.21 shows a ventricular escape beat. Fig. 2.20 Junctional (escape) rhythm Note • No P waves • Narrow QRS complexes and normal T waves Fig. 2.21 Ventricular escape beat Note • Three sinus beats are followed by a pause • There is then a single ventricular beat with a wide QRS complex and an inverted T wave • Sinus rhythm is then restored 83 The ECG in patients with palpitations and syncope: between attacks Fig. 2.22 Fig. 2.23 I VR V1 V4 II VL V2 V5 III VF V3 V6 I VR V1 V4 II VL V2 V5 III VF V3 V6 II 84 Patients with possible bradycardias First degree block Note Sinus rhythm PR interval 380 ms T wave inversion in leads III and VF suggests ischaemia • • • Long PR interval in lead III 2 SYNCOPE In a patient with syncopal attacks, ECG changes that would be ignored in a healthy person take on a greater significance. First degree block, itself of no clinical importance, may point to intermittent complete block, and complete block is much more likely when the ECG of a currently asymptomatic patient shows second degree block. The ECGs in Figures 2.22, 2.23 and 2.24 are from patients with syncopal attacks, all of whom needed permanent pacemakers. Left axis deviation usually indicates left anterior hemiblock, but a minor degree of left axis deviation with a narrow QRS complex can be accepted as a normal variant (Fig. 2.25). A QRS complex near the upper limit of the normal width with marked left axis deviation represents the full pattern of left anterior hemiblock (Fig. 2.26). Second degree block (Wenckebach) Note Sinus rhythm PR interval lengthens progressively from 360 ms to 440 ms and then a P wave is not conducted Small Q wave and inverted T wave in leads III and VF suggest an old inferior infarct • • • P waves 85 The ECG in patients with palpitations and syncope: between attacks Fig. 2.24 I VR V1 V4 II VL V2 V5 III VF V3 V6 II Fig. 2.25 86 I VR V1 V4 II VL V2 V5 III VF V3 V6 Patients with possible bradycardias 2 Second degree block (2 : 1) Note Sinus rhythm Alternate beats conducted and not conducted Lateral T wave inversion in leads I, VL, V6 suggests ischaemia • • • P waves Left axis deviation Note • Sinus rhythm • Dominant S waves in leads II and III: left axis deviation • Normal QRS complex duration • Lateral T wave inversion Dominant S waves in leads II and III 87 The ECG in patients with palpitations and syncope: between attacks Fig. 2.26 I VR V1 V4 II VL V2 V5 VF V3 V6 III Fig. 2.27 88 I VR V1 V4 II VL V2 V5 III VF V3 V6 Patients with possible bradycardias 2 Combinations of conduction abnormalities Left anterior hemiblock Note Sinus rhythm Left axis deviation Broad QRS complexes (122 ms) Inverted T waves in lead VL • • • • Dominant S waves and broad QRS complexes in leads II and III First degree block and left bundle branch block (LBBB) Note Sinus rhythm PR interval 300 ms LBBB pattern Broad QRS complexes • • • • Long PR interval in leads II and III ECG evidence of atrioventricular conduction abnormalities will not be associated with syncope unless there is intermittent second or third degree heart block with a bradycardia. It is, however, important to recognize the clinically less common conduction defects because they may be pointers to the cause of syncopal attacks. When first degree block is associated with left bundle branch block (Fig. 2.27), conduction must be delayed in either the AV node, the His bundle or the right bundle branch as well as in the left bundle branch. The combination of first degree block and right bundle branch block (RBBB) (Fig. 2.28) shows that conduction has failed in the right bundle branch and is also beginning to fail elsewhere. A combination of left anterior hemiblock and RBBB means that conduction into the ventricles is only passing through the posterior fascicle of the left bundle branch (Fig. 2.29). This is called ‘bifascicular block’. A combination of left anterior hemiblock, RBBB and first degree block suggests that there is disease in the remaining conducting pathway – either in the main His bundle or in the posterior fascicle of the left bundle branch. This is sometimes called ‘trifascicular block’ (Fig. 2.30). Complete conduction block in the right bundle and in both fascicles of the left bundle would, of course, cause complete (third degree) heart block. Right axis deviation is not necessarily a feature of left posterior hemiblock, but, when combined with other evidence of conducting tissue disease such as first degree block (Fig. 2.31), it usually is. A combination of second degree (2 : 1) block with left anterior hemiblock (Fig. 2.32) or with both left anterior hemiblock and RBBB (Fig. 2.33) suggests widespread conduction tissue disease. 89 The ECG in patients with palpitations and syncope: between attacks Fig. 2.28 Fig. 2.29 90 I VR V1 V4 II VL V2 V5 III VF V3 V6 I VR V1 V4 II VL V2 V5 III VF V3 V6 Patients with possible bradycardias 2 First degree block and right bundle branch block (RBBB) Note Sinus rhythm PR interval 328 ms Right axis deviation Broad QRS complexes RBBB pattern • • • • • Long PR interval and RBBB pattern in lead V1 Bifascicular block Note Sinus rhythm PR interval normal (176 ms) Left anterior hemiblock RBBB • • • • Left axis deviation and broad QRS complex in lead II RBBB in lead V1 91 The ECG in patients with palpitations and syncope: between attacks Fig. 2.30 Fig. 2.31 92 V1 V4 I VR II VL V2 V5 III VF V3 V6 I VR V1 V4 II VL V2 V5 III VF V3 V6 Patients with possible bradycardias 2 Trifascicular block Note Sinus rhythm PR interval 224 ms Left anterior hemiblock RBBB • • • • Left axis deviation in lead II RBBB in lead V1 Left posterior hemiblock Note Sinus rhythm First degree block (PR interval 320 ms) Right axis deviation This could represent right ventricular hypertrophy, but there is no dominant R wave in lead V1 • • • • Long PR interval and deep S wave in lead I 93 The ECG in patients with palpitations and syncope: between attacks Fig. 2.32 Fig. 2.33 94 I VR V1 V4 II VL V2 V5 III VF V3 V6 I VR V1 V4 II VL V2 V5 III VF V3 V6 Patients with possible bradycardias 2 Second degree block and left anterior hemiblock Note • Sinus rhythm • Second degree block (2 : 1 type) • Left anterior hemiblock • Poor R wave progression suggests possible old anterior infarct P waves in lead II Second degree block, left anterior hemiblock and right bundle branch block (RBBB) Note Sinus rhythm Second degree block (2 : 1 type) Left anterior hemiblock RBBB • • • • P waves and RBBB in lead V1 95 The ECG in patients with palpitations and syncope: between attacks AMBULATORY ECG RECORDING The only way to be certain that a patient’s symptoms are due to an arrhythmia is to show that an arrhythmia is present at the time of the symptoms. If symptoms occur frequently – say two or three times a week – a 24-h tape recording (called a ‘Holter’ record after its inventor) may show the abnormality. When symptoms are infrequent ‘event recorders’ are more useful, and these can either be patient-activated or programmed to detect rate or rhythm changes. Table 2.4 shows examples of these devices, and some of their advantages and disadvantages. Figures 2.34, 2.35 and 2.36 show examples of ambulatory records obtained from patients who complained of syncopal attacks, but whose hearts were in sinus rhythm at the time they were first seen. When an ambulatory record shows arrhythmias which are not accompanied by symptoms, it is difficult to be certain of their significance. When 24-h recordings are made from healthy volunteers, extrasystoles are found in about two-thirds of them, and a few will even show the R on T phenomenon. Episodes of supraventricular tachycardia are seen in about 3% of apparently healthy subjects, and ventricular tachycardia in about 1%. If an ECG can be recorded at the time when the patient has symptoms, then there can be little doubt about the relationship between the symptoms and the cardiac rhythm, and the next two chapters deal with ECGs that may be recorded when a patient has either a tachycardia or a bradycardia. Fig. 2.34 Ventricular tachycardia Note • Ambulatory recording • Initially sinus rhythm with ventricular extrasystoles • Then salvos (three beats) of extrasystoles, leading to a broad complex tachycardia • The change in the QRS complex conﬁguration suggests that the tachycardia is ventricular, but a 12-lead ECG would be necessary to be certain 96 Ambulatory ECG recording 2 Fig. 2.35 Ventricular standstill Note • Ambulatory recording • Top strip shows sinus rhythm with normal AV conduction • Second strip shows SA block, which was asymptomatic • Third strip shows second degree block, which was also asymptomatic • Bottom strip shows a ventricular extrasystole followed by ventricular standstill. The patient lost consciousness due to this Stokes–Adams attack 97 Table 2.4 Ambulatory cardiac monitoring devices Monitoring device Mode of use Holter monitor Usually three electrodes placed on chest wall for maximal signal; activation button can be used in association with patient diary to highlight symptomatic events Cardiac memo Device placed directly on to the skin by patient when symptomatic, or can be adapted to use with electrodes; traces can be downloaded by telephone Loop recorder Usually three electrodes placed on chest wall; position of electrodes may require rotation, especially if there is skin reaction Implantable loop recorder Requires subcutaneous implantation, a procedure taking around 20 min and with a low risk of infection Can be patient-activated 98 Duration and mode of recording Applications Comments Usually 24 h, but up to 7 days Usually 1–2 channels, but up to 12 leads possible Suitable for palpitations, syncope or presyncope occurring fairly frequently (e.g. daily) Analysis time-consuming, but aided by software 10–20 recordings of 30–60 s Suitable for palpitations lasting for several minutes, enabling patient to apply device and record trace Not suitable for syncope, because patient activation required Recording period programmable; usually 4 min pre- and post-activation Can record 2000–3000 periods (‘loops’) of ECG records, including patient-activated and autoactivated episodes Autoactivation function programmable, based on heart rate and on QRS complex duration and irregularity Increasingly replacing memo devices Useful for diagnosis of palpitations or syncope Can be kept in place for long periods, although batteries may need replacing periodically Highly programmable; autoactivation can be based on heart rate and on QRS complex duration and irregularity Especially useful for the diagnosis of rare rhythm disturbances and syncope Orientation and site of implantation can be optimized prior to implantation Up to 14 months’ battery life Surgical removal needed 99 The ECG in patients with palpitations and syncope: between attacks Fig. 2.36 Sudden death due to ventricular ﬁbrillation Note • Ambulatory recording • First strip shows sinus rhythm • Sinus bradycardia then develops, with inversion of the T wave suggesting ischaemia • Short runs of ventricular tachycardia (VT) lead to polymorphic VT • Ventricular ﬁbrillation then develops 100 The ECG when the patient has a tachycardia Mechanism of tachycardias 102 3 Tachycardias associated with the Wolff– Parkinson–White syndrome 147 Enhanced automaticity and triggered activity 102 Management of arrhythmias 150 Abnormalities of cardiac rhythm due to re-entry 105 What to do when an arrhythmia is suspected 150 Differentiation between re-entry and enhanced automaticity 111 What to do when an arrhythmia is recorded 150 Tachycardias with symptoms 113 Extrasystoles 152 Sinus rhythm causing symptoms 113 Sinus tachycardia 154 Extrasystoles causing symptoms 115 Atrial tachycardia 154 Narrow complex tachycardias causing symptoms 117 Atrioventricular nodal re-entry tachycardia (AVNRT, junctional tachycardia) 154 Broad complex tachycardias causing symptoms 126 Atrial ﬁbrillation and ﬂutter 154 Ventricular tachycardia 155 The Wolff–Parkinson–White syndrome 155 Special forms of ventricular tachycardia in patients with symptoms 144 101 The ECG when the patient has a tachycardia Electrophysiology and catheter ablation 155 Cardiac arrest 162 The endocardial ECG 156 Management of cardiac arrest 164 Catheter ablation 157 Causes of cardiac arrest 165 Arrhythmias amenable to ablation 158 Indications for electrophysiology 162 Implanted cardioverter deﬁbrillator (ICD) devices 165 The only tachycardia that can be (reasonably) reliably diagnosed from the patient’s history is sinus tachycardia. A patient may notice the irregularity of atrial fibrillation, but it is easy to confuse this with multiple extrasystoles. The heart rate may give a clue to the nature of the arrhythmia (Table 3.1) but there is really no substitute for the ECG. MECHANISM OF TACHYCARDIAS 102 Electrophysiology is the process of recording the ECG from inside the heart, using electrodes inserted via a peripheral vein. This is a highly specialized area, and yields additional information to that obtained from a conventional 12-lead ECG. The main purpose of electrophysiological studies is to identify the site of origin of an arrhythmia. Arrhythmias occur either because of an abnormality of focal depolarization of the heart, or because of re-entry circuits. If the origin can be localized, the arrhythmia may be prevented permanently by ablation. This technique uses local endocardial (or more rarely epicardial) cautery burns to abolish areas of abnormal cardiac electrical activity, or to interrupt re-entry circuits. Before the advent of electrical (ablation) therapy, the cause of arrhythmias was a fairly esoteric subject. Now, however, it is essential to understand the underlying electrical mechanisms, because they form the basis of ablation therapy. ENHANCED AUTOMATICITY AND TRIGGERED ACTIVITY If the intrinsic frequency of depolarization of the atrial, junctional or ventricular conducting tissue is increased, an abnormal rhythm may occur. This phenomenon is called ‘enhanced automaticity’. Single early beats, or extrasystoles, may be due to enhanced automaticity arising from a myocardial focus. The most common example of a sustained rhythm due to enhanced automaticity is ‘accelerated idioventricular rhythm’, which is common after acute myocardial infarction. The ECG appearance (Fig. 3.1) resembles that of a slow ventricular tachycardia, and that is the old-fashioned name for this condition. This rhythm causes no symptoms, and should not be treated. If the junctional intrinsic frequency is increased to a point at which it approximates to that of the SA node, an ‘accelerated idionodal rhythm’ results. This may appear to ‘overtake’ the P waves (Fig. 3.2). This rhythm used to be called a ‘wandering pacemaker’. The term ‘focal junctional tachycardia’ is used in the (probably rare) instances of a supraventricular tachycardia originating around the AV node, by mechanisms other than re-entry. Enhanced automaticity is also thought to be the mechanism causing some non-paroxysmal tachycardias, particularly those due to digoxin intoxication. Enhanced automaticity and triggered activity 3 Table 3.1 Physical signs and arrhythmias Pulse Heart rate (beats/min) Possible nature of any arrhythmia < 50 Sinus bradycardia Second or third degree block Atrial ﬂutter with 3 : 1 or 4 : 1 block Idionodal rhythm (junctional escape), with or without sick sinus syndrome Probable sinus rhythm Sinus tachycardia or an arrhythmia Probable atrial ﬂutter with 2 : 1 block Atrial tachycardia Atrioventricular re-entry tachycardia (AVRT) Atrioventricular nodal re-entry tachycardia (AVNRT; junctional (nodal) tachycardia) Ventricular tachycardia Probable ventricular tachycardia Atrial ﬂutter with 1 : 1 conduction Arterial pulse Regular 60–140 140–160 150 140–170 > 180 300 Irregular Marked sinus arrhythmia Extrasystoles (supraventricular or ventricular) Atrial ﬁbrillation Atrial ﬂutter with variable block Rhythm varying between sinus rhythm and any arrhythmia or conduction defect Jugular venous pulse More pulsations visible than heart rate Second or third degree block Cannon waves – third degree block Fig. 3.1 Accelerated idioventricular rhythm Note • After two sinus beats, there are four beats of ventricular origin with a rate of 75/min • Sinus rhythm is then restored 103 The ECG when the patient has a tachycardia Fig. 3.2 Accelerated idionodal rhythm Note • After three sinus beats, the sinus rate slows slightly • A nodal rhythm appears and ‘overtakes’ the P waves Fig. 3.3 I VR V1 V4 II VL V2 V5 III VF V3 V6 II 104 Abnormalities of cardiac rhythm due to re-entry 3 Fig. 3.4 Re-entry pathways in the pre-excitation syndromes The Wolff–Parkinson–White syndrome type A The Lown–Ganong–Levine syndrome LA RA LA LV RA LV Note RV RV • Broken lines indicate the potential re-entry pathways in AVRT Right ventricular outﬂow tract ventricular tachycardia (RVOT-VT) Note Broad complex tachycardia Left bundle branch block and right axis deviation, typical of RVOT-VT • • ‘Triggered activity’ results from late depolarizations which occur after normal depolarization, during what would normally be a period of repolarization. Like enhanced automaticity, this can cause extrasystoles or a sustained a