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

World Scientific
L Singapore New Jersey. London Hong Kong
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World Scientific Publishing Co. Re. Ltd.
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British Library Cataloguing-in-Publication Data

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First published 1998

Reprinted 2000

CLINICAL ELECTROCARDIOGRAPHY, 3rd Edition

Copyright 0 1998 by World Scientific Publishing Co. Re. Ltd.
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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 V
Acknowledgements vi
Preface vii

1. The Normal Electrocardiogram 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 108

Index 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
 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
-I 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 1 (300/1)
150 2 (300/2)
100 3 (30013)
75 4 (300/4)
60 5 (300/5)
50 6 (300/6)
43 7 (300/7)
38 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 Fig. 1.3 Diagram showing the hexaxial
system. reference system.

4
 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 aVR aV F

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-

aV R
4
II m aV F

v3 V6
v1
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 aVR aVL

v1 v3 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.

V6
V1 v3 VS
v2 v4

V8 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
 4iiLL
...
....
......
.....

. ~- .~
I

I I1 111 aV L aVF

v1 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 ST-
T 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.

T:.:.. . ... ..=.::.::.::IT._: ..

..

jf-7
.~ .-....

. . -... . .- ......... -
, . . . . ..... . . . . . ..... . . . . . . . . .
I

........ ,
,. . . .
I : .
: , 1:...........
...--
::::
.......
.
-. . . . .
_.
...
_.
... .
- .. r I --::I
.:. .:
.2:.
.
Vl 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 C

D 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
 v5 V6

V4 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 aVL aVF

Vl v2
Zk'IiEE v3
V4 VS
Fig. 2.19 ECG was recorded in a patient with angina pectoris during an episode of
V6

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),

-$njnp&
.
,....
~ ..
.......
. .. .. .. .. .. .. .. ....... . . . .

I lI
........
. . .... ...... .. .. .-

m
b
%
aVR aVL
.
...
. . .. . . .. . ..-

aVF

v1 v2 V3 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.

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
RESTING HYPERVENT a modified V 5 lead. The resting
1 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
IMMEDIATE PE 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
8 MIN PE 10 MIN PE 12 MIN PE T wave at 10 minutes. ( 5 ) Normal
ECG at 12 minutes.

26
 . . . I .. .. . . .I
.-.$-$-.

- __..
.. ..
.- . . . . . . . .
. . . . .

Vl
w-
.... __
II
. . .. . ..-.

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

..
m
. _ ._. . . . . . . . . . . . .

v3
. . .
aVF

v2 v4 . .. ........

v5 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 mid-
right 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

I II 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 aV F

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
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 aV R aV L aV F

V1 v2 v3 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).

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 post-
extrasystolic 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 post-
extrasystolic 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 post-
extrasystolic 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
:
I:.::
. . .
;

.... . . . .
1 : : :.
. ., .. .. .....
.
..
,
. . .
jI jj
. . . . . . . . .. .. . . ,. . .
, -.
. . -. . . .

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.

36
 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 B

NORMAL

--TL-
A
--T
--+
GRUSIN
I --

Fig. 3.1 Diagram showing

GRUSIN normal ECG pattern and the
Grusin pattern I and pattern I1
II (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.

.. -.
- . . -.- ..
-utcI.
.
aV L
I III aV R aVF

v3
v2
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)

I m
aV R aV L aV F

v5 V6
v4
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
...

,
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.

v2 v3
VI 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 two-
dimensional 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
& aVR
aVF
I aVL

fE v1
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:

1. S1,Q3,T3 pattern (i.e. S wave in lead I, Q wave and inverted T wave in lead 111)
2. Right axis deviation
3. Transient right bundle branch block (usually incomplete)
4. T wave inversion and ST segment elevation in the right praecordial leads V1 and V2
5. 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.

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 V3
v5

Fig. 3.12 Acute massive pulmonary embolism.The patient was a 34-year-old woman who suddenly
collapsed 1 day after caesarean section. Note: (1) S I . Q ~ , T
pattern.
~
@- V6

The S wave in I and the q wave

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
II
w aVR
*4Q&aV L
.-

aVF

Vr,
M v5
..

V6
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.

II m aVR
*P aVF

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
aVF
11 m aV L

-trtt V6
v1 v2 v5
v3 v4
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.

I m 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). Two-
dimensional 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
These include deeply inverted and wide T waves or less commonly,
intracranial haem~rrhage.~
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

v1

v4 v5 V6
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-
EE
v1
iT= #I+# V6
v2 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
 I
LhlJ-c-
aVR

aV 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
rn , ,

aVR
/ I
aVL
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

18 yrs

v1 v2 v3 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 II m aVR aVL aVF

V6
v1 VS

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.

58
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&$[-
V7R
I_

I
V6R
v4 R 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.

59
 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.

60
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 cardioverter-
defibrillator 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.

66
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

68
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 bradycardia-
tachycardia 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).

71
(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 aVL

v1 v2 v3 v4 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).

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.

73
(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.

74
(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.

75
 Fig. 5.13 Blocked atrial ectopic beat (arrow). Note: (1) Complete compensatory pause. (2) Post-
ectopic 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.

76
(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.

aVR v1
I

aV L
II
V5
m - 5 - I I 1--

V6

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.

77
 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).

I aVR v1

aV L

aVF v2
' m

v3

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.
a= 1
II
m
I , ,-.__----- r

aVR
- - v - - - - r

aVL
. I

aVF
, I

......

V6
vi v2
v4
v3
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.

. . .

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

- ...
.- ................
aV R 1..
- ............
.......
..
. . .
.
. .
..
I .

.... .... - . ___

. . ...
~ .,. .

.......
.~ -
......... . . . .. . . ’
~

. .. .. . . . . . . . :. .. . .
i
. ~-
.

.
. . . , . .. .

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.

79
 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 “post-
tachycardia 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 <O. 12 sec, and the QRS complex is prolonged by an initial
delta wave to 20.12 sec (Figs. 5.17 and 5.20). Both these ECG abnormalities are due to
premature depolarization (“preexcitation”) of the left or the right ventricle via an accessory
pathway with accelerated conduction (Bundle of Kent). In addition, the ECG may show
pathological Q waves in leads II,I n and aVF or other leads, thus closely simulating transmural
myocardial infarction (Fig. 5.20).
In 1945, Rosenbaum and his colleagues classified the WPW syndrome into a type A and
. ~the type A variety, the QRS complexes are dominantly positive in the
a type B ~ a r i e t yIn
right praecordial leads V1 and V2 (very frequently also positive in leads V3 to V,) and the
accessory pathway is left-sided. In the type B variety, the QRS complexes are dominantly
negative in leads V1 and V2 or in lead V1 alone, and the accessory pathway is right-sided. In
recent years, more accurate but at the same time more complicated ECG criteria for the
localization of the accessory pathway have been proposed.

80
 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
 I II I aV R aV L aV F

._
-1..I ;'...
. -. .
: .
. ... .
... . ..... ..,
~

ic: ::::- :;I:I:: :.

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.

I
m

aVF

n t lpJ3Il !I 1II

I . . . . I ....I .. , _ _ _ . I, . I , . .! I . &

v5
V6
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).

82
 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).

m aV R
FFW aV L m aV F

Vl

v3 V6
V5
v4
v2
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.

83
 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.
 %& aV R
aV L

v4 II I

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.

85
 A

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

86
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.

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.

a7
 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.

90
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.

91
favouring aberrant ventricular conduction for the same degree of prematurity. This
phenomenon is termed the “Ashman’s phenomenon” (Fig. 6.4).

aV F

. .-
v1 VS
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”.

92
 .

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.

94
-++
I
aVL f

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

96
 I I1 111

aVR aVL aVF

Vl v2 v3

V4 v5 V6
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.~

97
(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.

100
I n lrI aVR aV L aV F

Vl v2 v3 v4 v5 V6
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.

I m aVR aVL aVF

vl v2 v3 v4 v5 V6
Fig. 6.15 This normal ECG was recorded subsequent to Fig 6.14, after the termination of the
tachycardia.

101
 1 2 3 4 5 6 7 8 9 1011 1 2 1 3 1 4 1 5 1 6
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.

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

SA 7 I
1 7 1 1 I ‘I

A I

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

104
 Very recently, it has been shown that treatment with an implantable cardioverter-
defibrillator 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.

__ , . ~ .. - .

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.

107
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.

AV
NODE BUNDLE

FASCICLE

LEFT POSTERIOR
FASCICLE

Fig. 7.1 Diagram illustrating the conducting system of the heart

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).

A €3

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.

w
-

v2
V6
v3
vl v4
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).

I I1 111 aVR aVL aVF

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.

110
 I

v3 V6
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

Vl
v2
V6
v3 v5
v4

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.

111
 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.

I aVL

v5 V6
v1 v3
v4

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 pre-
set 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 Mobitz type I 114

Aberrant ventricular conduction 90 Mobitz type I1 114
Accelerated idioventricular rhythm 103 high grade 115
Accelerated junctional rhythm 83 third degree (complete) 116
Activation of the ventricles 6 Atrioventricular (AV) dissociation 83
Acute pericarditis 40 Axis deviation,
Acute pulmonary embolism 48 left 5
Adenosine 80 right 5
Amiodarone 97
Angina pectoris, B
stable angina 25 Beta-blocker 80
unstable angina 29 Bidirectional ventricular tachycardia 97
Prinzmetal’s angina 30 Bifascicular block 109
Aortic regurgitation 44 Bradycardia-tachycardia syndrome 71
Aortic stenosis 44 Bundle branch block,
Arrhythmias, left 112
classification of 68 right 109
diagnosis of 62 right with left anterior hemiblock 109
Ashman’s phenomenon 92 right with left posterior hemiblock 109
Athelete’s heart syndrome 56 Bundle of Kent 80
Atrial enlargement,
left atrial 47 C
right atrial 47 Cardiomy opathy,
bi-atrial 47 dilated 50
Atrial fibrillation 84 hypertrophic 50
Atrial flutter 86 Carotid sinus massage 71, 80
Atrial infarction 36 Chronic obstructive-lung disease 49
Atrial septa1 defect 110 Compensatory pause,
Atrial tachycardia, complete 90
with AV block 96 incomplete 90
multifocal 76 Complexes and segments 5
Atrioventricular (AV) block, Conducting system,
first degree 113 anatomy of 108
second degree 114 degenerative disease of 112
Coronary angiography 28

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Coupling interval 94 Junctional tachycardia 77
Juvenile T wave inversion 57
D
Deltawave 80 L
Dextrocardia 59 Lignocaine 102
Digitalis, Lown-Ganong-Levine (LGL) syndrome 83
effect 23
intoxication 96 M
Digoxin 80 Mitral regurgitation 43
Mitral stenosis 47
E Mitral valve prolapse 55
Early repolarization syndrome/pattern 38 Myocardial infarction,
Ebstein’s anomaly 47 location of 16
Einthoven triangle 4 anteroseptal 16
Electrical alternans 41, 78 anterolateral 16
Electrical axis 4 inferior 16
Electrophysiological testing 64 posterior 16
Exercise stress test 26 right ventricular 16
“hyperacute phase” of 13
F “fully evolved phase” of 14
Fusion beat 98 “resolution phase” of 15
“chronic phase” of 15
H old 15
Hemiblock, reinfarction 22
left anterior 112 subendocardial 19
left posterior 112 transmural 12
Hexaxial reference system 4 Qwave 21
Holter ambulatory ECG monitoring 62 non-Qwave 21
Horizontality of ST segment 23 Myxoedema 52
Hyperkalaemia 54
Hypersensitive carotid sinus syndrome 71 0
Hypertension 44 Oesophageal lead ECG 16,62
Hypocalcaemia 54
Hypokalaemia 52 P
Pacemaker,
I permanent 118
Idioventricular rhythm 105 temporary 118
Implantable cardioverter-defibrillator 105 Palpitation 64
Intracranial haemorrhage 52 Pathological Q wave 13
Pericardial effusion 41
J “P mitrale” 47
Junctional escape beat 73 “P pulmonale” 47
Junctional rhythm 72 Poor man’s exercise test 34

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Poor R wave progression 15 Syncope 64, 117
Post-extrasystolic T wave inversion 34
Post-tachycardia syndrome 80 T
Procainamide 102 T wave inversion 57
Pseudo-nomalization of T wave 19 Tetralogy of Fallot 45
Pulmonary hypertension 45 Tilt table test 64
Pulmonary stenosis 46 “Torsade de pointes” 104
Triaxial reference system 4
Q Trifascicular block 115
Q 111 58
QT prolongation 55, 104 U
Quinidine 65 U wave inversion 32

R V
rSr‘ 110 Ventricular aneurysm 15
Rule of bigeminy 94 Ventricular asystole 105
Ventricular bigeminy 94
S Ventricular ectopic beats,
S,,Q3,T3 pattern 48 Lown’s grading system 92
ST segment depression, uniform 92
horizontal 23 multiform 92
Jtype 22 consecutive 92
reciprocal 13 “R on T” 92
downsloping 23 unifocal, multiform 96
Sick sinus syndrome 7 1 Ventricular fibrillation 105
Sinoatrial block 70 Ventricular flutter 104
Sinus arrest 71 Ventricular hypertrophy,
Sinus arrhythmia 70 left 43
Sinus bradycardia 69 right 45
Sinus capture beat 98 Ventricular parasystole 106
Sinus tachycardia 69 Ventricular septa1 defect 110
Sotalol 80 Ventricular tachycardia 98
Stokes-Adams attack 116 Verapamil 80
Supraventricular ectopic beat,
unifocal 75 w
multifocal 75 Wandering pacemaker 74
non-conducted 76 Wenckebach phenomenon 114
with aberrant ventricular conduction 92 Wolff-Parkinson-White (WPW) syndrome
Supraventricular tachycardia, atrial fibrillation in 8 1
AV nodal re-entrant tachycardia 77 ECGin 80
AV reciprocating tachycardia 77 Q wavesin 80
atrial tachycardia 77 supraventricular tachycardia in 8 1
with aberrant ventricular conduction 100

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