Clinical Electrocardiography

Clinical E lectrocardiography Third Edition

Clinical E Zectrocardiography Third Edition

B L Chia MBBS, FRACP, FRCP (Edin), FAMS, FACC PROFESSOR OF MEDICINE NATIONAL UNIVERSITY OF SINGAPORE CHIEF; CARDIAC DEPARTMENT NATIONAL UNIVERSITY HOSPITAL SINGAPORE

L

World Scientific Singapore New Jersey. London Hong Kong

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First published 1998 Reprinted 2000

CLINICAL ELECTROCARDIOGRAPHY, 3rd Edition Copyright 0 1998 by World Scientific Publishing Co. Re. Ltd.

A11 rights reserved. This book, or parts thereoJ may not be reproduced in any form or by any means, electronic or mechanical, including photocopying, recording or any information storage and retrieval system now known or to be invented, without written permission from the Publisher.

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ISBN 981-02-3761-8 ISBN 981-02-3762-6 (pbk)

Printed in Singapore.

To John and Lin

ACKNOWLEDGEMENTS

It gives me great pleasure to express my thanks and gratitude to the following: (1) Assoc Professor Lim Yean-Teng (Senior Consultant) and the other members of the Cardiac Department, National University Hospital, Singapore who are listed below for their dedication and unfailing support and also for helping to create a stimulating environment where electrocardiography can enjoy a robust growth together with echocardiography, electrophysiology and interventional cardiology: (a) Drs Lim Tai-Tian, Ling Lieng-Hsi, Ng Kheng-Siang, Ng Wai-Lin, Tan Huay-Cheem and Ye0 Tiong-Cheng (all Consultant Cardiologists) (b) Drs Ho Kheng-Thye (Senior Registrar), Bernard Kwok and James Yip (Registrar) (2) Dr Lau Kean-Wah, Senior Consultant Cardiologist at the National Heart Centre, Singapore for reading through the manuscript and for his friendship, invaluable advice and help through the years. (3) Ms Christina Ng for her excellent typing and secretarial skills, without which this book could not have been completed. (4) Mr Tan Lip-Seng for his excellent photography. I would also like to thank the following: Dr Chan I t - Y e e for Fig. 5.18, Dr Bernard Ee for Figs. 2.6,7.9 and 7.13, Dr A Johan for Fig. 5.6, Dr Koo Chee-Choong for Figs. 6.14,6.15 and 7.12, Dr Quek Swee-Chye for Fig. 3.29 and Dr Arthur Tan for Fig. 2.8. The Managing Editor of Asian Medical News for permission to reproduce several of the ECG and cardiovascular quizes which I have previously published. The Editor of the Singapore Medical Journal for permission to reproduce from my previous publications Figs. 2.2 1, 2.27, 2.28, 2.29, 2.30 and 5.19. The Editor-in-Chief, The Canadian Journal of Cardiology for permission to reproduce from my previous publication, Fig. 7.3.

PREFACE

This is the third edition of “Clinical Electrocardiography” which was first published in 1985. There has been tremendous progress in the last 10 years since the second edition, especially in the electrocardiography of acute myocardial infarction. With the advent of the thrombolytic era, many important new insights into the electrocardiography of acute myocardial infarction have evolved. In this new edition, the sections on posterior myocardial infarction, supraventricular tachycardia, ventricular tachycardia and antiarrhythmic drug therapy have all been updated and revised. One of the strengths of the previous two editions has been the quality of the ECG illustrations. In keeping with this tradition, the ECG illustrations in this third edition have been further improved, with 54 (39%) out of the 139 illustrations being new. Books, monographs and scientific papers on electrocardiography abound and it would appear that there is little justification for yet another book on this subject. However, despite the voluminous publications, it is difficult to find books on electrocardiography which are simple, concise, accurate and relevant to patient care. This book is the culmination of about 30 years of experience in the teaching of electrocardiography to coronary care unit nurses, medical undergraduates, interns, residents and cardiology registrars. As the title of the book implies, the approach to the subject has been entirely from the viewpoint of a clinician. Hence, theoretical considerations have been kept to a minimum and clinical-electrocardiographic correlations have been emphasized throughout the text.

B L CHIA 1998

vii

CONTENTS

Dedications Acknowledgements Preface 1. The Normal Electrocardiogram

V

vi vii

2

2. Ischaemic Heart Disease

11

3. Miscellaneous Conditions

38

4. Cardiac Arrhythmias

62

5 . Supraventricular Arrhythmias

68

6. Ventricular Arrhythmias

90

7. Bundle Branch Block, Hemiblock and Atrioventricular (AV) Block Index

108

120

ix

Clinical Electrocardiography

1

CHAPTER 1

THE NORMAL ELECTROCARDIOGRAM

THE 12-LEAD ELECTROCARDIOGRAM The 12-lead electrocardiogram (ECG) consists of the following leads:

(I)

Bipolar Leads (i) Lead I (between right arm and left arm) (ii) Lead I1 (between right arm and left leg) (iii) Lead I11 (between left arm and left leg)

(11) Augmented Unipolar Leads (i) Lead aVR (right arm) (ii) Lead aVL (left arm) (iii) Lead aVF (left leg) (111) Unipolar Chest Leads These are designated as V leads. There are six V leads (from V1 to V,) depending on where the electrode is placed on the chest (Fig. 1.1). Lead V1 is recorded with the electrode in the fourth intercostal space just to the right of the sternum, and lead V2 in the fourth intercostal space just to the left of the sternum. Lead V3 is recorded at a position exactly mid-way between leads Vz and V4. Lead V4 is recorded in the fifth intercostal space in the mid-clavicular line. Leads V5 and V6 are recorded at the same horizontal level as lead V4, with lead V5 in the anterior axillary line and lead V6 in the mid-axillary line. Apart from the above conventional 12 leads, other leads are also frequently recorded. Right-sided chest leads such as leads V3R, V4R, VSRand V6R are recorded in positions which correspond to leads V3, V4, V5 and V6 respectively, except that the electrode is

2

-I

Fig. 1.1 Diagram showing the positions of the electrode when recording the different left and right-sided chest leads. 1 to 6 = leads V1 to V6 respectively. MCL = mid-clavicularline, AAL = anterior axillary line, MAL = mid-axillary line, V3R and V4R = right-sided chest leads.

now placed on the right side of the chest instead of on the left.' These leads (especially lead V4R) are particularly useful for the diagnosis of right ventricular infarction. Very recently, leads V7,Vg and Vg have been reported to be valuable in the diagnosis of posterior myocardial infarction. These 3 leads are recorded at the same horizontal level as lead Vg, with the electrode being placed in the left posterior axilliary line (V,), left mid-scapular line (V,) and at the left border of the spine (V9).2

CALCULATION OF HEART RATE The ECG is normally recorded at a speed of 25 m d s e c . The horizontal distance between 1 large square on the ECG paper recorded at this speed represents 0.20 sec. Since this distance spans the length of 5 small squares, each small square therefore represents 0.04 sec (Fig. 1.5). There are many different ways of calculating the heart rate. A simple way is to divide 300 by the number of large squares between 2 consecutive beats if the rhythm is regular. For example, the following are the heart rates corresponding to the number of large squares in between 2 consecutive beats.

3

Heart rate

Number of large squares between 2 consecutive beats

300 150 100 75 60 50 43 38

1 (300/1) 2 (300/2) 3 (30013) 4 (300/4) 5 (300/5) 6 (300/6) 7 (300/7) 8 (300/8)

The rationale for the above calculation is as follows. There are 300 fifths of a second in 1 minute (5 x 60). One fifth of a second (i.e. 0.20 sec) is represented by 1 large square. Therefore the heart rate is conveniently calculated by dividing 300 by the number of large squares between 2 consecutive beats.

CALCULATING ELECTRICAL AXIS The term "electrical axis" is used to describe the average direction of the electrical impulse of the heart as it is projected in the frontal, horizontal or sagittal plane. Although the P, QRS and T complexes each has an axis in these 3 planes, this term, when unqualified, usually refers to the axis of the QRS complex in the frontal plane. Like the calculation of the heart rate, there are numerous ways of calculating the electrical axis. To understand the logic behind the method of calculating the axis, one must be familiar with the concept of the Einthoven triangle and the hexaxial reference sy~tern.~ The latter is derived from a combination of the triaxial reference systems of both the standard bipolar leads and the augmented unipolar limb leads (Fig. 1.2). In the hexaxial reference system, which is diagrammed in Fig. 1.3, the frontal plane is divided into 30" intervals.

.' -150."

..

aVF Fig. 1.2 Diagram showing the triaxial reference system.

4

Fig. 1.3 Diagram showing the hexaxial reference system.

When calculating the axis of the heart, it is useful to assess all the limb leads (i.e. leads I, 11,111, aVR, aVL and aVF) and look for the lead where the QRS complex has the smallest or most equiphasic deflection. The axis is perpendicular to this lead. Using Fig. 1.4 as an example, the limb lead where the ventricular complex shows the least deflection is lead aVL. The axis which is perpendicular to lead aVL is therefore lead 11. Examination of lead I1 shows that the ventricular complex is upright and therefore the axis must be directed towards the positive pole of this lead (i.e. the axis is +60"). The following method is an alternative way of calculating the axis: (1) Calculate the algebraic sum of the QRS deflections in leads I and aVF and mark Off each value in arbitrary units in these 2 leads; (2) Draw lines perpendicular to leads I and aVF passing through these 2 points; and (3) Draw a line joining the point of intersection of the constructed lines to the point of intersection of leads I and aVE This line represents the axis. The normal axis is between -30" to +90". Left axis deviation is defined as an axis between -30" to -90" and right axis deviation as an axis between +90" to +180". When the axis is between -90" to -1 80" (i.e. upper right quadrant), the axis is termed "indeterminate".

wwww m

aV F

aVR

kki% v3

v2

V4

V5

Fig. 1.4 Normal 12-lead ECG.

COMPLEXES AND SEGMENTS P Wave The P wave represents atrial depolarization which normally proceeds downwards, anterogradely from the sinoatrial node. It is normally upright in leads I, 11, aVF and the left

5

Fig. 1.5 Diagram showing the various ECG complexes, segments and intervals.

praecordial leads V4 toV6, and inverted in lead aVR. The polarity of the P wave in all the other leads is variable. It should not be more than 0.12 sec in duration and 2.5 mm in height in the limb leads, and it should be less than 1.5 mm in height in the praecordial leads (Figs. 1.4 and 1.5).

PR Segment The PR segment is the portion between the end of the P wave and the beginning of the QRS complex.

QRS Complex The QRS complex reflects depolarization of the 2 ventricles. The nomenclature of the various segments of the ventricular complex is standardized. If the first deflection is downwards, it is called a Q wave. An upright deflection is called an R wave, whether it is preceded by a Q wave or not. Anegative deflection following an R wave is called an S wave, whether the R wave has been preceded by a Q wave or not. Depolarization of the ventricular myocardium begins in the septum, where it takes place in a left to right direction (sequence 1 in Fig. 1.6). Following this, both the left and right ventricles are depolarized simultaneously. However, since the left ventricle has a much larger physical and electrical mass, ventricular depolarization can be conveniently regarded electrically as depolarization of the left ventricle alone. This depolarization proceeds from right to left (sequence 2 in Fig. 1.6). An electrode which is orientated to the left ventricle (e.g. lead V,) will show an initial small q wave (due to septa1 depolarization moving away from the electrode), followed by a large R wave (due to the ventricular depolarization moving towards the electrode). A typical left praecordial lead complex is therefore a qR complex.

h

Fig. 1.6 Diagram showing normal sequence of ventricular depolarization and the ventricular complexes in V1 and V5. S = septum, RV = right ventricle, LV = left ventricle.

The same electrical events are recorded in an opposite fashion in an electrode orientated to the right ventricle (e.g. lead Vl). The initial deflection is a small r wave due to septa1 depolarization moving towards the electrode, followed by an S wave due to ventricular depolarization moving away from the electrode. A typical right praecordial lead complex is therefore an rS complex (Fig. 1.6). In the praecordial leads, rS complexes are seen in leads V1 and V2, and qR complexes in leads V4 to V6 There is a gradual increase in the height of the r wave and a corresponding decrease in the depth of the S wave from leads V1 to V3. In lead V3, which represents the transitional zone, the height of the R wave and the depth of the S wave are approximately equal. In the limb leads, the ventricular complexes may show either a left or a right praecordial lead pattern. The only exception is lead aVR, where the ventricular complex normally shows a negative deflection in the form of either a deep Q wave or a rS complex (Fig. 1.4). Normally, the 2 ventricles are depolarized simultaneously, resulting in a narrow QRS complex which is between 0.05 to 0.10 sec in duration. In ventricular ectopic beats, bundle branch block or supraventricular ectopic beats with aberrant ventricular conduction, the QRS complex is widened. There is a wide variation in the amplitude of the QRS complex. The generally accepted upper limit for the R wave in lead V5 is between 25 to 30 mm. However, voltages greater than this are commonly present in asthenic, normal, young individuals and in those whose ECG show the early repolarization pattern (see Chapter 3).

ST Segment The ST segment is that portion of the ECG between the end of the S wave and the beginning of the T wave. Normally, the ST segment blends smoothly and imperceptibly with the T wave. It is also normally isoelectric, i.e. at the same horizontal level as the T-P segment which is taken as the isoelectric line (Figs. 1.4 and 1.5). The ST segment may be either elevated or depressed with reference to the isoelectric line. T Wave The T wave comes after the ST segment and represents ventricular repolarization (Fig. 1.5). It is normally upright in leads I, 11, V4 to v6 and inverted in lead aVR. In all the other leads, the polarity of the T wave is variable. T wave inversion is commonly present in leads V1 to V4 in children up to the age of 14 years. After this age, it is considered abnormal except in lead V1 in males, and leads V1 and V2 in females. Rarely, T wave inversion may be present up to lead V3 in normal individuals. The 2 limbs of the T wave are usually asymmetrical and the apex is slightly rounded (Fig. 1.4). It is frequently stated that the height of the T wave should not exceed 5 mm in any standard limb lead and 10 mm in any praecordial lead. However, in subjects with the early repolarization pattern, tall T waves exceeding 10 mm are frequently encountered, even though there is no cardiac or other disease (see Chapter 3).

U Wave The U wave follows the T wave (Figs. 1.4 and 1.5). The genesis of the U wave is unclear but it has been postulated to be due to repolarization of the Purkinje fibres or the papillary muscles. It is normally of low voltage and has the same polarity as the T wave. It is usually most prominent in leads V2 to V, and generally does not exceed 2 mm or one quarter of the height of the preceding T wave (Fig. 1.5).

INTERVALS PR Interval The PR interval is measured from the onset of the P wave to the beginning of the QRS or rS complex (Fig. 1.5). It represents the time taken for the sinus impulse to travel across the atria, down the atrioventricular (AV) node, bundle of His, bundle branches, Purkinje fibres and finally to the ventricular myocardium. It is normally between 0.12 to 0.20 sec in duration. QT Interval The QT interval is measured from the onset of the QRS or rS complex to the end of the T wave (Fig. 1.5). Since the normal QT interval varies with the heart rate, the QTc or the corrected QT interval is used clinically instead of the QT interval. The QTc is calculated from the QT interval and the heart rate using the formula: QTc = QT interval divided by the square root of the R-R i n t e r ~ a l . ~ T hnormal e QTc should not exceed 0.42 sec.

8

REFERENCES 1. Tan CC, Hiew TM, Chia BL. Right chest electrocardiographic patterns in normal subjects. Chest 1990; 97: 572. 2. Matetzky S, Freimak D, Chouraqui P, et al. Significance of ST segment elevations in posterior chest leads (V, to V,) in patients with acute inferior myocardial infarction: application for thrombolytic therapy. J A m Coll Curdiol 1998; 31: 506. 3. Schamroth L. An Introduction to Electrocardiography, Blackwell Scientific Publications, Oxford, 7th ed., 1990; p. 35. 4. Bazett H 0.An analysis of the time relations of electrocardiograms. Heart 1920; 7: 353.

9

CHAPTER 2

ISCHAEMIC HEART DISEASE

The two major clinical applications of electrocardiography are the diagnosis of myocardial ischaemia and cardiac arrhythmias. The birth of electrocardiography more than 9 decades ago opened a new dimension in the study of the heart, by allowing the cardiac electrical currents (voltages, potentials) to be clinically recorded for the first time. This heralded a milestone in the diagnosis and treatment of coronary artery disease and cardiac arrhythmias. Despite the introduction in recent years of many new investigative techniques such as myocardial perfusion scintigraphy, stress echocardiography and coronary angiography, the electrocardiogram today still maintains its pivotal role in the evaluation of myocardial ischaemia, chiefly because it is very useful, very simple to perform, noninvasive and inexpensive. In this chapter, various ECG patterns in ischaemic heart disease will be discussed. The many problems and pitfalls that are frequently encountered in the ECG diagnosis of ischaemic heart disease will be highlighted in the next chapter which deals with ECG abnormalities seen in miscellaneous conditions.

DIAGNOSIS OF ISCHAEMIC HEART DISEASE Coronary artery disease may present in several different ways. A significant number of individuals who suffer from this disease have no symploms at all even though the disease is very severe. They have what is known as “silent myocardial ischaemia”.’Others, however, manifest with stable and unstable angina pectoris, acute myocardial infarction or “sudden death”. Whenever an ECG is recorded in a patient suspected of having ischaemic heart disease, the following questions should be routinely asked:

11

(1) Is the ECG normal or abnormal? (2) If it is abnormal, do the abnormalities indicate myocardial infarction or angina pectoris? (3) If the ECG is indicative of myocardial infarction, do the changes suggest an acute or an old myocardial infarction?

These questions are of obvious importance, because the clinical significance in terms of urgency of management in patients suffering from acute myocardial infarction versus patients suffering from stable angina pectoris or chronic ischaemic heart disease is completely different.

MYOCARDIAL INFARCTION Early diagnosis of acute myocardial infarction is of crucial importance because (1) Mortality is highest in the first few hours; and (2) Thrombolytic therapy, which is today frequently given, is most effective if it is administered within 3 hours after the onset of infarction. In the evaluation of a patient who is suspected of suffering from acute myocardial infarction, the 3 principal parameters are: (1) Clinical history (2) ECG (3) Serum markers of acute myocardial infarction such as creatine phosphokinase (CK), CKMB fraction (CKMB) and troponin T. Since the levels of the serum markers of acute myocardial infarction may not be significantly elevated in the first few hours after the onset of the infarction, early diagnosis frequently must depend on the clinical history and ECG.

TRANSMURAL (Q WAVE) MYOCARDIAL INFARCTION Every year in Singapore, which has a population of about 3 million people, approximately 1300 patients aged 20-64 years suffer from acute myocardial infarction.2 Acute myocardial infarction is very often due to a thrombus which is superimposed on a ruptured atherosclerotic plaque resulting in total obstruction of coronary blood flow. In transmural myocardial infarction, the whole thickness of the myocardium is involved. There is a central core of necrotic myocardium which is surrounded in turn by a shell of injured tissue, and then a zone of ischaemic tissue. An ECG lead which is placed over the site of infarction will record the following changes: (1) Pathological Q waves reflecting tissue necrosis (2) Elevated ST segments reflecting tissue injury (3) T wave inversion reflecting tissue ischaemia. These ECG changes have been described as “the indicative changes” of acute transmural myocardial infar~tion.~

12

Normally, small and narrow q waves are always present in the left praecordial leads. The following are the characteristics of a pathological Q wave which distinguish it as being abnormal: (1) It is broad (0.04 sec or longer in duration); (2) It is deep (greater than 4 mm in depth); ( 3 ) It is usually associated with a substantial loss of the height of the R wave resulting in a Q wave/R wave ratio which is 25% or greater; and (4) It is frequently seen in multiple leads. For example, in inferior infarction, it is present in leads 11, I11 and aVF and in anterolateral infarction, it is seen in leads V4, Vg, Vg, I and aVL. Lastly, to be significant, the pathological Q wave must be present in leads which do not normally show wide and deep Q waves, e.g. lead aVR. In the “hyperacute phase” (i.e. during the first few hours), the ST segments are elevated with a slope which is either straight upwards to the apices of tall and widened T waves or concave upwards. ST segments in leads overlying normal myocardium which are opposite to the infarct site will show “reciprocal” ST segment depression. In this phase of acute myocardial infarction, pathological Q waves and T wave inversion are not seen (B in Fig. 2.1). It is important to note that the initial ECG shows the classical “hyperacute” changes in only about 50% of patients. In another 45% of cases, the ECG shows either ST segment depression or nondiagnostic abnormalities, and in the remaining 5% of cases, no ECG abnormality is d e t e ~ t e d If . ~ the initial ECG is normal or shows nondiagnostic abnormalities, it is crucial to repeat 12-lead ECG recordings every 15-30 minutes, because serial ECGs will very frequently show diagnostic changes in patients who have suffered a myocardial infarction. All the studies so far have shown that thrombolytic therapy is beneficial only in acute myocardial infarction patients presenting with ST segment elevation.

NORMAL

iYPERACUTE

‘ULLY EVOLVED

RESOLUTION

CHRONIC

kf k-

3n +A

C

E

Fig. 2.1 Diagram showing the ECG changes in transmural myocardial infarction. Top panel shows the ECG changes in the leads facing the infarct site (i.e. “indicative changes”). Bottom panel shows the ECG changes in the leads facing the opposite normal myocardium (i.e. “reciprocal changes”).

13

Generally, within 24 hours of the onset of acute myocardial infarction, the ST segment elevation decreases and pathological Q waves start to develop. The elevated ST segments, unlike those seen in the “hyperacute phase”, are now convex upwards. Later in this phase which is called “the fully evolved phase”, deep and symmetrically inverted arrowhead T waves are seen (C in Fig. 2.1 and Fig. 2.4).

Fig. 2.2 “Hyperacute phase” of transmural anterior infarction in a 51-year-old man. Note: (1) Markedly elevated ST segments (concave upwards) in V2 to V,, I and aVL, merging with tall T waves in V2 to V4 (ST segment and T wave in V2 = 10 mm and 20 mm respectively). (2) Reciprocal ST segment depression in 11, I11 and aVE Coronary angiography revealed a 90% stenosis of the proximal left anterior descending artery.

II-

II

v1

m v3

aV R

4 aV F

V6

Fig. 2.3 The ECG was recorded approximately 24 hours after Fig. 2.2. It shows the “fully evolved phase” of transmural anterior infarction as reflected by: (1) Pathological Q waves in V1 and V2. (2) Elevated ST segments in V, to V3. (3) Deep and symmetrically inverted T waves in V2 to V,, I and aVL.

Figures 2.2 and 2.3 are ECGs of a patient with transmural, anterior myocardial infarction recorded about 2 and 24 hours respectively, after the onset of chest pain. Figure 2.2 shows ECG changes reflecting the “hyperacute phase” and Fig. 2.3, the “fully evolved phase” of transmural, anterior myocardial infarction.

14

I

v1

aVR

v3

aVL

V6

Fig. 2.4 “Fully evolved phase” of transmural anterior infarction. Note: (1) Pathological Q waves in V, to V3. (2) Elevation of the ST segment (convex upwards) and T wave inversion in V , to v,.

Following the “fully evolved phase”, the ECG begins to show the “resolution phase”. During this period, the ST segments fall to the isoelectric line, but the T waves remain inverted (D in Fig. 2.1 and Fig. 2.8). Still later, in the “chronic phase”, the T waves become upright and all that remains are the pathological Q waves (E in Fig. 2.1 and Fig. 2.5). The terms “chronic phase” of myocardial infarction and “old myocardial infarction” are frequently used synonymously. In some patients, the pathological Q waves become less prominent or may even disappear completely after several months or years. With the passage of time, small r waves are occasionally resurrected in leads which originally showed pathological Q waves. If this occurs in leads V1 to V3, the height of the r waves may not increase progressively as in the normal ECG. This phenomenon is referred to as “poor r wave progression”, which often indicates an old anteroseptal infarction (Fig. 2.5). This abnormality may also be seen in left ventricular hypertrophy and dilated cardiomyopathy. To illustrate the sequence, an ECG abnormality shown in B in Fig. 2.1 indicates a very recent myocardial infarction perhaps a few hours old, in C slightly later in time, in D a few weeks old and in E a few months old. However, it is important to note that all these evolutionary changes described above may be accelerated with thrombolytic therapy or percutaneous transluminal coronary angioplasty. In some patients, especially those with anterior myocardial infarction, there is persistent elevation of the ST segment. This usually suggests a ventricular a n e ~ r y s m . ~

aV R

aVL

aVF

V6

v3 Fig. 2.5 ECG of a 70-year-old man showing the “chronic phase” of transmural anterior and inferior infarction. Note: (1) Very deep and wide pathological Q waves in leads 111 and aVF (arrowheads) reflecting old inferior infarction. (2) Poor r wave progression from V1 to V3 reflecting old anterior infarction. Coronary angiography showed severe triple vessel disease.

LOCALIZATION OF INFARCT SITE The presence of the “indicative” ECG infarct pattern in certain leads suggest that myocardial infarction has occurred in specific sites of the heart, e.g. leads 11, I11 and aVF - inferior infarction, leads V1 to V3 - anteroseptal infarction, leads V4, V5, V6, I and aVL - anterolateral infarction of the left ventricle. The conventional 12-lead ECG does not directly record electrical currents from the posterior wall of the left ventricle. Therefore, infarction at this site does not manifest the usual “indicative” infarct pattern in any of the conventional 12 leads. However, “indicative changes” of posterior infarction can be detected in leads V7, V8 or Vg (Fig. 2.7) or in the oesophageal lead (ie ECG recorded from an electrode placed in the oesophagus facing the posterior wall of the left ventricle) which is seldom performed today because of its inconvenience. Posterior wall infarction can also be diagnosed from the 12-lead ECG using indirect criteria, such as reciprocal ST segment depression in leads V1to V4in the “hyperacute phase” (Figs. 2.6 and 2.7), or tall R and tall T waves in leads V1 and V2 in the “resolution phase” (Figs. 2.8 and 2.9). In the past 20 years, there has been considerable controversy over whether ST segment depression in the praecordial leads V1 to V4 in patients with acute inferior infarction, reflects reciprocal changes or represent additional ischaemia in the anterior myocardial waK6 Very recently however, this ST segment depression has been confirmed to be due to reciprocal changes from acute posterior infarction which frequently accompanies inferior infarction7. A major advance in recent years has been the finding that right ventricular infarction, which is present in approximately 30% of patients with inferior infarction of the left ventricle, can be accurately diagnosed from right-sided chest leads, especially lead V4R.8Figures 2.6 and 2.7 are examples of the “hyperacute phase” of right ventricular infarction, as well as inferior and posterior infarction of the left ventricle.

16

~~

.-

___ - - - -

v1

V6

V4R

V5R

V6R

Fig. 2.6 Acute inferior, posterior and right ventricular infarction in a 60-year-old woman. Note: (1) Elevated ST segments in 11, I11 and aVF, merging with tall T waves and reciprocal ST segment depression in I and aVL reflecting the “hyperacute phase” of transmural inferior infarction. (2) ST segment depression in V2 to V, reflecting the reciprocal changes of acute posterior infarction. (3) Pathological Q waves and elevated ST segments in V,R, VSR and V6R reflecting acute right ventricular infarction.

V1

V6 v2

V8

v3

v4

VS

V9

V4 R

VSR

V6R

Fig. 2.7 Acute inferior, posterior and right ventricular infarction in a 49-year-old man. Note: (1) Elevated ST segments in 11,111 and aVF (associated with pathological Q wave in 111) and reciprocal ST segment depression in I and aVL reflecting acute, transmural inferior infarction. (2) ST segment elevation in V7, Vg, V, and ST segment depression in V1 to V3 reflecting acute posterior infarction. (3) ST segment elevation and pathological Q waves in V4R, V5R and V6R reflecting acute right ventricular infarction. (4) First degree AV block (PR interval = 0.28 sec). Coronary angiography showed subtotal occlusion of the right coronary artery.

17

I

II

Ill

aVR

aVL

aV F

Fig. 2.8 ECG of a 39-year-old man showing inferolateral and posterior transmural myocardial infarction. Note: (1) Pathological Q waves and T wave inversion in 11, 111, aVF, V5 and V6 reflecting the “resolution phase” of transmural inferolateral infarction. (2) Tall R and T waves in V1 to V3 reflecting the “resolution phase” of posterior infarction.

Fig. 2.9 Top panel is an enlargement of Vl to V3 shown in Fig. 2.8. Bottom panel was obtained from a photograph of the top panel but it was printed upside down. Note: (1) Pathological Q waves and deeply inverted T waves in Vl to V3 in the bottom panel. These are the ECG abnormalities which would have been seen in an oesophageal lead ECG, if it had been done in this patient. (2) The tall R and tall T waves in V, to V, in the top panel represent reciprocal changes of the pathological Q wave and the deeply inverted T wave respectively in the oesophageal lead ECG.

18

SUBENDOCARDIAL (NON-Q WAVE) INFARCTION In subendocardial infarction, only the inner half of the myocardium is involved. The clinical history of patients with subendocardial infarction and those with transmural infarction is similar. However, the ECG diagnosis of subendocardial infarction is not as precise as that for transmural infarction, since similar changes may occur in stable angina (i.e. angina induced by exercise or emotion) or unstable angina. The diagnosis of subendocardial infarction must therefore be based on the clinical history, together with ECG and biochemical abnormalities. In patients with subendocardial infarction, no pathological Q waves or elevated ST segments are seen. Instead, there are either deep and symmetrically inverted arrowheadT waves which are usually associated with ST segment depression (Fig. 2.10), or ST segment depression occurring alone. Unlike angina pectoris, these ECG abnormalities are usually persistent and may last for several hours or days. There is also an associated rise in the levels of the serum markers of acute myocardial infarction.

SUBENDOCARDIAL INFARCTION Fig. 2.10 Diagram showing ECG pattern of subendocardial infarction. Note deep and symmetrically inverted arrowhead T wave (T).

Figure 2.11 is the ECG of a 65-year-old woman with subendocardial infarction showing deep and symmetrically inverted arrowhead T waves and ST segment depression in leads V2 to V6, 11, I11 and aVF. Coronary angiography showed severe narrowing of the proximal left anterior descending artery. In this patient, the T wave inversion persisted for 3 years. She then suffered another attack of acute myocardial infarction. The ECG recorded at that time showed that all the previously inverted T waves had become upright (Fig. 2.12). This phenomenon of inverted T waves becoming upright during an episode of acute myocardial ischaemia is termed “pseudo-normalization”of the T wave.

19

Fig. 2.11 Subendocardial infarction. ECG of a 65-year-old woman with acute subendocardial infarction. Note: (1) Deep and symmetrically inverted T waves with ST segment depression in V2 to v,,f 11,111 and aVF. ( 2 ) Axis of about - 45’ reflecting left anterior hemiblock. Coronary angiography showed severe narrowing of the proximal left anterior descending artery.

I

111

aV R

aV L

aV F

Fig. 2.12 The ECG shown in Fig. 2.11 remained unchanged for 3 years. The patient then suffered another attack of acute myocardial infarction. This ECG was recorded at that time and it shows that all the deeply inverted T waves have become upright - “pseudo-normalization” of the T waves. Ventricular ectopic beats are seen in V1, V3 and vf,.

Figure 2.13 is the ECG recorded from another patient with subendocardial infarction and it shows very marked ST segment depression (downsloping and horizontal type) in multiple leads.

20

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... ....

......

.

~-

.~

I

I

I1

v1

111

aVF

aV L

V6

v2

Fig. 2.13 Subendocardial infarction. The patient was a 54-year-old man who presented with severe chest pain and cardiogenic shock. Note that there is very deep depression of the ST segments (downsloping and horizontal) in multiple leads - Vz to V6, I, 11,111and aVF. The deepest ST segment depression (14 mm) is seen in V5 (arrowhead).

In recent years, some experts have suggested that the ECG differentiation of transmural and subendocardial infarction should be a b a n d ~ n e d They .~ opined that many patients showing Q waves do not have full thickness (i.e. transmural) myocardial infarction. Furthermore, many other patients showing ST-T wave changes do not have infarction which is limited to the inner half of the ventricular wall. Because of this, they proposed that the ECG diagnosis of myocardial infarction should be described as either “Q wave infarction” (i.e. presence of pathological Q waves), or “non-Q wave infarction” (i.e. absence of pathological Q waves but presence of STT wave changes). Nevertheless, it is important to note that Q wave infarctions, although not always transmural in pathology, are in general significantly larger than non-Q wave infarctions.

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_.

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I

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V2

v3

v5

V6

Fig. 2.14 Reinfarction. The ECG is from a patient who had previously suffered an acute myocardial infarction. Top panel is his usual ECG which shows old, transmural anterior infarction as reflected by pathological Q waves in V2 to V4 and loss of R wave voltage with T wave inversion in V4 to Vs. The bottom panel was recorded soon after he suffered a reinfarction and shows ST segment elevation in V, to V4, deepening of the T wave inversion in V4 to v g , deepening of the Q wave and loss of R wave in V4 and a further decrease in the height of the R waves in v5 and vg.

21

REINFARCTION A frequent clinical problem is the diagnosis of reinfarction in a patient who had previously suffered a myocardial infarction and now complains of chest pain. In this situation, it is important to compare the present ECG with those recorded in the recent past. If the current ECG shows new ST segment elevation, new Q waves or new T wave inversion, then most likely reinfarction has occurred. In addition, the serum markers of acute myocardial infarction will be elevated. Figure 2.14 shows an example of reinfarction.

CHRONIC ISCHAEMIC HEART DISEASE The hallmark ECG abnormality of chronic ischaemic heart disease is ST segment depression. Normally, the ST segment is isoelectric and blends smoothly and imperceptibly with the ascending limb of the T wave. In the J type or junctional ST segment depression, there is depression of the proximal part of the ST segment beginning at its junction with the QRS complex. The slope of the ST segment is upwards and its distal part merges gently and imperceptibly with the T wave (B in Fig. 2.15). J type ST segment depression may be present in normal subjects and is not significant unless it is very marked and its upward slope is so gradual as to appear nearly horizontal.

B

D

C

E

Fig. 2.15 Diagram showing the different types of ST segment depression indicated by arrows. (A) Isoelectric ST segment. (B) Junctional or J type. ( C ) Mirror image of the pass sign (/) “digitalis effect”. (D) Horizontal. (E) Downsloping (Sagging).

22

Figure 2.16 is an ECG showing J type ST segment depression in a 34-year-old man with atypical chest pain during treadmill exercise stress testing. C in Fig. 2.15 shows a type of ST segment depression which resembles a mirror image of the pass sign (v). This ECG finding, termed the “digitalis effect”, is seen in patients who have been given digitalis and is not a sign of digitalis toxicity. Figure 2.17 shows the ECGs of a patient recorded before and during digoxin administration. The other 2 types of STsegment depression shown in Fig. 2.15 are horizontal (plane depression) in D, and downsloping (sagging depression) in E. They are both abnormal and are seen in ischaemic heart disease. Before an ST segment depression is regarded as significant, it should be at least 1 mm in depth. In horizontal ST segment depression, there is, in addition, a sharp angle between the ST segment and the proximal limb of the T wave. This sharp angle ST-T junction is sometimes one of the earliest signs of coronary artery disease. It may be present even though the ST segment is not depressed. In this situation, the ST segment appears to hug the baseline giving an appearance of “horizontality” (Fig. 2.18).

Fig. 2.16 The ECGs (top and bottom panels) were recorded during treadmill exercise stress testing in a 34-year-old man. Top panel was recorded at rest and the bottom panel soon after exercise, in the recovery period. Arrowheads indicate J type ST segment depression.

23

V4

v5

V6

v5

V6

Fig. 2.17 “Digitalis effect”. Top panel was recorded in a patient before and bottom panel after the administration of digoxin. Note ST segment depression resembling the mirror image of the pass sign (/) in the bottom panel (arrowheads).

Fig. 2.18 “Horizontality” of the ST segment in a 62-year-old man with coronary artery disease which was confirmed by coronary angiography. Top panel was recorded at rest and is normal Bottom panel was recorded 15 minutes after the termination of an attack of chest pan. Note the sharp angle (arrow) between the ST segments and the proximal limbs of the T waves and

24

In a patient with stable angina, the ST segment depression is transient and is frequently present only during chest pain. If the history is typical of angina but the resting ECG is normal, the diagnosis of ischaemic heart disease cannot be excluded. Figures 2.19 and 2.20 show the ECGs of a patient with angina pectoris when he was having chest pain and when he was free of chest pain respectively.

I

v2

Vl

Zk'IiEE

aVL

aVF

VS

V6

v3

V4

Fig. 2.19 ECG was recorded in a patient with angina pectoris during an episode of chest pain. Note: ( 1 ) Marked horizontal ST segment depression in Vz, I and I1 (arrowhead in V2), (2) Marked downsloping ST segment depression in V3 to v6 (arrowhead in V3) associated with U wave inversion (arrow in V3),

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..

.......

........

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.

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aVR

aVL

aVF

v4

v5

V6

Fig. 2.20 Normal ECG recorded from the same patient whose ECG is shown in Fig. 2.19 during a pain-free period.

25

EXERCISE STRESS TEST In patients who are suspected of suffering from coronary artery disease but who have a normal resting ECG, an exercise ECG stress test should be done. This test may reveal ECG abnormalities (usually associated with angina) during exercise. In most laboratories or clinics, treadmill exercise stress test is performed using the Bruce protocol.1° Figure 2.21 is the treadmill exercise stress test ECG in a patient with angina and a normal resting ECG. During exercise, chest pain and marked ST segment depression were induced. Subsequent coronary angiography showed severe triple vessel disease. Figure 2.22 is the treadmill exercise stress test ECG of an asymptomatic 63-year-old woman. It shows marked, horizontal ST segment depression in multiple leads. No chest pain was noted during the test. Subsequent coronary angiography showed triple vessel disease (Figs. 2.24 and 2.25) indicating that the ST segment depression which was seen during the exercise stress test was indeed a reflection of “silent myocardial ischaemia”. After coronary artery bypass surgery was performed, the repeat treadmill exercise stress test ECG was normal, indicating an absence of myocardial ischaemia as a result of successful myocardial revascularization (Fig. 2.23). In recent years, Holter ambulatory ECG monitoring has also been frequently used to detect ST segment abnormalities, especially for the diagnosis of “silent myocardial ischaemia” and Prinzmetal’s angina.

RESTING

HYPERVENT

1

IMMEDIATE PE

8 MIN PE

26

10 MIN

PE

12 MIN PE

Fig. 2.21 Treadmill exercise stress testing in a 52-year-old man with angina pectoris. The patient experienced chest pain during Stage I of the Bruce exercise stress test protocol and the test was stopped. ECG was recorded using a modified V 5 lead. The resting ECG and that recorded after hyperventilation (HYPERVENT) are both normal. There is 3 mm ST segment depression (arrowhead) in Stage I. The following changes are seen in the post-exercise (PE) period. (1) Horizontal ST segment depression (arrowhead) and U wave inversion (arrow) in the immediate phase. (2) Downsloping ST segment depression (arrowhead) at 3 minutes. (3) Deeply inverted T wave (arrow) at 4 minutes. (4)“Horizontality” of the S T segment (arrowhead) and flat T wave at 10 minutes. ( 5 ) Normal ECG at 12 minutes.

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.

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.. - .... . .... . . . .. . .-. . .

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. . .

v2

..

. . .

v3

v4

.

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........

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V6

Fig. 2.22 12-lead ECG was recorded during treadmill exercise stress testing in a 63-year-old asymptomatic woman with familial hypercholesterolaemia. It shows the following: (i) The heart rate is about 15O/minute. (ii) Marked ST segment depression in V3 to v6, 11, 111 and aVF. The ST segment depression in V4 to v6 is horizontal and is about 2 mm deep (arrowheads in V5and V6). In the absence of chest pain, the ST segment depression could be interpreted as representing a false positive result. However, subsequent coronary angiogram revealed triple vessel disease (Figs. 2.24 and 2.25), thus indicating that the ST segment depression was truly a reflection of “silent myocardial ischaemia”

aVF

VI v2

v3

v5

V6

Fig. 2.23 12-lead ECG recorded at peak exercise during treadmill exercise stress testing in the same patient whose ECG is shown in Fig. 2.22, after successful coronary artery bypass surgery. It is now completely normal, indicating an absence of myocardial ischaemia.

27

Fig. 2.24 Left coronary angiogram (lateral view) in the same patient whose ECGs are shown in Figs. 2.22 and 2.23. Arrowhead indicates a discrete 99% stenosis of the left anterior descending artery (LAD). The circumflex artery is absent and was found to be totally occluded at operation. The patient’s right coronary angiogram is shown in Fig. 2.25.

Fig. 2.25 Right coronary angiogram in the left anterior oblique view. Arrowhead indicates a 50% discrete stenosis of the midright coronary artery (RCA).

28

UNSTABLE ANGINA Unstable angina is defined as a clinical syndrome which is between stable angina and acute myocardial infarction, with a wide variety of severity and presentation. In the more severe form, the patient presents with chest pain at rest and ST segment depression and/or T wave inversion in the ECG (Fig. 2.26). Pathological Q waves and elevated ST segments are not seen and the serum CK and CKMB levels are not elevated.

v1 v2

@ v3

VS

V6

Fig. 2.26 ECG of a 75-year-old woman with unstable angina recorded during an episode of chest pain occurring at rest. Note: (1) Marked ST segment depression in V2 to Vs (arrowheads in V3 and V4). (2) Tall P wave in I1 (“Ppulmonale”) reflecting co-existing chronic lung disease. (3) Complete right bundle branch block.

29

PRINZMETAL’S ANGINA Prinzmetal’s angina or variant angina is quite uncommon and is due to vasospasm of the coronary arteries which are either normal or are mildly or severely diseased. Such patients, unlike those with stable angina, usually experience chest pain spontaneously, especially in

II

I

Ill

aV R

aV L

aVF

Fig. 2.27 Prinzmetal’s angina in a 52-year-old man. ECG was recorded during a spontaneous attack of chest pain occurring at rest. Note: ( 1 ) ST segment elevation in I, I1 and aVL. (2) Reciprocal ST segment depression in 111, aVR, aVF and V1 to V3. (3) Deep T wave inversion in v4 to vg.

I

II

II I

aVR

aV L

Fig. 2.28 This ECG was recorded several minutes after Fig. 2.27, at a time when the chest pain had been relieved following sublingual glyceryl trinitrate administration. Note: (1) ST segments are now isoelectric. (2) Widespread, deep T wave inversion.

30

aV F

the early hours of the morning. The ECG recorded during an attack of chest pain will show elevated ST segments in certain leads, with reciprocal ST segment depression in the opposite leads, thus resembling very closely the “hyperacute phase” of transmural myocardial infarction. However, unlike acute myocardial infarction, the ECG quickly becomes normal when the chest pain subsides either spontaneously or following sublingual glyceryl trinitrate administration (Figs. 2.27,2.28 and 2.29). Cardiac arrhythmias such as frequent ventricular ectopic beats, ventricular tachycardia, ventricular fibrillation and atrioventricular (AV) block may all be encountered during an attack of Prinzmetal’s angina (Fig. 2.30).

I

I1

II I

V1

v2

v3

aV R

aV L

aV F

v5

Fig. 2.29 This ECG was recorded about 30 minutes after Fig. 2.27 and is essentially normal except for flat or isoelectric T waves in multiple leads. Coronary angiography showed severe triple vessel disease.

Fig. 2.30 Ventricular bigeminy during an attack of Prinzmetal’s angina. This ECG and Fig. 2.27 were recorded from the same patient. Note: ( 1 ) Elevated ST segment (arrowheads). (2) Ventricular ectopic beats (E) occurring in bigeminy.

31

U WAVE INVERSION In recent years, the importance of U wave inversion as a specific ECG marker of heart disease such as ischaemic, hypertensive and myocardial disease has been re-emphasized (Figs. 2.31,3.8 and 3.17). In ischaemic heart disease, U wave inversion is usually associated with ST segment depression (Fig. 2.19). However, it may rarely be the sole abnormality. Figure 2.32 was recorded in a 50-year-old man with stable angina. It shows isolated U wave inversion in leads V2 and V3. Subsequent coronary angiography showed critical stenosis of the proximal left anterior descending artery. In ischaemic heart disease patients showing U wave inversion in the mid- or left praecordial leads, the coronary arteries which are stenosed are nearly always the left main coronary artery or the left anterior descending artery. l1

A

6

C

Fig. 2.31 Diagram showing: (A) Normal upright U wave (arrowhead). (B) IsolatedU wave inversion (arrowhead). (C) U wave inversion (arrowhead) associated with ST segment depression (arrow).

I

II

111

aVR

aV L

aVF

Fig. 2.32 Isolated U wave inversion in a 50-year-old man with stable angina pectoris. U wave inversion, without ST segment depression, is seen in V2 and V3 (arrowheads). The axis is about -40' reflecting left anterior hemiblock. Coronary angiography showed a 99% narrowing of the proximal left anterior descending artery.

32

VENTRICULAR ECTOPIC BEATS The polarity of the T wave in ventricular ectopic beats is opposite to that of the QRS complex. It is therefore inverted when the ventricular complex shows a predominant R wave, and upright when it shows a predominant S wave. The ST segment blends smoothly and imperceptibly with the T wave whose 2 limbs are asymmetrical (Fig. 2.33). The following deviations in the morphology of the ventricular ectopic beat suggest underlying ischaemic or myocardial disease: (1) Deep and symmetrically inverted arrowhead T wave (Fig. 2.34); (2) T wave polarity identical to that of the qRS complex; (3) presence of a q wave in a ventricular ectopic beat with a predominant R or Rs complex (Fig. 2.35).

I

Fig. 2.33 “Benign” ventricular ectopic beats in a normal individual. Note the following characteristics of the ectopic beats. (1) The ST segments merge gently with the proximal limbs of the T waves. ( 2 )The T waves are opposite in polarity to the R waves or the S waves and their 2 limbs are asymmetrical. These features are best seen in the ventricular ectopic beats (E) in I1 and 111.

33

Fig. 2.34 This ECG is an enlargement of V3 in Fig. 2.12. Note deep and symmetrically inverted arrowhead T wave of the ventricular ectopic beat (E).

Fig. 2.35 ECG of a patient who had previously suffered a transmural myocardial infarction. Although the rS complex of the sinus beat is essentially normal except for a slightly coved ST segment, the ventricular ectopic beat (E) shows a pathological Q wave (arrowhead) indicating an old, transmural myocardial infarction.

Sometimes, the sinus beat immediately following either a ventricular or a supraventricular ectopic beat shows certain changes such as T wave inversion, ST segment depression or U wave inversion which are not present in the sinus beats preceding the ectopic beat (Figs. 2.36 and 5.13). All these changes suggest underlying ischaemic or myocardial disease. The postextrasystolic T wave changes have been termed by Levine as “poor man’s Master’s test”, since they indicate cardiac disease and the patient may thus be spared the cost of a formal exercise stress test.’* However, some investigators have suggested that post-extrasystolic T wave inversion is not specific for cardiac disease, claiming that it is also seen quite commonly in normal individ~a1s.l~ In the author’s experience, however, marked postextrasystolic T wave inversion is associated with ischaemic or myocardial disease in most instances.

34

Fig. 2.36 Post-extrasystolic T wave inversion. Note the inverted T wave (arrow) in the first postextrasystolic sinus beat. (E = ventricular ectopic beat).

ELECTROCARDIOGRAPHIC DIFFERENTIAL DIAGNOSIS OF ISCHAEMIC HEART DISEASE On the other side of the coin, there are many non-coronary causes of ST-T wave abnormalities. Table 2.1 lists the conditions which may produce ST segment depression and

TABLE 2.1* NON-CORONARY CAUSES OF ST-T WAVE ABNORMALITIES PHYSIOLOGICAL RACE, ADOLESCENCE PHARMACOLOGICAL DIGITALIS, ANTI-DEPRESSANT DRUGS PATHOLOGICAL CARDIAC VENTRICULAR HYPERTROPHY, MYOCARDITIS, CARDIOMYOPATHY EXTRA CARDIAC HYPOKALAEMIA, HYPOTHYROIDISM, INTRACRANIAL HAEMORRHAGE

ARTEFACTUAL FAULTY MACHINE (*Adapted from D Short. Br Heart J 1969; 31: 531-537 and withpermissionfforn the BMJ Publishing Group)

35

T wave abnormalities which may mimic ischaemic heart disease.I4 They must be excluded before myocardial ischaemia is diagnosed. Most of these abnormalities will be discussed in the next chapter.

ATRIAL INFARCTION Atrial infarction is reported to occur in about 17% of patients with infarction involving the ventricular myocardium in necropsy studies. However, in clinical practice, ECG evidence of atrial infarction is much less frequently encountered. The main ECG abnormality in atrial infarction is elevation of the PR segment as shown in Fig. 2.37.

1: -1; i 7;I ii 1

jI jj

: ; 1 : : :. . ., .. .. ..... , I:.:: . . . . , -. . . . . . . . . . . . .. .. . . ,. . . .... . . . . .. . . -. . . .

Fig. 2.37 Atrial infarction in a 70-year-old woman. Note: (1) Elevated PR segments in 11, I11 and aVF (arrowheads) reflecting atrial infarction. (2) Pathological Q waves, elevated ST segments and T wave inversion in 111 and aVF reflecting acute, transmural inferior infarction.

REFERENCES 1. Deedwania PC, Carbajal EV. Silent myocardial ischaemia. Arch Intern Med 1991; 151: 2373. 2. Source: The Singapore Myocardial Infarction Registry, Ministry of Health, Singapore. 3. Schamroth L. The 12 Lead Electrocardiogram. Blackwell Scientific Publications, Oxford, 1st ed., 1989; p. 145. 4. Fisch C. Electrocardiography. In Heart Disease edited by E Braunwald, W B Saunders Company, Philadelphia, 5th ed., 1997; p. 129. 5. Chou TC. Electrocardiography in Clinical Practice. WB Saunders Company, Philadelphia, 4th ed., 1996; p. 181. 6. Shah PK, Berman DS. Implications of precordial ST segment depressions in acute inferior myocardial infarction. Am J Cardioll981; 48: 1167.

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7. Wong CK, Freedman SB, Bautovich G, et al. Mechanism and significance of precordial ST segment depression during inferior myocardial infarction associated with severe narrowing of the dominant right coronary artery. Am J Cardiol 1993; 71:1025. 8. Reddy GV, Schamroth L. The electrocardiology of right ventricular myocardial infarction. Chest 1986; 90: 756. 9. Phibb B. “Transmural” versus “subendocardial” myocardial infarction: an electrocardiographic myth. J A m Coll Cardiol 1983; 1: 561. 10. Faris J, McHenry P, Stephen N. Concepts and applications of treadmill exercise testing and exercise electrocardiogram. Am Heart J 1978; 95: 102. 11. Gerson MC, McHenry PL. Resting U wave inversion as a marker of stenosis of the left anterior descending coronary artery. Am JMed 1980; 69: 545. 12. Levin HD, Lown B, Streeper RB. The clinical significance of post-extrasystolic T wave changes. Circulation 1952; 6: 358. 13. Engel TR. Postextrasystolic T wave changes and angiographic coronary disease. Br Heart J 1977; 39: 371.

37

CHAPTER 3

MISCELLANEOUS CONDITIONS

NORMAL VARIANT In 1954, Grusin from South Africa described certain distinctive ECG patterns which differed from the usual ECGs seen in the white population, but which were apparently quite common amongst the blacks.’ In his description, pattern I showed deeply inverted T waves (especially in the praecordial leads) simulating subendocardial infarction (Fig. 3.1). This pattern is very rare in the normal Asian population. In contrast, pattern 11, which is also known as the early repolarization syndrome or pattern, is seen in approximately 30% of young healthy males of Indian, Chinese and Malay ethnic rigi in.^.^ Here, there is elevation of the ST segment, concave upwards. The T wave is tall and asymmetrical with a gently sloped ascending limb and a sharp descending limb ending in a prominent U wave. These changes are most prominent in the mid- and left praecordial leads V2 to Vg. The QRS voltages in the left praecordial leads are also increased (Figs. 3.1 and 3.2). Unlike the “hyperacute phase” of transmural myocardial infarction, there is no reciprocal ST segment depression. It is important to recognize the early repolarization pattern because it may be mistaken for the “hyperacute phase” of transmural myocardial infarction, acute pericarditis, left ventricular hypertrophy and hyperkalaemia. The points of differentiation will be discussed in the sections below.

A

NORMAL

GRUSIN

I

GRUSIN

II

B

--TL-

A --T

--+

--

Fig. 3.1 Diagram showing normal ECG pattern and the Grusin pattern I and pattern I1 (early repolarization syndrome) normal variants. A = right praecordial lead, B = left praecordial lead.

Fig. 3.2 Early repolarization syndrome in a 61-year-old asymptomatic man. Note: (1) The ST segments are elevated (concave upwards) in Vz to V6 (arrowhead in V4) and they merge with very tall T waves (T = 17 mm in V4) . (2) Rightward displacement of the transition zone resulting in a positive QRS complex in V3. (3) Tall R waves in V4 to Vg.

39

ACUTE PERICARDITIS In acute pericarditis, there is widespread elevation of the ST segments (concave upwards). Frequently, ST segment depression is present only in lead aVR and the ST segment is isoelectric in lead aVL (Fig. 3.3). This is because in acute pericarditis, the ST segment vector in the frontal plane is directed towards lead 11, resulting in maximum ST segment elevation in this lead, isoelectric ST segment in lead aVL, and ST segment depression in lead aVR.4 In contrast, in the “hyperacute phase” of transmural, inferior myocardial infarction, the maximum ST segment elevation is very often in lead 111. Maximal elevation of the ST segment in lead 11, together with widespread ST segment elevation in the praecordial leads, also help to distinguish acute pericarditis from acute, transmural myocardial infarction and the early repolarization pattern. A further point of distinction between acute pericarditis and the early repolarization pattern is that the height of the T waves in the former is normal, whereas it is considerably increased in the latter. As a result of this, the ST/T ratio (i.e. the height of ST segment elevation divided by the amplitude of the T wave) in lead V6 and other left praecordial leads is >0.25 in acute pericarditis, and <0.25 in the early repolarization att tern.^ Lastly, in acute pericarditis, there is often depression of the PR segment which is frequently maximal in lead 11. The QRS voltages in patients with acute pericarditis, but without pericardial effusion, are normal.

..

.

III

I

v2

-utcI.

-.

- . . -.- ..

aV L

aV R

aVF

v3

Fig. 3.3 Acute pericarditis. Note: (1) Elevated ST segments (concave upwards) in V2 to y h ,11,111 and aVF (arrowheads). The ST segment elevation in the limb leads is maximal in 11. (2) ST segment depression in aVR (arrow). (3) Depressed PR segment in I1 (arrow). (4)Normal QRS and T wave voltages.

40

PERICARDIAL EFFUSION In large pericardial effusions, the QRS as well as the P wave and T wave voltages are all considerably diminished in all the limb and praecordial leads (Fig. 3.4). Occasionally, electrical alternans of the ventricular complexes (i.e. alternation of the height of the QRS complexes) is present, especially in very large, malignant pericardial effusions (Fig. 3.6). In recent years, echocardiography has enabled the diagnosis of pericardial effusion to be confirmed easily and accurately. Figure 3.5 is the two-dimensional echocardiogram of the patient whose ECG is shown in Fig. 3.4, demonstrating a very large pericardial effusion.

._ ......

....

Fig. 3.4 ECG of a 38-year-old woman with a very large pericardial effusion due to metastasis from carcinoma of the breast. The P,QRS, T wave voltages are all extremely small.

41

Fig. 3.5 Two-dimensional echocardiogram of the patient whose ECG is shown in Fig 3.4. The frame was recorded in the parasternal long-axis view in diastole. A large pericardial effusion (PE) is seen. Arrowhead indicates collapse of the right ventricle (RV) reflecting pericardial tamponade. In the real-time study, excessive movement of the heart in the pericardial cavity was noted indicating a “swinging heart”, which is an echocardiographic sign of a large pericardial effusion. (LA = left atrium, LV = left ventricle)

m

I aV R

v4

aV L

v5

aV F

V6

Fig. 3.6 Electrical alternans in a patient with a very large pericardial effusion. Note: (1) Low voltages of the P, QRS and T complexes. (2) Electrical alternans of the QRS complexes which is best seen in V, and V, (arrowheads).

42

VENTRICULAR HYPERTROPHY In left ventricular hypertrophy, tall R waves are seen in leads V5 and v6 and deep S waves in leads V1 and Vz. Many different criteria have been proposed for the diagnosis of left ventricular hypertrophy but none is entirely satisfactory.The most commonly used criterion states that SV, + RV5/RV6is greater than 35 mm. (Fig. 3.7). However, in a population of normal, young, asthenic males, this criterion is usually too sensitive, and a sum greater than 40 mm may be more appropriate. Furthermore, in the early repolarization pattern, the marked increase in left praecordial lead voltages frequently simulates left ventricular hypertrophy.

.. .L_._

...

j i

i

i

I

,

1--

i I

v1

v2

v3

V4

v5

V6

Fig. 3.7 Left ventricular hypertrophy in a 36-year-old man with severe rheumatic mitral regurgitation. Note: (1) Tall R wave in Vs (45mm) and deep S waves in Vl(32 mm) and V2 reflecting left ventricular hypertrophy. (2) Wide, bifid P waves ("P mitrale") in V2 and V, (arrowheads), and widening and slurring of the negative component of the biphasic Pwave in V, (arrowhead) reflecting left atrial enlargement.

43

In severe left ventricular hypertrophy, ST segment depression and T wave inversion accompany tall R waves in leads V5 and V6 - the so-called “left ventricular hypertrophy with strain” pattern. Unlike in ischaemic heart disease, T wave inversion in left ventricular hypertrophy is usually asymmetrical, with a distal limb which is steeper than the proximal limb (Fig. 3.8). The important causes of left ventricular hypertrophy are hypertension, valvular heart disease such as aortic stenosis, aortic regurgitation and mitral regurgitation, hypertrophic and dilated cardiomyopathy, ventricular septal -defect and patent ductus arteriosus.

I

v2 VI

v3

V6

Fig. 3.8 Left ventricular hypertrophy with strain in a 71-year-old man with severe uncontrolled hypertension of around 230/125 mmHg. The left ventricular hypertrophy was confirmed by twodimensional echocardiography. Note: (1) Very tall R waves in the left praecordial leads (R in V4 and V, = 42 mm and 40 mm respectively). (2) Deep S wave in V, (28 mm). (3) ST segment depression and deeply inverted and asymmetrical T waves in V4 to Vg. (arrowhead in Vs). (4) U wave inversion in V4 to V6 (arrow in Vs).

44

In right ventricular hypertrophy, tall R waves are seen in the right praecordial leads and deep S waves in the left praecordial leads. In lead V1, the amplitude of the R wave is greater than that of the S wave and frequently measures 7 mm or greater. As in left ventricular hypertrophy, ST segment depression and T wave inversion may accompany the tall R waves if the right ventricular hypertrophy is severe (Figs. 3.9 and 3.10). Very frequently, there is also right axis deviation. The important causes of right ventricular hypertrophy are pulmonary arterial hypertension which may be due to mitral stenosis, intracardiac shunts or chronic lung disease and congenital heart disease such as pulmonary stenosis and tetralogy of Fallot.

n I

fE v1

& aVR

aVF

aVL

V6

Fig. 3.9 Severe right ventricular hypertrophy and right atrial enlargement. Note: (1) Very tall R wave in V, (21 mm) associated with ST segment depression and asymmetric deep T wave inversion, and deep S wave in V5 (19 mm) and V6 (9 mm) reflecting right ventricular hypertrophy with strain. (2) Tall and peaked P wave in I1 (3.5 mm) (arrowhead) reflecting right atrial enlargement.

45

aV R

I aV L aV F

m

V?

v2

V6

v4

v5

v3 Fig. 3.10 Severe mitral stenosis with pulmonary hypertension in a 50-year-old woman. Note: (1) Left atrial enlargement as reflected by: (a) A wide (0.12 sec) and bifid P wave (“P mitrale”) in multiple leads, but especially prominent in I (arrowhead) and (b) Widening and slurring of the negative component of the P wave in V I (arrowhead). (2) Severe right ventricular hypertrophy as reflected by a very tall R wave in V 1 (18 mm) associated with ST segment depression and deep T wave inversion, a deep S wave in lead V6 (15 mm) and a right axis deviation of about +120°.

In 1952, Cabrera and Monroy introduced the overload concept for the ECG patterns of left and right ventricular hypertrophy.6 Systolic overload of the left ventricle occurs when it has to pump against an increased resistance in systole, as in systemic hypertension and aortic stenosis. The ECG manifestation of left ventricular systolic overload is reflected by the left ventricular hypertrophy with strain pattern described above (Fig. 3.8). Diastolic overload of the left ventricle occurs when it is overfilled in diastole, as in aortic and mitral regurgitation and ventricular septal defect. The ECG pattern of left ventricular diastolic overload is reflected by tall R waves which are preceded by deep but narrow q waves, isoelectric ST segments and tall T waves in the left praecordial leads (Fig. 3.7). Systolic and diastolic right ventricular overload patterns have also been described. The right ventricular systolic overload ECG pattern is as described above (i.e. tall R waves with ST segment depression and T wave inversion in the right praecordial leads) and is seen in pulmonary hypertension and pulmonary stenosis (Figs. 3.9 and 3.10). In contrast, a right ventricular diastolic overload pattern, classically seen in atrial septal defect, manifests as a right bundle branch block pattern. In bi-ventricularhypertrophy, various ECG patterns may be encountered. They include: (1) Tall R waves in the left praecordial leads (V, and V,) as well as in the right praecordial leads (V, and V2); and (2) Presence of right axis deviation despite ECG evidence of left ventricular hypertrophy.

46

ATRIAL ENLARGEMENT In left atrial hypertrophy or dilatation, the P wave is wide (greater than 0.12 sec in duration) and bifid in shape - the so-called “P mitrale” pattern. The time interval between the 2 peaks of the P wave is greater than 0.04 sec. These changes are often best seen in leads I and I1 and leads V4 to V6. In lead V1, the P wave is biphasic, with the negative component being widened and slurred (Figs. 3.7 and 3.10). Left atrial hypertrophy or dilatation is seen in mitral valve disease, hypertensive heart disease, ischaemic heart disease and cardiomyopathy. In right atrial hypertrophy or dilatation, the P waves, which are often best seen in the inferior leads 11, 111and aVF (especially lead 11) and also in the right praecordial leads V1 and V2, are tall and peaked - the so-called “P pulmonale” pattern because these abnormalities are commonly seen in chronic pulmonary disease. The height of the P wave is greater than 2.5 mm in lead 11, and greater than 1.5 mm in lead V1 (Figs. 3.9 and 3.14). The important causes of right atrial hypertrophy or dilatation are chronic obstructive lung disease, pulmonary stenosis, tetralogy of Fallot, pulmonary hypertension, Ebstein’s anomaly and tricuspid atresia. In bi-atrial hypertrophy or dilation, the P waves are both wide and tall.

vi

v2

v3

v4

v5

V6

Fig. 3.11 ECG of a 34-year-old man with severe mitral stenosis and left atrial dilatation confirmed by two-dimensional echocardiography. Note wide (0.12 sec) and bifid P waves in 1,II, 111, V4 to V6 (arrowheads in 11, V4 and V,) indicating “P mitrale”, which is a reflection of left atrial enlargement

47

ACUTE PULMONARY EMBOLISM The ECG changes in acute massive pulmonary embolism are many and varied. However, the classical ECG pattern is as follows: S1,Q3,T3 pattern (i.e. S wave in lead I, Q wave and inverted T wave in lead 111) Right axis deviation Transient right bundle branch block (usually incomplete) T wave inversion and ST segment elevation in the right praecordial leads V1 and V2 Clockwise rotation of the heart round its longitudinal axis, resulting in rS complexes in both the right and the left praecordial leads 6. “P pulmonale” 7. Sinus tachycardia.

1. 2. 3. 4. 5.

None of these taken alone is diagnostic of acute pulmonary embolism. Often, however, more than 1 of these abnormalities are seen (Fig. 3.12) and they are particularly significant if an ECG recorded in the recent past shows that they were previously a b ~ e n t . ~

v1 v2

f

@V6

v5

V3

Fig. 3.12 Acute massive pulmonary embolism.The patient was a 34-year-old woman who suddenly pattern. ~ The S wave in I and the q wave collapsed 1 day after caesarean section. Note: (1) S I . Q ~ , T in I11 are indicated by arrowheads and the inverted T wave in 111 by an arrow. ( 2 ) Incomplete right bundle branch block. (3) Clockwise rotation of the heart round its longitudinal axis resulting in rS complexes in V Lto V5.(4)Sinus tachycardia. Pulmonary angiography confirmed massive pulmonary embolism.

48

=I

w aVR

II

*4Q& .-

aV L

aVF

M ..

v5

V6

Vr,

Vl

v3 Fig. 3.13 This ECG was recorded subsequent to Fig 3.12, 4 days after successful pulmonary embolectomy. It is now essentially normal except for flat, isoelectric or mildly inverted T waves in multiple leads.

CHRONIC OBSTRUCTIVE LUNG DISEASE In chronic obstructive lung disease such as emphysema (Fig. 3.14), a distinctive ECG pattern is often seen: 1. “P pulmonale” 2. fight axis deviation 3. Clockwise rotation of the heart round its longitudinal axis, resulting in an rS pattern in leads V to V5or V 6 4. Low QRS voltages especially in the left praecordial leads 5 . “Lead I sign”, which is reflected by isoelectric P, QRS and T complexes in lead I.

I..

I

II

m

aVR

aV L

aVF

v1

v2

v3

V4

v5

V6

Fig. 3.14 Chronic obstructive lung disease. Note: (1) “Ppulmonale”. This is best seen in 11,111and aVE The P wave in I11 is peaked and measures 5 mm in height (arrowhead). (2) Clockwise rotation of the heart round its longitudinal axis resulting in rS complexes in V1 to V,. (3) Relatively low QRS voltages. (4)“Lead I” sign - isoelectric P, QRS and T complexes in I

49

CARDIOMYOPATHY There are many ECG abnormalities associated with the cardiomyopathies. In hypertrophic cardiomyopathy, the commonest ECG changes are left ventricular hypertrophy, ST and T wave abnormalities (Fig. 3.15) and pathological Q waves which are usually seen in the inferolateral leads8 (Fig. 3.16). In dilated cardiomyopathy, left ventricular hypertrophy and pathological Q waves (usually seen in the right and mid-praecordial leads) are frequently present (Fig. 3.17). The pathological Q waves in both hypertrophic and dilated cardiomyopathy are often misdiagnosed as old transmural myocardial infarction.

*P

aVF

II

m

aVR

aVL

v2 V6 .

v3

.

V5

Fig. 3.15 ECG was recorded in a 63-year-old woman with hypertrophic cardiomyopathy which was confirmed by two-dimensional echocardiography. Coronary angiography showed normal findings. Note tall R waves in V2 to Vs associated with ST segment depression and deep T wave inversion.

50

aV R

II

m

11

v1

aV L

V6

-trtt v2

aVF

v3

v4

v5

Fig. 3.16 Hypertophic cardiomyopathy. ECG of a 26-year-old woman with hypertrophic cardiomyopathy which was confirmed by two-dimensional echocardiography. Note pathological Q waves in 11,111, aVF, Vs and v6 (arrowheads). The Q waves in 111 and aVF are extremely deep.

m

I .... ...... . . .

aVR

aV L

aV F

. ... .,

v1 V6 v2

v3

Fig. 3.17 Dilated cadiomyopathy in a 46-year-old man. Note: (1) Very deep, pathological Q waves in V1 to V3. (2) Inverted U waves in V5 and v6 (arrowheads). (3) “P mitrale” in I (arrowhead). Twodimensional echocardiography and left ventricular angiography confirmed the diagnosis of dilated cardiomyopathy. Coronary angiography showed normal coronary arteries.

INTRACRANIAL HAEMORRHAGE Some of the most bizarre ECG changes are seen in patients with subarachnoid and intracranial haem~rrhage.~ These include deeply inverted and wide T waves or less commonly, prominent, upright T waves in the praecordial leads. The QT interval is also markedly prolonged (Fig. 3.18).

a VR

aV L

I

v1

v2

v3

v5

V6

Fig. 3.18 ECG was recorded in a 75-year-old woman with proven subarachnoid haemorrhage. Note: (1) T waves which are very deeply inverted and very wide in multiple leads but especially in V3 to V,. In Ill and aVF, the inverted T waves are bizarre looking. (2) The QTc interval (0.69 sec) is markedly prolonged. (3) The P waves are flat and abnormal looking indicating that they are most likely atrial in origin and the PR interval is very short (approximately 0.08 sec).

MYXOEDEMA In myxoedema (Fig. 3.19), the following changes are seen: 1. Sinus bradycardia 2. Widespread decrease in the voltages of the QRS complexes 3. Flat or inverted T waves.

HYPOKALAEMIA The ECG is a very useful tool for the diagnosis of both hypokalaemia and hyperkalaemia. As the serum potassium falls, the U wave becomes more prominent and the T wave becomes flatter.'OTherefore, an accurate sign of hypokalaemia is a U wave equal to or greater than the T wave in height (Fig. 3.20). In severe hypokalaemia, there is T wave inversion and ST segment depression. In this situation, an upright and prominent U wave can be mistaken for

52

I

I 1 1 1 aVR

aVL

aVF

v5

V6

v1

v4

Fig. 3.19 Myxoedema in a 62-year-old woman. Note: (1) Sinus bradycardia (56/min). (2) Low voltages of the QRS complexes. (3) Flat or isoelectric T waves.

a T wave and the ECG pattern may be easily misdiagnosed as ischaemic heart disease. It is possible to use the ECG to grossly estimate the degree of hypokalaemia. For example, if the U waves are taller than the T waves, the serum potassium is around 2.7 m E q L or less.

I

m

avt-

#I+#

EE i T = v1 v2

V6

v5

Fig. 3.20 Severe hypokalaemia (serum potassium = 1.6 mmoVL) in a 23-year-old man with thyrotoxic periodic paralysis who presented with weakness in all 4 limbs. Note: (1) Tall U waves (arrowheads) in multiple leads. In some leads (eg Vz, V3), the U waves are very prominent (4 mm in V3). (2) T wave inversion/ST segment depression in V1 and V2.

53

Fig.3.21 This normal ECG was recorded from the same patient whose ECG is shown in Fig. 3.20, at a time when treatment had restored the serum potassium to a normal level.

HYPERKALAEMIA The main ECG abnormality in hyperkalaemia is the presence of tall T waves. However, very tall T waves are also a hallmark of the early repolarization pattern. Just as important as the actual height of the T wave for the diagnosis of hyperkalaemia is its shape. In contrast to the early repolarization pattern, the T wave in hyperkalaemia is not only tall but also symmetrical, peaked, slender, scooped inwards and “tented”, resembling closely the Eiffel Tower in Paris (Fig. 3.22). With further elevation of the serum potassium, the QRS widens and the P wave disappears.

A J

v1

v3 v2

V4

v5

V6

Fig.3.22 Hyperkalaemia (serum potassium = 8.1 mmoVL) in a 53-year-old woman with chronic renal failure. Note that the T waves (arrowheads) are not only tall in V2 and V, (15 mm in V2), but are also unique in their morphology. They are narrow-based, slender, symmetrical and peaked, resembling the Eiffel Tower in Paris. This unique T wave morphology is also seen in V4, even though the amplitude of the T wave in this lead is not increased.

HYPOCALCAEMIA AND HYPERCALCAEMIA In hypocalcaemia, the QT interval is prolonged and this is due mainly to lengthening of the ST segment which hugs the baseline (Fig. 3.23). In hypercalcaemia, the QT interval is shortened. 54

aVR

I

LhlJ-caV L aV F

* v2

v5 v3

V6

Fig. 3.23 Hypocalcaemia (serum calcium = 1.71 mmoVL) in a 52-year-old man with chronic renal failure. Note that the QTc is prolonged (0.51 sec) and this is due mainly to prolongation of the ST segment which hugs the base-line (arrowheads in V5 and v6).

MITRAL VALVE PROLAPSE This common condition occurs in approximately 5 % of most populations. Electrocardiographicchanges such as T wave inversion or ST segment depression are often present in the inferolateral leads (Fig. 3.24).

I

II

II I

aVR

aV L

aVF

Fig. 3.24 Mitral valve prolapse. ECG of a 25-year-old woman with mitral valve prolapse which was confirmed by two-dimensional echocardiography. Note shallow T wave inversion in the inferolateral leads, 11, 111, aVF and Vq to v6 (arrowheads).

55

ATHLETE’S HEART SYNDROME In highly trained athletes, certain ECG changes are commonly seen. They include sinus bradycardia, first degree AV block and tall QRS voltages in the praecordial leads. In approximately 2% of cases, T wave inversion simulating ischaemic heart disease may also be seenll (Fig. 3.25).

* I

aVL

rn

,

,

/

aVR

I

a aVF

Fig. 3.25 Athelete’s heart. ECG of a 31-year-old male athlete. Note: (1) Tall R wave in V5 and very deep S wave in V,. ( 2 ) Deep T wave inversion in V4 to V,. In I1 and aVF, the T wave is less deeply inverted. (3) Sinus bradycardia (57/min). Two-dimensional echocardiography showed normal findings.

JUVENILE ECG PATTERN T wave inversion in leads V1 to V4 is usually present in the child (Fig. 3.26). After about 14 years of age, T wave inversion is uncommon beyond lead V1 in males and beyond leads V1 and V2 in females, except in the black population.

56

13 yrs.

v1

‘v2

v3

v1

v2

v3

18 yrs

v4

v5

Fig. 3.26 Juvenile ECG pattern. Top panel, which was recorded when the male was individual was 13 years old, shows deep T wave inversion in V1 to V3 (arrowheads). Bottom panel was recorded when he was 18 years old and shows disappearance of theT wave inversion except in Vi (arrowhead).

FLAT OR INVERTED T WAVES Flat or mildly inverted T waves often cause confusion as to their significance. Although ischaemic heart disease is frequently suspected, it is important to remember that such T wave changes are non-specific. Apart from ischaemic heart disease, mild T wave inversion may be seen in normal individuals (Fig. 3.27), in mitral valve prolapse (Fig. 3.24), and also in many situations such as hyperventilation, change in posture, drinkmg ice water, eating and emotional upset.

aVR

aVL

aVF

V1

v3 Fig.3.27 Shallow, non-specific T wave inversion from V1 to V6 (arrowheads) in an asymptomatic 60-year-old man. Coronary angiography showed minor, insignificant coronary artery disease and dobutamme stress echocardiography test was normal.

57

ISOLATED Q I11 Occasionally, the presence of a prominent Q wave in only limb lead I11 (QIII) poses a dilemma as to its diagnostic significance. Such a finding may be seen in normal people, but is also seen in old inferior myocardial infarction and acute pulmonary embolism. The QIII is likely to be abnormal if it is wide or if Q waves are also present in leads aVF and 11. Although disappearance or diminution of the Q wave in inspiration is a point in favour of it being benign, organic cardiac disease cannot be completely excluded as illustrated in Fig. 3.28.

I

v1

II

m

aVR

aVL

VS

aVF

V6

Fig. 3.28 ECG of a 60-year-old asymptomatic man showing a deep and wide pathological Q wave which is present only in I11 (arrowhead). The top and bottom panels of the rhythm strip shown below (recorded in lead 111) is continuous. Arrow indicates the beginning of deep inspiration which has resulted in a disappearance of the Q wave. Two-dimensional echocardiography shows hypokinesia of the inferior wall of the left ventricle, due most likely to a previous silent inferior infarction.

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DEXTROCARDIA In dextrocardia, the P and T waves are inverted and the QRS is negative in lead I. The P wave is also inverted in lead aVL but upright in lead aVR. Leads V1 to V6 show ventricular complexes of decreasing amplitude.A left ventricular complex pattern is seen in right-sided chest leads (Fig. 3.29).

v4

v5

V6

SL&$[

--

I_

I

v4 R

-

V6R

V7R

V5R

Fig. 3.29 Mirror-dextrocardia in a normal 17-year-old male with a normal heart. Note: (1) Inverted P wave, negative QRS complex and inverted T wave in I. ( 2 ) Inverted P wave in aVL and upright P wave in aVR. (3) rS pattern in V I to V3 (4) R waves in VSR, V& and V7R.

REFERENCE 1. Grusin H. Peculiarities of the African's electrocardiogram and the changes observed in serial studies. Circulation 1954; 9: 860. 2. Burns-Cox CJ, Lau LC, Toh BH. The electrocardiogram of healthy young Chinese and Malay men. J Electrocardiol 1971; 4: 211. 3. Chia BL. Personal unpublished observations. 4. Schamroth L. The 12 Lead Electrocardiogram, 1st ed., Blackwell Scientific Publications, Oxford, 1989; p. 294. 5. Ginzton LE, Laks MM. The differential diagnosis of acute pericarditis from normal variant: new electrocardiographiccriteria. Circulation 1982; 65: 1004. 6. Cabrera CE and Monroy JR. Systolic and diastolic loading of the heart. Am Heart J 1952; 43:66 1. 7. Sreeram N. Cheriex EC, Smeets J, et al. Value of the 12 lead electrocardiogramat hospital admission in the diagnosis of pulmonary embolism. Am J Cardiol 1994; 73: 298.

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8. Savage D, Seides S, Clark C, et al. Electrocardiographic findings in patients with obstructive and nonobstructive hypertrophic cardiomyopathy. Circulation 1978; 58: 402. 9. Burch GE, Meyers R, Abildskow JA. A new electrocardiographic pattern observed in cerebrovascular accidents. Circulation 1954; 9: 179. 10. Chou TC. Electrocardiography in Clinical Practice, 4th ed., WB Saunders Company, Philadelphia, 1996; p. 535. 11. Hanne Paparo N, Drory Y, Shoenfeld Y et al. Common ECG changes in athletes. Cardiology 1976; 61: 267.

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CHAPTER 4

CARDIAC ARRHYTHMIAS

INTRODUCTION Cardiac arrhythmias are frequently encountered in clinical practice. They must be diagnosed and carefully evaluated, especially as to their significance and whether treatment is required or not.

ASSESSMENT Two principles are of paramount importance: (1) The exact diagnosis of the cardiac arrhythmiamust be made. This is because different arrhythmias frequently have markedly different clinical significance. For example, a patient presenting with a regular tachycardia of about 170/min may have either supraventricularor ventricular tachycardia. Both these arrhythmiashave vastly different prognostic implications and require different therapeutic approaches.Although the clinical history and examination may provide clues about the arrhythmia, an ECG is necessary for precise definition.A 12-lead ECG together with a long “rhythm strip”, usually recorded in either leads II or V1, are invaluable. Identifying P waves is crucial because the temporal relationship of the P and QRS complexes often is the key to the exact diagnosis of the type of arrhythmia present. If P waves are not clearly identifiable, the oesophageal lead ECG (i.e. ECG recorded from an electrode placed in the oesophagus) can be done. P waves are greatly magnified in the oesophageal lead and are therefore clearly visible (Fig. 4.1). However, because of the inconvenience of this technique, it is today seldom performed. Since cardiac arrhythmias are often intermittent,they may not be detected in a routine recording of the 12-lead ECG. Twenty-four hour Holter ambulatory ECG monitoring

62

Fig. 4.1 Top panel shows ventricular tachycardia. There are no clearly visible P waves. Bottom panel was recorded at the same time as the top panel using an oesophageal lead (Oe. LD). Note that large, biphasic P waves (closed circles) are clearly seen. The ventricular complexes are labelled V.

Fig. 4.2 Holter ambulatory ECG monitoring in a patient who complained of palpitations. The top, middle and bottom panels were recorded at different times of the day. Top panel shows frequent, uniform ventricular ectopic beats, middle panel ventricular bigeminy and bottom panel ventricular ectopic beats occurring in pairs and in 3 consecutive beats.

63

is indicated if an arrhythmia is suspected but not confirmed in the routine ECG (Fig. 4.2). Exercise stress test can also be used to detect cardiac arrhythmias. In selected cases, an electrophysiological study is indicated especially in: (a) Cases of supraventricular tachycardia which are resistant to conventional pharmacological therapy; (b) Patients with sustained ventricular tachycardia or ventricular fibrillation in the absence of an acute myocardial infarction; and (c) Patients presenting with Stokes-Adams attacks (syncopal episodes caused by periods of cardiac arrest) who may have atrioventricular (AV) block or sinus arrest, but whose resting ECG or Holter ambulatory ECG recording fail to confirm these arrhythmias. In patients presenting with syncope, a tilt-table test is also useful. (2) The clinical setting in which a cardiac arrhythmia occurs is very important, especially in deciding whether treatment is necessary or not. For example, frequent ventricular ectopic beats in a person with a normal heart are completely benign and do not require treatment except when there are distressing symptoms. However, an identical arrhythmia in the background of severe left ventricular dysfunction usually connotes a significantly increased risk of ventricular fibrillation.

CLINICAL PRESENTATION The commonest clinical presentation of cardiac arrhythmias is palpitation, which is usually caused by ventricular ectopic beats or atrial fibrillation. Prolonged episodes of supraventricular tachycardia or rapid atrial fibrillation, especially in the background of heart disease, may lead to congestive heart failure or hypotension. Severe bradycardia, which may be seen in third degree (complete) AV block or the sick sinus syndrome, often results in giddiness, syncope or heart failure. Ventricular fibrillation, if uncorrected, will inevitably result in death. Indeed, the most common cause of “sudden death” is ventricular fibrillation. However, it is important to realize that many individuals with cardiac arrhythmias are asymptomatic and are unaware of their cardiac rhythm abnormalities. TABLE 4.1

CAUSES OF CARDIAC ARRHYTHMIAS (1) Coronary artery disease

(2) Hypertensive heart disease (3) Cardiomyopathy

(4) Valvular heart disease, e.g. rheumatic valvular heart disease, mitral valve prolapse

(5) Drugs - digitalis, quinidine, flecainide, amitriptyline, phenothiazines ( 6 ) Electrolyte disturbances e.g. hypokalaemia

64

AETIOLOGY Table 4.1 summarizes the common causes of cardiac arrhythmias. In every patient with a cardiac arrhythmia, a possible aetiology should always be sought for by a careful history, clinical examination, resting 12-lead ECG and chest X-ray. In selected cases, further investigations such as exercise stress test, echocardiography, myocardial perfusion scintigraphy and coronary angiography may be indicated. However, it is important to realize that in a significant number of cases, no cause may be found despite exhaustive investigations.

MANAGEMENT In many patients with cardiac arrhythmias, specific treatment may not be necessary. However, if treatment is required, one or more of the following therapeutic approaches may be employed:

(1) Physiological (a) Carotid sinus massage (b) Valsalva manoeuvre (2) Pharmacological Drugs commonly used in the treatment of cardiac arrhythmias are: (a) Atropine, digoxin and adenosine (b) Class I antiarrhythmic drugs such as quinidine, procaineamide (both Ia), lignocaine (Ib) and propafenone (Ic) (e) Class I1 drugs which are the beta-blockers (especially sotalol which has both beta-blocker as well as amiodarone-like properties) (f) Class I11 drugs such as amiodarone (g) Class IV drugs such as verapamil.

(3) Electrical (a) Cardioversion (b) Cardiac pacing (c) Radiofrequency catheter ablation (d) Implantable cardioverter-defibrillator In the last few years, it has become very clear that although many of the more potent antiarrhythmic drugs (e.g. Class Ic drugs such as flecainide) are extremely effective in suppressing cardiac arrhythmias, they are paradoxically also potentially proarrhythmic (i.e. they may aggravate preexisting arrhythmias or induce new arrhythmias), especially in patients with significant structural heart disease.’ Very recently, it has been shown that treatment with an implantable cardioverterdefibrillator can significantly reduce total mortality in patients who have been successfully resuscitated from cardiac arrest, as compared to antiarrhythmic drug therapy.2

65

~

REFERENCE 1. Garratt C, Ward D, Camm AJ.Lessons from the cardiac arrhythmia suppression trial. Br Med J 1989; 299: 805. 2. Kuck KH. Cardiac Arrest Study Hamburg (CASH). JAm Coll Curdiol 1998; 1: 1.

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CHAPTER 5

SUPRAVENTRICULAR ARRHYTHMIAS CLASSIFICATION OF CARDIAC ARRHYTHMIAS Table 5.1 is a simple classification of the cardiac arrhythmias. TABLE 5.1 CLASSIFICATION OF CARDIAC ARRHYTHMIAS SUPRAVENTRICULAR Sinus tachycardia Sinus bradycardia Sinus arrhythmia Sinoatrial block Sinus arrest Junctional (nodal) rhythm Junctional (nodal) escape beats Wandering pacemaker Supraventricular ectopic beats Supraventricular tachycardia Multifocal atrial tachycardia Accelerated junctional rhythm Atrial fibrillation Atrial flutter Wolff-Parkinson-White Syndrome VENTRICULAR Ventricular ectopic beats Ventricular tachycardia Accelerated idioventricular rhythm “Torsade de pointes” Ventricular flutter Ventricular fibrillation Idioventricular rhythm Ventricular asystole Ventricular parasystole BUNDLE BRANCH BLOCK AND ATRIOVENTRICULAR (AV) BLOCK Right and left bundle branch block Left anterior and left posterior hemiblock First, second and third degree AV block

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THE NORMAL CARDIAC RHYTHM Normally, the cardiac impulse arises from the sinoatrial node and the resting heart rate is around 70/min. In sinus tachycardia, the sinus rate exceeds 100/min and in sinus bradycardia, it is slower than 60/min.

(1) SINUS TACHYCARDIA Sinus tachycardia at rest is nearly always secondary to an underlying condition such as anxiety, heart failure, fever or thyrotoxicosis. The ECG shows regular, normal P waves which are usually between 100 to 140/min (Fig. 5.1). Management is directed towards treatment of the underlying condition. In cases of anxiety or thyrotoxicosis, beta-blockers are particularly effective in suppressing the tachycardia.

Fig. 5.1 Sinus tachycardia. The ECG was recorded in a 30-year-old woman during treadmill exercise stress test. The top panel was recorded at rest and shows a sinus rate of around 88/min. The bottom panel was recorded in the recovery period soon after termination of exercise and it shows a sinus tachycardia of around 149/min. Arrowheads in this ECG and in all other subsequent ECGs in Chapters 5 , 6 and 7 indicate sinus P waves unless stated otherwise.

Arrowheads in Fig. 5.1 and in all other subsequent ECGs in Chapters 5, 6 and 7 indicate sinus P waves unless stated otherwise.

(2) SINUS BRADYCARDIA Sinus bradycardia is common and may be found in health as well as in disease. The ECG shows normal P waves which are less than 60/min (Fig. 5.2). Physically fit individuals usually have slow resting heart rates of around 40 to 60/min due to a high degree of vagotonia. Sinus bradycardia may also be due to beta-blocker therapy, the sick sinus syndrome or digitalis intoxication.

Fig. 5.2 Sinus bradycardia. ECG of a 66-year-old man with previous myocardial infarction. The sinus bradycardia of around 53/min is due to beta-blocker therapy.

69

(3) SINUS ARRHYTHMIA In this arrhythmia, the sinus rate increases with inspiration and decreases with expiration (Fig. 5.3). Sinus arrhythmia is often a normal physiological phenomenon and is particularly accentuated in infants and young children.

Fig. 5.3 Sinus arrhythmia. There is marked variation in the sinus rate as it increases with inspiration (beats 1, 2, 3,6 and 7) and decreases with expiration (beats 4,5 and 8).

(4) SINOATRIAL BLOCK In sinoatrial block, there is sudden failure of either the sinoatrial node to discharge or the sinus impulse to be conducted to the atrium, resulting in absence of the P wave in the ECG (Fig. 5.4). The P-P intervals of the long pauses are multiples of the normal sinus cycle. For example, in a 2: 1 or a 3: 1 sinoatrial block, they are twice or three times the normal sinus cycle respectively. Sinoatrial block may be due to the sick sinus syndrome, digitalis intoxication, acute myocarditis or acute myocardial infarction. No specific treatment is required if the pauses are of short duration or if the patient is asymptomatic. However, if the pauses are long and especially if they are associated with syncope, cardiac pacing is indicated.

Fig. 5.4 2:1 sinoatrial block. The time interval is approximately 0.76 sec between the f i s t and second, fourth and fifth and fifth and sixth P waves and approximately 1.54 sec between the second and third and third and fourth P waves. The longer intervals are double the shorter intervals indicating a 2: 1 sinoatrial block. The following abbreviationsare used in this and all subsequent laddergrams in Chapters 5 , 6 and 7. SA = sinoatrial node, A = atrium, AV = atrioventricular node, V = ventricles.

The following abbreviations are used in the laddergram shown in Fig. 5.4 and in all subsequent laddergrams in Chapters 5, 6 and 7. SA = sinoatrial node, A = atrium, AV = atrioventricular node, V = ventricles. 70

Patients with the sick sinus syndrome may present with a wide variety of arrhythmias such as sinus bradycardia, sinoatrial block, and sinus arrest.’ In the “alternating bradycardiatachycardia syndrome”, which is another presentation of the sick sinus syndrome, periods of sinus bradycardia or sinus arrest alternate with episodes of rapid supraventricular tachycardia, atrial fibrillation or atrial flutter (Fig. 5.5). This condition is usually difficult to treat with drugs alone and frequently requires a combination of cardiac pacing and drug therapy.

4.9 sec Fig. 5.5 Alternating bradycardia - tachycardia syndrome in a 62-year-old woman who complained of syncope. The top and bottom ECG strips (non-continuous) are taken from a 24-hour Holter ambulatory ECG monitoring test. The top strip shows atrial fibrillation with a rapid ventricular rate, The bottom strip shows spontaneous termination of the atrial fibrillation. This is followed by a pause of about 4.9 sec due to sinus arrest. Arrowhead indicates a junctional escape beat.

Sinus arrest is sometimes due to the hypersensitive carotid sinus syndrome. In this condition, massage of the carotid sinus, or sometimes mere movement of the head, may cause sinus arrest and syncope (Fig. 5.6).

CSM

Fig. 5.6 Hypersensitive carotid sinus syndrome in a 64-year-old man who presented with recurrent syncope. ECG shows: (1) A pause of 4.6 sec due to sinus arrest induced by gentle carotid sinus massage (CSM) (2) Atrial escape beat (E).

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(5) JUNCTIONAL (NODAL) RHYTHM In junctional rhythm, normal P waves are absent and inverted P waves are seen instead in leads 11,111,V5 and Vg. The P wave is upright in lead aVR. The abnormal P waves may either precede, be buried within, or come after the QRS complexes which have a normal morphology (Figs. 5.7 and 5.8). Junctional rhythm is seen in normal individuals, particularly in those who are physically fit and have increased vagotonia.

I

II

III

aVR

v1

v2

v3

v4

aVL

V6

Fig. 5.7 Junctional rhythm. Note: (1) Inverted P waves in 11,111, aVF (arrowheads) and V2 to Vg, (2) Upright P wave in aVR (arrowhead).

12

Fig. 5.8 Junctional rhythm. Lead I1 of the same ECG which is shown in Fig 5.7. Arrowheads indicate inverted P waves due to retrograde depolarization of the atria.

(6) JUNCTIONAL (NODAL) ESCAPE BEAT In patients with sinus bradycardia, sinoatrial block or sinus arrest, the depression or absence of sinus activity may allow the emergence of a subsidiary pacemaker in either the atria, AV junction or the ventricles, resulting in what is termed as an escape beat (Fig. 5.9).

I

Fig. 5.9 Junctional escape beat. Note: (1) The interval between the third and fourth, fourth and fifth and fifth and sixth P waves is double the interval between the first and second and the second and third P waves, indicating a 2:1 sinoatrial block. (2) Junctional escape beats (J). (3)AV dissociation.

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(7) WANDERING PACEMAKER In this arrhythmia which is frequently associated with sinus bradycardia, multiple atrial escape beats are seen (Fig. 5.10). Wandering pacemaker is a benign arrhythmia and is usually seen in normal individuals.

Fig. 5.10 Wandering pacemaker. Top and bottom panels are continuous. Arrowheads indicate sinus P waves and arrows indicate atrial escape beats.

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(8) SUPRAVENTRICULAR ECTOPIC BEATS Supraventricular ectopic beats may arise in either the atrium or the AV node junction, giving rise to atrial or junctional (nodal) ectopic beats. They may be unifocal or multifocal. Figure 5.11 shows unifocal supraventricular ectopic beats occurring in bigeminy while Fig. 5.12 shows multifocal supraventricular ectopic beats. A supraventricular ectopic beat may be conducted normally or with aberrant ventricular conduction (Fig. 6.3), a phenomenon which is discussed in Chapter 6. A very premature supraventricular ectopic beat may not be conducted, and if there is a complete compensatory pause, a 2: 1 sinoatrial block is closely simulated (Fig. 5.13). Supraventricularectopic beats usually occur in normal individuals and require no treatment. They may also be seen in mitral valve disease and cor pulmonale. In these 2 conditions, frequent supraventricular ectopic beats may lead to atrial fibrillation, atrial flutter or atrial tachycardia.

Fig. 5.11 Unifocal atrial ectopic beats occurring in bigeminy. Note: (1) Premature and inverted P waves which are indicated by arrowheads. (2) The atrial ectopic beats occur in bigeminy after the first ectopic beat - rule of bigeminy. (3) The compensatory pause is almost complete.

Fig. 5.12 Multifocal atrial ectopic beats. Note: (1) Different coupling intervals and morphologies of the 2 atrial ectopic beats (arrowheads). (2) Incomplete compensatory pause.

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Fig. 5.13 Blocked atrial ectopic beat (arrow). Note: (1) Complete compensatory pause. (2) Postectopic ST segment depression. The ST segment of the first sinus beat after the blocked atrial ectopic beat is more deeply depressed and more horizontal (arrowhead) than the ST segments of the other sinus beats, indicating the possibility of ischaemic or myocardial disease.

(9) MULTIFOCAL ATRIAL TACHYCARDIA (CHAOTIC ATRIAL MECHANISM) In this arrhythmia, normal sinus rhythm is replaced by a variety of atrial beats. The following features distinguish multifocal atrial tachycardia from multifocal atrial ectopic beats: (1) P waves of at least 3 different morphologies; (2) Varying P-P intervals; (3) Varying P-R intervals; and (4)Absence of a dominant pacemaker (Fig. 5.14). The commonest cause of multifocal atrial tachycardia is chronic obstructive lung disease.2

Fig. 5.14 Multifocal atrial tachycardia in a 71-year-old man with heart failure. Top and bottom panels are continuous. Note: (1) P waves of multiple morphologies. (2) Varying P-P intervals. (3) Varying PR intervals. (4) Absence of a dominant pacemaker.

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(10) SUPRAVENTRICULAR TACHYCARDIA Supraventricular tachycardia is a common arrhythmia and comprises several distinct entities: (1)AV nodal re-entranttachycardia; (2)AV reciprocating tachycardia (associated with the Wolff-Parkinson-White syndrome); (3) Atrial tachycsrdia; and (4) Junctional (nodal) tachycardia. Of these, AV nodal re-entrant tachycardia is the most common and is usually seen in individuals who have no organic heart disease. It can be divided into 2 varieties: (1) The slow-fast variety; and (2) The considerably rarer fast-slow variety. Like AV nodal re-entrant tachycardia, AV reciprocating tachycardia is also very common. Atrial tachycardia is much less common and junctional tachycardia is very rare.

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v3 Fig. 5.15 SupraventricularAV nodal re-entrant tachycardia in a 35-year-old woman who presented with palpitations. Note: (1) Regular, narrow QRS tachycardia of around 200/min. (2) No P waves are visible. Subsequent electrophysiological study confirmed that the patient was suffering from supraventricularAV nodal re-entrant tachycardia.

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The ECG in supraventricular tachycardia shows regular, narrow QRS complexes at a rate of around 170/min or more. Electrical alternans of the QRS complexes may sometimes be seen during the tachycardia (Fig. 5.21). In AV nodal re-entrant tachycardia of the slow-fast variety, the P waves are usually hidden because they are buried within or appear just after the QRS complexes (Fig. 5.15). In AV reciprocating tachycardia, the P waves are clearly visible as they occur shortly after the QRS complexes, with the RP interval being shorter than the PR interval (Fig. 5.16). In atrial tachycardia, each QRS complex is preceded by a P wave which is different in morphology from the normal sinus P wave, with the RP interval being longer than the PR interval3 (Fig. 5.18).

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V6 Fig. 5.16 Supraventricular reciprocating tachycardia associated with the Wolff-Parkinson-White syndrome in a 34-year-old man presenting with palpitations. Note: (1) Regular, narrow QRS tachycardia of around 166/min. (2) Clearly visiblepwaves in V1 (arrowheads), 11, I11 and aVE They occur soon after the QRS complex resulting in a RP interval which is much shorter than the PR interval.

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Fig. 5.17 This ECG was recorded from the same patient whose ECG is shown in Fig. 5.16 after termination of the supraventricular tachycardia. Note the Wolff-Parkinson-White syndrome ECG pattern as reflected by: (1) Short PR interval (about 0.08 sec). (2) Wide QRS complex ( 0.12 sec). (3) Delta waves in Vq. V5, Vs (arrowheads), I, I1 and aVL.

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Fig. 5.18 Recurrent atrial tachycardia in a 2-month-old baby. Note: (1) Regular, narrow QRS tachycardia of around 225/min. (2) Clearly visible Pwaves (arrowheads in V,) (3) RPinterval equal to or longer than PR interval.

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The ECG during and after an attack of supraventricular tachycardia may show ST segment depression which may persist for several hours or days. The latter is known as the “posttachycardia syndrome”. Although these ECG changes may mimic ischaemic heart disease, many such patients have normal coronary arteries and no known cardiac disease. Attacks of supraventricular tachycardia may be frequent (e.g. weekly), or infrequent (e.g. yearly), and each episode may be transient (e.g. a few minutes), or prolonged (e.g. a few hours). In the initial management of supraventricular tachycardia, a vagotonic stimulus such as carotid sinus massage or the valsalva maneouvre is employed. If this is unsuccessful and if the attack is prolonged, pharmacological therapy is often required. Intravenous adenosine (6-12 mg) or verapamil (5-10 mg) are the 2 drugs of ~ h o i c e The . ~ rate of conversion to sinus rhythm is approximately 90% in AV nodal re-entrant tachycardia and AV reciprocating tachycardia, but much lower in atrial tachycardia. If the supraventricular tachycardia is resistant to drug therapy, or if the patient presents with hypotension or heart failure, cardioversion is indicated. The need for long term prophylactic drug treatment depends largely on the frequency and the severity of presentation of the attacks. The most common drugs that are used for this purpose are: (1) Digoxin, beta-blockers (especially sotalol) or verapamil in AV nodal re-entrant tachycardia and atrial tachycardia; and (2) Beta-blockers (especially sotalol) and a Class I drug such as procaineamide in AV reciprocating tachycardia. In recalcitrant cases of AV nodal re-entrant tachycardia or AV reciprocating tachycardia, radiofrequency catheter modification of the AV node or ablation of the accessory pathway respectively is strongly indicated.

(11) WOLFF-PARKINSON-WHITE (WPW) SYNDROME The WPW syndrome is seen in approximately 0.1% to 0.3% of the general population. The PR interval is shortened to
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The commonest arrhythmia in the WPW syndrome is an AV reciprocating tachycardia, with the cardiac impulse travelling anterogradely down the AV node and retrogradely through the accessory pathway (Fig. 5.16). This arrhythmia is also known as AV reciprocating orthodromic tachycardia as opposed to the much less common antidromic tachycardia where the impulse travels anterogradely down the accessory pathway and retrogradely through the AV node. Atrial fibrillation is infrequent in the WPW syndrome. Here, the ECG shows an irregular rhythm and the QRS complexes are variably widened, depending on how much of the ventricle has been depolarized via the accessory pathway (Fig. 5.19). If the ventricular rate is very rapid, there is a significant risk of ventricular fibrillation6. Drugs that impede conduction through the AV node (e.g. digoxin, verapamil or beta-blockers) are contraindicated as they will result in more impulses passing through the accessory pathway. As a result of this, the ventricular rate will be even faster, thus further increasing the risk of ventricular fibrillation. Intravenous procaineamide is the drug of choice in atrial fibrillation associated with the WPW syndrome. If this drug is inefficacious, cardioversion should be performed.

I

11

v1

v2

Fig. 5.19 Atrial fibrillation in a 22-year-old man with the WPW syndrome. Note: (1) Irregular rhythm and very rapid ventricular rate. (2) The QRS complexes are variably widened.

81

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Fig. 5.20 Type B WPW syndrome. ECG was recorded 15 minutes after Fig. 5.19, after the arrhythmia was converted with intravenous disopyramide. Note: (1) Short PR interval (about 0.10 sec). (2) Delta waves in V2 to Vg. I and aVL, (arrowheads). (3) Pathological Q waves in 111, aVF and VI, simulating myocardial infarction.

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Fig. 5.21 Supraventricular tachycardia in a 16-year-old man. Note: (1) Regular, narrow QRS tachycardia of around 2141min. (2) Clearly visible Pwaves in V, (arrowheads). (3) Electrical alternans of the QRS complexes which is best seen in V4 (arrowheads).

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A variant of the WPW syndrome is the Lown-Ganong-Levine (LGL) syndrome which consists o f (1) Short PR interval; (2) Normal QRS complex; and (3) Supraventricular tachyarrhythmias (Figs. 5.21 and 5.22).

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Fig. 5.22 This ECG was recorded from the same patient whose ECG is shown in Fig. 5.21, after termination of the supraventricular tachycardia. Note the Lown-Ganong-Levine (LGL) ECG pattern, as reflected by a short P-R interval (about 0.10 sec) and a normal QRS complex.

(12) ACCELERATED JUNCTIONAL RHYTHM (NON-PAROXYSMAL JUNCTIONAL TACHYCARDIA) This arrhythmia is due to acceleration of the junctional pacemaker. The ECG shows normal QRS complexes at a rate of approximately 100/min. Since the junctional rate is faster than the sinus rate, the ventricles are depolarized by the junctional pacemaker and the atria by the sinoatrial node. Depolarization of the ventricles and the atria by 2 different pacemakers at different rates results in the phenomenon of atrioventricular (AV) dissociation. A sinus P wave, which occurs fortuitously at a time when the AV node is nonrefractory, will be conducted anterogradely to depolarize the ventricles, giving rise to a sinus capture beat (Fig. 5.23). Accelerated junctional rhythm is seen in acute myocardial infarction, digitalis intoxication, acute myocarditis and after cardiac surgery. It is usually a transient arrhythmia and requires no specific treatment.

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Fig. 5.23 Accelerated junctional rhythm. Note: (1) Accelerated junctional pacemaker rate of 83/ min. (2) AV dissociation. (3) Sinus capture beat (C). Laddergram illustrates mechanism of AV dissociation and sinus capture.

(13) ATRIAL FIBRILLATION Atrial fibrillation is a very common arrhythmia. The most important aetiologies are mitral valve disease, thyrotoxicosis, ischaemic heart disease, hypertension and congestive heart failure of any cause. In those cases where no aetiology can be found, the patient is diagnosed as having “idiopathic atrial fibrillation”. The ECG in atrial fibrillation shows no P waves but instead fibrillary “f” waves, which result in an undulating baseline, are seen (Fig. 5.24) Atrial fibrillation is described as fine or coarse depending on the size of the “f” waves. If these “f” waves closely resemble atrial flutter waves but are not completely regular, the ECG is described as showing “flutter fibrillation”. The ventricular rate in undigitalized patients is usually rapid and may vary between 140 to 180/min, and the rhythm is totally irregular (Fig. 5.25). Digoxin, a beta-blocker or verapamil is used to reduce the ventricular rate in rapid atrial fibrillation by decreasing conduction in the AV node. Excessively slow ventricular rates in undigitalized patients suggest co-existing disease of the AV node. One of the most important complications of atrial fibrillation is systemic thromboembolism, resulting in a stroke. The risk of this complication is considerably increased when the atrial fibrillation is associated with cardiac disease or in elderly patient^.^ In such high risk patients, anticoagulant therapy is indicated if there are no contraindications.

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Fig. 5.24 Atrial fibrillation in a 36-year-old woman with severe rheumatic mitral regurgitation. Note: (1) Totally irregular rhythm and a rapid ventricular rate of around 134/min. (2) No P waves are seen. They are instead replaced by fibrillary ("f") waves.

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A

B

C

Fig. 5.25 Atrial fibrillation. Panel A is the ECG of a 36-year-old woman with rheumatic mitral stenosis. It shows atrial fibrillation with a very rapid ventricular rate. Panel B was recorded from the same patient after digitalization. The ventricular rate is now excessively slow, due to too much digoxin. Panel C, which was recorded from a 60-year-old man, shows atrial fibrillation with third degree (complete) AV block. The ventricular rate is very slow (3l/min) and regular. Panel D is the ECG of a 26-year-old man with rheumatic mitral and aortic valve disease. The “f” waves are much bigger in amplitude compared to those in Panels A to C. This type of atrial fibrillation is termed “coarse atrial fibrillation” in contrast to the atrial fibrillation in panels B and C which can be described as “fine atrial fibrillation”.

(14) ATRIAL FLUTTER Atrial flutter is considerably less common than atrial fibrillation. The causes of atrial flutter and atrial fibrillation are somewhat similar. The ECG in atrial flutter is characteristic and is reflected by “saw-tooth” “F” waves. These are most apparent in leads I1 and 111. However, in lead V1, discrete P waves are very often seen (Fig. 5.26). The ventricular rate, as well as the regularity of the rhythm, depends on the ratio of AV conduction. Atrial flutter is particularly difficult to diagnose if there is a 2: 1 AV conduction, because the “F’waves may not be apparent when they are buried within the T waves or QRS complexes. Carotid sinus massage or intravenous adenosine may reveal the concealed “F” waves by increasing the AV conduction ratio (Fig. 5.27). However, a good clue to the diagnosis of atrial flutter with 2:l AV conduction is a regular tachycardia with narrow QRS complexes at a rate of 150/min. This is because the “F’waves in atrial flutter are usually at a rate of around

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300/min, and a 2: 1 AV conduction will thus result in a ventricular rate of 150/min. In patients with atrial flutter who have been given quinidine or other class I anti-arrhythmic drugs, the rate of the "F" waves may be markedly reduced (Fig. 5.28). As in atrial fibrillation, digoxin, a beta-blocker or verapamil are the drugs of choice if the ventricular rate is rapid. However, atrial flutter is easily terminated by low energy cardioversion, and this method of treatment is frequently employed if the arrhythmia is persistent.

m aVR

aVF

v1 v3

v4

V6

Fig. 5.26 Atrial flutter. Note: (1) Rapid (about 280/min), saw tooth, flutter ("F") waves in 11, I11 and aVF'(arrowheads in the bottom rhythm strip). (2) The ventricular rate is around 70/min due to 4: 1 AV conduction.

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Fig. 5.27 Atrial flutter with 2: 1 AV conduction. During 2: 1 AV conduction, the flutter (“F’)waves are hidden as they are buried within the QRS complexes and the ST/T wave segments. They are evident only when the AV conduction ratio is increased resulting in a slower ventricular rate (arrow). Arrowheads indicate flutter (“F’)waves.

Fig. 5.28 Top panel, which was recorded in 11, shows atrial flutter with 4:l AV conduction. The flutter (“F”) waves are clearly seen and have a saw-tooth appearance (arrowheads). The rate of the “F’waves is unusually slow (214/min). In the bottom panel, which was recorded in V1, discrete P waves are seen (arrowheads) and the AV conduction ratio is variable.

REFERENCE 1. Belic N, Talano JV. Current concepts in sick sinus syndrome. Arch Intern Med 1985; 145: 722. 2. Kastor J. Multifocal atrial tachycardia. N Engl J Med 1990; 322: 1713. 3. Wu D, Denes P, Amat-Y-Leon F, et al. Clinical, echocardiographic and electrophysiologic observations in patients with paroxysmal supraventricular tachycardia. A m J Cardioll978; 41: 1045. 4. Ganz L, Friedman P. Supraventricular tachycardia. N Engl J M e d 1995; 332: 166. 5. Rosenbaum FF,Hecht HH, Wilson FN, Johnston FD. The potential variations of the thorax and the esophagus in anomalous atrio-ventricular excitation (Wolff-Parkinson-White syndrome). A m Heart J 1945; 29: 281. 6. Klein GJ, Bashore T, Sellers T, et al. Ventricular fibrillation in the Wolff-Parkinson-White syndrome. N Engl J M e d 1979; 301: 1080. 7. Lip GVH, Lowe G. Antithrombotic treatment for atrial fibrillation. Br Med J 1996,312: 45. 88

CHAPTER 6

VENTRICULAR ARRHYTHMIAS

Ventricular arrhythmias are common and frequently present a challenge as well as a dilemma to the clinician.

(1) VENTRICULAR ECTOPIC BEATS (VENTRICULAR EXTRASYSTOLES, PREMATURE VENTRICULAR CONTRACTIONS) Ventricular ectopic beats are commonly seen and they often present as palpitations. However, it is important to know that many people with frequent ventricular ectopic beats are completely asymptomatic. The ECG recognition of a ventricular ectopic beat depends on the following criteria: (1) It occurs prematurely (2) The widened and bizarre-looking QRS complex is not preceded by a premature P wave ( 3 ) The compensatory pause is usually complete. The compensatory pause is described as being “complete” when the interval between the 2 sinus beats flanking an ectopic beat is equal to 2 sinus cycles, and “incomplete” when it is shorter (Figs. 5.12, 6.1 and 6.2). A complete compensatory pause results when the sinoatrial node is not discharged by an ectopic beat and the sinus cycle is not reset, whereas an incomplete compensatory pause is seen when the sinoatrial node is prematurely discharged. Frequently, the compensatory pause following a ventricular ectopic beat is complete, whereas that following a supraventricular ectopic beat is incomplete, but there are many exceptions to this rule. The main differential diagnosis of a ventricular ectopic beat is a supraventricular ectopic beat with aberrant ventricular conduction - a term used to describe a supraventricular beat which is conducted to only 1 ventricle because of transient bundle branch block. This phenomenon occurs because the refractory periods of the 2 bundle branches are frequently unequal. The right bundle branch usually has a longer refractory period compared to the left.

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A late supraventricular beat will be conducted through both bundle branches because they will have fully recovered from the previous depolarization. A very early supraventricular beat will find both bundle branches refractory and the impulse will be blocked. A supraventricular beat of intermediate prematurity may find 1 bundle branch (usually the right bundle branch) still refractory, while the other has recovered fully. This beat will be conducted through the recovered branch, giving rise to a ventricular complex with a bundle branch block pattern. This phenomenon is termed “aberrant ventricular conduction”. Although the QRS complex is widened in a supraventricular ectopic beat with aberrant ventricular conduction, it is less bizarre looking than a ventricular ectopic beat, being frequently triphasic (rSr’) in morphology, thus closely resembling a right bundle branch block pattern (Fig. 6.3). A longer preceding R-R interval increases the refractory period of the bundle branches, thus

Fig. 6.1 This ECG is the second panel of Fig. 6.5. It shows frequent uniform ventricular ectopic beats. Arrows indicate P waves which have resulted from retrograde depolarization of the atria. Arrowheads indicate sinus Pwaves. Note that the compensatory pause is incomplete. This is because the ventricular ectopic beats are conducted retrogradely through the AV node and across the atria to the sinoatrial node which is prematurely discharged. This results in a resetting of the sinus cycle.

Fig. 6.2 This ECG is the third panel of Fig. 6.5. Note: (1) Multiform ventricular ectopic beats. (2) AV dissociation. (3) Complete compensatory pause.

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favouring aberrant ventricular conduction for the same degree of prematurity. This phenomenon is termed the “Ashman’s phenomenon” (Fig. 6.4).

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Fig. 6.3 Atrial ectopic beats with aberrant ventricular conduction. Arrow indicates atrial ectopic beat and arrowheads, sinus P waves. Note: (1) Ventricular complex following each atrial ectopic beat has a right bundle branch block morphology. (2) Incomplete compensatory pause.

Fig. 6.4 Ashman’s phenomenon. ECG shows a run of supraventricular tachycardia which terminates spontaneously for a brief period before it is resumed. The ventricular complex labelled with an arrow shows a right bundle branch block morphology due to aberrant ventricular conduction, although it is not earlier than all the other ventricular complexes which are normally conducted. This is because it is preceded by a longer R-R interval. This phenomenon is known as the “Ashman’s phenomenon”.

Figure 6.5 shows the Lorn’s grading system for ventricular ectopic beats which is widely used.2The grading is as follows: Grade 0 -none; Grade 1 - occasional (<30/hour); Grade 2 - frequent (230/hour); Grade 3 - multiform; Grade 4A - 2 consecutive ventricular ectopic beats (couplets); Grade 4B - 3 or more consecutive ventricular ectopic beats; Grade 5 “R on T”.

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.

Fig. 6.5 Lown’s grading system of ventricular ectopic beats. Grade 1 = uniform and infrequent (e30/hr). Grade 2 = uniform and frequent (30 or >/hr). Grade 3 = multiform. Grade 4A = 2 consecutive beats (pairs or couplets). Grade 4B = 3 or more consecutive beats. Grade 5 = “R on T”.

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Uniform ventricular ectopic beats have the same coupling interval (i.e. the interval between the ectopic beat and the preceding sinus beat) and morphology. Multiform ventricular ectopic beats have different coupling intervals and morphologies, indicating that they arise from different foci. “R on T” ventricular ectopic beats occur very prematurely at the apices or the downslope of the T waves of the preceding sinus beats. The risk of ventricular fibrillation becomes greater with increasing grades of ventricular ectopic beats. For example, Grade 1 ventricular ectopic beats are usually benign. On the other hand, there is a high risk of ventricular fibrillation in patients with grade 5 (“R on T”) ventricular ectopic beats, especially in those with early acute myocardial infarction, hypokalaemia or the prolonged QT syndrome (Fig. 6.6).

Fig. 6.6 “R on T” ventricular ectopic beats and ventricular fibrillation in a patient with acute inferior infarction. Note: (1) “Hyperacute” changes of transmural inferior infarction as reflected by raised ST segment in 11. (2) “R on T” ventricular ectopic beats (E) initiating ventricular fibrillation (VF).

The first ventricular ectopic beat sometimes starts a run of ventricular bigeminy. This is because the compensatory pause which follows results in a longer R-R interval preceding the next sinus beat, and this encourages the emergence of another ventricular ectopic beat. This phenomenon is called the “rule of bigeminy” which is seen in both ventricular as well as supraventricular ectopic beats (Fig. 5.11). Figure 6.7 shows a case of ventricular bigeminy.

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Fig. 6.7 Ventricular bigeminy. Note: (1) Uniform ventricular ectopic beat (arrowheads in V, and V,) follows every sinus beat resulting in ventricular bigeminy. (2) ECG inside the left hand box was recorded before exercise and shows ventricular bigeminy. ECG inside the right hand box was recorded during exercise. It shows sinus tachycardia and a complete suppression of the ventricular ectopic beats.

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The following arrhythmias occurring either alone, or especially in combination, are highly suggestive of digitalis intoxication: (1) Unifocal but multiform ventricular ectopic beats (Fig. 6.8) - these ventricular ectopic beats have identical coupling intervals but different morphologies, implying that they may have arisen from the same focus but have varying intraventricular conduction; (2) Atrial tachycardia with block (Fig. 6.9); (3) Mobitz type I (Wenckebach phenomenon) second degree and third degree AV block with narrow QRS complexes; (4)Accelerated junctional rhythm; ( 5 ) Sinoatrial block; (6) Bidirectional ventricular tachycardia. This very uncommon arrhythmia is nearly always due to digitalis intoxication. The ECG shows alternation in the polarity of the ventricular complexes (Fig. 6.10).

Fig. 6.8 Unifocal, multiform ventricular ectopic beats in a patient with digitalis intoxication. Note the constant coupling interval but varying morphologies of the ventricular ectopic beats (arrowheads).

Fig. 6.9 Digitalis intoxication. The patient, an elderly man with previous anterior infarction, presented with deterioration of his heart failure. ECG shows atrial tachycardia with 2: 1 AV block and ventricular ectopic beats (E). Arrowheads indicate atrial P waves.

Ventricular ectopic beats may be due to coronary artery, hypertensive and valvular heart disease (especially mitral valve prolapse), cardiomyopathy, digitalis intoxication and hypokalaemia. However, they are also frequently seen in individuals who have no heart disease. In every patient presenting with ventricular ectopic beats, a careful assessment is always necessary. It is important to remember that the significance of any type of ventricular

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I

I1

111

aVR

aVL

aVF

Vl

v2

v3

V4

v5

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Fig. 6.10 Bidirectional tachycardia in a 58-year-old woman with digitalis intoxication. Note that the polarity of the consecutive QRS complexes is alternately positive and negative in all the leads except for V1 and Vz.

ectopic beat depends greatly on whether it is associated with a normal or a diseased heart. An appropriate analogy is that of the relationship between seed and soil. For a seed to blossom, fertile soil is necessary. Similarly, for ventricular ectopic beats to degenerate into ventricular fibrillation, a diseased heart is nearly always required. In the presence of a normal heart, ventricular ectopic beats, whatever their grade and however frightening they may appear, are mere cosmetic blemishes in the ECG and do not require any treatment except when the patient is distressed by symptoms such as severe palpitations. On the other hand, in patients with cardiac disease (especially in those with severe left ventricular dysfunction) and ventricular ectopic beats which are frequent, multiform, consecutive or “R on T”, the risk of ventricular fibrillation or sudden death is considerably increased. Unfortunately however, the results of antiarrhythmic drug therapy in this group of patients have generally been very disappointing mainly because of the proarrhythmic effects of these drugs.3 However, if drug therapy is considered necessary, amiodarone should be given. This recommendation is based largely on a very recent meta-analysis study which showed that amiodarone was beneficial when given to high risk patients with recent myocardial infarction or with congestive heart fai1u1-e.~

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(2) VENTRICULAR TACHYCARDIA Ventricular tachycardia is defined as 3 or more consecutive ventricular ectopic beats (4B in Lown’s grading of ventricular ectopic beats). It is described as sustained when it lasts longer than 30 sec and nonsustained when it is shorter. The 1Zlead ECG in ventricular tachycardia shows widened and bizarre looking QRS complexes at a rapid rate of between 140 to 200/rnin5 (Figs. 6.11 and 6.12). The ECG differentiation of ventricular tachycardia from supraventricular tachycardia with aberrant ventricular conduction is important and is usually possible, but requires some experience and skill. The points in favour of ventricular tachycardia are:

AV dissociation (Fig. 6.11) An indeterminate QRS axis (Fig. 6.12) “Concordant pattern” which means that the polarity of all the QRS complexes in the praecordial leads is either positive or negative (Fig. 6.13) Sinus capture beats with narrow QRS morphology, in the midst of rapid and wide ventricular complexes (Fig. 6.1 1) Fusion beats (Fig. 6.11).

Fig. 6.11 Ventricular tachycardia in a patient with acute myocardial infarction. Note: (1) Regular, wide QRS tachycardia of around 166/min. (2) The QRS morphology superficially resembles a left bundle branch pattern, except that the r waves in V1 and V2 (arrowheads) are broad thus favouring ventricular ectopy. (3) The rhythm strip in the lower part of the ECG shows fusion beats (arrowheads) which are of different morphologies. There is also a suggestion of AV dissociation, because some corresponding parts of the STm wave segments of the consecutive ventricular complexes have slightly different morphologies and appear deformed, due most likely to the superimposition of P waves occurring at a rate which is different from that of the QRS complexes.

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Fig. 6.12 Ventricular tachycardia. Note: (1) Rapid ventricular rate of 158/min. (2) Regular and wide (0.16 sec) QRS complexes. (3) Monophasic R wave in V1. (4)rS complex in V5 and Vg. ( 5 ) Indeterminate axis of approximately -170'.

99

On the other hand, the ECG in supraventricular tachycardia with aberrant ventricular conduction frequently shows a 1:l P-QRS relationship (i.e. one P wave to every QRS complex) and widened QRS complexes with a right bundle branch block morphology (Fig. 6.14).

Fig. 6.13 Ventricular tachycardia showing the concordance pattern. Note: (1) Regular, wide QRS tachycardia (190/min). (2) All the QRS complexes in the praecordial leads from V, to V6 are negative in polarity.

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Fig. 6.14 Supraventricular tachycardia with aberrant ventricular conduction induced in the electrophysiological laboratory in a 25-year-old man presenting with palpitations. Note: (1) Rapid heart rate of 160/min. (2) Regular and wide QRS complexes (0.12 sec) with a typical right bundle branch block configuration (triphasic rSR pattern in Vl). (3) No clearly visible P waves.

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Fig. 6.15 This normal ECG was recorded subsequent to Fig 6.14, after the termination of the tachycardia.

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Fig. 6.16 Supraventricular tachycardia with aberrant ventricular conduction. The top and bottom panels are not continuous. Top panel shows atrial ectopic beat (arrow) with aberrant ventricular conduction. Bottom panel shows atrial ectopic beat (arrow) initiating an episode of supraventricular tachycardia (either AV nodal re-entrant tachycardia or reciprocating tachycardia). Arrowheads indicate inverted P waves occurring after every QRS complex due to retrograde depolarization of the atria. During the supraventricular tachycardia, beats 1 to 10 show a widened QRS complex due to aberrant ventricular conduction. However, beats 11 to 16 show normal ventricular conduction.

Unfortunately, AV dissociation is seen in only about 50% of cases and an indeterminate QRS axis, sinus capture beats, fusion beats and a concordant pattern are all seldom present, being seen in approximately less than 5% of cases. Because of this, there has been much emphasis in recent years on the analysis of the morphology of the ventricular complexes in the 12-lead ECG, especially in leads V1 and v6. A ventricular complex with a right bundle branch block pattern and particularly a triphasic pattern in lead V1, strongly favours supraventricular tachycardia with aberrant ventricular conduction (Fig. 6.14). On the other hand, both a monophasic R wave or a diphasic qR complex in lead V1 and a rS or QS complex in lead v6, strongly favour the diagnosis of ventricular tachycardia6 (Fig. 6.12). When the QRS complexes show a left bundle branch block pattern, both ventricular tachycardia and a supraventricular tachycardia with aberrant ventricular conduction (presenting with the much less common manifestation of a left bundle branch block) have to be considered. A wide r wave and a slow S wave descent in leads V 1 N 2 and a qR pattern in lead V6 both strongly favour the diagnosis of ventricular tachycardia (Fig. 6.1 1). Sustained ventricular tachycardia is usually associated with coronary artery or myocardial disease. It is a serious condition since it may deteriorate to ventricular fibrillation. Intravenous lignocaine is the drug of choice. If this is ineffective, intravenous procaineamide should then be given. If there is no response to pharmacological therapy, cardioversion is necessary (Fig. 6.17) 102

Fig. 6.17 Successful cardioversion (arrow) in a patient with ventricular tachycardia.

(3) ACCELERATED IDIOVENTRICULAR RHYTHM This variant of ventricular tachycardia is known by several names such as “accelerated idioventricular rhythm” and “slow ventricular tachycardia”. It is usually seen in patients with acute myocardial infarction associated with sinus bradycardia. The ECG resembles the classical type of ventricular tachycardia except for a slow ventricular rate of around 50 to 1lO/min. Fusion beats (i.e. ventricular complexes due to simultaneous depolarization of the ventricles by both the sinus as well as the ventricular ectopic beats) are common at the beginning and end of each episode of accelerated idioventricular rhythm (Fig. 6.18). These fusion beats have varying morphologies intermediate between the sinus and ventricular ectopic beats. Accelerated idioventricular rhythm is a benign arrhythmia and requires no treatment as it is usually transient and well tolerated.

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Fig. 6.18 Accelerated idioventricular rhythm. Note: (1) Termination and onset of accelerated idioventricular rhythm. (2) AV dissociation. (F = fusion beat).

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(4) “TORSADE DE POINTES” Recently, the importance of a unique ventricular tachycardia known as “torsade de pointes” or “polymorphic ventricular tachycardia” is r e ~ o g n i z e d In . ~ this arrhythmia, the QRS complexes appear to twist and turn, resulting in their apices being positive and negative for a few beats at a time (Fig. 6.19). “Torsade de pointes” is usually associated with a prolonged QT interval due to either type Ia and Ic antiarrhythmic drugs such as quinidine or flecainide, hypokalaemia, or certain non-cardiac drugs such as the phenothiazines. Continuation of these drugs will aggravate the arrhythmia, which is best treated by intravenous magnesium and temporary cardiac pacing. If hypokalaemia is present, it must be promptly corrected.

Fig. 6.19 “Torsade de pointes”. Note the twisting and turning of the QRS complexes resulting in their apices being positive and negative for a few beats at a time.

(5) VENTRICULAR FLUTTER Ventricular flutter is characterized by: (1) A very rapid ventricular rate of around 260 to 300/min; (2) Undulation of the QRS complexes; (3) No differentiation of the QRS or the T complexes (Fig. 6.20). If left uncorrected, it frequently degenerates into ventricular fibrillation.

Fig. 6.20 Ventricular flutter in a terminally ill patient with stroke. Note: (1) Rapid ventricular rate of about 286/min. (2) Undulation of the QRS complexes. (3) No differentiation of the QRS and T complexes.

(6) VENTRICULAR FIBRILLATION Ventricular fibrillation is the most serious of all cardiac arrhythmias because it results in cardiac arrest. It is the commonest cause of “sudden death”. Irreparable brain damage results if cardiopulmonary resuscitation or termination of the arrhythmia is not attempted within 3 to 4 minutes. Immediate defibrillation is crucial and if successful, should be followed by an intravenous infusion of lignocaine. The ECG in ventricular fibrillation shows completely irregular and chaotic deflections of varying amplitude and shape (Figs. 6.6 and 6.21).

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Very recently, it has been shown that treatment with an implantable cardioverterdefibrillator can decrease total mortality in patients who have been successfully resuscitated from cardiac arrest as compared to antiarrhythmic drug therapy. This mode of therapy should therefore be considered in all such very high risk patients.

Fig. 6.21 Ventricular fibrillation in a patient with acute myocardial infarction. All 3 panels are continuous. After cardioversion (arrow in bottom panel), sinus rhythm was restored.

(7) IDIOVENTRICULAR RHYTHM AND VENTRICULAR ASYSTOLE In idioventricular rhythm, there is an extreme bradycardia with very wide and bizzare looking QRS complexes and absence of P wavesiIn ventricular asystole, only a straight line is seen (Fig. 6.22). Both these arrhythmias usually represent the final expression of a dying heart and resuscitative measures are often unsuccessful.

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Fig. 6.22 Idioventricular rhythm and ventricular asystole in a terminally ill patient. Top and bottom panels are non-continuous. Top panel shows idioventricular rhythm. Note: (1) Absence of P waves. (2) Very wide and bizarre looking QRS complexes with an extremely slow ventricular rate (36/min). Bottom panel, which was recorded a little later, shows a straight line reflecting ventricular asystole.

105

(8) VENTRICULAR PARASYSTOLE This is an uncommon arrhythmia which is seen in patients with diseased hearts and very rarely in normal individuak8The ventricular ectopic pacemaker is protected from the sinus beats and discharges regularly on its own. The following are the criteria for diagnosis: (1) Coupling intervals which are widely variable (2) Inter-ectopic intervals which are multiples of a common denominator (3) Fusion beats (Fig. 6.23).

Fig. 6.23 Ventricular parasystole in an asymptomatic 16-year-old male who has no cardiac disease. All 3 panels are continuous and were recorded in V1. Closed circles indicate parasystolic beats which are manifested in the ECG.Open circles indicate parasystolic beats which have occurred during the refractory period of the ventricles and are therefore not manifested. Note: (1) Widely varying coupling intervals of the parasystolic beats. (2) The inter-ectopic intervals are all multiples of a common denominator - 1.88 sec. (3) Fusion beats (F) which are indicated by half closed circles.

REFERENCE 1. Marriot HJ, Sandler I. Criteria, old and new, for differentiating between ectopic ventricular beats and aberrant ventricular conduction in the presence of atrial fibrillation. Prog Curdiovusc Dis 1966; 9: 181. 2. Lown B, Wolf M. Approaches to sudden death from coronary heart disease. Circulation 1971; 43:130. 106

3. CAST Investigators. Preliminary report: effect of encainide and flecainide on mortality in a randomised trial of arrhythmia suppression after myocardial infarction. N Engl JMed 1989; 321: 406. 4. Amiodarone Trials Meta-analysis Investigators. Effect of prophylactic amiodarone on mortality after acute myocardial infarction and in congestive heart failure: meta-analysis of individual data from 6520 patients in randomised trials. Lancet 1997; 350: 1417. 5 . Schamroth L. Ventricular extrasystoles, ventricular tachycardia, and ventricular fibrillation: clinical-electrocardiographic considerations. Prog Cardiovas Dis 1980; 23: 13. 6. Wellens HJ,Bar FW,Lie KI. The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex. Am JMed 1978; 64: 27. 7. Cleland J, Krikler D. Torsade de pointes: chaos, sixteen years on? Br Heart J 1992; 67:1. 8. Myburgh OP, Lewis BS. Ventricular parasystole in healthy hearts. Am Heart J 1971; 82: 307.

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CHAPTER 7

BUNDLE BRANCH BLOCK, HEMIBLOCK AND ATRIOVENTRICULAR (AV) BLOCK

The conducting system of the heart comprises the AV node and the bundle of His which divides into a right and a left bundle branch. The right bundle branch is a discrete structure from its origin to its termination, but the left bundle branch quickly divides into an anterior (superior) and a posterior (inferior) fascicle (Fig. 7.1). The infra-Hisian portion of the conducting system is therefore essentially trifascicular, consisting of the right bundle branch and the anterior and posterior fascicles of the left bundle branch.

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BUNDLE

FASCICLE

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108

Block in conduction may be at the level of either the AV node, bundle of His, right or left bundle branch or the 2 fascicles of the left bundle branch, occurring singly or in different combinations. An isolated lesion of either the anterior or posterior fascicle of the left bundle branch is termed a hemiblock. The combination of right bundle branch block and either left anterior or posterior hemiblock is termed bifascicular block, because 2 of the 3 fascicles of the conducting system are involved.' (1) BUNDLE BRANCH BLOCK The ECG in right bundle branch block shows: (1) Widened ventricular complexes with either an M (RsR') or a triphasic (rSR') pattern and secondary T wave inversion in leads V1 and V,; (2) Widened and slurred S waves in leads Vg, V6 and I (Figs. 7.2 and 7.3). The right bundle branch block is described as being complete if the width of the QRS complex is 0.12 sec or greater, and incomplete if it is less than 0.12 sec. The axis in isolated right bundle branch block is normal. An axis greater than -30" or.+ 120"indicates co-existing left anterior and posterior hemiblock respectively (Figs. 7.4 and 7.5).

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Fig. 7.2 Diagram showing the morphologies of the ventricular complexes in right bundle branch block (top panel) and left bundle branch block (bottom panel). Note: (1) Top panel. rSR and M pattern in V1 are seen in A and B respectively. C shows widening and slurring of the S wave (arrowhead) in Vg. D shows rSr' pattern in V1. Arrowhead indicates r' wave. (2) Bottom panel. Monophasic (QS)and rS ventricular complexes in V, are seen in Aand B respectively. Widened and slightly notched R wave and M shaped R wave in V, are seen in C and D respectively.

Right bundle branch block is seen in atrial septal defect (about 90% of cases and usually the incomplete variety), acute myocardial infarction, ischaemic and hypertensive heart disease, degenerative disease of the conducting system and after operation for tetralogy of Fallot and ventricular septal defect. Complete right bundle branch block also occurs in approximately 0.2%of the general population.

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Fig. 7.3 Complete right bundle branch block in an 80-year-old woman with hypertension. Note: (1) rSR pattern in V1. The QRS complex is 0.12 sec in width (2) Widening and slurring of the S wave in V5, v6, I and aVL (arrowheads in v5 and I).

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Fig. 7.4 Complete right bundle branch block and left anterior hemiblock in a patient with acute anterior infarction. Note: (1) RsR pattern in V1. The QRS is 0.12 sec in width. ( 2 )The axis is about -55", reflecting left anterior hemiblock. (3) ST segment elevation in V1 to V5 (arrowheads in V2 and V,) and deep pathological Q waves in Vg, v6 and I reflecting acute, transmurd anterior infarction.

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Fig. 7.5 Complete right bundle branch block and left posterior hemiblock in a 53-year-old man with acute myocardial infarction. Note: (1) Elevated ST segments and pathological Q waves in V1 to V4 reflecting acute, transmural anterior infarction. (2) qR pattern in V1 to V3 and widening and slurring of the S wave in I (arrowhead) reflecting right bundle branch block. The QRS complex is widened to 0.12 sec. (3) The axis is about +150" reflecting left posterior hemiblock.

It is important to recognize the rSr' pattern in lead V1, caused by a secondary wave (r') which is usually either lower or similar in height to the r wave (Figs. 7.2 and 7.6). The duration of the QRS complex is normal or borderline. This ECG abnormality is seen in 2 to 5% of the normal population, in subjects with pectus excavatum or the straight back syndrome, and in acute pulmonary embolism. The rSr' pattern may also be an expression of incomplete right bundle branch block.2

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Fig. 7.6 rSr' pattern in a 57-year-old asymptomatic woman. The ECG inside the box is an enlargement of V 1 in the 12-lead ECG. Note: (1) The height of the r' wave (arrowhead) is less than that of the r wave in V,. (2) The QRS complex is not widened.

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In left bundle branch block, the widened ventricular complexes are usually monophasic and slightly notched in leads V5 and V6. Less commonly, they are M shaped. There is also secondary ST segment depression and T wave inversion and an absence of q waves in these 2 leads. The right praecordial leads (i.e. leads V1 and V,) usually show deep Q waves and less commonly, rS complexes (Figs. 7.2 and 7.7). As with right-bundle branch block, left bundle branch block may either be complete (20.12 sec) or incomplete (e0.12 sec). Left bundle branch block seldom occurs in normal people. The common causes are acute myocardial infarction, ischaemic and hypertensive heart disease, dilated cardiomyopathy and degenerative disease of the conducting system.

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v1

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Fig. 7.7 Complete left bundle branch block in a 67-year-old woman. Note (1) Wide M shaped QRS complex (0.16 sec) with an absence of q wave in V5 and Vg. (2) rS pattern in V, and V2.

(2) HEMIBLOCK Left anterior hemiblock is diagnosed when the left axis deviation is greater than -30". There is also a positive terminal r wave in lead aVR. The width of the QRS complex is either normal or minimally widened (Fig. 7.8). Left posterior hemiblock is considerably less common than left anterior hemiblock and it is also more difficult to diagnose with confidence. The diagnosis can be made if the axis is greater than +120°, but right ventricular hypertrophy and a vertical heart (both of which can cause this degree of right axis deviation) must first be excluded. The causes of hemiblock and bundle branch block are similar.

112

aVR

aV F

Fig.7.8 Left anterior hemiblock. Note: (1) Axis of approximately -45". ( 2 ) Positive terminal r wave in aVR (arrowhead). (3) QRS complex is narrow.

(3) ATRIOVENTRICULAR (AV) BLOCK Atrioventricular block may be either first, second or third degree (complete AV block). In first degree AV block, every P wave is conducted.The PR interval is constant and is prolonged beyond 0.20 sec. It is commonly seen in fit, healthy individuals and no specific treatment is required. First degree AV block is also seen in patients with acute inferior infarction and in patients who are on beta-blockers or digoxin (Fig. 7.9).

Fig. 7.9 Fist degree AV block in a 56-year-old woman with acute inferior infarction. Note: (1) "Hyperacute phase of transmural inferior infarction as reflected by elevated ST segment. (2) Prolonged PR interval of 0.28 sec.

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Second degree AV block can be divided into Mobitz type I (Wenckebachphenomenon), Mobitz type 11,2:1 and high grade AV block? In Mobitz type I AV block, the ECG shows progressive prolongation of the PR interval, culminating in a dropped QRS complex, following which the whole sequence is repeated (Fig. 7.10). It may occur in highly trained athletes because of excess vagotonia and also in patients with acute inferior infarction or digitalis intoxication. The site of block is nearly always at the AV node and the prognosis is good.

Fig. 7.10 Mobitz type I second degree AV block (Wenckebach phenomenon) in a patient with acute inferior infarction. Note: (1) Pathological Q wave, slightly elevated and coved ST segment, and T wave inversion reflecting the “resolution phase” of transmural inferior infarction. (2) Progressive prolongation of the PR interval culminating in non-conduction of the fourth P wave, following which the whole sequence is repeated.

In Mobitz type II AV block, the conducted beats show a constant PR interval and there is sudden failure of P wave conduction. The QRS complexes frequently show a bundle branch block pattern (Fig. 7.1 1). The lesion is very often at the bundle branches and the prognosis is considerably less favourable than Mobitz type I AV block, as it frequently proceeds to complete AV block and ventricular standstill! The two common causes of Mobitz type 11 AV block are anterior myocardial infarction and degenerative disease of the conducting system.

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Fig. 7.11 Mobitz type I1 second degree AV block. Note: (1) Constant PR interval of 0.16 sec. (2) Sudden failure of conduction of the sixth P wave. (3) Wide QRS complexes.

In 2: 1 AV block, every second P wave is not conducted. In high grade AV block, the AV conduction ratio is 3: 1 or higher. If the 2: 1 AV block or high grade AV block has followed a Wenckebach sequence and if the QRS complexes are narrow, the block is very often at the AV node. On the other hand, if the QRS complexes are widened or if a Mobitz type I1 AV block has preceded the 2: 1 or high grade AV block, the lesion is very frequently at the level of the bundle branches (Fig. 7.12).

Fig. 7.12 2: 1 second degree AV block. Note: (1) Every second P wave is blocked. (2) The conducted beats show a constant PR interval of 0.12 sec. (3) The QRS complexes show a complete right bundle branch block pattern. The site of the block is most likely at the level of the bundle branches.

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In third degree or complete AV block, there is a failure of conduction of all the P waves. Third degree AV block may be due to a lesion at the AV node or the bundle branches. In the latter case, all 3 fascicles of the conducting system are blocked and the situation is essentially a trifascicular block. If the block is at the AV node as in inferior infarction or congenital heart block, the escape pacemaker is situated at the AV junction and the QRS complexes are narrow. The ventricular rate, which is often around 50 to 60/min, can frequently be increased with intravenous atropine and Stokes-Adams attacks are uncommon (Fig. 7.13). Cardiac pacing is usually unnecessary, except when the patient presents with Stokes-Adams attacks or heart failure, or when the ventricular rate is less than 40/min in an asymptomatic patient. On the other hand, in third degree (complete) AV block due to trifascicular block, the escape pacemaker is situated within the ventricles. The QRS complexes are widened and the ventricular rate, which is often very slow at around 30 to 40/min, usually cannot be increased with intravenous atropine. Stokes-Adams attacks are frequent and cardiac pacing is usually necessary (Figs. 7.14 and 7.15). Common causes of trifascicular block are acute anterior infarction, chronic degenerative disease of the conducting system, chronic ischaemic heart disease, post-cardiac surgery and acute myocarditis.

Fig. 7.13 Third degree (complete) AV block in acute inferior infarction. This ECG was recorded a few hours later than Fig 7.9. Note: (1) Failure of conduction of all the P waves (2) Slow ventricular rate of 46/min (3) Narrow QRS complexes.

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Fig. 7.14 ECG of a patient presenting with third degree (comp1ete)AV block. The aetiology of the AV block most likely was idiopathic degeneration of both the bundle branches. Note: (1) Failure of conduction of all the P waves. (2) Very slow ventricular rate of 33/min. (3) Wide QRS complexes.

Fig. 7.15 ECG of a 16-year-old male with acute viral myocarditis. The ECG in the upper box shows third degree (complete) AV block, wide QRS complexes and a very slow ventricular rate of around 4O/min. The ECG rhythm strips in the lower box are continuous and show third degree (complete) AV block and ventricular standstill resulting in syncope (Stokes Adams attacks) and convulsons which have caused artifacts in the ECG (arrow).

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In patients with third degree (complete) AV block who require cardiac pacing, either temporary cardiac pacing or implantation of a permanent pacemaker may be performed. If the complete AV block is temporary as most often is the case in acute inferior myocardial infarction, only temporary cardiac pacing is required. However, if it is chronic, which is frequently so in degenerative disease of the bundle branches, a permanent cardiac pacemaker will be required to be implanted. In patients with pacemakers employing the ventricular mode of pacing, the ECG shows spikes (due to ventricular pacemaker inpulses) which are immediately followed by widened QRS complexes (Fig. 7.16). In dual chamber pacing, each P wave is preceded by an atrial spike and this is followed, after a pre-set interval, by a ventricular spike which depolarizes the ventricles (Fig. 7.17).

Fig. 7.16 Ventricular pacing in a patient with third degree (complete) AV block. Note: (1) Pacemaker spikes (arrows). (2) Wide QRS complex following each pacemaker spike because of asynchronous depolarization of the 2 ventricles. Arrowheads indicate sinus P waves.

Fig. 7.17 Dual chamber pacing. Note atrial spikes (arrows) followed immediately by P waves in the first 3 beats. The next three P waves (arrowheads) are the patient’s own sinus beats. After a preset interval of 0.20 sec, ventricular spikes (open arrows) are seen. They are followed immediately by wide QRS complexes reflecting asynchronous ventricular depolarization.

REFERENCE 1. Chou TC. Electrocardiography in Clinical Practice, 4th ed., WB Saunders Company, Philadelphia, 1996, p. 111. 2. Marriott H. Practical Electrocardiography, 7th ed., Williams & Williams, Baltimore, 1983, p. 80.

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3. Narula 0. Wenckebach type I and type I1 atrio-ventricular block (revisited). In Fisch C, Brest AN, eds., Complex Electrocardiography,Vol6, Philadelphia, FADavis, 1974, p. 1. 4. Haft J. Clinical implications of atrio-ventricular and intraventricular conduction abnormalities. In: Rios J, ed., Clinical ElectrocardiographicCorrelates,Vol8, Philadelphia, FADavis, 1977, p. 41.

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INDEX A Aberrant ventricular conduction 90 Accelerated idioventricular rhythm 103 Accelerated junctional rhythm 83 Activation of the ventricles 6 Acute pericarditis 40 Acute pulmonary embolism 48 Adenosine 80 Amiodarone 97 Angina pectoris, stable angina 25 unstable angina 29 Prinzmetal’s angina 30 Aortic regurgitation 44 Aortic stenosis 44 Arrhythmias, classification of 68 diagnosis of 62 Ashman’s phenomenon 92 Athelete’s heart syndrome 56 Atrial enlargement, left atrial 47 right atrial 47 bi-atrial 47 Atrial fibrillation 84 Atrial flutter 86 Atrial infarction 36 Atrial septa1 defect 110 Atrial tachycardia, with AV block 96 multifocal 76 Atrioventricular (AV) block, first degree 113 second degree 114

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Mobitz type I 114 Mobitz type I1 114 high grade 115 third degree (complete) 116 Atrioventricular (AV) dissociation 83 Axis deviation, left 5 right 5

B Beta-blocker 80 Bidirectional ventricular tachycardia 97 Bifascicular block 109 Bradycardia-tachycardia syndrome 71 Bundle branch block, left 112 right 109 right with left anterior hemiblock 109 right with left posterior hemiblock 109 Bundle of Kent 80

C Cardiomy opathy, dilated 50 hypertrophic 50 Carotid sinus massage 71, 80 Chronic obstructive-lung disease 49 Compensatory pause, complete 90 incomplete 90 Complexes and segments 5 Conducting system, anatomy of 108 degenerative disease of 112 Coronary angiography 28

Coupling interval 94

D Deltawave 80 Dextrocardia 59 Digitalis, effect 23 intoxication 96 Digoxin 80

E Early repolarization syndrome/pattern 38 Ebstein’s anomaly 47 Einthoven triangle 4 Electrical alternans 41, 78 Electrical axis 4 Electrophysiological testing 64 Exercise stress test 26

F Fusion beat 98

H Hemiblock, left anterior 112 left posterior 112 Hexaxial reference system 4 Holter ambulatory ECG monitoring 62 Horizontality of ST segment 23 Hyperkalaemia 54 Hypersensitive carotid sinus syndrome 71 Hypertension 44 Hypocalcaemia 54 Hypokalaemia 52

I Idioventricular rhythm 105 Implantable cardioverter-defibrillator 105 Intracranial haemorrhage 52

J Junctional escape beat 73 Junctional rhythm 72

Junctional tachycardia 77 Juvenile T wave inversion 57

L Lignocaine 102 Lown-Ganong-Levine (LGL) syndrome 83

M Mitral regurgitation 43 Mitral stenosis 47 Mitral valve prolapse 55 Myocardial infarction, location of 16 anteroseptal 16 anterolateral 16 inferior 16 posterior 16 right ventricular 16 “hyperacute phase” of 13 “fully evolved phase” of 14 “resolution phase” of 15 “chronic phase” of 15 old 15 reinfarction 22 subendocardial 19 transmural 12 Qwave 21 non-Qwave 21 Myxoedema 52

0 Oesophageal lead ECG 16,62

P Pacemaker, permanent 118 temporary 118 Palpitation 64 Pathological Q wave 13 Pericardial effusion 41 “P mitrale” 47 “P pulmonale” 47 Poor man’s exercise test 34

121

Poor R wave progression 15 Post-extrasystolic T wave inversion 34 Post-tachycardia syndrome 80 Procainamide 102 Pseudo-nomalization of T wave 19 Pulmonary hypertension 45 Pulmonary stenosis 46

Q

Syncope 64, 117

T T wave inversion 57 Tetralogy of Fallot 45 Tilt table test 64 “Torsade de pointes” 104 Triaxial reference system 4 Trifascicular block 115

Q 111 58 QT prolongation 55, 104 Quinidine 65

U

R

V

rSr‘ 110 Rule of bigeminy 94

Ventricular aneurysm 15 Ventricular asystole 105 Ventricular bigeminy 94 Ventricular ectopic beats, Lown’s grading system 92 uniform 92 multiform 92 consecutive 92 “R on T” 92 unifocal, multiform 96 Ventricular fibrillation 105 Ventricular flutter 104 Ventricular hypertrophy, left 43 right 45 Ventricular parasystole 106 Ventricular septa1 defect 110 Ventricular tachycardia 98 Verapamil 80

S S,,Q3,T3 pattern 48 ST segment depression, horizontal 23 Jtype 22 reciprocal 13 downsloping 23 Sick sinus syndrome 7 1 Sinoatrial block 70 Sinus arrest 71 Sinus arrhythmia 70 Sinus bradycardia 69 Sinus capture beat 98 Sinus tachycardia 69 Sotalol 80 Stokes-Adams attack 116 Supraventricular ectopic beat, unifocal 75 multifocal 75 non-conducted 76 with aberrant ventricular conduction 92 Supraventricular tachycardia, AV nodal re-entrant tachycardia 77 AV reciprocating tachycardia 77 atrial tachycardia 77 with aberrant ventricular conduction 100

122

U wave inversion 32

w Wandering pacemaker 74 Wenckebach phenomenon 114 Wolff-Parkinson-White (WPW) syndrome atrial fibrillation in 8 1 ECGin 80 Q wavesin 80 supraventricular tachycardia in 8 1