Bedside Approach To Electrocardiography Japyee

Bedside Approach
to
Electrocardiography
Bedside Approach
to
Electrocardiography
Gami NK MRCP(Edin) FRCP(Edin)

Formerly Consultant to the
Wessex Regional Hospital Board, UK
Formerly Physician and Cardiologist to the
Department of Medicine
Darbhanga Medical College and Hospital
Consultant Physician and Cardiologist at
Darbhanga (Bihar)
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Bedside Approach to Electrocardiography
© 2001, Gami NK
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First Edition 2002
Publishing Director: RK Yadav
ISBN 81-7179-892-6
Typeset at JPBMP typesetting unit

Printed at Lordson Publishers (P) Ltd., C-5/19, R P Bagh, Delhi 110 007
To
My Parents
and
To my beloved daughters
Reeta, Kavita and Tanuja
Foreword
All of us have looked forward for a book which would provide a ready store of intelligible and important
facts in a difficult but interesting discipline of medicine, like electrocardiography. The student, introduced
for the first time to the intricacies of electrocardiography, is frequently bewildered, sometimes
overwhelmed, by complicated method of presentation.
Dr NK Gami FRCP (Edin) has been practising and teaching of electrocardiography both here and
abroad. This book is the artistic synthesis, distilled elexir of all these experiences.
The electrocardiography can have as much precision as mathematic is aptly revealed by reading this
book. Theoretical considerations have been reduced to a minimum, emphasis being placed on practical
and clinical aspects.
It is especially interesting and pleasing to realise that this excellent book is written by a physician
who has spent major part of his professional life in our smaller towns. This book is also a testimony that
there are excellent teachers outside the confines of medical colleges.
It is meant for teachers, students, physicians and general practitioners who wish to refresh the
knowledge. The specialist physicians and cardiologists may systematise their knowledge and at least it
will help him in bedside quick orientation and diagnosis.
NP Mishra MD FRCP (Edin)

Physician
Laheriasarai
Darbhanga
Preface
“ The lord hath sought him a man after his own heart”
— Samuel
“ The heart has its reason which reason does not know”
— Blaise Pascal
This book is a bedside approach to the electrocardiography. Despite of astonishing advances in

electrophysiological sciences and laboratory investigations an ECG is no match. It is a simple procedure
and, like mathematics, is an exact science based on electro-physiological principles. It gives power to
the clinicians to solve urgent problems immediately at the bedside and decisions must be made and
action taken, occasionally at electric speed.
The book is intended mainly for clinicians and students and arm them with such clinical knowledge
that the uncertainty will vanish. They will stand on a firm footing. It is important to interpret the tracings
in the light of clinical picture.
I cannot claim this book is fully comprehensive. I have intentionally avoided undue details and
extreme views. Many controversies exist. An attempt is made to identify major clear-cut diagnostic
clues. Each wave, segment and interval is identified as individual entity and each unit is approached
individually to reach the definitive diagnosis. Where certain specific diagnostic patterns are detected,
they are rationally discussed and diagnostic flow chart are devised to reach the quick diagnosis. The
approach is a logical step-by-step flow chart to reach the diagnosis in a very short time. It prepares the
mind for a methodical and systematic approach to abnormalities of different components of ECG tracings
(waves, segments, intervals, specific patterns such as bundle branch block, ventricular hypertrophy,
ischaemia and infarction). Tables and figures are lavishly used to summerise and clarify the facts. I have
tried to hand over the cup of knowledge to the young without froth.
The subject of cardiac arrhythmias is dealt with some detail because I think it is a difficult part of
ECG tracings. I have tried my level best to simplify its interpretation in a rational way
I welcome this opportunity to express my gratitude to my colleagues, my students and teachers
specially cardiologists Dr Gilchrist, Dr RW Turner of Edinburgh from whom I have learnt a lot. I am
very grateful for this opportunity to thank my adviser and teacher Dr JW Wade MD FRCP (London),
Cardiologist of Manchester Royal Infirmary for his considerable help and interest during the period in
which it has been my fortune to work under him and to learn intricacies of the ECG tracings.
I am really grateful to the publishers Jaypee Brothers and especially the Director (Publishing)
Mr RK Yadav for meticulous supervision, helpful suggestion and presentation of the book.
Finally I would like to thank Professor NP Mishra MD FRCP (Edinburgh) for writing the foreword and
my wife for putting up with long period of silence without complaining.
NK Gami
x Bedside Approach to Electrocardiography
Acknowledgements
I wish to acknowledg my indebtedness to the following authors, Publishers, whose books and articles I
have consulted in particular:
Books
1. Schamroth’s “An Introduction to Electrocardiography”.
2. Lipman and Massie’s “Clinical Scalar Elecrocardiography”.
3. McLachlan’s “Fundamentals of Electrocardiography”.
4. Goldman’s “Principles of Clinical Electrocardiography”.
5. Armstrong’s “Electrocardiograms, a Systematic Method of Reading Them”.
6. Marriott’s “Practical Electrocardiography”.
Articles
1. Wolff L: Syndrome of short P-R interval with abnormal QRS complexes and paroxysmal tachycardia
(Wolff-Parkinson-White syndrome), Circulation 10: 282, 1954.
2. Wood P: Pulmonary embolism: Diagnosis by chest lead electrocardiograms, Brit. Heart J. 3: 21,
1941.
3. Wilson FN: Einthoven’s triangle, Am. Heart J, 32: 277, 1946.
4. Sodi-Pillares D: The importance of Electrocardiographic patterns in Congenital Heart Disease, Am.
Heart J. 49: 202.
5. Scott RC: The electrocardiogram pattern of right ventricular hypertrophy in chronic cor pulmonale,
Circulation 11: 927, 1955.
6. Murnaghan D: Pulmonary embolism, special reference to the electrocardiogram, Am. Heart J, 25:
573, 1943.
7. Lepeschkin E: The U wave of the electrocardiogram, A.M.A Arch. Int. Med. 96: 600, 1955.
8. Johnston FD: Reflections on electrocardiography, Circulation 15: 801, 1957.
9. Goldbreger E: The electrocardiographic pattern of ventricular aneurysm, Am. J Med., 4: 248, 1948.
Contents xi
Contents
Basic Principles
1. Impulse Generation in the Heart ..... .... ..... 1

2. Leads of the Clinical Electrocardiogram ..... .... ..... 6
3. Normal ECG Complex ..... ..... .... ..... 9
4. Heart Position ..... ..... .... ..... 11
5. Axis Deviation ..... ..... .... ..... 15
Waves, Intervals and Segments
6. P-Wave .... ..... ..... .... ..... 16

7. Q-Wave .... ..... ..... .... ..... 25
8. T-Wave .... ..... ..... .... ..... 40
9. U-Wave .... ..... ..... .... ..... 44
10. S-T Segment . ..... ..... .... ..... 45
11. P-R Interval ... ..... ..... .... ..... 57
12. Q-T Interval ... ..... ..... .... ..... 60
13. Significance of Abnormal Waves, Segments and Intervals in Different ECG Leads 62
Myocardial Infarct
14. ECG Changes in Myocardial Infarct ..... .... ..... 66
Ventricular Hypertrophy
15. Left Ventricular Hypertrophy .. ..... .... ..... 74

16. Right Ventricular Hypertrophy ..... .... ..... 77
Cardiac Arrhythmias
17. Cardiac Arrhythmia ..... ..... .... ..... 80

18. Classification of Cardiac Arrhythmias ..... .... ..... 82
19. Classification of Arrhythmia Based on ECG Patterns .... ..... 84
20. Mechanism of Arrhythmias .... ..... .... ..... 86
21. Tachyarrhythmias ..... ..... .... ..... 90
22. Bradyarrhythmias ..... ..... .... ..... 99
23. Arrhythmias Other than Tachyarrhythmias and Bradyarrhythmias ..... 105
xii Bedside Approach to Electrocardiography
24. Approach to Atrial Premature Beats ..... .... ..... 108

25. Summary of Premature Beats ..... .... ..... 113
26. Approach to Paroxysmal ATRIAL Tachycardia (PAT) .... ..... 114
27. Approach to Atrial Fibrillation and Flutter ..... .... ..... 119
28. Junctional or Nodal Arrhythmia ..... .... ..... 124
29. Approach to Ventricular Premature Beat ..... .... ..... 127
30. Approach to Ventricular Tachycardia (VT) ..... .... ..... 132
31. Heart Block (Atrioventricular) . ..... .... ..... 135
32. Disorders Produced by Two Independent Pacemakers .... ..... 140
33. Atrioventricular Dissociation . ..... .... ..... 142
34. Hemiblock of Left Bundle Branch Block ..... .... ..... 145
35. Bundle Branch Block ..... ..... .... ..... 148
36. Accelerated Conduction or Preexcitation Syndrome or
Wolff-Parkinson-White Syndrome ..... .... ..... 154
37. Sick Sinus Syndrome ..... ..... .... ..... 156
38. How to Read the ECG of Arrhythmias ..... .... ..... 158
Other Abnormal ECG Patterns
39. Electrographic Patterns in Aquired Heart Disease .... ..... 163

40. Electrocardiographic Patterns in Congenital Heart Disease ... ..... 164
41. Other Electrocardiographic ECG Patterns ..... .... ..... 168
42. ECG Report ... ..... ..... .... ..... 172
Index .... ..... ..... .... ..... 175

Basic Principles
1 Impulse Generation
in the Heart
INTRODUCTION
The most important feature of heart is to contract. Each contraction maintains the rhythmicity of heart
due to excitation wave of electrical activity preceding contraction. The electrocardiograph records this
electrical impulse. The electrical impulse starts in the sinus node and spreads from there to the atrio-
ventricular node through the specialised tissues in the atrium and then proceeds also through the
specialised conducting tissues (Tables 1.1 and 1.2). “Anatomy and Physiology of specialised conducting
tissues.”
Table 1.1: Anatomy of specialised tissues
Site Blood supply Nerve supply
1. Sinus node: Right atrium near junction Right coronary artery Vagus slows rate of impulse
of superior vena cava with transmission
lateral right atrial wall Sympathetic increases it
2. AV node: Right of upper margin of Right coronary artery — Do —
intervent septum
3. Other specialised
tissues:
• In atria: 3 internodal conducting pathways which channelise impulses from
SA node to AV node activating atria longitudinally
• In ventricle:
1. Bundle of His and its two branches—right and left bundle branch.
The right branch runs right side of interventricular septum and left
branch crosses to the left side of septum dividing into anterior
fascicle spreading anteriorly and the posterior fascicle spreading
inferiorly. Ventricle is activated transversely.
2. Purkinje fibers in LV muscle.
Table 1.2: Physiology of specialised conducting tissues
Rate of activation Remarks

Sinus node 60-100/mt Impulse travels in a wave like fashion and longitudinal way towards AV
node. No retrograde conduction
AV node 50-60/mt Unique capacity to delay passage of impulse to maintain proper sequence of
atria followed by ventricular contraction
Ventricle 30-35/mt Ventricle activated in transverse fashion from endocardium to epicardium
2 Bedside Approach to Electrocardiography
Electrical Activity in Cardiac Muscle
The resting cardiac muscle cell is in a state of electrical equilibrium keeping positive charges on the
outer surface of the cell and negative charges on the inner surface and this state is termed polarised state.
When the muscle is stimulated the charges are reversed so that the outer surface becomes negative and
the inner surface positive and this is termed depolarised state. The current of stimulation will have
positive head and a negative tail. A unipolar electrode facing the oncoming head of this current will
record a positive or upward deflection and an electrode facing the receding tail will record a negative or
downward deflection (Fig. 1.1).
+ + + + + + + + Record
+ – – – – – – – + Resting state
+ – – – – – – – +
+ + + + + + + +
Polarised cell
(Resting stage)
| ↑
Stimulation Recovery
↓ | Positive
– – – – – – – – – Deflection
| + + + + + + + + |
+ +
| + + + + + + + + |
– – – – – – – – –
Depolarised cell
(Activated state)
Fig. 1.1: Electrical activity in cardiac muscle
Depolarisation and Repolarisation of Cardiac Muscles
Electrographically the ventricles are composed of three muscle groups—interventricular septum, free
wall of right ventricle and free wall of left ventricle. Depolarisation commences in the left side of
septum and spreads through the septum from left to right. This is the first stage of depolarisation (indicated
in Fig. 1.2). The depolarisation then proceeds outward simultaneously through the free wall of both
ventricles from endocardial to epicardial surfaces. This is the second stage of depolarisation (indicated
in Figs 1.3 and 1.4). The free wall of left ventricle has a larger muscle mass possessing larger potential
electrical force than the free wall of the right ventricle, produces larger deflection in the ECG nullify the
smaller force of the right ventricle. An electrode facing the left ventricle therefore writes an initial
downward deflection “q” due to spread of the impulse away from the electrode through the septum,
followed by a large deflection or “R” wave due to spread of the impulse towards the electrode through
the left ventricular free wall producing a “qR” wave called the left ventricular complex (Fig. 1.5) and
while the electrode facing the right ventricle will show an initial small upright deflection “r” due to
Impulse Generation in the Heart 3
Fig. 1.2: First stage of depolarisation of ventricles Fig. 1.3: Second stage of depolarisation of ventricles
Fig. 1.4: Depolarisation of the ventricles Fig. 1.5: Left ventricular complex
in a simplified form
Fig. 1.6: Right ventricular complex

ECG Waves Cardiac Cycle Heart Sounds
QRS interval First heart sound occurs during QRS

T-wave Diastole occurs after T-wave, starting Second heart sound occurs after termi-
from end of T-wave to beginning of next nation of T/U-wave occurs after 2nd HS
Q-wave T occurs during systole
QT interval Systole corresponds to QT interval
Fig. 1.7: Relation of systole and diastole with ECG waves and heart sounds
spread of the impulse towards the electrode through the septum followed by a large downward deflection
a “S” due to spread of the impulse away from the left ventricular free wall producing an “rS” termed
right ventricular complex. See Table 1.3 “Sequence of depolarisation and repolarisation in cardiac cycle”.
Figure 1.7 shows relation of systole and diastole with ECG waves and heart sounds.
Table 1.3: Sequence of depolarisation and repolarisation in cardiac cycle
 At atria
• Impulse starts at sinoatrial node at 60-100 per minute
• Passes through atrial muscles and 3 specialized conducting pathways (Internodal bundles)
writing P-wave

 At junctional tissue
• Then impulse reaches atrioventricular node, Bundle of His and main left and right bundle
branch (Junctional tissues) responsible for P-R segment where impulse is delayed. So rapid is
the transmission of impulses that the delay in AV node is necessary to maintain the proper
sequence of atrial followed by ventricular, contraction. Grant says: “There is no parallel
elsewhere in biology or in physics for an electrical impulse delayed for so long an interval in
so small a region without undergoing decrement or becoming extinguished”. P-R interval
represents the time taken for atrial activation plus the time taken for the impulse to traverse
AVN and Bundle of His

Contd....
Impulse Generation in the Heart 5
Contd....

 Ventricle activation/and repolarisation
• First stage of ventricular activation: IVS activation:
– Impulse after passing through junctional tissues activates interventricular septum from left
side via bundle branches writing in electrocardiogram normal small q-wave in left sided
leads (I, aVL, V5-V6) and small r-wave in right sided chest leads (V1-V2)

• Second stage of ventricular activation:
– Further spread of impulses occur down the bundle branches to simultaneous activation of
both ventricles via Purkinje fibers and is responsible for R and S-wave

• Third stage of ventricular activation:
– The final stage of activation occurs from endocardium to epicardium of ventricle. The total
time taken for ventricular activation is responsible for QRS interval

• Fourth stage of ventricular repolarisation (recovery) :
– Following completion of ventricular activation, there is period of electrical inactivity shown
by the S-T segment in ECG when all parts of ventricle are in depolarised state. Finally,
repolarisation of ventricle occurs writing T-wave
2 Leads of the Clinical

Electrocardiogram
Bipolar or Standard Leads
If leads from electrode facing the end of a muscle strip are connected to a galvanometer, then each lead
will show its own potential and both leads record simultaneously any electrical activity occurring in the
muscle strip. The resultant tracing is the composite recording of both electrodes. This is the basis of
bipolar or standard leads in electrocardiography (Fig. 2.1). It is not possible to apply electrodes to the
surface of the heart. Recordings are taken by electrodes attached to the body surface, limbs and chest
wall. All electrocardiographs are so built that the positive and negative galvanometer connections of the
various leads are arranged in an universal fashion. Three combinations of bipolar leads are used and
these at a given moment record three different ECG patterns:
Bipolar or Standard Lead I: With the positive electrode on the left arm and negative
on the right arm.
Lead II: Positive electrode on left leg and negative on right arm.
Lead III: Positive electrode on left leg and negative on left arm.
Unipolar Leads
The heart may be considered to lie in the centre of an equilateral triangle the apices of which are the
right arm, left arm and left foot originally proposed by W Einthoven in 1901. According to Einthoven
physiologist in Leyden and inventor of string galvanometer, the algebraic sum of the potentials of these
electric forces at any instant is zero. Thus, if these three leads are connected to a central terminal, the
potential of this will be zero. If this terminal (also called the neutral or indifferent electrode) is now
connected to one lead of a galvanometer, that lead will always have a potential value of zero. The
electrode connected to the other lead of the galvanometer will then record the true potential value at any
given point. This electrode is termed the exploring electrode. This unipolar system is devised by FN
Wilson in 1935.
Nine unipolar leads are recorded, one from each of the three limbs (right arm, left arm and left leg)
and 6 from the chest wall. The unipolar leads are so arranged that the positive electrode is applied to the
site to be explored, and the negative or indifferent connection to the galvanometer is made up of a
combination terminal from all the three limb electrodes—the central terminal with potential value zero
(Figs 2.1 and 2.2). In this way the single exploring electrode records only the electrical forces from the
site at which it is applied hence the name “Unipolar”.
VR lead: Right arm has connections from both the exploring and neutral electrodes
VL lead: Left arm has connections from both the exploring and neutral electrodes
VF lead: Left foot has connections from both the exploring and neutral electrodes.
Leads of the Clinical Electrocardiogram 7
RA _______ VR
LA __________ V1
— Extremity leads LF _____________ VF
RA LA EE
— NE — G —
EE
LF — Chest leads
V1,V2,V3,V4,V5,V6
Fig. 2.1: Unipolar electrode connection without augmentation

Key: NE = Neutral electrode or central or indifferent electrode;
EE = Exploring electrode; RA = Right arm ; LA = Left arm;
LF = Left foot
RA LA
NE ______ G ______ EE aVR
LF
RA LA
NE ______ G ______ EE aVL
LF
LA
RA
NE ______ G ______ EE aVF
LF
Fig. 2.2: Augmented unipolar electrode connections broken line indicates served connections
The electrocardiographic waves from the unipolar limb leads are found to be of low amplitude, so a
method of augmentation was devised by Goldberger. He omitted the connection of the neutral terminal
to the limb being explored by the positive electrode and letting it hang free. The addition of a small “a”
(for augmentation) was used to prefix the name of these leads:
Lead aVR: Omitting the right arm connection from neutral electrode
Lead aVL: Omitting the left limb connection from neutral electrode
Lead aVL: Omitting the left foot connection from neutral electrode.
Table 2.1 Shows electrocardiographic leads
Table 2.1: Electrocardiographic leads

Standard Bipolar Leads Unipolar Leads
Lead I = RA lead + LA lead  Extremity leads
Lead II = RA lead + LF lead • VR lead:
Lead III = LA lead + LF lead RA + LA + LF combine to form neutral terminal with
exploring electrode to RA
• VL lead:
RA + LA + LF forms neutral terminal with exploring
electrode to LA
• VF lead:
RA + LA + LF forms neutral electrode with exploring
electrode to LF
• aVR lead:
Omitting connection of RA
• aVL lead:
Omitting connection LA
• aVF lead:
Omitting connection to LF
 Chest leads:
V1 to V6
3
Normal ECG Complex
THE NORMAL WAVES, COMPLEXES, AND INTERVALS

The ECG complex is composed of different waves with intervals between them. Their mechanism of
production, direction, duration and amplitude are given in Table 3.1.
Table 3.1: Normal ECG waves
Waves Mechanism Direction Duration Amplitude Remarks
P-wave Represents electrical Upright in I, II, avf and Not more than Not more than Best seen in II and V1
activity throughout atria V3 to V6 0.10 second 2.5 mm
starting from sinoatrial Inverted in aVR and aVL,
node (Atrial depolari- biphasic in V1 and some-
sation) times in V2
Sometimes inverted in III.
QRS Represents total ventri- Negative in aVR 0.14 to 0.11 second
complex cular depolarisation time
S-T seg- Represents ventricular From nil to 0.15 second varies ST segment normally
ment and recovery after ventricular inversely with cardiac rate isoelectric but may
T-wave depolarisation vary from 0.5 to +2.0
mm occurs normally
in I, aV1, V4 to V6
Q-wave Represents ventricular Less than 0.01 Depth less than
depolarisation second 2 mm in II and III
R-wave R in V6 and S in V1 represents Less than 0.01 In V1 height of R small and S deep,
S-wave left ventricular electrical activity second as one passes across chest R gradually
increases and S decreases
T-wave Represents ventricular Upright in all leads Higher than 5 mm in standard
recovery (Ventricular except in aVR. May leads 10 mm in chest leads
repolarisation) be inverted in III,
aVF, V1, V2. Inverted
T in I, II, V3 to V6
always abnormal
Inverted T in aVL not
abnormal if P also
inverted and if QRS
is of low amplitude
U-wave Represents slow repolarisation of intra- Usually upright Best seen in V3
ventricular conduction system with period
of greatest excitability of ventricle
Contd...
Contd...
Waves Mechanism Direction Duration Amplitude Remarks
P-R Represents atrioventricular time (Time taken Duration 0.12 to 0.20 second
interval starting from sinoatrial node to be corrected with heart rate
giving of ventricular excitation)
QT Represents total time taken for depolari- Maximum duration 0.40 second
interval sation and repolarisation of ventricular for heart rate of 70/minute
muscle. It measures duration of electrical
systole
Fig. 3.1: Nomenclature
How they are present in different leads are depicted in the Table 3.2.
Table 3.2: Normal ECG waves and intervals in different leads
Leads P Q R S T Remarks
Lead I Upright Small q Major deflection Small s Upright
Lead II Upright Often small q Major deflection R Upright
Lead III Upright may be Occasionally Usually present Upright or Deep Q and inverted T
biphasic or inverted very deep inverted can only be considered
abnormal if they are pre-
sent in lead II and aVF
or with changes in I and
aVL reciprocal
Lead aVR Usually inverted Usually Major QRS deflection
inverted downward
Lead aVL Resembles Lead I Occasionally P inverted
Occasionally T inverted
if P inverted and QRS
amplitude small
Lead aVF Resembles Lead III If P and T inverted they
are more significant than
in lead III
Chest Often inverted or biph- Small q in V5, Small r in V3R, S shows reverse T upright in R and S of equal
Leads asic in V3R, V1 and V6; Deep Q V1 and increases trend as we move all leads. Can amplitude in V3 and V4
V2. Upright P in V3-V6 can occur in in size as we across chest be inverted
V1 and V2 move across towards V6 in V1 and V2
towards V6
Heart Position 11
4 Heart Position
HEART POSITION IN ECG
Position of the heart influences the ECG patterns resulting from electrical spread of excitation. Electrical
heart position is not synonymous with anatomical position of heart.
Rotation of heart on the following three axis:

|
Anteroposterior axis running Longitudinal axis running Transverse axis running on a
on a frontal plane through obliquely from base to apex sagittal plane through centre of
centre of heart from anterior of heart on horizontal plane heart from one lateral surface to
to posterior surfaces other lateral surface
Resulting in: Resulting in (changes viewed by Results in:
1. Horizontal position—left an observer looking up at the 1. Frontal rotation
ventricular apex facing left heart from below the diaphragm)
shoulder and right ventricle 1. Clockwise rotation—right ventri-
faces left hip cle moving anteriorly and right
ventricular wall and interventri-
cular septum will lie parallel to
anterior chest wall
2. Vertical position—left ventri- 2. Counterclockwise rotation— 2. Backward rotation
cular apex facing left hip left ventricle rotating ante-
riorly facing anterior chest wall
ECG PATTERN (Fig. 4.1)
Left ventricular complex Right ventricular complex Other changes

qR as found in V5, V6 rS as found in V1, V2
Horizontal position: aVL and V5-V6 shows aVf shows rS pattern
qR pattern
Vertical position: aVF and V5-V6 shows aVL shows rS pattern Right axis deation usually
qR pattern present
Clockwise rotation: Left ventricular complex V1-V6 show rS pattern • Tall R or QR in aVR in
(qR) does not appear marked clockwise rotation
until V7 to V9 • Prominent S in V5 and V6
+ RS pattern in V5 and V6
in marked clockwise rota-
tion (Figs 4.2 and 4.3)
Contd...
Contd...
Left ventricular complex Right ventricular complex Other changes
qR as found in V5, V6 rS as found in V1, V2
• Vertical position usually
associated
• Left axis deviation usually
present
Counterclockwise V2, V3, V4, and V6 V1, V2 (V3) show rS qR pattern beings in V4 and
rotation: show qR pattern pattern rS pattern in V1 in marked
counterclockwise rotation
(Figs 4.4 to 4.6)
aVL aVF aVL aVF
HORIZONTAL HEART POSITION VERTICAL HEART POSITION

qR complex in aVL rS in aVF qR complex in lead aV F rS in aVL
V3 V3
V2 V4 V2 V4
V5 V1 V5
V1
RIGHT VENTRICLE LEFT VENTRICLE
V6 V6
INTER
VENTRICULAR LEFT VENTRICLE RIGHT VENTRICLE
SEPTUM INTER
VENTRICULAR
SEPTUM
Clockwise rotation Anti-clockwise rotation
V1 or V2 R V3 or V4
R V5 V4 R
R
a
S S S
Diagrammatic representation of clockwise rotation of Diagrammatic representation of anti-clockwise rotation of

the heart the heart
Equal R and S in V5 and V4. Right ventricle assumes Left ventricle and right ventricle assume anterior position.
anterior position and left ventricle posterior. Prominent Equal R and S in V1 and V2. qR in V3
S in V5 and V6
Fig. 4.1: ECG pattern in different heart positions
Heart Position 13
Fig. 4.2: Marked clockwise rotation:

QR complex in aVR and V1. Prominent
S wave in left chest leads
Fig. 4.3: Clockwise rotation: Standard leads show vertical heart position.
Transition zone displaced to left. RS complex still present in V6
Fig. 4.4: Counterclockwise rotation:

Shift of transition zone to the right
between V1 and V2 (Tall R-wave in V2
and deep S-wave in V1
Fig. 4.5: Extreme clockwise rotation
Fig. 4.6: Counterclockwise rotation: Transition zone displaced to right-left ventricular complex in V2
5 Axis Deviation
There are two types of axis deviation (Fig. 5.1).

Left Axis Deviation Right Axis Deviation
 Position: Left axis lies between +0 and –120 Right axis lies between +90 and –180
 Rough and simple Main direction of QRS complex upward Main direction of QRS complex
method of finding in Lead I and downward in aVF, i.e. points downwards in Lead I and up-
out axis deviation Lead I and aVF divulge away from one ward in Lead aVF, i.e. Lead I and aVF
another especially associated with S- converge towards one another
wave in Lead II equal to or larger than
R-wave
 Causes: • Left anterior hemiblock • Right ventricular hypertrophy
• Left bundle branch block • Right bundle branch block
• Right ventricular ectopic rhythm • Left posterior hemiblock
• Mechanical shift of heart due to • Dextrocardia
elevated diaphragm • Left ventricular ectopic rhythm
• Normal in 10 percent cases • Normal variation
• Ischaemic heart disease • Children under 8 years
• WPW syndrome
• Pulmonary emphysema
LEAD I LEAD II LEAD III LEAD I LEAD II LEAD III
A. LEFT AXIS DEVIATION B. RIGHT AXIS DEVIATION

Fig. 5.1: Right and left axis deviation
Fig. 5.2: Left axis deviation. QRS axis greater than 15.
S in (negative complexes) III and aVF. R (positive complexes) in I and aVL
Waves, Intervals and Segments
6 P-Wave
The P-wave represents the spread of electrical activity throughout the atria. It is upright in leads I, II,
aVF and V2 to V6; positive or negative in lead III; inverted in aVR and in either direction in aVL.
Duration: Usually 0.08 second, maximum 0.11 second.
Height: Maximum 2.5 mm.
Best seen in leads II and V1
Causes of Abnormal P-Waves
P-wave may be revealed or not revealed (absent P-wave).
I. Causes of absent P-waves

|
| | | | |
P-wave replaced by P-wave superim- P burried in QRS PQRST dropped Other causes
posed on T-waves
• Fibrillary waves: • Paroxysmal atrial Nodal rhythm Sinoatrial block • Hyperpotassemia
auricular fibrillation tachycardia
• Flutter waves: • Paroxysmal ventri-
auricular flutter cular tachycardia
Fig. 6.1: Auricular fibrillation P-waves are replaced by fibrillary waves (F)
ventricular rate completely irregular
Approach
First note whether P is revealed or not revealed.
II. Causes of abnormalities of revealed P-waves
|
| | |
Distorted P-wave P-wave not followed by QRS Inverted P-wave
• Broad P-wave due to (Isolated P or multiple P) (upright P in aVR)
left auricular enlarge- | |
ment or hypertrophy | | | |
• Peaked P due to right P not related with QRS P-wave related with QRS Inverted P in aVF or II Inverted P in lead I
auricular enlargement (with varying P-R | • Inverted P preceding • Dextrocardia
or hypertrophy interval) | | QRS • Technical dextro-
• Changing shape of P • Complete heart With gradually With constant – High AV nodal cardia
due to wandering block increasing P-R P-R interval extrasystole
pacemaker, PAT with • Atrioventricular interval • Mobitz type II – Low atrial extra-
AV block, multiple dissociation • Mobitz type I second degree systole
extrasystole second degree heart block • Inverted P following
heart block • PAT with 2:1 QRS:
block – Low AV nodal
• Blocked atrial extrasystole
extrasystole
P-Wave 17
A. P not revealed (absent P): Note the rate, rhythm and abnormal waves (fibrillary waves—irregular
undulating waves; flutter waves—saw-toothed or picket-fence appearance). Also note the height of
T-wave. See Table
|
| |
Rhythm Rate
| | | | |
Irregular rhythm Regular rhythm Nodal rhythm Slow rate Fast rate
• Auricular fibril- Atrial flutter Due to retro- Sinoatrial block: Types • Paroxysmal atrial
|
lation (auricular with fixed AV grade conduc- | | tachycardia (150-
rate or ‘f’-waves block (flutter tion causing P- Normal QRS Bizarre QRS 250 per minute)
350-550 per min.)waves 200-400 wave to be bur- with ventri- with ventri- starts and stops
Note whether f per min) Carotid ried in the QRS cular rate 50 cular rate 30- abruptly, carotid
wave is fine (IHD sinus pressure per min. 40 per min. sinus pressure
or hypertension) increases AV ↓ ↓ either stops it or
or coarse (mitral block revealing Nodal escape Ventricular has no effect, P
stenosis or thyro- flutter waves Table escape Table difficult to iden-
toxicosis) more clearly) See also note tify)
• Auricular flutter below • Ventricular tachy-
with varying cardia (150-200
atrioventricular per minute, starts
block and stops abrup-
tly, carotid sinus
pressure has
no effect, QRS
bizarre, P often
B. P revealed hidden in QRS)
First note the shape and size of P-wave
|
| |
Broad and notched P Tall, narrowed and peaked Changing shape of P
due to left auricular P due to right auricular 1. Wandering pacemaker (also varying P-R
enlargement or hyper- hypertrophy or enlargement interval)
trophy (P-mitrale) (P-pulmonale) 2. PAT with block
↓ 3. Multifocal extrasystole
Then note is P is not followed by QRS, e.g. isolated P or multiple P.
Determine whether P is related with QRS or independent of it and also note P-R interval:
|
| |
P independent of QRS P related with QRS
with varying P-R interval |
• Complete atrioventricular block | |
With gradually increasing With constant P-R interval:
P-R interval: Mobitz type • Mobitz type II second
I second degree AV block degree AV block
(Wenckebach) • PAT with 2:1 block
Contd...
P-Wave 19
Contd...
• Atrioventricular dissociation (P-R • Blocked atrial extrasystoles
interval progressively shorter)
↓
Next note relation between atrial and ventricular rate
|
| |
Atrial rate faster than Atrial rate slower than
ventricular rate ventricular rate
↓ ↓
Suggests complete heart Suggests AV dissociation
block (CHB) due to causes other than
↓ complete heart block
Finally note the shape
of ventricular complex
in CHB |
| |
Normal shaped QRS Bizarre QRS
suggests 2nd pacemaker suggests 2nd pacemaker
in AV node (1st pace- in the ventricle (1st pace-
maker in the SA node) maker in the SA node)
↓
Next note any inverted P-wave: P is normally inverted in aVR. If P is upright in aVR, look for inverted P
in other leads and its relationship with QRS
|
| |
Inverted P in lead aVF Inverted P in lead I
suggesting retrograde atrial conduction:
• Inverted P in aVF preceding QRS as in: • True dextrocardia (also inverted T in lead I,
— High AV nodal premature focus (taller R in lead V1-2 and deeper S in lead V5-6)
as in nodal extrasystole • Technical dextrocardia, i.e. reversal of right
— Low atrial focus as in low atrial or left arm leads
extrasystole
• Inverted P in aVF following QRS as in:
low AV nodal focus as in nodal extrasystole
Sinoatrial Block (SA Block)
Suppression of SA node is SA block. It is characterised by a prolonged pause (due to dropping of a

complete cycle, i.e. PQRST, the next cycle appears at double the normal interval) and escape rhythm.
When the SA node fails, the AV node starts the impulse (nodal escape) and if the AV node is also
suppressed, the ventricle starts the impulse (ventricular escape). The nodal escape (50-60 per minute)
is slower than the SA rhythm (70-80 per minute) and the ventricular escape (30-40 per minute) is slower
than the nodal escape. The nodal escape had normal shape of QRS, the ventricular escape has bizarre
QRS.
Illustrative ECG Showing Absent or Modified P-wave (Figs 6.1 to 6.5)
Fig. 6.1: Auricular fibrillation. P-wave replaced by fibrillary waves (f) ventricular rate irregular
Fig. 6.2: Auricular flutter: Flutter waves (F) have a saw-tooth appearance. P-waves replaced by F-waves
Fig. 6.3: SA block without any atrial activity resulting in an escape rhythm with ventricular rate of 27 beats
per minute and bizarre QRS complexes—Ventricular escape rhythm. Note absent P-waves
Fig. 6.4: Hyperpotassemia: P-wave absent

P-Wave 21
Fig. 6.5: Nodal premature beat (N). P buried in QRS
Illustrative ECG Showing Inverted P-wave (Figs 6.6 and 6.7)

Fig. 6.6: The second beat is premature (occurs earlier
in the cardiac cycle (E) than expected. E is preceded
by inverted P-wave. An atrial ectopic. Low atrial focus
Note:
Nodal ectopic: (a) In high AV nodal focus inverted P
precedes QRS complex in aVF
(b) In low AV nodal focus inverted P follows QRS
complex in aVF
Fig. 6.7: True dexocardia: Inverted P in lead I. Lead I is the mirror image of normal aVR.
In chest leads R in V1 becomes smaller as we move across towards V6, reverse holds are S-wave
Illustrative ECG Showing Abnormal Shapes of P-wave (Figs 6.8 to 6.10)
Fig. 6.8: Wandering auricular pacemaker. Varying shaped P-wave and varying P-R interval
Fig. 6.9: Acute pulmonary embolism: Large P-wave in lead II and III. Right bundle branch block in V1 (usually transient).
Clockwise rotation. T-wave inversion in right chest with S-T segment depression
Fig. 6.10: AB + BC = greater than CD + DE i.e. compensatory pause incomplete
Illustrative ECG Showing Multiple or Isolated

(not followed by QRS) P-wave (Figs 6.11 to 6.15)
Fig. 6.11: Supraventricular tachycardia with 2:1 AV block.

2 P-waves can be seen for each QRS complex multiple P-waves are seen
P-Wave 23
Fig. 6.12: Complete heart block. Multiple P-waves
Fig. 6.13: Some P-waves occur prematurely (B) but are not followed by QRS
complexes—blocked premature atrial beat note multiple P-waves
Fig. 6.14: Wenckebach phenomenon (Mobitz type I AV block): Multiple P-waves.

P=R interval gradually increases until after the 4th QRS-T complex a P-wave
appears which is not followed by QRS—more P than QRS (multiple P-waves)
Fig. 6.15: 2nd degree AV block (Mobitz type II) 1,2,3 and 4 is of sinus origin.
Isolated P is not followed by QRS (Beat is dropped)
A Few More ECG Showing Abnormalities of P-wave (Figs 6.16 to 6.21)
Fig. 6.16: AV nodal rhythm: P follows Fig. 6.17: Left atrial hypertrophy: Biphasic prominent
QRS. P are inverted P-wave. P mitraile
Fig. 6.18: Right atrial hypertrophy. Prominent P, P-Pulmonale
Fig. 6.19: Atrial flutter: Saw-toothed flutter waves seen in II, III, aVF regular atrial rhythm. 4:1 ventricular response
Fig. 6.20: Auricular fibrillation: P-waves replaced by Fig. 6.21: Complete heart block: Multiple P-waves. Auricular
fibrillary waves. Ventricular rhythm irregular rate 100 per minute, ventricular rate 60 per minute. P-R interval
varies
Q-Wave 25
7 Q-Wave
Mechanism
Q-wave is formed as a result of septal activation during ventricular depolarisation. Q normally presents in lead
aVL when heart is vertical and in lead aVF when the heart is horizontal; and in V1 and V2.
Duration: less than 0.04 second (25% of total QRS duration).
Depth: less than 2 mm in lead I and II.
Various configurations of the Q-waves:
QR QRS QS (Q is the only deflection)
Causes of Pathological Q-wave

A. Q-wave in multiple leads
|
| |
Infarct Q-wave Non-infarct Q-wave
Q in lead II,III,aVF: ______→ Recent inferior infarct ______→ • Acute pulmonary embolism
• Old inferior infarct • Emphysema
Q in lead V1-3 and V3R: __→ Recent antero-septal infarct → • Cor pulmonale (Acute)
• Old antero-septal infarct • Rules out right bundle branch block (RBBB)
Q in lead V4-6 and lead I: → Recent antero-lateral infarct → • Cardiomyopathies
• Old antero-lateral infarct • Rules out left bundle branch block (LBBB)
QR in aVR______________________________________________________→ Marked clockwise rotation
Approach
Find out in which lead Q is present (whether in multiple leads or in isolated lead). Also note whether associated
with elevated S-T segment. Elevated S-T suggests infarction Q-wave of recent onset.
I. Q-wave in leads II, III, aVF:
Look for whether S-T segment is elevated or not
|
| |
With elevated S-T segment Without elevated S-T segment
↓ ↓
Suggests recent inferior infarct (associated • Remember important causes: Old inferior
with inverted T-wave) and acute pulmonary wall infarct (with or without inverted T-
embolism (associated with inverted T and wave) and pulmonary embolism
Contd...
depressed S-T in V1 and V2, peaked P, • Posterior infarct (old) (confirmed by tall
right axis deviation, S1Q3T3 syndrome and T-wave in chest leads)
incomplete right bundle branch block). • WPW syndrome
‘Whenever ECG shows inferior infarct plus
antero-septal infarct, suspect massive pulmo-
nary embolism as the alternative diagnosis’
II. Q-wave in right chest leads (V1 to V3):

|
| |
↓ ↓
Recent antero-septal infarct (associated with • Remember important causes: Very old antero-
initial R-wave and inverted T in V3R and V4R) spetal infarct (with or without inverted T), acute
cor pulmonale (associated with right ventricular
hypertrophy and strain, peaked P)
• Rules out right bundle branch block (RBBB)
III. Q-wave in left chest leads (V4 to V6): or lead I and aVL:

|
| |
↓ ↓
Recent antero-lateral infarct • Remember important causes: Very old antero-
lateral infarct (with or without inverted T), left
ventricular hypertrophy (50% cases)
• Rules out left bundle branch block.
IV. Q-wave in multiple leads: Cardiomyopathy (generalised low voltage and left axis deviation).
V. Q-wave in isolated leads:

|
| | | |
Q in lead III Q in aVR Q in aVL Q in aVF
• S1Q3T3 syndrome • Right ventricle • S1S2S3 syndrome • Inferior wall infarct
in acute pulmonary hypertrophy See table • Acute cor pulmonale
embolism • Emphysema • Normally present • WPW syndrome
• Q normally present • Marked clockwise in vertical heart • Obese persons in recum-
in lead III rotation bent position
• Inferior wall infract • Right bundle
See table branch block
Q-Wave 27
Showing Q in Illustrative ECG of Acute Pulmonary Embolism (Fig.

7.1)
Fig. 7.1: Acute pulmonary embolism

causing acute cor pulmonale. Deep S-
wave in leads I,II, and III. Clockwise
rotation. Inverted T in III and aVF
Illustrative ECG Showing Q in Acute Myocardial Infarction (Fig.

7.2)
Fig. 7.2: Q-waves in leads V1, V2 and V3. Chest leads show inverted T-waves.
Suggests recent antero-septal infarct (elevated S-T)
Illustrative ECG Showing Q in Old Infarction (Figs 7.3 and 7.4)
Fig. 7.3: Deep Q-waves in lead I and aVL and inverted T suggesting old antero-lateral infarct (no S-T elevation hence
suggests old infarct). Normal gradual increase of R-wave from V1 to V6 has not occurred (poor R-wave progression)
sometimes the only indication of old anterior infarct
Q-Wave 29
Fig. 7.4: Small q-waves in leads II, III, and aVF. The tall T-waves in V2-V4 confirms
posterior infarction. Non-elevation of S-T segment points to old infarct
Illustrative ECG Of Q in Miscellaneous Conditions (Figs 7.5 and

7.6)
Q in WPW syndrome
Fig. 7.5: WPW syndrome. Short P-R interval. The initial limb of R-wave is
slurred in leads I, aVL, V2-6. Q in aVF, II and III
Q in marked clockwise rotation
Fig. 7.6: Right ventricular hypertrophy with clockwise rotation and right axis deviation.
Marked clockwise rotation suggested by QR in aVR and deep S-wave in V5, V6
Q-Wave 31
QS Abnormalities
QS Complex in V 1 , V 2 , V 3 and V 4
A. Antero-septal infarction
B. Left ventricular hypertrophy
QS in Leads I and V 1 -V 3
A. Anterior infarct
B. Emphysema Fig. 7.7: Anterior infarction
C. Right ventricular hypertrophy
QS in Leads II, III and aVF
A. Inferior infarction
B. Emphysema
C. Right ventricular hypertrophy
Fig. 7.8: QS complex in leads I and V1-3(4)
Inferior Infarction
Fig. 7.9: QS complex in leads II,III and aVF Fig. 7.10: Antero-septal infarction
Fig. 7.11: Left ventricular hypertrophy

Significance of Q-wave in Lead III in Inferior Wall Infarction
1. Q-wave must be 0.04 second or more in duration and more than 4 mm in depth.
2. Q should be present in lead II and aVF.
3. R in lead III must be at least 5 mm in height.
4. P in lead III must be upright.
Causes of S 1 S 2 S 3 Syndrome
1. Normal.
2. Congenital heart disease with right ventricular hypertrophy.
3. Cor pulmonale.
4. Acute myocardial infarction.
5. Pregnancy.
6. Right ventricular hypertrophy in a child.
Q-Wave 33
QRSCOMPLEX
The QRS complex represents ventricular depolarisation. It is always negative in lead aVR.
Normal duration: 0.04 to 0.11 second
Height: It is measured in standard limb leads—more than 5 mm.
Different configuration of QRS complexes:
QR QRS QS RS RSR’ Rr’ RSR‘S’
Causes of Abnormal QRS Complex
Wide QRS Complex
It varies according to the shape of QRS complexes.

|
| | | | |
Bundle branch 1. Ventricular Hyperpotassemia Quinidine effect WPW syndrome
block rsR or ‘M’ ectopic Wide Wide QRS with Wide QRS with Wide QRS with
wave pattern QRS with dep- tall peaked T short and wide T slurring of proximal
ressed S-T limb of QRS
and T point- (delta-wave)
ing opposite
to QRS
1. Right bundle (Late effect → (Q-T prolonged)

branch block P absent)
(RBBB)—
rsR in V1, V2 (short P-R interval)
and V3R (QRS (Premature, constant
more than 0.12 coupling interval, full
second and compensatory pause)
wide S1 in lead I)
2. Left bundle
branch block
(LBBB) —
rsR in V4-7 and I
(QRS more than VPB
0.12 second and 2. Parasystole: shape
absence of Q in of QRS like ventri-
V4-7 and I) cular ectopic (varying
coupling interval,
occasional fusion
beat, not premature)
Wide Bizarre QRS Complex

|
| | | |
Aberrant ventricular Ventricular tachycardia: Ventricular fibrillation: Ventricular flutter:
conduction: Burst of bizarre wide and Burst of completely Burst of large undefinable
Wide, notched notched QRS irregular rapid bizarre rapid-waves
bizarre QRS oscillations
(related to P, RBBB
pattern in V1, qRS in
V6, this bizarre complex
may interrupt auricular
fibrillation or a run of
rapid beats)
Abnormal Voltage of QRS Complex

|
| | |
High voltage: Low voltage: Varying heights of QRS:
• Ventricular hypertrophy: • Hypothyroidism (bradycardia, • Pericardial effusion
– Left ventricular hypertrophy flattened or inverted T, S-T • Electrical alternans
(R in V6 more than 27 mm, normal)
R in I, aVL: more than 13 • Pericardial effusion (often electri-
mm, SV1 + RV6 (or RV5) cal alertnans)
more than 35 mm • Chronic constrictive pericarditis
– Right ventricular hypertrophy (flattened and inverted T)
(R in V1 more than 7 mm) • Myocardial infarct (Q, elevated S-T
• Thin chest wall and inverted T)
• Emphysema (Right axis deviation
Peaked P Clockwise rotation)
• Serve cardiac failure
Illustrative ECG Showing Wide QRS Complex (Figs 7.12 to 7.22)
Fig. 7.12: Ventricular fibrillation: Rapid, irregular, chaotic and deformed deflections
Q-Wave 35
Fig. 7.13: Quinidine toxicity. Wide and bizarre QRS resulting in slow ventricular tachycardia. No atrial activity is seen
Fig. 7.14: Complete right bundle branch block: Right axis deviation. Wide QRS in right chest leads.
Wide slurred S-wave in leads I, V5, V6. Absent Q in right chest leads
Fig. 7.15: It looks like ventricular tachycardia but each complex is preceded by a P-wave.
Atrial tachycardia with aberrant ventricular conduction. Wide bizarre QRS
Fig. 7.16: 2,4 and 6th complexes are normal beats. 1st, 3rd, 5th and 7th complexes are wise and bizarre like ventricular
ectopics. But each ectopic beat is preceded by a small P-wave, hence, they are atrial ectopic with aberrant ventricular
conduction
Fig. 7.17: Ventricular tachycardia. Slightly irregular rhythm. Wide slurred QRS
Fig. 7.18: Incomplete right bundle branch block. QRS less than 0.12 second.
Right axis deviation. Right ventricular hypertrophy (tall R in V1 and V2)
Fig. 7.19: Right bundle branch block
Fig. 7.20: Left bundle branch block

Q-Wave 37
Fig. 7.21: (A) Ventricular pre-

mature beat (VPB), (B) Bige-
minal ventricular premature
beat (VPB), (C) Interpolated
ventricular premature beat
(VPB). QRS-T complexes of
VPB are wide and bizarre with
depressed S-T and T pointing
opposite to QRS. Compen-
satory pause are complete
in A and B. In C VPB occurs
between two normal beats
without compensatory pause
Fig. 7.22: Wolff-Parkinson-White syndrome. Short

P-R interval. Wide QRS complex with slurring of
the ascending limb of QRS in leads in I, aVL, V5 and
V6 and descending limb in III, aVF, V1 and V2
Illustrative ECG Showing Voltage Abnormalities of QRS (Figs 7.23

to 7.25b)
Fig. 7.23: Electrical alternans. Varying heights of QRS

Fig. 7.24: Right ventricular hypertrophy. Tall R in V1 and deep S in V5-V6. Right axis deviation. Clockwise rotation
Figs 7.25a and b: Left ventricular hypertrophy. Deep S-wave in V1, V2, and tall R-wave in V5, V6.
Left axis deviation. Tall R in aVL. S-T depression and inverted T in V5, V6
Q-Wave 39
Fig. 7.26: Left ventricular hypertrophy. Deep S in V2, Tall R in V5
Fig. 7.27: Right ventricular hypertrophy. Tall R in V1

8 T-Wave
Repolarisation of the ventricles is depicted by T-waves. T-wave is usually more

than 2 mm in height. Its maximum height in the standard leads is 5 mm and in the
chest leads is 10 mm. It is normally upright in all the leads except in aVR. It may be
normally inverted in leads III, aVF, V1 and V2 but inverted T in leads I, V3-6 is
abnormal. An inverted T in aVL with vertical heart is normal. The curve of T is
usually smooth, if it is sharp or notched (see adjacent figure) one should suspect
superimposed P on T-wave. T-wave may be inverted, flat or upright in lead III
without clinical significance.
Causes
Flattened T-wave
• Ischaemia • Pericarditis
• Chronic constrictive pericarditis • Myxoedema
• Cardiomyopathy • Quinidine toxicity.
Deep Inversion of T-wave
A. Symmetrical inversion:
1. In leads II, III and aVF:
• Inferior wall infarction
• Inferior wall ischaemia
• Subendocardial infarction.
2. In leads I, aVL and V2-6:
• Anterior infarction
• Anterior ischaemia
• Subendocardial infarction.
B. Asymmetrical inversion:
1. In leads I, aVL and V4-6 (left chest leads):
• Left ventricular hypertrophy
• Left bundle branch block
• Left ventricular strain
• Myocarditis
• Cardiomyopathy
• Anxiety
• Prolonged tachycardia
• Hyperthyroidism.
T-Wave 41
2. In leads V1-3 and V3R (right chest leads):

• Right ventricular hypertrophy
• Right bundle branch block
• Right ventricular strain
• Acute pulmonary embolism
• Normal child (juvenile pattern)
• Negro male.
3. Other causes:
• Isolated T negativity syndrome (normal variant) in leads V3 and V4
• Late stage of pericarditis
• Chronic constrictive pericarditis
• WPW syndrome
• Anemia.
Tall Peaked T-wave
• Hyperkalemia • Posterior infarct • Normal variant.
Approach
I. Approach to flattened T-wave:

Determine the voltage (low or normal) and position of S-T segment (depressed or isoelectric).
Flattened T
|
| |
Low voltage Normal voltage
| | | |
With isoelectric S-T With depressed S-T With isoelectric S-T With depressed S-T
segment segment segment segment
↓ ↓ ↓ ↓
Myxoedema (also Cardiomyopathy (also Pericarditis (late) 1. Quinidine toxicity
bradycardia and pro- deep Q, left axis deviation, (Fig. 8.2)
longed PR) (Fig. 8.1) prolonged QT and PR) 2. Digitalis toxicity
Fig. 8.1: ECG criteria of myxoedema Fig. 8.2: ECG criteria of quinidine toxicity
II. Approach to deep inversion of T-wave:

Note whether inversion is symmetrical (both limbs of T equal) or asymmetrical (limbs of T unequal). Note
the specific leads in which T is inverted.
In symmetrical inversion (Fig. 8.3), note whether Q is absent or present and S-T elevated or isoelectric.
In asymmetrical inversion, look for configuration of QRS, position of S-T and abnormalities of PR and
QT intervals.
Symmetrical inversion of T-wave (Fig. 8.3)
| |
In leads II, III, aVF In leads I, aVL, V4-6
| | | |
With Q and elevated Depressed or isoelectric With Q and elevated Depressed or isoelectric
S-T: S-T: S-T: S-T:
Recent inferior Subendocardial infarct. Recent anterior Subendocardial infarct.
wall infarct Inferior wall ischaemia. infarct Anterior ischaemia
Late inferior wall infarct Late anterior infarct
Subendocardial infarct Acute myocardial infarct Myocardial ischaemia
Fig. 8.3: Differential diagnosis of symmetrical T-wave inversion
Asymmetrical Inversion of T-wave (Fig. 8.4)

I. In left chest leads:
1. Left ventricular hypertrophy (also tall R, wide QRS, depressed S-T).
2. Left bundle branch block (also ‘M’ type QRS, depressed S-T).
3. Left ventricular strain (also normal R and QRS, S-T depressed).
4. Myocarditis (also prolonged QT and PR, depressed S-T and arrhythmia).
5. Cardiomyopathy.
6. Anxiety, tachycardia and hyperthyroidism.
II. In right chest leads:
1. Right ventricular hypertrophy (also tall R, wide QRS and depressed S-T).
2. Right bundle branch block (‘M’ type QRS with depressed S-T).
3. Right ventricular strain (also normal R and QRS, depressed S-T).
4. Acute pulmonary embolism (also peaked P, depressed S-T, right bundle branch block).
5. Juvenile pattern in child and negro.
III. In any lead except aVR:
1. Late pericarditis (isoelectric S-T).
2. Anemia.
3. Chronic constrictive pericarditis.
4. Hypokalemia (also prolonged PR and QT, depressed S-T and prominent U).
5. WPW syndrome (short PR and slurred QRS).
T-Wave 43
Bundle branch WPW syndrome Ventricular Ventricular Ventricular

block (‘M’ type (short PR and hypertrophy strain (normal extrasystole
QRS) slurred QRS) (tall R) R and QRS) (bizarre QRS)
Myocarditis Tachycardia Peaked P, ST Right bundle

(prolonged PR and Anxiety depressed, T branch block
QT; ST depressed) Hyperthyroidism inverted in V1-3
1. Chronic constrictive
pericarditis
2. Juvenile pattern in V1-3
} Acute pulmonary embolism
Hypokalemia (prolonged PR and QT;

ST depressed; prominent U-wave)
Fig. 8.4: Differential diagnosis of asymmetrical T-wave inversion

III. Approach to tall peaked T-wave:
Note the affected leads
| | |
All leads except aVR and Lead III and aVF: Lead V1-4
aVL with vertical heart:
↓ ↓ ↓
Hyperkalemia (absent P) Anterior infarct Posterior infarct (tall R in V1)
9 U-Wave
The U-wave represents the period of greatest excitability and is considered to represent slow depolarisation of
the interventricular conducting septum. It is best seen in V3. It is usually upright and in the same direction as
the T-wave. The U-wave occurs after the second heart sound.
Approach
Note whether the U-wave is prominent, i.e. taller than the T-wave or inverted. Note also the affected leads.
|
| |
Prominent U-wave: Inverted U-wave:
Bradycardia. a. Inverted U in left chest leads (I, aVL, V4-6):
Hypokalemia (prolonged Antero-lateral ischaemia
PR and depressed ST) Left ventricular hypertrophy
Left ventricular strain
b. Inverted U in right chest leads (V1-3):
Antero-septal ischaemia
Right ventricular hypertrophy
Right ventricular strain
Fig. 9.1: Hypokalemia—T-waves depressed. Prominent U-wave. Depressed S-T segment in chest leads.
QT prolonged in some leads where separation from U-wave is not distinct
S-T Segment 45
10 S-T Segment
S-T segment represents the process of recovery (repolarisation) after ventricular excitation (depolarisation)
and may be followed by a small U-wave.
↑ ↑
Repolarisation
Depolarisation
The duration of S-T segment is nil to 0.15 second. It is normally isoelectric. Slight S-T segment elevation
upto 1 mm may be normally found especially in V1 and V2. When determining S-T segment shift, the junction of
P-R segment with the QRS complex as reference level has been recommended by the American Heart Association.
This reference line is unsatisfactory in cases of early repolarisation. This S-T segment elevation in such a case
is compared with the T-P interval.
A.
S-T segment in A at first glance appears elevated
but is within normal limits when compared with
the following T-P baseline. This is due to early
repolarisation. S-T segment in B is elevated
B. pathologically in comparison to the T-P line.
Causes of Abnormal S-T Segment

I. S-T segment elevation:
a. Convex elevation:
01. Acute myocardial infarction
02. Ventricular aneurysm.
b. Concave elevation:
01. Pericarditis
02. Prinzemetal’s angina
03. Normal variant in young adult negroes
04. Metastatic tumours of the heart.
II. S-T segment depression:

a. Concave depression:
01. Digitalis effect.
b. Horizontal or oblique depression:
1. Ischaemic heart disease
2. Subendocardial infarction
3. Acute pulmonary embolism.
c. Oblique depression:
01. Ischaemic heart disease 02. Left ventricular hypertrophy
03. Right ventricular hypertrophy 04. Left bundle branch block
05. Right bundle branch block 06. Left ventricular strain
07. Right ventricular strain 08. Ventricular premature beat
09. Drugs: digitalis, quinidine, emetine 10. Myocarditis
11. Cardiomyopathy 12. Overventilation, anxiety
13. Tachycardia.
Approach
I. Elevated S-T segment

Note the shape of elevation whether concave or convex. Also note the affected leads and other special
features.
|
| |
Concave elevation Convex elevation
| | | |
I, aVL, V4-6 All leads except II, III, aVF I, aVL, V4-6
↓ aVR, V1 and aVL ↓ ↓
• Prinzemetal angina with vertical heart: • Recent inferior wall • Recent anterior infarct
• Young negro (S-T ↓ infarct (associated (associated with Q and
may become isoelec- Acute pericarditis with Q and inverted T) inverted T)
tric after exercise) • Ventricular aneurysm • Ventricular aneurysm
(infarction pattern per- (infarction pattern per-
sists instead of healing sists instead of healing
with time) (See Fig. 10.1) with time)
Fig. 10.1: Types of convex S-T elevation

S-T Segment 47
Different types of concave S-T elevations Diseases Affected leads

Pericarditis All the leads except aVR
and V1 and in aVL in
vertical heart
Prinzemetal angina I, aVL, V4-6
Young negroes Left chest leads
Cardiac trauma Any lead—localised or

diffuse
Fig. 10.2: Types of concave S-T elevation
II. Depressed S-T segment

Note the shape of the S-T depression, affected leads and any other associated features.
First note the shape of the S-T depression. It may be concave, convex, horizontal or oblique depression:
Horizontal
depression
Horizontal Convex
depression
Oblique
depression { Ischaemia
Sub-endocardial infarct.
Acute pulmonary embolism
______________
Concave (Hammock or Oblique (Correction → Digitalis effect
boat shaped) mark shaped)
Ventricular hypertrophy
Bundle branch block
Ventricular strain
Oblique depression
{ Anxiety
Anemia
Over-ventricular
Ventricular premature beat
Myocarditis
Cardiomyopathy
Ischaemia
Oblique depression Sub-endocardial infarct
Then note the affected leads and any other associated features:
Then note the affected leads and any other associated features:
| | |
Any lead Left chest leads, I and aVL: Right chest leads:
a. Concave depression: Horizontal or oblique depression: Horizontal or oblique depression:
Digitalis (with or without 1. Left ventricular hypertrophy 1. Right ventricular hypertrophy
flattened or inverted T; AV (tall R, wide QRS) (tall R, wide QRS)
Block, premature beats) 2. Left ventricular strain (normal 2. Right ventricular strain (normal
b. Horizontal or oblique R and QRS) R and QRS)
depression: 3. Left bundle branch block 3. Right bundle branch block
1. Ischaemia (with or (rSR’ pattern in V4-6). (rsR pattern in V1-2).
without inverted T; 4. Cardiomyopathy (inverted T, 4. Acute cor pulmonale or pulmo-
any arrhythmia) prolonged P-R and Q-T, low nary embolism (Q and symmetri-
2. Subendocardial infarction voltage, arrhythmia, left axis cally inverted in III and aVF like
(symmetrically inverted T) deviation) inferior wall infarct but S-T is
3. Exercise test 5. Overventilation and anxiety isoelectric in III and aVF; dep-
4. Quinidine (depressed T, 6. Ischaemic heart disease. ressed S-T)
conduction disturbance, 5. Normal in children.
prolonged Q-T)
5. Hypokalemia (flattened
or inverted T, prominent U)
6. Ventricular
7. WPW syndrome
(short P-R, slurred QRS).

Finally, note effect of modifying factors (Valsalva manoeuvre, exercise, head tilting and
atropine injection).
Causes of S-T depression: Modifying factors Effect on ECG
Digitalis Valsalva manoeuvre, exercise Increases S-T depression
and head tilting and T-wave changes
Overventilation and anxiety Atropine intravenous injection Abnormal T-wave becomes normal
Angina Exercise Horizontal depression of S-T
Diagnosis of Angina
Diagnosis of myocardial anoxia is confirmed by depressed S-T and flattened or inverted T during
(1) spontaneous angina or (2) coronary insufficiency induced by exercise tests. But a normal exercise ECG does
not exclude the diagnosis of angina. A careful history is more important (central chest pain on exertion and
relieved by rest). The ECG is usually normal in angina. Serial ECG are taken at rest and (1) immediately after, (2)
two minutes after, (3) six minutes after two-step (Master) exercise test and if the last record is still normal, ECG
is taken 10 minutes after.

Result of exercise and criteria of positive test
1. S-T segment depression or elevation of 1 mm or more in lead I, or 1.5 mm or more in
lead II, or 1.5 mm or more in lead III and of 2 mm or more in chest leads.
S-T Segment 49
Horizontal depression Down-slopping S-T segment Depressed S-T junction

↓ ↓ ↓
Positive Probably Negative Negative
2. Diphasic or inverted T in leads II or III or chest leads.

3. Bundle branch block
4. Ventricular ectopic.
5. Inversion of W-wave.
Ventricular hypertrophy: Ventricular strain: Coronary ischaemia: Bundle branch block:

Tall R, wide QRS, asym- Normal R and QRS, limbs of T, symmetri- ‘M’ type of QRS, asymme-
metrically inverted T symmetrical limbs cal, and sharp pointed trical limbs of T
of T vertex of T
Fig. 10.3: Different types of inverted T associated with S-T depression.

Most of the S-T depressions are associated with flattened or inverted T-wave
Ventricular hypertrophy: Bundle branch block: Ventricular premature beat: WPW syndrome:
Tall R, wide QRS ‘M’ type QRS Bizarre QRS Short P-R with wide and slurred
QRS
resembling bundle branch block
Fig. 10.4: Different types of QRS associated with S-T depression
Illustrative ECG Showing S-T Segment Shift (Fig. 10.5 to 10.22)
Fig. 10.5: Ventricular premature beat (ectopic beat). Note S-T segment depression and
inverted T-wave and wide bizarre QRS complex
RT Bundle Branch Block

Fig. 10.6: Right bundle branch block. Oblique depression of S-T segment in
V1, V2, V3 with wide notched R-wave (M complex)
Fig. 10.7: Digitalis effect. Note Hammock shaped S-T segment depression
Fig. 10.8: Exercise test for angina pectoris. Note S-T depression in lead aVL and V3 S-T
elevation in aVR after exercise
Fig.10.9: Angina, S-T segment depression
LEAD FACING INJURED SURFACE
LEAD FACING UNINJURED SURFACE
PHASE I PHASE 2 PHASE 3 PHASE 4
Fig. 10.10: Shift of S-T segment in myocardial infarction. Lead facing injured surface in acute myocardial
infarction shows elevated S-T segment. Lead facing uninjured surface shows S-T depression
S-T Segment 51
Fig. 10.11: Left branch block. Oblique depression S-T segment V5, V6 with wide QRS (M complex)
Fig. 10.12: Note S-T segment depression after exercise
Fig. 10.13: Ventricular premature beats followed by run of ventricular tachycardia.

Note S-T segment depression with wide QRS and inverted T in VPB
Fig. 10.14: Hypokalaemia. Note S-T depression
Fig. 10.15: Ventricular premature beats (1 and 2). Note S-T depression with inverted T and wide QRS in VPB
Fig.10.16: Ischaemia. S-T segment depression and T inversion

S-T Segment 53
Fig. 10.17: Atrial ectopic with aberrant ventricular conduction 1, 3, 5 and 7 look like ventricular ectopic but each of these
ectopics are preceded by a small P-wave hence it is atrial ectopic with aberrant ventricular conduction. Note the S-T
depression and inverted T-wave in ectopic complex
Fig. 10.18: Acute cor pulmonale. S1Q3 pattern. Depres-

sed S-T segment in lead I and II. Lead III shows changes
of inferior wall infarction without shift of S-T segment
Fig. 10.19: Complete sino-auricular block with ventricular escape rhythm. Note absent P-wave resulting in ventricular
escape rhythm with slow ventricular rate. Note bizarre ventricular complex with oblique depression of S-T segment and
inverted T-waves
Fig. 10.20: Ventricular aneurysm. Note the curved elevation of S-T segment in V5 and V6.
The diagnosis is confirmed if S-T segment changes persist over a prolonged period
Fig.10.21: Acute cor pulmonale (acute pulmonary embolism)
Fig. 10.22: Paroxysmal atrial tachycardia. Note S-T segment depression
Fig. 10.23: Acute anterior myocardial infarction. Note shift of S-T segment
S-T elevation in I, II and aVL S-T depression in III and aVF
Fig. 10.24: Digitalis effect: Correction mark abnormally of S-T segment

S-T Segment 55
Fig. 10.25: Anterior subsendocardial infarction. Note shift of S-T segment both
elevation (reciprocal) in aVR and depression in V2-V6, I and aVL
Fig. 10.26a: Pericarditis. All leads facing the injured

surface show concave raised S-T segment
Fig. 10.26b: Pericardial effusion. When pericarditis subsides S-T segment returns to base line and flat or inverted T-waves
occur. After full recovery the ECG returns to normal. If the condition progresses to constrictive pericarditis or to pericardial
effusion, T-waves remain inverted and QRS complexes show low voltage
Fig. 10.27: Posterior infarct. S-T segment depression in V1, V2, V3, V4, V5, V6, aVL. S-T elevation in aVF
Fig. 10.28: Left ventricular hypertrophy and strain. Depression of S-T segment in lead I, aVL, V4 and V5. Left axis deviation. Horizontal line
Fig. 10.29: Right ventricular hypertrophy and strain. S-T segment depression in V1-V6. Right axis deviation. Vertical line
Fig. 10.30: Digitalis effect: S-T segment depression resembling inverted hockey stick is typical of digitalis effect
P-R Inverval 57
11 P-R Interval
P-R interval measures atrioventricular conduction time. Transit time for excitation to travel from SA node,
through atrial and AV node down the bundle of His to reach the ventricles is depicted as P-R interval. It varies
from 0.12 to 0.20 second. Maximum is 0.22 second. It must be correlated with heart rate.
Causes of Abnormal P-R Interval

A. Prolonged P-R interval:
1. Digitalis effect
2. First degree heart block due to digitalis, ischaemic heart disease, active rheumatic carditis and
hypokalemia
3. Beta-blocker
4. Atrial septal defect
5. Myxoedema.
B. Shortened P-R interval:
1. WPW syndrome
2. Lown-Ganong-Levine syndrome
3. Nodal rhythm with inverted P preceding QRS
4. Normal.
C. Varying P-R interval:
1. Second degree heart block with Wenckebach phenomenon
2. Wandering pacemaker
3. Complete heart block
4. Atrioventricular dissociation.
Approach
Prolonged P-R Interval
Note the associated special features:
Causes Other special features
Digitalis • Sagged or scooped or hammock-shaped S-T depression. Any type
of arrhythmia and atrioventricular block
Rheumatic carditis • Prolonged Q-T interval
Quinidine • Widened QRS, ventricular arrhythmia and atrioventricular block
Hypokalemia • U-wave, S-T depression, T-wave inversion
Atrial septal defect • Incomplete right bundle branch block
Beta-blocker • Sinus bradycardia
Shortened P-R Interval

Note the associated special features
Causes Other special features
WPW syndrome • Slurred QRS (thickened upstroke of QRS called the delta wave)
Lown-Ganong-Levine syndrome • No other abnormality
Nodal rhythm • Inverted P preceding QRS
Fig. 11.1: Wandering auricular pacemaker. Note different shapes of P and varying P-R interval
Varying P-R Interval
Note the P-P and R-R interval

| |
Varying P-R with constant P-P and R-R intervals Varying P-R with varying R-R interval
↓ ↓
suggests: suggests
1. Complete heart block 1. Wandering pacemaker (Fig. 11.1)
2. AV dissociation 2. Second degree heart block (Wenckebach)
↓
Note atrial and ventricular rate
| |
Atrial rate faster Ventricular rate
than ventricular rate faster than atrial rate
↓ ↓
Complete heart block AV dissociation
Illustrative ECG Showing abnormalities of P-R Interval (Figs 11.2 to 11.4)
Fig. 11.2: Complete heart block. P-R interval varies. Independent and regular atrial and
ventricular rate—Atrial rate 72 per minute and ventricular rate 64 per minute
P-R Inverval 59
Fig. 11.3: First degree heart block. P-R interval prolonged
Fig. 11.4: First degree heart block. Prolonged P-R interval

12 Q-T Interval
Q-T interval represents total time taken for depolarisation and repolarisation of ventricle muscles. Maximum
duration is 0.43 second in males and 0.42 second in females for a heart rate of 70 per minute. The electrical
systole coincides with Q-T interval.
Causes
I. Prolonged Q-T interval:
1. Hypocalcemia
2. Active rheumatic carditis
3. Ventricular hypertrophy
4. Hypopotassemia
5. Myocardial ischaemia
6. Quinidine effect
7. Diphtheritic heart
8. Severe liver disease.
II. Shortened Q-T interval:
1. Digitalis effect
2. Hypercalcemia.
Clinical Notes
1. Q-wave normally presents in aVR and III. Pathological Q in I, II, aVF and aVL except when QRS axis
more than +60 degree, indicate myocardial infarction.
2. R-wave progression in chest leads: Loss of height of R+ normal height of on both sides of infarcted zone
or the previous ECG shows normal height of R in the infarcted zone, suggest myocardial infarction.
Abnormal decrease in the height of R without their disappearance in chest leads suggest infarction.
3. Flattened T, diaphasic T or inverted T occur not only in acute myocardial infarction but also in myocarditis,
pericarditis, digitalis toxicity and electrolyte imbalance.
4. Depth of Q is directly proportional to relative thickness of dead zone of infarcted tissue and height of
R-wave is directly proportional to amount of living tissue that escapes death.
5. Some elevation of S-T segment is normal in V1-2 (1-2 mm) and does not indicate acute infarction. If
elevation is concave in the direction of QRS deflection does indicate infarction.
6. If changes of infarction in I and aVl leads, record ECG in 3rd or even 2nd interspace to exclude high
lateral infarct.
7. Changes of acute inferior wall infarction + changes of acute antero-lateral infarct indicate the following
differential diagnosis:
a. Acute pulmonary embolism (transient changes only for a few hours and no Q-wave in lead II)
Q-T Inverval 61
Fig. 12.1: Hypocalcemia. Prolongation of Q-T interval
b. Inferior wall infarction (Infarction changes last for days and weeks and Q in lead II)
c. Antero-septal infarct (changes of infarct go to V4-6).
8. Always suspect posterior infarct when tall R in V1 and V2 is associated with inferior infarction changes.
Also suspect posterior infarction if tall R-waves in chest leads is associated with inferior wall infarction.
9. Differential diagnosis of tall R in V1 or V3R:
a. Posterior infarction
b. Right ventricular hypertrophy
c. Right bundle branch block
d. Pre-excitation syndrome.
10. Features of sub-endocardial infarction:
a. Deep symmetrically inverted T-waves without deep Q-wave
b. S-T segment depression
c. Reciprocal S-T segment elevation in aVR
d. Reduction in R-wave voltage
e. Upright high voltage T-waves
f. Order for SGOT, LDH and CPK-MB tests to confirm the diagnosis of infarction.
11. Differential diagnosis of causes of S-T segment depression and inverted T-waves:
Angina, chronic coronary insufficiency, hyperthyroidism, electrolyte imbalance, shock, digitalis effect
and metabolic disorders.
13
Abnormalities
Significance
Leads Significance
of Abnormal
Waves, Segments and Intervals
in Different ECG Leads
Abnormalities Leads Significance

P-wave abnormalities
1. Wide, bifid I, aVL, V4-6 Left atrial hypertrophy
Wide and negative (diphasic) V1
2. Tall, peaked II, III, aVF and V1 {•• Pulmonary
Right atrial hypertrophy
hypertension
3. Varying shape In any lead {• Wandering pacemaker
• Multifocal atrial premature beat
4. Ratio of width of P and P-R V1, V2 Right atrial enlargement

interval greater than 1
5. Inverted P In I
+
Upright P In aVR • Dextrocardia
• Transposition of right and left arm leads
6. Inverted P In aVF
+
Upright P In aVR • Ectopic atrial focus low in atrium or in AV
node
• Coronary sinus rhythm (P-R shortened)
7. Inverted P In any lead Ventricular premature beat with retrograde
conduction
8. P not followed by QRS In any lead • AV block (second and third degree)
(Isolated P) • Blocked atrial premature beat
• Supraventricular tachycardia with AV
block (2:1 or 3:1)
9. Inverted P aVR, I, III aVF Normal
QRS complex abnormalities
{
• Left axis deviation, coronary artery disease
1. QRS diaphasic, upright I • Left ventricular hypertrophy
2. S greater than R in QRS II • Emphysema
• Antero-lateral peri-infarction block
3. QRS upright, diaphasic or aVF • Right axis deviation
inverted in • Right ventricular hypertrophy and strain
• Diphragmatic per-infarction block
4. Wide QRS (RR pattern) V1 Right bundle branch block
5. Wide QRS (RR Pattern) V1 Right bundle branch block
Contd...
Significance of Abnormal Waves, Segments and Intervals in Different ECG Leads 63

6. Wide QRS (RR or RSR pattern) I, V4-V6 Left bundle branch block
7. Wide QRS Most of leads • Hyperkalemia
• WPW syndrome
Q-wave abnormalities
1. Q-wave II, III, • Right ventricular hypertrophy
aVF • Pulmonary emphysema
2. Deep Q with S-T and T changes I, aVL, V4-6 Antero-lateral infarct
3. Deep Q V3R, V1, V2, V3 • Antero-septal infarct
4. QR aVR, V3R • Pulmonary emphysema
V1 • Clockwise rotation
• Cor pulmonale
5. QS and inverted T in III + deep Acute pulmonary embolism
S in I + Right ventricular strain
6. QS V1-3, V1-2 or V1-4 • Antero-septal infarct
7. QS I and V1-3 • Anterior infarction
• Emphysema
8. QS in II, III, • Inferior infarction
aVF • Emphysema
R-wave abnormalities
 Voltage abnormalities
1. Greater than 13 mm in aVL or Left ventricular hypertrophy
27 mm in V5 or V6 or tallest R
in V6 + deepest S in V1 more
than 35 mm
2. R greater than S in V3R and V1 Right ventricular hypertrophy
3. R greater than S in V3R, V1-V4 Posterior infarct
 Width
1. RR pattern in V3R or V1- or V1-V2 Right bundle branch block
2. RR’ pattern in V5-V6 Left bundle branch block
-do- aVL in horizontal heart
-do- aVF in vertical heart
 Small R (specially with Q) but V3-V4 Anterior infarct
if enough viable muscle is pre-
sent in epicardial layer,
abnormal Q is not registered
instead only low R is found
 Slurred R in I, aVl, V-V_ WPW syndrome
Contd...

S-wave abnormalities
Deep S In V5-V6 • Pulmonary emphysema
• Clockwise rotation
• Pulmonary embolism
In V1 Left ventricular Hypertrophy
In I, II, III Acute cor pulmonale due to pulmonary
embolism
Deep broad S In I, aVL, • Right bundle branch block
V5-V6 • Pulmonary embolism
S-T segment abnormalities
 Elevation a. In all leads except • Pericarditis
in aVR and in aVL • Myocarditis
in vertical lie
b. In II, III, aVF Inferior infarct (Even without Q) and
ventricular aneurysm
c. I, aVl, V-V6 • Anterior infarct
• Ventricular aneurysm
• Angina
d. In V1-V2 (even with Left bundle branch block
Q)
 Depression
1. Oblique depression or a. In any lead except • Angina
horizontal depression aVR and aVLwith • Sub-endocardial infarct
vertical lie • Digitalis toxicity
• Anxiety
• Tobacco
2. Oblique or horizontal b. In V1, V2, V3 • Ischaemia
• Right bundle branch block
• Angina—exercise induced depression
1-3 mm
c. I, aVL, V4-V6 • Left ventricular hypertrophy
• Ischaemia
• Reciprocal S-T depression in inferior wall
infarct
d. II, III, aVF Reciprocal S-T depression in anterior wall
infarct
e. Secondary or pseu- • Tachycardia
dodepression • Anxiety
Contd...
Significance of Abnormal Waves, Segments and Intervals in Different ECG Leads 65

T-wave abnormalities
 Inversion of T-wave
1. Symmetrical inversion
a. In any lead except • Infarction
in aVR and aVL in • Ischaemia
vertical lie • Anemia
b. In I, aVL, V4-V6 Anterior infarct
c. In II, III, aVF Inferior wall infarct
d. V1, V2, III, aVF Normal
e. In any lead • Overventilation
• Tachycardia
• After drinking iced water
• Excess glucose ingestion
2. Asymmetrical inversion
with S-T depression
a. In I, aVL, V4-V6 • Left ventricular hypertrophy strain
with tall R • Left bundle branch block
b. in II, III, aVF, V5-V6 Left ventricular hypertrophy
with tall R
c. In V1-V3 with tall R • Right bundle branch block
d. In all leads • Right ventricular strain
Hypokalemia
 Tall T-wave
a. In all leads except Hyperkalemia
aVR and aVL in Posterior infarction
vertical lie
b. In V1-V4
 Flattened T-wave
a. In all leads • Myxoedema
• Cardiomyopathies
b. In V1-V4, V3R Pulmonary embolism
c. In I, II, III, aVL, Pericarditis
aVF, V2-V6
d. II, III, aVF without Right ventricular strain
tall R in chest leads
U-wave abnormality
Upright U-wave, taller than T-wave Hypokalemia
specially in V2-V4
Myocardial Infarct
14 ECG Changes in Myocardial Infarct
ECG in myocardial infarction may point to:

1. Thickness of infarction
2. Localisation of infarction
3. Age of infarction (Stage of evolution in time).
Thickness Localisation
1. Sub-endocardial infarction:- | |
symmetrically inverted T Infarcted area Leads affected
without Q-wave 1. Antero-septal V1-3
2. Complete transmural (entire 2. Anterior V2, V3, V4
thickness of myocardium) 3. Antero-lateral I, aVL, V4-6
infarction: Q, elevated S-T 4. Inferior II, III, aVF
and inverted T 5. Infero-lateral II, III, aVF, V5-6
6. Posterior V1, V2
Age of Infarct
Q S-T change T change

Recent infarct (appears Deep Q appears 1. Horizontal elevation in Inverted T does not appear
within few hours of leads overlying infarc-
infarct) ted area
2. In opposite leads S-T
depression, i.e. in anterior
infarct S-T depression in
II, III, aVF; in inferior
infarct in I, aVL and V2-6
Regressive changes Deep Q persists 1. S-T elevation becomes 1. T starts inverting
(appear within hours convex (Fig. 14.1) 2. Tall T in V2-4 in true
and days) 2. Reciprocal S-T depression posterior infarct
becoming less and less
Old infarct (appear Deep Q persists S-T becomes isoelectric 1. T symmetrically and
after 4-5 days and may deeply inverted
last upto several weeks) 2. Tall peaked T may per-
sist in true posterior
infarct (No tall T in
inferior infarct)
Very old infarct (appear Pathological Q S-T isoelectric T becomes upright. But
in 4-5 weeks and may persists inverted T may persist
last for years) (Fig. 14.2)
Contd...
ECG Changes in Myocardial Infarct 67
Q S-T change T change

Q may gradually dis-
appear and be replaced
by R-wave which has
poor progression from V1-6
Age of infarction Infarcted leads Cavity leads (aVR, aVL) and

opposite leads (180° from
the infarct)
1. Recent infarct:
Elevated S-T with straight top

Reciprocal S-T depression
(In inferior infarct—S-T depres-
sion in I, aVL, chest leads.
In anterior infarct—S-T depres-
sion in II, III, aVF)
2. Regressive changes S-T elevation becomes convex
in recent infarct:
3. Old infarct S-T becomes isoelectric

Fig. 14.1: S-T changes in myocardial infarction
Age of infarct: Over infarct Over opposite leads

(180° from the infarct)
1. Recent infarct: T begins to
start inverting
‘Cove-plane T’ Symmetrical inversion of T Tall and symmetrical upright

with convex elevated S-T T-wave in leads showing S-T
segment depression
‘Coronary T’ Symmetrical inversion of T

or ‘Pardee T’ with isoelectric but convex S-T
2. Old infarct: The T-wave may remain inverted for the remainder of the patients’
life, or after many months the T-wave may gradually revert to the normal
Fig. 14.2: T-wave changes in myocardial infarction
Branches of Coronary Artery and Sites of Infarction (Fig. 14.3)
Coronary arteries affected Site of infarction Localisation of infarct in ECG
Anterior descending 1. Anterior infarction Lead I, aVL, V1-V5

2. Antero-lateral infarct Lead I, aVL, V5-6
3. Antero-septal infarct V1-3. Reciprocal changes in aVR
4. Apical V5-6
Circumflex branch of High lateral infarct I, aVL. Spaces above (3rd, 4th intercostal
left coronary artery spaces) in the usual precordial sites.
Right coronary artery Inferior infarct II, III avf. Ischaemic changes in V5, V6
Posterior infarction (pure without Tall T-waves in chest leads specially right
extension to inferior surface) chest leads
Esophageal leads will confirm the diagnosis
Fig. 14.3: Branches of coronary artery and sites of infarction
Degree of Damage to Myocardium

due to
Obstruction of Coronary Artery
(Fig. 14.4)
1. Ischaemic tissue: First degree damage recognised by

symmetrically inverted T-waves
2. Injured tissue: Second degree damage recognised by
S-T segment elevation
3. Dead tissue (infarcted area): Third degree damage Q-
wave, S-T elevation and inverted T-wave.
Fig. 14.4: Degree of damage
Illustrative ECG of Acute Myocardial Infarction (Figs 14.5 to

14.12)
Fig. 14.5: Posterior infarct: Always suspect posterior infarct when tall R-wave in V1-4 + infarct pattern in II, III, aVF + S-
T depression V3-6. In inferior wall infarction, infarct pattern is II, III, aVF + S-T depression in chest leads
Fig. 14.6: Antero-septal infarct: Q-wave, elevated S-T segment and inverted T-wave in lead V2, V3, V4. Depressed S-T
segment in aVF. In antero-lateral infarction infarct pattern found in leads V4-V7. In antero-apical infarction infarct pattern
found in V3–V5
Fig. 14.7: Antero-septal infarct:Convex elevation of S-T segment from V4-V7.

Inverted T in V5, V6, V7. Pathological Q-wave in V4 to V7
Fig. 14.8: Extensive anterior infarct: Q-wave, elevated S-T segment and inverted T-wave in chest leads,
lead I (not shown) and aVL. Depressed segment in aVF and lead III (not shown).
Lead facing injured surface Lead facing uninjured surface

Fig. 14.9: Evolution of the infarction pattern: S-T elevation in injured area;
S-T depression and flattening (reciprocal depression in uninjured area)
Fig. 14.10: Anterior and lateral wall infarction, acute because of elevated S-T segment.
Q with inverted T and elevated S-T in lead I, aVL and V4-V6
Fig. 14.11: Acute antero-lateral infarction: Elevated S-T in I, aVL, V4, V6 leads.
Reciprocal depression of S-T segment in II, III, aVF
Fig. 14.12: Acute inferior wall infarction. Elevated S-T in II, III, aVF + Depressed S-T in I, aVL, V4-6
Illustrative ECG of Late and Old Myocardial Infarction (Figs

14.13 to 14.19)
Fig. 14.13: Old inferior wall infarction (Phase IV). Only evidence of infarction is deep Q-waves in II, III and aVF
Fig. 14.14: Late antero-lateral infarction. Inverted T and Q in I, aVL, V4, V6
Fig. 14.15: Late inferior wall infarction (Phase II): Deep Q in II, III and aVF.
S-T segment becomes isoelectric. Deepening of T inversion in lead II, III and aVF
Fig. 14.16: Old anterior and lateral infarction: Deep Q in I, aVL, V4, V6. S-T isoelectric. T returns to normal
Fig. 14.17: Old antero-septal infarction: QS complex in V1-V3 with or without inverted T-waves in V1, V2, aVL
Fig. 14.18: Old high antero-lateral infarction: Small Q in I, aVL. Inverted T in I, aVL, 3rd interspace leads show
QS in 3V2-3V4. Poor R-wave progression
Fig. 14.19: Old posterior infarction. Q-waves and inverted T-waves persist in III and aVF.
Tall peaked T-waves in V2, V3. Which confirms posterior infarction
Illustrative ECG of Sub-endocardial Infarction (Fig. 14.20)
Fig. 14.20: Anterior and lateral sub-endocardial infarction: Wide deep symmetrically inverted
T-waves in I, II, aVL, V5, V6. No Q-wave. S-T segment isoelectric
Illustrative ECG for the Evolution of Acute Infarct (Figs 14.21

and 14.22)
Normal Normal
Phase I: Occurring within a few hours of days after onset of Phase I: Acute. Q =+ elevated S-T + inverted T in
infarction Q + raised S-T + inverted T V1-V6
Phase II: Following few weeks of infarction S-T isoelectric Phase II: S-T isoelectric + inverted symmetrical T in
+ Inverted T V1-V6
Phase III: Following a month or two after infarct T becomes Phase III: T-wave returning to normal
normal Phase IV: T-waves normal. Only evidence of old
Phase IV: Following month or year after infarction only infarction is Q in leads V4-V6
Q persists
Fig. 14.22: Evolution of anterior infarction in chest leads
Fig. 14.21: Evolution of anterior acute infarction in limb leads.
Reciprocal S-T depression in leads III, aVF and aVR
Clinical Notes
1. Q-wave normally presents in aVR and III. Pathological Q in I, II, aVF and aVL except when QRS axis more
than +60 degree, indicate myocardial infarction.
2. R-wave progression in chest leads: Loss of height of R+ normal height of on both sides of infarcted zone
or the previous ECG shows normal height of R in the infarcted zone, suggest myocardial infarction.
Abnormal decrease in the height of R without their disappearance in chest leads suggest infarction.
3. Flattened T, diaphasic T or inverted T occur not only in acute myocardial infarction but also in myocarditis,
pericarditis, digitalis toxicity and electrolyte imbalance.
4. Depth of Q is directly proportional to relative thickness of dead zone of infarcted tissue and height of R-
wave is directly proportional to amount of living tissue that escapes death.
5. Some elevation of S-T segment is normal in V1-2 (1-2 mm) and does not indicate acute infarction. If
elevation is concave in the direction of QRS deflection does indicate infarction.
6. If changes of infarction in I and aVL leads, record ECG in 3rd or even 2nd interspace to exclude high lateral
infarct.
7. Changes of acute inferior wall infarction + changes of acute antero-lateral infarct indicate the following
differential diagnosis:
a. Acute pulmonary embolism (transient changes only for a few hours and no Q-wave in
lead II)
b. Inferior wall infarction (Infarction changes last for days and weeks and Q in lead II)
c. Antero-septal infarct (changes of infarct go to V4-6).
8. Always suspect posterior infarct when tall R in V1 and V2 is associated with inferior infarction changes.
Also suspect posterior infarction if tall R-waves in chest leads is associated with inferior wall infarction.
9. Differential diagnosis of tall R in V1 or V3R:
a. Posterior infarction
b. Right ventricular hypertrophy
c. Right bundle branch block
d. Pre-excitation syndrome.
10. Features of sub-endocardial infarction:
a. Deep symmetrically inverted T-waves without deep Q-wave
b. S-T segment depression
c. Reciprocal S-T segment elevation in aVR
d. Reduction in R-wave voltage
e. Upright high voltage T-waves
f. Order for SGOT, LDH and CPK-MB tests to confirm the diagnosis of infarction.
11. Differential diagnosis of causes of S-T segment depression and inverted T-waves:
Angina, chronic coronary insufficiency, hyperthyroidism, electrolyte imbalance, shock, digitalis effect and
metabolic disorders.
Ventricular Hypertrophy
15 Left Ventricular Hypertrophy
Left ventricular hypertrophy causes increased bulk and thickness of left ventricular wall to which myocardial
fibrosis is added latter on. Leads oriented towards the left ventricle (leads V5-V6 and I and aVL) show ECG
changes (Tall R). Conversely, right ventricular oriented leads (V1, V3 and aVF) show deep S-wave changes
(Figs 15.1A to C). See below the flow diagram:
Fig. 15.1A: Left ventricular wall thickened

Fig. 15.1B: Left ventricular hypertrophy
Left ventricular hypertrophy causes

| |
Increased bulk and thickness of left ventricular Myocardial fibrosis and endocardial
wall resulting in increased voltage of R-wave change resulting in S-T depression
in V5 and V6 due to increased electrical force
in hypertrophied ventricle
| |
Leads to delay in conduction Leads to relative ischaemia due
time resulting in wider to disproportion between muscle
QRS interval mass and available blood supply
resulting in inverted T-wave and
S-T depression in V5,V6, I and aVL
Left Ventricular Hypertrophy 75
Fig. 15.1C: Left ventricular hypertrophy: High voltage R-wave in V5 and V6. Deep S-wave in V1 and V2. S in V1 + R in V5 or
V6 over 35 mm. S-T segment depression and T-wave inversion in V5 and V6. Vertical heart with high voltage R in aVF (this
pattern of aVF is not diagnostic of left ventricular hypertrophy). R increases in amplitude and S decreases as it progresses
from right to left chest leads
Mechanism (See Fig. 15.1B)
V1 shows initial small upright deflection (r) due to spread of stimulus towards V1 through septum, followed
by large downward deflection (S) due to spread of stimulus away from V1 through large left ventricular mass.
V6 shows downward deflection (q-wave) due to spread of stimulus away from V6, followed by large upward
deflection (R) due to spread of stimulus towards V6 through large ventricular mass due increased electrical
forces in hypertrophied wall.
Clinical Approach to ECG Pattern of Left Ventricular Hypertrophy: Flow Diagram
First ascertain minimum diagnostic criteria for LVH:

R in aVL or I > 13 mm
or
R in V5-V6 > 27 mm
or
S in V1 + R in V5-V6 > 35 mm

Next find out associated evidence:
| | |
Chest leads Limb leads Standard leads
1. Prolonged QRS > 0.1 | | |
second in V5-V6 Horizontal heart Vertical heart R in I and S in III
2. R > 27 mm in V5-V6 1. R in aVL = or R in aVF 20 mm > 26 mm (Gubner)
(Sokolov and Lyon) > 13 mm (Sokolov (Sokolov and Lyon)
and Lyon)
3. S-T segment depres- 2. Left axis deviation
sion and T inversion associated with
in V5-V6 horizontal heart
Contd.....
4. Q in V5-V6 in 50%
cases, usually not
present in V5-V6
(Lipman and Massie)

Then, look for rotation of the heart
| | |
Clockwise rotation Counterclockwise rotation
Since the transition zone shifts to the left, Since the transition zone shifts to the right,
LVH pattern may not be seen until V7 to V9 a LVH pattern may be seen upto V2 or V3

Differential Diagnosis:
1. Left axis deviation: It may occur in thin chest individual but if left axis
deviation is associated with horizontal heart,
suggests LVH
2. S in V1 + R in V5-V6 greater than 35mm: It may occur in thin chest individual
3. Tall R in V5-6: It may also occur in fever, thyrotoxicosis, anemia and
other high output failure

Lastly, find out the aetiology:
1. Aortic regurgitation
2. Aortic stenosis
3. Hypertension
4. Mitral regurgitation
5. Ischaemic heart disease
6. Cardiomyopathy
7. Patent ductus arteriosus
8. Coarctation of aorta
9. Tricuspid atresia
Right Ventricular Hypertrophy 77
16
Right Ventricular Hypertrophy
In right ventricular hypertrophy right ventricular oriented leads (V2, V1, III and aVR) show tall R-waves and left
ventricular leads (V5, V6, I, and aVL) show S-waves. (Figs 16.1A to C).
Fig. 16.1A: RVH (Right ventricle hypertrophy)

Right ventricular wall thickened
Mechanism
V1 shows large upward deflection due to spread of
stimulus towards V1through septum and large mass Fig. 16.1B: Right ventricular hypertrophy
of right ventricle (arrow 1a and 1b). Depressed S-T and inverted T occur due to relative ischaemia of hypertrophied
right ventricle. Conspicuous S in V5 due to late depolarisation of a remote region of right ventricle (arrow 3).
Electrocardiographic Pattern
Chest Leads
V1 and V3R V2,V3 and V4 V5 and V6
• Tall R = or > 7mm • R decreases and S increases as • S-T isoelectric T upright
leads progressing from right to left
• qR • Clockwise rotation • Normal VAT .035 to .055 second
• VAT > 0.03 second • Deeper S than R (normal less than 1)
• S-T depression and T inversion • R/S ratio less than 1 (normal greater
than 1)
Contd...
V1 and V3R V2,V3 and V4 V5 and V6

• R/S ratio greater than 1
(normal less than 1)
• QRS not wide
• R in V1 + S in V6 greater than 10.5 mm
• Incomplete right bundle branch block
Fig. 16.1C: Right ventricular hypertrophy:

Tall R-wave in V1 and deep S in V5, V6.
Lead aVF resembles V1 right axis
deviation. Right BBB. Clockwise rotation
Standard Leads
• Right axis deviation 1 + 110° or more
• Deep S in I, II, III (S1 S2 S3)
• Depressed S-T and inverted T in II or III
These patterns alone do not point to RVH, unless accompanied by changes in chest leads.
Limb Leads
• Tall R in aVR 5 mm or more
• Tall R with depressed S-T and inverted T in aVF. These patterns alone do not point to RVH, unless
confirmed by changes in chest leads.
Approach to ECG Pattern of RVH
First, look for minimum diagnostic criteria for RVH
Rs or qR in V1 or V3R + VAT greater than 0.03 second Right axis deviation.

Next, look for other evidence. See electrographic pattern.
In the absence of tall R in V1,V3R the following criteria suggest RVH:
Very tall or notched P-waves and clockwise rotation
or
Right Ventricular Hypertrophy 79
Depressed S-T and T inversion in V3R and V1 to V3

or
Incomplete or complete right bundle branch block

Finally, remember the aetiology of RVH: Mitral stenosis, cor pulmonale,
tetralogy of Fallot, pulmonary stenosis, Eisenmenger’s syndrome.

Also remember the ECG criteria of cor pulmonale, i.e. tall peaked P in II
and III vertical heart, clockwise rotation, right axis deviation, right ventricular
hypertrophy, low voltage usually in V5 and V6 due to emphysema and inverted
T in chest leads.
NORMAL HEART
First stage of depolarisation spreads through septum

from left to right (arrow 1). Second of depolarisation
then proceeds outward simultaneously through the
free walls of both ventricles from endocardial to
epicardial surfaces (arrow 2 and 2A) V1 lead shows
initial small upright deflection due to spread of
stimulus towards V1 through septum, followed by a
large downward deflection (S-wave) due to spread of
stimulus away from V1 through left ventricular mass.
V6 lead shows an initial downward deflection (wave)
due to spread of stimulus away from V6 through
septum, followed by a large upward deflection (R-
wave) due to spread of stimulus towards V6 through Fig. 16.2: Both atria thin walled; left ventricular
left ventricular mass (Figs 16.2 and 16.3). wall thickened
Fig. 16.3: Normal heart

Cardiac Arrhythmias
17 Cardiac Arrhythmia
Cardiac arrhythmias are produced by the disturbances in:

i. the rate
ii. the impulse formation
iii. the impulse conduction
Impulse is formed and conducted either through specialised conduction tissues or elsewhere in the heart
(ectopic foci): |
| |
Through specialised conducting tissue Ectopic foci
Impulse originates in SAN at the inherent Impulses originate in ectopic foci
rate of 76/minute in atrium and ventricle
↓
Pass through specialised conducting For example premature beats, auri-
pathways registering P-wave cular fibrillation, flutter
↓
Goes to AVN which discharges at the
inherent rate of 60/min to bundle of
His, bundle branches, Purkinje fibers
and ventricular musculature at the
inherent rate of 30-40/minute register-
ing in ECG QRS-T complex
See “Classification of Arrhythmias”, and “Mechanism of Arrhythmias”.
For diagnosis of arrhythmias, following points should be analyzed and noted in the ECG:
• Heart rate
• Sequence of depolarisation and repolarisation
• Relationship of P-wave and QRS-T complex
• Special characteristics of P-wave specially in lead V1 or one space higher than V1.
Heart Rate
The ECG paper is divided into large and small squires (Fig. 17.1).
0.1mv
1mm
123456
123456
123456
123456
123456
1 second ← 0.2 second →
Fig. 17.1: ECG-Paper
Cardiac Arrhythmia 81
Time in seconds (Horizontal line)

Each large squire represents 0.2 second
5 large squires represent 1 second
300 large squires represent 1 minute that is 300 large squires
pass the writing stylus each minute. So to measure ventricular
rate we count the number of large squires between corresponding
peaks of R-waves of adjacent QRS complexes and divide this
number into 300.
Fig. 17.2: Second degree AV block, Type 2, 2:1 AV response
In the figure there are 8 large squires between R-waves of adjacent complexes so that the ventricular rate
= 300 divided by 8 or about 37 beats per minute. Atrial rate is measured by counting number of large squires
between consecutive P-wave and dividing the number into 300. In the above figure there are 4 large squires
between adjacent P-waves so that the atrial rate is 300 divided by 4 or about 70 per minute.
Voltage in millivolt (Amplitude or vertical height)

Height of large squire = 1 mm = 0.1 millivolt
Height of 5 large squire = 5 mm = 0.5 mV
Height of 10 large squires = 10 mm = 1 mV = Unit of standardisation
18 Classification of Cardiac
Arrhythmias
Arrhythmias Arising from Conduction System (Table 18.1)

Table 18.1: Arrhythmias arising from conduction system
Disorders of impulse formation Disorders of impulse conduction
SA Node • Respiratory arrhythmia I. SA block:

• Sinus tachycardia • Ist degree
• Sinus bradycardia • 2nd degree (Wenckebach)
• Sinus arrest • 3rd degree
II. WPW syndrome (Accessory pathway)
AV Node AV nodal rhythm: III. A V Block:
• Without retrograde conduction with absent A. Partial or incomplete
P-wave a. First degree
• With early retrograde conduction with inverted b. Second degree:
P preceding QRS • Mobitz type I (Wenckebach)
• With late retrograde conduction with P • Mobitz type II: With irregularly dropped beats
follows QRS with regularly dropped beats
• With retrograde conduction B. Complete or third degree heart block
depolarising simultaneously auricle IV. Intraventricular conduction defect
and ventricle with P merged with QRS V. Bundle branch block:
AV nodal escape beat a. Right bundle branch block
AV nodal tachycardia • Incomplete
Ventricle • Complete
b. Left bundle branch block
• Incomplete
• Complete
VI. Fascicular block:
a. Left anterior hemiblock
b. Left posterior hemiblock
c. Bifascicular block
d. Trifascicular block
Arrhythmias Arising from Ectopic Focus
Auricular
• Auricular ectopic
• Paroxysmal atrial tachycardia
• Paroxysmal atrial tachycardia with variable block
Classification of Cardiac Arrhythmias 83
• Atrial flutter
a. With fixed AV block
b. With varying AV block
• Atrial fibrillation
Nodal
Nodal ectopic
Ventricular
• Ventricular ectopic
• Ventricular tachycardia
• Ventricular flutter
• Ventricular fibrillation.
Parasystole
• Sinus parasystole
• Auricular parasystole
• Nodal parasystole
• Ventricular parasystole.
19 Classification of Arrhythmia
Based on ECG Patterns
A. Arrhythmia with PQRST change

|
| |
PQRST present PQRST absent
| |
| | | |
Rhythm regular Rhythm irregular With Pause PQRST replaced by
a. With normal rate: Rate increases during a. Sinus arrest. a. Regular oscillations of
Sinus rhythm inspiration, decreases Pause more than large amplitude sug-
b. With rate above during expiration: Sinus double the normal gests ventricular flutter
100/minute: arrhythmia interval b. Very irregular waves
Sinus tachycardia  with varying amplitude
c. With rate less than Prolonged sinus arrest points to ventricular
60/minute leads to fibrillation
 i. Nodal escape (Pause
Sinus bradycardia followed by only
QRS without P)
ii. Ventricular escape
(Pause followed by
bizarre QRS with-
out P)
b. Sino-auricular block.
Pause is exactly double
the normal interval
B. Premature Beats
|
| |
With normal shaped QRS With wide bizarre QRS
| | |
With normal configu- With abnormal `P’ due to retrograde, 1. Ventricular premature beat
ration of premature P conduction, P inverted or follows QRS 2. Aberrant ventricular conduc-
  tion
Atrial premature beat Nodal premature beat
Classification of Arrhythmia Based on ECG Patterns 85
C. Arrhythmia with P-wave changes

|
| | |
Arrhythmia with deformed Arrhythmia with inverted Arrhythmia with multiple P
P-wave P-waves specially in lead I or isolated P-wave
a. Fibrillary P-wave with a. Nodal rhythm a. With constant P-R: interval
irregular ventricular rhythm. b. True dextrocardia Mobitz type II AV block
Auricular fibrillation b. With gradually increasing P-R
b. Flutter waves replacing P-wave interval with dropped beat:
with (fixed AV block) or Mobitz type I with Wenckebach
without (varying AV block) phenomena
regular rhythm. c. With varying P-R: interval and P
Auricular fibrillation independent of QRS: complete
heart block
20 Sinoatrial node Atrium Atrioventricular node
Mechanism of Arrhythmias
Ventricle
MECHANISM OF ARRHYTHMIAS (Table 20.1)
Sequence of Events
Sequence of events (impulse formation and conduction) at different sites.

Table 20.1: Sequence of events (Impulse formation and conduction) at different sites
Sinoatrial node Atrium Atrioventricular node Ventricle
Auricular Rapid totally irregular Showered by rapid Ventricle irregularly

fibrillation beating of auricle from irregular impulses. stimulated resulting in
multiple ectopic foci. Only some strong rapid irregular ventri-
Rate varies from 350 to impulses are conduc- cular response. QRS
550/minute P absent, ted to ventricle complex normal
replaced by irregular f-
waves. Fine f wave
suggest IHD and hyper-
tensive heart disease;
coarse f-waves suggest
thyrotoxicosis and mitral
valve disease. Atrium no
longer responds comple-
tely to such fast rate
hence chaotic contrac-
tion occurs
Auricular Rapid but regular Usually AV block i. Fixed AV block
flutter impulses initiated in an exists which is fixed produces regular
ectopic focus in atrium. -2:1, 3:1, 4:1 ventricular beat
Auricular rate 200 to Occasionally
400/minute P-wave AV block varies ii. Variable AV block
replaced by flutter produces irregular
waves (saw-toothed and ventricular beat
regular) simulating auricular
fibrillation
Atrial pre- Arises from ectopic Normal conduction Normal contraction of
mature beat focus in atria with P of ectopic impulse ventricle with normal
appearing earlier (pre- through AVN QRS
mature) than expected
Contd...
Mechanism of Arrhythmias 87

and compensatory pause
is incomplete. If focus in
upper atria, normal con-
duction in atria produ-
cing normal P; if focus in
lower atria, retrograde
conduction of P to SAN
occurs resulting in up-
right P in aVR and aVL
and inverted P in aVF
Paroxysmal Ectopic focus in atria — Do — — Do —
atrial tachy- producing rapid
cardia series of atrial pre-
mature beats resulting
in tachycardia
APB with Ectopic focus in atria Impulse follows un-
ventricular usual pathways through
aberration ventricle producing
deformed QRS
Blocked Ectopic focus in atria Do not respond to too
APB premature P, hence no
ventricular contraction,
no QRS
Multifocal Two or more ectopic foci
APB produce two or more types
of APB-P are of different
configuration in the same
lead
Wandering Shift of focus bet- Varying shapes of P Normal ventricular con-
pacemaker ween SAN and varying P-R interval traction, normal QRS
Sinus AVN
tachycardia Impulse formed P normal Normal conduction Normal conduction.
above 100/minute Normal QRS
Sinus Impulse formation P normal Normal conduction Normal conduction.
bradycardia less than 60/minute Normal QRS
Sinus Impulse formation Normal atrial contrac- Normal conduction Normal contraction of
arrhythmia varies with respiration. Normal P ventricle.
tion—increases with Normal QRS
inspiration and dec-
reases with expiration
Sinoatrial Impulse formed in Conduction interfered Conduction interfered Conduction interfered.
block SAN but conduction No P formed No QRS
interfered
Contd...
Sinus arrest SAN fails to initiate No P-wave AVN initiates impulse Or ventricle may initi-
impulse due to prolonged sinus ate impulse leading to
arrest–Nodal escape ventricle escape produ-
Normal QRS without P cing normal QRS
Nodal pre- Due to retrograde con- Impulse arises in AVN, Antegrade conduction
mature beat duction from AVN to goes both to SAN to ventricle produces
SAN P may be upright (retrograde) and to normal QRS
in aVR and aVL, inver- ventricle (antegrade
ted in II, III and aVF conduction)
and V3 to V6 and
diphasic in V1 and V2.
P-R interval short
Nodal tachy- Due to retrograde con- Impulses arise in rapid QRS-T normal due to
cardia duction P usually fol- succession from an antegrade conduction
lows QRS, when P pre- ectopic focus in AVN from AVN to ventricle
cedes QRS it is usually
inverted in I, II and aVF;
upright in aVR. If rate is
rapid no, P-wave is visible.
Ventricular Retrograde conduction Retrograde conduction Shape of QRS bizarre.
premature from ventricle to atrium from ventricle to If ectopic focus is in the
beat occurs resulting in up- atrium right ventricle, QRS
right P in aVR and aVL, resembles QRS of left
inverted in aVF. V3-V6 bundle branch block and
and diaphasic in V1, V2 if in left ventricle, QRS
resembles QRS of right
bundle branch block. If
multiple foci are present
in ventricle, different
shapes of QRS in the
same lead occur
Ventricular Atrial P not disturbed Rapid series of impul- Ectopic foci in ventricle
tachycardia but hidden in QRS-T if ses originating in ven- bizarre shaped QRS at
retrograde conduction tricle passes through rate 150-200/minute
from ventricle to atrium AVN in retrograde Slightly irregular unlike
occurs fashion PAT. Carotid sinus
pressure has no effect
Ventricular Absence of normal P Ectopic foci in ventri-
flutter cle. Abnormal conduc-
tion in ventricle.
Normal QRS absent but
fairly normal oscilla-
Contd...
Mechanism of Arrhythmias 89

tions without isoelectric
interval occur.
Ventricular Ectopic foci in ventricle.
fibrillation Abnormal conduction
in ventricle results in
completely irregular of
varying amplitudes and
shapes of QRS-250-
500/minute
First degree Impulse delayed at
heart block AVN-prolonged con-
duction time represen-
ted by prolonged P-R
Second degree Conduction interrup- QRS normal
heart block ted in AVN resulting
in:
i. Regularly dropping
of beats (Mobitz
type III)
ii. Irregularly dropping
of beats (Mobitz
type II)
iii. Progressively longer
P-R interval until a
beat is dropped
(P not followed
by QRS)
Third degree P has no relation with Ventricle has its own
heart block QRS, it has its own rate, rate, slower than auri-
regular, normal shape cular rate. QRS defor-
and faster than ventri- med if ventricular
cular rate impulse originates in
right ventricle or left
ventricle. QRS normal
shaped if ventricular
impulse originates in
just below the AVN.
Atrioventri- One pacemaker Atria has its own rate, Another pacemaker in SAN impulse produces
cular dis- in SAN driving slower than ventricular AVN. Driving ventri- normal ventricular beat.
sociation auricle producing rate (In AV dissociation cle. 2 pacemakers are AVN impulse produces
sinus beat due to complete heart due to failure of trans- nodal type of ventri-
block auricular rate fas- mission through AVN cular beat (normal QRS
ter than ventricular rate) producing nodal beat without P)
21 Tachyarrhythmias
Causes of Tachyarrhythmia
Due to abnormal impulse formation at:

|
| | | |
SA node Atria AV node Ventricle
1. Sinus tachycardia 1. PAT 1. Nodal ectopic 1. Multiple ventricular extra-
2. Sinus arrhythmia 2. Auricular fibrillation 2. Nodal tachycardia systole
3. Auricular flutter 2. Paroxysmal ventricular tachy-
4. Multiple atrial pre- cardia (VT)
mature beats 3. Ventricular fibrillation
5. PAT with 2:1 block 4. Ventricular flutter
Approach
Look for rate, rhythm, P-wave, QRS-wave and effect of carotid sinus pressure.
I. Rate: Note the ventricular and atrial rate (R-R and P-P interval) and their ratio:
Sinus PAT PAT with Nodal VT Atrial Atrial
tachycardia 2:1 block fibrillation flutter
Ventricular usually more usual 150 80 60 to 140 usual 150 variable 150
rate: than 100 to 180; to 200;
max. 250. max. 220.
Atrial rate: same as ven- same as ven- 160 70 (ventri- 500 300
tricular rate. tricular rate. cular rate
faster than
atrial rate)
A:V 1:1 1:1 2:1 2:1
3:1
II. Rhythm: Note the rhythm, whether it is absolutely regular (PAT, sinus tachycardia, auricular flutter with
fixed AV block, PAT with fixed AV block), slightly irregular (VT) or irregular (auricular and ventricular
fibrillation; auricular flutter with varying AV block, PAT with varying AV block, multiple premature beats.
III. P-wave: Note whether P is present or absent due to superimposition of P on QRS-T complex.
A. P-wave present: Note the shape of P and its relation with QRS:
1. Shape of P:
a. P normal shaped suggests sinus tachycardia.
b. P replaced by fibrillary waves in atrial fibrillation and by flutter waves in atrial flutter.
c. P progressively altered in PAT with block.
2. Relation with QRS:
Tachyarrhythmias 91
a. P preceding normal QRS suggests normal antegrade conduction (from atria to ventricles). It
occurs in sinus tachycardia, PAT and sinus arrhythmia.
b. Inverted P preceding or following normal QRS in leads II, III, aVF, V3-6 suggests retrograde
conduction (from AV node and ventricle to the atria). It occurs in nodal.
c. P independent of QRS suggests VT.
d. Premature P in atrial premature beats.
B. P-wave absent:
a. Absent P with bizarre QRS suggests VT.
b. Absent P with normal QRS suggests PAT and nodal tachycardia.
IV. QRS-wave: Note any abnormality of QRS. |

| |
Abnormal QRS Normal QRS
(wide, bizarre or slurred)
1. Bizarre QRS: Multiple ventricular premature beats, Sinus tachycardia, PAT, atrial fibrillation
VT, ventricular fibrillation, ventricular flutter. atrial flutter, nodal tachycardia and ectopic,
2. Wide QRS: PAT with bundle branch block, multiple atrial ectopics.
PAT with aberrant ventricular conduction,
atrial fibrillation with bundle branch block.
3. Slurred QRS in WPW syndrome with tachycardia.
V. Effect of carotid sinus pressure:

PAT May terminate or no effect
Sinus tachycardia Temporary slowing
Atrial flutter Increases AV block, more flutter
waves revealed
PAT with AV block More P-waves revealed
VT No effect.
Flow Diagram for Tachycardia
If heart rate above 100/minute, tachycardia exists:


Determine ventricular and atrial rate
|
| |
Ventricular rate Atrial rate
|
|
| | | |
Above 100 Above 150 Same as ventricular Atrial rate above Ventricular rate
  rate ventricular rate; above atrial rate;
Suggests sinus Suggests PAT, VT   
• Sinus tachy- • PAT with block • VT.
cardia • Atrial fibrillation
• PAT. • Atrial flutter with block.


Next note rhythm

|
| |
Regular Irregular
• Sinus tachycardia • VT (slightly irregular)
• PAT • Atrial fibrillation
• Atrial flutter with fixed • Ventricular fibrillation
AV block • Atrial flutter with varying block
• PAT with fixed AV block. • PAT with varying AV block
• PAT with aberrant ventricular conduction.

Also note the character of P-wave:
| |
P present P absent
| | • PAT
P normal P abnormal • VT
| | | • Nodal
(Normal configuration Abnormal Abnormal
and normal relation with configuration relation with QRS
QRS complex) • P replaced by fibrillary waves • P independent of QRS:
• Sinus tachycardia.  
• PAT Atrial fibrillation VT
• Sinus arrhythmia • P replaced by flutter waves: • Premature P (P occurs earlier
 than expected)
Atrial flutter 
• P progressively altered: Premature beat

PAT with AV block
• Inverted P:

Nodal tachycardia

Next, note character of QRS:
| |
Abnormal (Wide, bizarre QRS) Normal QRS
• Multiple ventricular premature beat • Sinus tachycardia
• Ventricular fibrillation • PAT
• VT • Auricular fibrillation
• Ventricular flutter • Auricular flutter
• PAT with bundle branch block • Nodal tachycardia
• PAT with aberrant ventricular conduction. • Nodal and atrial ectopic.

Finally, note the effect of carotid sinus pressure
| |
Effective Not effective
• PAT • VT
• Sinus tachycardia (Temporarily slowing) • Some case of PAT
• Atrial flutter (Increase AV block, more
Tachyarrhythmias 93
flutter waves revealed)

• PAT with AV block (More P-waves revealed)
Table 21.1: Distinction between ventricular tachycardia and paroxysmal atrial tachycardia
Ventricular tachycardia Paroxysmal atrial tachycardia
Rate Usual heart rate 130 to 170/minute Usual rate above 170/-minute
Onset An initial ventricular premature beat An initial atrial premature beat followed by
followed by ventricular tachycardia paroxysmal atrial tachycardia
Axis Left axis deviation
P-wave P-wave may be absent (P superimposed onOnly in very fast PAT P may be absent (P
merged
T-wave) P not related with QRS with T-wave)
Ventricular capture beat May be present Absent
Fusion beat May be present Absent
Effect of carotid sinus pressure No effect May terminate or no effect
Illustrative ECG of Tachyarrhythmias
Sinus Tachyarrhythmias (Figs 21.1A to 21.3)
Fig. 21.1A: Sinus tachy-

cardia—Rate more than 100/
minute P at regular interval
followed by QRS-T complex
Fig. 21.1B: Axis -60 degree (Left axis). Sinus tachycardia. Antero-lateral infarction. (Left axis, small q in aVL,
small q in V5, QS in V3 and V4. Left anterior hemiblock (Left axis, small r in II,III and aVF)
Fig. 21.1C: Sinus tachycardia—The carotid sinus

pressure gradually slowing the heart rate in both the B
strips
Fig. 21.2: Brief run of ventricular tachycardia: The second complex is a VPC as are 4, 5, 6 and 8.
The complexes 4, 5 and 6 constitute ventricular tachycardia
Fig. 21.3: Ventricular fibrillation: Completely irregular waveforms. No ventricular complexes are seen
Tachyarrhythmias 95
Ventricular Tachycardia (Figs 21.4A to D)
Fig. 21.4A: Ventricular tachycardia. Slightly irregular. P-waves are indicated
Fig. 21.4B: Ventricular tachycardia: Its initial wave is not identical with those of the conducted beats and
the first peak is taller than its second, hence the form is not right bundle branch block
Fig. 21.4C: Ventricular tachycardia: The ventricular complexes and T-waves are
merged and the resulting waveform is almost symmetrical
Fig. 21.4D: The first part shows VT from left ventricle and the second half shows a change to right sided VT
Atrial Tachycardia (Figs 21.5 to 21.7)
Fig. 21.5: Paroxysmal auricular tachycardia: Upright and regular P-wave followed by QRS.
Rate varies between 150-250 per minute. Shape of QRS normal. S-T depression
PAT with aberrant ventricular

conduction
Fig. 21.6: Bizarre appearance of

QRS suggestive of ventricular
tachycardia but each QRS
complex is preceded by P-wave
points to PAT with aberrant
ventricular conduction
Fig. 21.7: Isolated P-waves show altered shapes
Atrial Tachycardia (Fig. 21.8)
Fig. 21.8: Supraventricular tachycardia with aberrant ventricular conduction.

Evidence of acute myocardial infarction
Tachyarrhythmias 97
Fast atrial fibrillation (Figs 21.9 and 21.10)
Fig. 21.9: Atrial fibrillation with rapid ventricular response
Fig. 21.10: Aberrant ventricular conduction associated with auricular fibrillation
Illustrative ECG for Nodal Tachyarrhythmia (Figs 21.11 to 21.14)
Fig. 21.11: Junctional tachycardia. Atrial complexes not seen

Fig. 21.12: Junctional (Nodal) tachycardia. An inverted P-wave follows QRS complex
Fig. 21.13: Nodal tachycardia: QRS is followed by P-wave which is retrograde in nature
Fig. 21.14: Conversion of junctional tachycardia (1, 2, 3) to sinus rhythm by intravenous verapamil
Bradyarrhythmias 99
22 Bradyarrhythmias
Bradyarrhythmias are produced under three circumstances:

1. P-wave normally related with QRS but impulse initiation at SA node is slower:
Sinus bradycardia
2. Whole cycle, i.e. P-QRS-T is dropped:
a. Sinoatrial block
b. Sinus arrest
3. P-wave not followed by QRS complex (Isolated P): Conduction interrupted at AVN:
Atrioventricular block:
a. Second degree AV block:
Mobitz type I (Weckebach)
Mobitz type II
b. Third degree AV block (Complete heart block)
Approach
P normally related P=QRS=T dropped P not followed by QRS (Isolated P)

with QRS | | Suggests AV block. Next differentiate 2nd
Suggests sinus Sinoatrial Sinus arrest and 3rd degree AV block
bradycardia block (Pause (Pause prolonged) | |
double the Conductism interrupted Conduction interruted
normal cycle) intermittently at AVN constantly at AV node,
resulting in periodic auricle and ventricle have
dropping of beats independent rates point-
 ing to 2 pacemakers (one
Suggests 2nd degree in SA node, another AV
AV block node or ventricle
| 
| | Note P-P and R-R interval
Progressively prolonged P-R P-R constant with vari- | |
interval until a dropped ation in auricular-ventri- P-P greater P-P slower
ventricular beat occurs. R-P cular ratio viz. 2P:IV or than R-R than R-R
preceding the pause shorter 3P:IV  
than R-R following the pause  Complete AV dissocia-
 Suggests Mobitz type II heart block tion
Suggests Mobitz type I AV block 
AV block (Wenckebach) Note the shape of QRS
Contd...
Note the shape of QRS

| | | |
Normal shaped QRS Deformed QRS Resemble right pre- Resemble left prema-
  mature beat or right ture beat or left
Suggests 2nd pace- Suggests 2nd bundle branch block bundle branch block
maker in just below pacemaker in  
AV node ventricle Suggests 2nd pace- Suggests 2nd pace-
maker in right maker in left ventri-
ventricle cle
Causes of Bradyarrhythmia Based on ECG Patterns

|
| |
PQRST absent Variation in P-waves
|
SA block | |
Sinus arrest P related with QRS Multiple P or Isolated P Nodal type of P (P follows
Sinus bradycardia a. With constant P-R: Mobitz QRS or inverted P precedes
type II AV block QRS in II, III, aVF, V3 to
b. With gradually increasing V6 or diphasic P in V1 and
P-R with dropped beat: V2 or upright P in aVR)
Mobitz type I with Wenckebach 
c. With varying P-R: Nodal rhythm
• Third degree heart block
• AV dissociation.
Differential Diagnosis of Bradyarrhythmia
Effect of effort Effect of atropine Cervical venous pulsation

2nd degree heart block No effect No effect
3rd degree heart block No effect No effect Cervical venous pulsation
unrelated to ventricular beats
SA block Rate doubles Rate doubles
Sinus bradycardia Quickens Quickens
Nodal rhythm Quickens Quickens
ILLUSTRATIVE ECG OF BRADYARRHYTHMIAS
Sinus Bradyarrhythmias (Figs 22.1 to 22.5B)
Fig. 22.1: Sinoauricular block: Due to interference in transmission of impulse initiated in SA node.
Duration of pause equal to double the normal interval between beats P-QRS-T dropped
Bradyarrhythmias 101
Fig. 22.2: Sinus arrest: Due to momentary failure of sinus node to initiate impulse.
Prolonged pause with absence of P and QRS-T
Fig. 22.3: SA block with dropped beat: Pause = Double the normal beat interval. P-QRS-T absent during pause
Fig. 22.4: SA block with every second beat dropped
Fig. 22.5A: Sinus bradycardia: Rate less than 60/minute
Fig. 22.5B: Sinus bradycardia following a VPB (Ventricular premature beat)
Illustrative ECG of Heart Block Bradyarrhythmias (Figs 22.6 to 22.14)
Fig. 22.6: Partial heart block with irregularly dropped beats: Isolated P, P-P constant, P-R constant, varying R-R interval
Fig. 22.7: Partial auriculoventricular block with regularly dropped beats. Isolated P, P-R constant, R-R constant
Fig. 22.8: Complete heart block: Complete independence of auricular and ventricular rhythm. QRS look normal, hence
impulses originate in bundle of His, above branching and just below the AV node. P-P and R-R constant, P-R varies
Fig. 22.9: Second degree heart block: With two auricular beats (P-wave) to each ventricular beat (QRS-T):
2:1 AV block (Mobitz type II AV block)
Fig. 22.10: AV block with 3:1 ratio that is three auricular beats to each ventricular beat (Mobitz type II)
Fig. 22.11: The Wenckebach Phenomenon: Progressive lengthening of P-R interval until a beat is dropped. The following
beat has a short P-R interval. Isolated P, varying P-R and R-R
Fig. 22.12: Complete heart block: P-waves bear no relationship to QRS complexes QRS are deformed, hence impulses
originate in ventricular musculature. P independent of QRS. Isolated P. P-R varies
Bradyarrhythmias 103
Fig. 22.13: Complete heart block: The pacemaker shifts in ventricular musculature
from time to time, hence QRS complexes vary in form
Fig. 22.14: P-R interval lengthens followed by dropped ventricular beat that is P-wave not followed by
QRS-T complex. Isolated P, P-P constant with varying P-R and R-R. Wenckebach
ILLUSTRATIVE ECG OF IDIOVENTRICULAR BRADYARRHYTHMIA (Figs 22.15 and 22.16)
Fig. 22.15: SA block: No atrial activity resulting in ventricular escape rhythm

(Idio-ventricular rhythm)—QRS complex looks bizarre with slow rate
Fig. 22.16: The first two cycles (1,2) are of sinus origin. The third is (3) a fusion beat, followed by two complexes (4,5) of
idioventricular rhythm, a VPC (6) one more fusion beat (7) and then a run of (8 to 12) idioventricular rhythm
ILLUSTRATIVE ECG OF NODAL BRADYARRHYTHMIAS (Figs 22.17 to 22.20)
Fig. 22.17: Nodal rhythm: There is increasing delay in retrograde atrial activation. The P-wave progressively approaches the
QRS in the first, second, third, fourth and fifth complexes untill it disappears in the sixth complex. The sixth, seventh and
eighth complex are nodal complexes without P-waves.
Fig. 22.18: The first, third, fifth and seventh complexes are of sinus origin with first degree AV block. Each of these are
followed by a blocked APC (A, B, C) which is in turn followed by a nodal escape beat (2, 4, 6) showing some aberrant
ventricular conduction
Fig. 22.19: Complexes 1 and 2 are nodal rhythm with aberrant ventricular conduction. Complex 3 is a VPC of left
ventricular origin. Complex 4 is a sinus complex. Complex 5 is a VPC. Complexes 6 to 10 are of sinus origin
Fig. 22.20: The first complex is a sinus one (1) followed by a sinus pause, followed by a nodal escape beat (2), then a
fusion beat (3) and then a sinus beat. The sequence is repeated
Arrhythmias other than Tachyarrhythmias and Bradyarrhythmias 105
23 Arrhythmias other than

Tachyarrhythmias and
Bradyarrhythmias
Few of these arrhythmias are also described in the chapters on Tachyarrhythmias, Bradyarrhythmias and in
other chapters.
Atrial Arrhythmias
a. Atrial premature beat—See Chapter on “Approach to Atrial Premature Beat”
b. Wandering pacemaker
c. Atrial fibrillation—See Chapter on “Atrial Fibrillation and Flutter”
d. Atrial flutter—See Chapter on “Atrial Fibrillation and Flutter”
e. Sino-atrial block and sinus arrest—See Chapter on “Bradyarrhythmias”
f. Sinus arrhythmia (Fig. 23.1).
Fig. 23.1: Respiratory sinus arrhythmia: Inspiration quickens and expiration slows rate
Junctional Arrhythmias
a. Atrio-ventricular block—See Chapter on “Heart Block (AV block)”
b. Nodal arrhythmias—See Chapter on “Nodal Arrhythmias”
c. Nodal premature beat—See Chapter on “Nodal Arrhythmias”.
Ventricular Arrhythmias
a. Ventricular premature beat—See Chapter on “VPB”
b. Intraventricular conduction defect (Fig. 23.2).
Miscellaneous Arrhythmias
a. Parasystole—See Chapter on “Parasystole”
b. AV dissociation—See Chapter on “AV Dissociation”
c. WPW syndrome—See Chapter on “WPW Syndrome”
Fig. 23.2: Intraventricular conduction defect: Evidence of anterior infarction (QS in V3-4, inverted T in V3-6) + evidence of
inferior wall infarction (Deep Q and inverted T in II,III,aVF) + Widened QRS intervals
d. Monofascicular block:
i. Left anterior hemiblock—See Chapter on “Hemiblock”
ii. Left posterior hemiblock—See Chapter on “Hemiblock”
e. Bifascicular block: (2 branches out of 3 branches of coronary artery blocked):
i. Right bundle branch block + Left anterior hemiblock
ii. Right bundle branch block + Left posterior hemiblock
f. Trifascicular block (All the 3 branches block) (Fig. 23.3)
i. Bifascicular block + Prolonged P-R
ii. Left bundle branch block + Prolonged P-R
iii. Alternating right bundle branch block and left bundle branch block
Fig. 23.3: Trifascicular block—(1) 1st degree AV block—P-R interval prolonged; (2) Left anterior hemiblock: Left axis
deviation + small r and deep S-wave in II, III, aVF; (3) Right bundle branch block: Wide “M” complex in V1
Arrhythmias other than Tachyarrhythmias and Bradyarrhythmias 107
g. Peri-infarction block (Fig. 23.4)

h. Sick sinus syndrome—See Chapter on “Sick Sinus Syndrome”.
Fig. 23.4: Antero-lateral peri-infarction block. Left axis deviation + Antero-lateral infarction
(Q in I, aVL + tall R in lead I and deep S in II, III and aVF
24 Approach to Atrial Premature Beats
Atrial premature beat arises from an ectopic focus in either auricle other than SA node, travels to AV node via
atrial muscle rather than usual conducting pathway resulting in variable shape and occasionally inverted P
with normal QRS.
ECG Pattern
Observe the waves, intervals and frequency
|
| | | |
P-wave P-R, R-R and Shape of QRS Frequency
P-P intervals Multiple APB
i. Shape: Often slightly a. P-R shorter or longer a. Usually QRS normal a. Occasionally two or
abnormal because than the basic P-R shaped. Occasionally more APB occur in
impulse travels through depending on how QRS deformed and succession, called
atrial muscle.** far the ectopic focus wide suggests APB multiple APB
ii. Direction: Depends on is from AV node with aberrant ventri- b. Occasionally multiple
where is the ectopic b. The sum of the inter- cular conduction and APB give rise to PAT
impulse in atria. Normally vals before and after this may be confused c. Atrial bigemini: APB
P inverted in aVR and APB will be less than with ventricular ecto- occurring after every
upright in aVF: the sum of 2 consecu- pic → QRS of APB normal beat
a. Ectopic focus in upper tive intervals. Hence, preceded by and rela- d. APB with PAT: Run
atrium results in compensatory pause ted to P. In VPB is not of PAT with APB.
upright P in aVF is incomplete** related to P and often
b. Ectopic focus in lower c. P-P interval of nor- P not seen at all.
end of atrium results in mal complex longer b. QRS normal shaped in
upright P in aVR and than P-P of APB nodal escape and wide
inverted in aVF complex. So always and bizarre in ventri-
iii. Relation with QRS:
measure P-P in arrhy- cular escape.
a. Usually P followed by
thmia.
normal QRS
b. Occasionally P not
followed by QRS,
points to blocked or
non-conducted APB
c. APB with nodal or
ventricular escape:
Escape beats not pre-
ceded by P-wave. See
shape of QRS in escape
beats.
**If shape of P varies when two or more APB occurs in the same lead, multifocal APB is suggested
Approach to Atrial Premature Beats 109

Finally, find out the aetiological diagnosis:
• Normal individual
• Anxiety
• Any organic heart disease
• Digitalis
• May precede atrial fibrillation or paroxys-
mal atrial tachycardia especially in mitral
stenosis and thyrotoxicosis.
ECG ILLUSTRATIONS OF ATRIAL PREMATURE BEAT
Blocked Atrial Premature Beats (Figs 24.1 to 24.5)
Fig. 24.1: Compensatory pause following a blocked premature atrial beat (third complex). The T-wave of the third complex is
distorted by a premature P-wave (P). No QRS follows it. This is the commonest cause of a pause in an otherwise regular
tracing.
Fig. 24.2: Complexes 1, 2, 3, 4 and 5 are blocked APB not followed by QRS
Fig. 24.3: Blocked atrial premature beat: The third complex is followed by a premature small p-wave distorting the T-wave-
blocked atrial premature beat. A compensatory pause follows at the end of which is a junctional escape beat with no related
P-wave
Fig. 24.4: Blocked premature atrial contraction: P-wave not followed by QRS.
J is a junctional escape beat not preceded by P-wave
Fig. 24.5: Blocked atrial premature beats: 1, 2, 3, 4 beats are blocked atrial premature beats not followed by QRS
complex 5, 6, 7 and 8 are regular sinus beats
APB with Aberrant Ventricular Conduction (Figs 24.6 to 24.9)
Fig. 24.6: Complexes 1, 3, 5, 6, 7, and 9 are sinus beats. The complexes 2, 4, and 8 are examples of aberrant ventricular
conduction of right bundle branch type. All have preceding P-waves and are coupled to the preceding sinus beat
Fig. 24.7: The second complex in each pair is a premature beat with compensatory pause with aberrant
ventricular conduction of right bundle branch type
Fig. 24.8: Atrial premature beat with aberrant ventricular conduction (1, 2)
Fig. 25.9: Atrial premature beat

with aberrant ventricular con-
duction: The T-wave of complex 3
is distorted by a premature P-wave.
The APB (4) shows aberrant ventri-
cular conduction with incomplete
compensatory pause
Approach to Atrial Premature Beats 111
Atrial Bigemini (Figs 24.10 to 24.12)
Fig. 24.10: Atrial bigemini: Complexes 2, 4, 6 are atrial premature complexes.

Complexes 1, 3, 5, 7 and 8 are of sinus in origin
Fig. 24.11: APB with PAT: Atrial premature contractions and atrial tachycardia. Complexes 1 and 2 are of sinus origin.
Complex 3 is an APC, followed by an incomplete compensatory pause. Complex 4 is of sinus origin. Complexes 5-8 represent
a run of atrial tachycardia also followed by an incomplete compensatory pause. Complex 9 is of sinus origin
Fig. 24.12: APB with ventricular escape beat: The 3rd complex is a atrial premature beat. The incomplete compensatory
pause is followed by 2 ventricular escape beats (4, 5). Sinus beats are present in complex 6 and 7. QRS of ventricular escape
beat is wide and bizarre and without P-wave
ILLUSTRATIVE ECG OF ATRIAL AND JUNCTIONAL PREMATURE BEATS
Junctional Premature Beats (Figs 24.13 to 24.16)
Fig. 24.13: Junctional premature beat: The fourth complex is a nodal premature beat and no P-wave
related to it. NPB = Nodal premature beat. QRS of Junctional premature beat is normal shaped
Fig. 24.14: APB distorting preceding T-wave: Atrial premature contraction. The premature P-wave
has coincided with and distorted the preceding T-wave
Fig. 24.15: Interpolated APB: Complex 3 is an interpolated APC
Fig. 24.16: High atrial focus APB: P inverted in aVR, P upright in aVF,
Low atrial focus APB: P upright in aVR and inverted in aVF
Summary of Premature Beats 113
25 Summary of Premature Beats
Characteristics of different types of premature beats occur earlier in the cardiac cycle than expected.
Atrial premature beat Nodal premature beat Ventricular premature beat

1. Compensa- Incomplete Incomplete Complete
tory pause:
2. Shape of Normal except APB with Normal Wide and bizarre
QRS: aberrant ventricular
conduction.
3. Site of a. High atrial focus: P upright a. High AV nodal: Upright P a. Unifocal: All VPB of
focus: in aVF inverted in aVR in aVR and inverted in aVF same shape
b. Low atrial focus: P upright b. Mid AV nodal: P burried b. Multifocal: VPB’s have
in aVR and inverted in aVF in QRS different shapes
c. Low AV nodal: Upright P c. Left ventricular VBP:
in aVR and inverted in aVF Main deflection of VPB
upright in V1 and down-
ward in V6
d. Right ventricular VPB:
Main deflection of VPB
downward in V1 and
upward in V6
4. Variations: a. Blocked APB: Premature P a. Bigemini: VPB occurring
not followed by QRS after every normal beat
b. APB with aberrant ventricular b. Trigemini: VPB after two
conduction: Premature P normal beats
followed by wide QRS c. VPB followed by nodal
c. Atrial bigemini: APB occur- escape
ring after every normal beat d. “R” on “T” VPB: R-wave
d. APB with run of atrial tachy- of VPB distorting preced-
cardia ing T-wave.
e. APB with nodal or ventricular
escape beat. Escape beats not
preceded by P-wave. QRS
normal in nodal escape and
wide and bizarre in ventricular
f. APB occurring symmetrically
between 2 normal beats without
compensatory pause. P and QRS
normal shaped. Interpolated APB
26 Approach to Paroxysmal Atrial

Tachycardia (PAT)
PAT is due to rapid series of impulses arising regularly in an ectopic focus in either auricle resembling a series
of APB (atrial premature beat) occurring in quick succession.
ECG Pattern: Diagnostic Flow-Chart

First observe waves
| | |
P-waves QRS-waves T-waves and ST changes
a. Occasionally difficult to identify. May a. Normal shaped Prolonged PAT producing
be burried in preceding QRS or T b. wide and slurred if ventri- myocardial ischaemia resulting
b. Shape: Direction: Depends on site of cular aberration or bundle in S-T depression and inverted
origin as described in the approach to branch block associated T- wave. May result in heart
to APB. If focus arises in upper atrium failure
normal direction of P occurs, if arises
in lower end of atrium upright P in
aVR and inverted P in aVF occurs
c. Relation with QRS: Each P followed
by QRS unless there is AV block

Next, look for rate and rhythm
| | |
Rate Rhythm Effect of carotid sinus pressure
150-250/minute Regular Either stops it or no effect
Starts and stops abruptly 
Next, differentiate tachycardias (Differential diagnosis)
Rate and Rhythm ECG pattern Effect of Effect of Effect of carotid
exercise atropine sinus pressure
Sinus tachy- Above 100 PQRST normal Marked change Quickens Slight gradual slow-
cardia: regular ing, quickens on
release
PAT: Atrial rate See above No effect No effect No effect or stops it
160-220 1:1
Multiple ecto- Irregular See APB and Disappears Disappears May exaggerate
pics: VPB
Fast auricular Atrial rate above Fibrillary waves Worsens Worsens Slowing but no
fibrillation: 350 irregular change in rhythm
Contd...
Approach to Paroxysmal Atrial Tachycardia (PAT) 115
Auricular flutter: Atrial rate Flutter No effect — Abrupt slowing to ½.

220-350 waves Reversed on release.
Reveals hidden flutter
waves on release
VT: Ventricular rate Wide QRS. No effect No effect No effect
150-200, not as P often hidden in
fast as PAT. QRS and T
Slightly irregular

Finally, find out the cause of PAT:
Normal, emotional tension, mitral valve disease, less common in IHD
ILLUSTRATIVE ECG SHOWING ATRIAL TACHYCARDIA

WITH WIDE QRS (Figs 26.1 to 26.4)
Fig. 26.1: Supraventricular tachycardia with left

bundle branch block. Wide QRS also suggests
ventricular tachycardia but the previous record
during normal sinus rhythm was associated with
bundle branch block. Further the rate is very
regular. P-waves are suspected near the apices
of T-wave which are too much pointed
Fig. 26.2: PAT with aberrant ventricular conduction. QRS wide and bizarre
Fig. 26.3: PAT: Wide QRS complexes are

due to pre-existing bundle branch block.
The rhythm is quite regular. P is not
revealed. P and T are fused
Fig. 26.4: PAT with aberrant ventricular conduction. The rhythm is completely regular unlike VT.
Each wide QRS is preceded by P-wave unlike VT
ILLUSTRATIVE ECG SHOWING PAT WITH NARROW QRS COMPLEX (Figs 26.5
to 26.9)
PAT with Manifest P-wave
Fig. 26.5: Paroxysmal auricular tachycardia

Approach to Paroxysmal Atrial Tachycardia (PAT) 117
PAT with Superimposed P and T-wave
Fig. 26.6: APB occurring in runs

producing brief period of PAT. P and T
are fused during paroxysm.
Fig. 26.7: PAT: The T and P-waves are superimposed
PAT with AV block
Fig. 26.8: PAT with varying AV block.

IN V1 multiple P-waves are seen
Fig. 26.9: Paroxysmal atrial tachycardia with block. P not followed by QRS complexes. There is atrial arrest following
the 3rd QRS complexes. Complexes 3, 4, 5, are of sinus origin, with first degree AV block
Focus of Stimulation of APB (Figs 26.10 and 26.11)
Fig. 26.10: PAT: P-waves are upright in aVR and inverted in aVF suggesting ectopic focus low in atrium
Fig. 26.11: Multifocal PAT. Complexes 2, 3, 4 and 5 have similar P-waves. Complexes 1, 9, 10 and 13 have different
inverted P-waves. Complexes 8, 11, 12 and 14 have different P-waves. All suggest different pacemakers
PAT with APB (Fig 26.12)
Fig. 26.12: PAT with APB

Approach to Atrial Fibrillation and Flutter 119
27 Approach to
Atrial Fibrillation and Flutter
ATRIAL FIBRILLATION
Mechanism
Atrium
Ectopic focus in atrium discharging at variable rates and so fast (above 350-400/minute) that atrium can no
longer respond completely to each stimulus resulting in chaotic and asynchronous contractions of atrium. In
ECG, P-wave is replaced by irregular undulating waves of varying amplitude and shapes and sizes known as
fibrillary waves.

AV Node
Only strongest atrial stimuli stimulate AV node at rapid and irregular intervals. Weak stimuli are not conducted
through AV node.

Ventricle
Likewise ventricle responds rapidly and irregularly usually 120 to 150 beats per minute. ECG shows very
irregular ventricular rhythm.
ECG Pattern
Approach
First observe P-wave and QRS complex:

P-wave QRS complex
P replaced by fast different sized fibrillary waves. Normal configuration
Best seen in V1

Next observe ventricular rhythm:
Completely irregular. Carotid sinus pressure produces
ventricular slowing but no change in rhythm


Then differentiate auricular fibrillation from auricular
flutter, flutter-fibrillation and paroxysmal auricular
tachycardia
Auricular Flutter Flutter-fibrillation PAT
Ventricular rhythm usually regular Occasionally the rhythm may alternate Rhythm is regular as
unless varying AV block present. between flutter and fibrillation in a against fibrillation.
Saw-toothed like flutter waves are single tracing. Both types of waves are Carotid sinus pressure
characteristic. Carotid sinus pressure seen stops PAT or no effect
will increase AV block and reveals
more flutter waves

Lastly find out the aetiology:
• Coronary artery disease
• Mitral valve disease
• Thyrotoxicosis
AURICULAR FLUTTER
Mechanism
Atrium
A rapid series of impulses starts in an ectopic focus in either auricle. The auricular rate varies between 200 to
400 beats per minute. P-wave in ECG replaced by flutter waves (picket fence or saw-toothed appearance) but
regular with no isoelectric intervals, i.e. continuously wavy line.

AV Node
Like atrial fibrillation, all atrial stimuli are not transmitted through AV node and there is often some degree of
AV block.

Ventricle
Likewise, ventricle is unable to respond to so rapid an atrial rate. Usually AV block is regular resulting in 2:1,
3:1 or 4:1 AV block. Occasionally, block is irregular causing irregular ventricular rhythm. ECG shows normal
QRS complex, usually regular
ECG Pattern: Approach Flow Chart
First observe P-wave and QRS complex:

P-wave QRS complex

P replaced by saw-toothed flutter waves Regular and normal QRS
best seen in II, III, avf and V1

Then observe for AV block by noting number of flutter waves and QRS complex and their ratio:
| | |
Usually regular 2:1 AV block, Occasionally varying degree of Carotid sinus pressure increases
less often 3:1, 4:1, 5:1 or 6:1 AV block resulting in irregular AV block, slowing ventricular rate
block, resulting in more flutter ventricular beats simulating and allowing flutter waves to become
waves than ventricular beats auricular fibrillation more evident clarifying the diagnosis

Differential diagnosis:
See atrial fibrillation

Lastly, find out the aetiological diagnosis.
See auricular fibrillation
ILLUSTRATIVE ECG SHOWING AURICULAR FIBRILLATION AND

ATRIAL FLUTTER (Figs 27.1 to 27.10)
Fig. 27.1: Auricular fibrillation: Note irregular ventricular beats. P-waves replaced by irregular oscillations (Fibrillary waves)
of varying amplitude, contour and spacing. No definite P-waves. Fibrillary waves are fast (usually 300 to 600 per minute)
Fig. 27.2: Auricular flutter with 3:1 AV block: Note saw-toothed appearance of
flutter waves with regular ventricular beats
Fig. 27.3: Auricular flutter with 4:1 auriculoventricular block: Note saw-toothed base line due to flutter waves (F)
Fig. 27.4A: Atrial flutter with 4:1 AV block. Characteristic flutter waves are present.
There are 4 flutter waves to each QRS complex
Fig. 27.4B: Atrial flutter with 2:1 and 3:1 AV block. Saw-toothed and fence like baseline
Fig. 27.5: Atrial flutter: Saw-toothed appearance of F (flutter) waves replace P-wave.
Three F-waves before each QRS: Atrial flutter with 3:1 AV block
Fig. 27.6: Atrial fibrillation: Fibrillary waves (f-waves) replace P-wave with irregular ventricular rhythm
Fig. 27.7: Atrial flutter: Saw-toothed flutter waves with 2:1 and 3:1 AV block
Fig. 27.8: Atrial fibrillation, complete AV block

Fig. 27.9A: Atrial fibrillation. The first five cycles (1, 2, 3, 4, 5) show aberrant ventricular conduction.
The conduction returns to sinus beat with the sixth beat
Fig. 27.9B: Atrial fibrillation: Diminutive ventricular complexes with coupled VPB
Fig. 27.10: Myocardial Infarction + Auricular fibrillation. Only apex of R-wave visible
28 Junctional or Nodal Arrhythmias
In nodal arrhythmia, ectopic focus arises in the AV node. The impulse spreads upwards (retrograde conduction)
into the atrium and downwards (antegrade) into the ventricle. The QRS complexes are normal. The configuration
of P-wave depends on the presence of retrograde conduction and the site of ectopic focus in the AV node
whether it is in the upper part, lower part or mid-part of the AV node.
High AV nodal focus Mid AV nodal focus Low AV nodal focus
Upright P in aVR and inverted P P absent, buried in QRS due to retro- Upright P in aVR and inverted P in
in aVF preceding QRS due to grade and antegrade conduction are aVF following QRS. Due to ante-
retrograde conduction faster than of the same rate grade conduction faster than retro-
antegrade conduction grade conduction
Diagnosis
First, establish the presence of retrograde conduction by noting the configuration of P-wave and its position
relative to QRS complex: |
| |
P absent P present
|
| |
Upright P Inverted P
follows QRS |
| |
Inverted P follows Inverted P precedes
QRS QRS
All the above abnormalities of P suggest retrograde configuration

Next, find out the special forms of nodal arrhythmias:
A. Nodal tachycardia
B. Nodal premature beat
C. Nodal escape
Nodal Tachycardia
Rate 150-250/minute. If P is identifiable, it may precede, follow, QRS complex. They may be inverted in II,
III, aVF, and V3-4, upright in aVR and aVL, and diphasic in V1-V2.
Often, it is impossible to differentiate atria, tachycardia from nodal tachycardia if P-wave is absent and
rate is rapid. Differentiation clinically is not important and the two conditions are called supraventricular
tachycardia.
Junctional or Nodal Arrhythmias 125
Nodal Premature Beat
Note the compensatory pause which is usually complete. P-wave may or may not be identified. Identifiable
P-wave will appear after QRS or inverted P may precede or follow QRS.
Nodal Escape (See Further)
Finally, find out the site of focus in the AV node: (See starting of the chapter)
| | |
High AV nodal focus Mid AV nodal focus Low AV nodal
Nodal Escape
This nodal arrhythmia is characterized by normal QRS complex without P-wave following a pause due to
sinoauricular block or sinus arrest. In SA block and sinus arrest the SA node fails to initiate an impulse
following the pause (i.e. a period of no electrical activity) the AV node may initiate the impulse (Nodal
escape) or the ventricular musculature may start the impulse (Ventricular escape):
|
| |
Nodal escape Ventricular escape
QRS normal shaped with absent P-wave or if P QRS complex wide and bizarre with absent P-wave
identifiable it is either inverted follows or precedes or if identifiable it is either inverted following or pre-
QRS or upright following QRS complex ceding QRS or upright following QRS complex
Note: Junctional arrhythmia arises somewhere about the junctional region. They used to be called nodal, but
the term junctional is now favoured, as it is uncertain that the AV node is the actual site of origin; rather it is
somewhere in the adjacent junctional tissue.
ILLUSTRATIVE ECG SHOWING NODAL ARRHYTHMIAS
Nodal Arrhythmias with Upright P-wave (Figs 28.1 and 28.2)
Fig. 28.1: Nodal rhythm with late retrograde conduction. P-wave follows QRS
Fig. 28.2: Complex 1-4 are of sinus origin. Complex 5, 6, 7, 8, 9, and 10 are run of nodal beats in which P-waves follow
the QRS complexes. The QRS complexes show aberrant ventricular conduction
Nodal Arrhythmias with Absent P-wave (Figs 28.3 to 28.5)
Fig. 28.3: Nodal rhythm. P-wave absent
Fig. 28.4: Nodal escape beat (V): Note P-wave absent in nodal escape beat and shape of QRS normal
Fig. 28.5: Junctional (Nodal) tachycardia: No P-wave preceding QRS. Retrograde atrial
activation seen, P-wave immediately following QRS complex
Nodal Arrhythmia with Inverted P-wave (Figs 28.6 to 28.9)
Fig. 28.6: Nodal escape (N): It follows prolonged period of sinus arrest. Note inverted P-wave. QRS-t normal
Fig. 28.7: Nodal rhythm with early retrograde conduction. Inverted P preceding QRS
Fig. 28.8: Paroxysmal nodal tachycardia. Rate varies between 120-220/minute. Inverted P occurs regularly and QRS normal
Fig. 28.9: Nodal rhythm: The first two beats are of sinus origin. The remainder P-waves are inverted and of junctional in origin
Approach to Ventricular Premature Beat 127
29 Approach to Ventricular
Premature Beat
Ventricular premature beat (VPB) is initiated by ectopic focus in either ventricle characterized by bizarre
shaped QRS.
ECG Pattern: Flow Chart
First, observe the changes in waves and intervals.

P-wave Changes in shape of QRS R-R interval
a. May be absent a. Usually wide and slurred The sum of R-R interval
b. Retrograde conduction may b. Sources in ventricle: If QRS is shaped between pre and post VPB is
occur. recognized by configu- like left bundle branch block, VPB has exactly equal to 2 normal R-R
ration of P (upright in aVR arisen in right ventricle; similarly if intervals. Hence compensa-
and aVL; inverted in aVF, QRS of VPB is shaped like right bun- tory pause is complete
V3, V4, V5, V6 and diaphasic dle branch block, VPB is originated
in V1 and V2) in left ventricle
c. Multifocal VPB characterized by at least
2 abnormal QRS complexes of different
shapes in the same lead. Unifocal VPB:
Beats are of same configuration and
direction suggests single focus

Next note the VPB as related with normal beats:
A. Bigeminal or coupled rhythm: Characterized by grouping of pulse beats in pairs associated with
short or long run of VPB following every normal beat.
B. Trigemini: Grouping of pulse beats in groups of three associated with two successive VPB
follow a normal beat or one VPB follows every two normal beat.
C. Interpolated VPB: A VPB occurs immediately between two normal beats, not followed by
compensatory pause.

Note one differential diagnosis: Atrial premature beat with aberrant ventricular conduction gives rise to bizarre
QRS simulating VPB.

Finally, find out the aetiological diagnosis:
• Any form of organic heart disease, especially IHD and myocarditis
• Quinidine
• Digitalis
• Less common in normal individuals.
ILLUSTRATIVE ECG SHOWING VENTRICULAR PREMATURE BEATS (Figs 29.1 to 29.17)
Fig. 29.1: Ventricular premature con-

traction—Unifocal premature ventricular
contractions. Note wide and bizarre QRS.
Compensatory pause complete
Fig. 29.2: Ventricular premature beats

(trigeminal rhythm). VPB occurring regu-
larly after two normal beats
Fig. 29.3: Sinus rhythm with VPB. Complexes 2, 5, and 8 are ventricular premature contractions. The notches on their
T-waves are P-waves occurring at the expected time. The last complex in the strip is a nodal escape beat. VPB=Ventricular
premature beat, SB=Sinus beat, NEB=Nodal escape beat
Fig. 29.4: Multiform VPC: Complex 4 is a VPC. Complex 6 is a VPC of different focal origin
Fig. 29.5: Two VPC from different foci: The first shows marked distortion.
The second occurs in the P-R segment of the preceding beat
Fig. 29.6: Multifocal ventricular ectopic beats: Different configuration of ectopic points to different ectopic foci
Fig. 29.7: Bigeminal or coupled rhythm or premature ventricular beats (v) occurring after every
normal beat. Unifocal VPB—all VPB of same shape and direction
Fig. 29.8: Left ventricular ectopic beat. AB + BC = CD + DE i.e. compensatory pause complete
Fig. 29.9: Complex 2 is an interpolated VPB. Complex 6 is a VPB occurring after a longer coupling interval
Fig. 29.10: “R” on “T” VPB
Fig. 29.11: VPC and right bundle branch block: The basic rhythm is sinus rhythm with right bundle branch block (Complexes
1, 2, 3, 5, 6, 7). Complexes 4 and 8 are ventricular premature beat—their initial waves do not resemble the small r-wave of
the other right bundle branch block complexes. The beat following the second VPB is a nodal escape beat
Fig. 29.12: The complex is a VPC and at the apex of its T-wave a second VPC is initiated (3, 3A). The second pair of VPC (6,
6A) are further separated from each other and T-wave interruption does not occur. The first pair of VPC (3A, 3) are very close
so that T-wave interruption occurs
Fig. 29.13: Interpolated ventricular premature contraction (V) between two normal beats without compensatory pause
Fig. 29.14: Multiple VPB producing VT
Fig. 29.15: VPB occurring

before completion of the
T-wave of preceding beat.
They occur during the refrac-
tory period
Fig. 29.16: VPB showing compensatory pause. The R-R

interval between first and third sinus beats is double the R-R
interval between the 3rd and 4th sinus beat
Fig. 29.17: Run of VT with fusion beats (F)

30 Approach to Ventricular
Tachycardia (VT)
Produced by rapid and regularly occurring ectopic beats arising in either ventricle manifested on the ECG by
bursts of bizarre, wide, notched QRS complexes in rapid succession resembling VPB.
ECG Pattern
First observe rate and rhythm and effect of carotid sinus pressure
| | |
Rate Rhythm Effect of carotid sinus pressure
150-200 not as fast as Slightly irregular No effect
SV tachycardia

Then observe following waves: |
| |
P-wave QRS complex
• Often no P can be made out it may be • Bizarre, wide and slurred QRS
hidden in QRS and T. At times special • T slopes off from QRS in the opposite direction with no inter-
leads over right chest leads taken to vening S-T segment
demonstrate P • Deflection of QRS is in the same direction throughout chest
• In some cases P is independent of QRS leads from V1 to V6
• Occasionally retrograde conduction • QRS complex do not have the usual smoothness of ventri-
occurs and the direction and relation cular fibrillation
of P to QRS varies (See VPB) • Due to rapid rate it is not possible to separate QRS from
 S-T segment and T-wave
Next, differentiate VT from PAT, PAT with bundle branch block and PAT with ventricular aberration:
|
| | | |
Ascertain P and its QRS pattern Compare ECG pattern Effect of carotid
relation with QRS taken before and after sinus pressure
paroxysm when rate is slow
a. if P is upright and fol- a. Right BBB pattern in • Presence of BBB pat- • May or may not stop,
lowed by QRS suggests V1 and QRS in V6 tern points to PAT points to PAT, PAT
PAT, PAT with BBB favours PAT with with BBB with BBB or aberration
or PAT with ventri- aberration and • If shape of QRS resem- • No effect, points to VT
cular aberration PAT with BBB bles shape of QRS of
b. P not related with b. QS or rS in V6 and VT suggests VT
QRS or evidence of RS in V1 favours VT
retrograde conduc-
tion suggests VT
Approach to Ventricular Tachycardia (VT) 133
c. P hidden in QRS and T points to VT

d. If auricular wave in neck vein are
slow and at the same time rapid
ventricular rate occurs indicates VT

Finally, find out the cause of VT
• Recent myocardial infarction
• Hypertension
• Digitalis
ILLUSTRATIVE ECG SHOWING DIFFERENT TYPES OF VT
VPB Producing VT (Fig. 30.1)
Fig. 30.1: Run of VT. The 2, 4, 5, 6 and 8 are VPB. The 4, 5 and 6 show brief run of VT
VT Showing P-wave (Fig. 30.2)
Fig. 30.2: Ventricular tachycardia. The rhythm is slightly irregular. P-waves are pointed by arrows
VT with Capture Beat, or Fusion Beat (Figs 30.3 to 30.5)
Fig. 30.3: Ventricular tachycardia with one ventricular capture beat (CB)
Fig. 30.4: Ventricular tachycardia. The first half shows left ventricular VT and
the later half shows right ventricular VT. VC is ventricular capture beat
Fig. 30.5: A short run of ventricular tachycardia started by a fusion beat (FB)
Heart Block (Atrioventricular) 135
31 Heart Block (Atrioventricular)
Classification
First degree heart block

Second degree heart block:
a. Constant (2nd degree AV block with regular dropping of ventricular beats)-Mobitz type II
b. Periodic (2nd degree AV block with irregular dropping of beats)-Mobitz type II
c. 2nd degree AV block with Wenckebach phenomenon-Mobitz type I.
Third degree heart block (Complete heart block)
Mechanism
Defective conduction of supraventricular impulse from auricle to

ventricle above bundle of His results AV block. It is due to
|
| |
Pathological disorders such as acute rheumatic Functional disorders as in increased vagal stimu-
fever, digitalis, quinidine, coronary artery dis- lation by carotid sinus pressure
ease, diphtheria, and certain congenital heart lesion

There are three types of AV block
| | |
Conduction of atrial If some of the atrial impulses Complete heart block
impulse to ventricle simply del- are conducted to ventricle inter- If no impulse is conducted to ventri-
ayed and all atrial impulses con- mittently and others are not cle and a second pacemaker, either
ducted to ventricle with prolonged  in ventricle or AV node stimulates
P-R (greater than 0.20 sec) Results in 2nd degree heart block ventricle with atrial rate greater than
  ventricular rate and P-R variable
Ist degree heart block Three types
| | |
Periodic 2nd degree AV block: Constant 2nd degree AV block: Conduction increasingly impaired
Periodic interruption to AV con- Regular interruption to AV con- and finally fails and a beat is drop-
duction results in periodic absence duction resulting in regular absence ped with increasingly prolonged
of ventricular beats (dropped of ventricular beats with constant P-R interval
beats) with variation in A:V ratio A:V ratio with fixed P-R interval 
  Mobitz type I. 2nd degree heart
Mobitz type II with irregularly Mobitz type II. 2nd degree AV block with Wenckebach
dropped beats block with regularly dropped beats
Approach
First exclude Ist degree AV block by noting prolonged (greater than 0.20 second)
and constant P-R interval

Next, count the number of P-waves and QRS complex.
P more than QRS suggests 2nd degree and 3rd degree AV block

Then note whether there is a ratio between P and QRS (A:V ratio) or
P is completely independent of QRS. Also note P-R and R-R intervals
|
| |
Ratio between P and QRS exists, e.g. 2P to 1QRS, P completely independent of QRS pointing to
3P to 1 QRS, 4P to 1 QRS and so on CHB or AV dissociation
 
Suggests 2nd degree AV block observe Next, find out atrial rate (P-P interval) and ventricle
P-R interval and R-R interval | rate (R-R interval) |
| | | |
Constant P-R interval Progressively increasing Atrial rate greater than Ventricular rate greater
 P-R till a beat is dropped ventricular rate and than auricular rate with
Suggests Mobitz and also progressively R-R constat R-R interval irregular due
type II AV block shorter R-R until a beat  to capture beats***
 is dropped Suggests 3rd degree 
Next note R-R interval  AV block Suggests AV dissociation
Suggests Mobitz type I 
with Wenckebach Find out shape of QRS |
| | | |
Regular R-R interval Irregular R-R interval Normal Deformed
   
Suggests Mobitz type II Suggests Mobitz type II Suggests 2nd pacemaker Suggests 2nd pacemaker
with regular dropping of with irregular dropping in bundle of His above in right or left ventricle
of beats beats branching below AV
node
*** Capture beat: A P-wave expected to be transmitted through AV junction and activate the ventricle, is called a
ventricular capture beat.
ILLUSTRATIVE ECG SHOWING ATRIOVENTRICULAR BLOCK

First Degree AV Block (Figs 31.1 and 31.2)
Fig. 31.1: First degree heart block. Prolonged P-R interval

Fig. 31.2: First degree AV block. Prolonged

P-R interval. P seen sitting on the tops of
the preceding T-waves
Second Degree AV Block
2nd Degree AV Block (Periodic) with Irregularly

Dropping of Beats (Mobitz Type II) (Figs 31.3 to 31.8)
Fig. 31.3: 4th P is isolated without producing QRS. P-R intervals are constant,
hence 4th P is not premature. D/D blocked APB
Constant AV Block with Regularly Dropping of Beats (Mobitz Type II)
Fig. 31.4: 2nd degree 2:1 AV block. After two atrial beats there is one ventricular beat
Fig. 31.5: 2:1 AV block. Alternate ventricular response to P-wave. Regular P-P intervals.
Regular drop of beats with regular P-P intervals suggests 2nd degree AV block
2nd Degree AV Block with Wenckebach Phenomenon (Mobitz Type I)
Fig. 31.6: Second degree AV block with

Wenckebach phenomenon. P-R interval
gradually increasing till QRS is dropped
Fig. 31.7: 2nd degree AV block with Wenckebach phenomenon. The P-R interval gradually increases till
the 5th P-wave is not followed by RS-T complex. There are 7 atrial beats to 6 ventricular beats
Fig. 31.8: Mobitz type I AV block with Wenckebach phenomenon. The P-R interval gradually
increases until 4th P is not followed by a QRS-T complex
Complete AV Block
CHB with Normal QRS (Figs 31.9 and 31.10)
Fig. 31.9: Complete heart block. Atrial and ventricular rates are independent of each other. QRS complex is normal shaped
hence the second pacemaker is near AV node. P-R intervals vary. Atrial and ventricular rhythm is regular but ventricular
rate is slower than atrial rate
Fig. 31.10: Complete AV block. Rate of P-P and R-R intervals vary. P-P is faster, R-R is slower. P-R intervals vary
CHB with Wide and Bizarre QRS (Figs 31.11 and 31.12)
Fig. 31.11: Complete AV block. QRS wide (2nd pacemaker in ventricular wall).
Atrial rate is independent of ventricular rate. P-R interval varies
Fig. 31.12: Complete heart block. P-waves bear no relationship to QRS. Ventricular rate is slow and QRS is bizarre
(2nd pacemaker is in ventricular wall). Atrial rate is faster than ventricular rate. P-R interval varies
32 Disorders Produced by
Two Independent Pacemakers
Parasystole
Occasionally, two independent pacemakers exist: one in SAN and other in ectopic foci in atria or AVN or
ventricle. This condition could not exist unless the most rapid rhythm were somehow prevented from assuming
complete charge of the heart. This protective mechanism is due to a “protective block” or “entrance block”.
The two pacemakers are independent of each other and activate ventricle at different times. There are two
types of arrhythmias produced due to presence of two pacemakers depending upon the conduction of sinus
impulse:
|
| |
No blocking of conduction of normal sinus Blocking of sinus impulse
impulse through AV node through AV node
 
Parasystole a. AV dissociation
Two pacemakers: One in SAN, the other is ectopic b. Complete heart block: One
focus in the atria or ventricle or AVN pacemaker in SAN and the
| | other in AVN or ventricle
Pacemaker in SAN (Sino- Pacemaker in ectopic foci in 
atrial node): Rate faster atria or ventricle: Slower than See Chapter on AV dissociation
than the ectopic focus rate. sinus pacemaker. Shaped like
Beat behaves like sinus ectopic beat specially resembles
beat-normal shaped ventricular premature beat

Time relationship:
— Parasystolic beats have a varying coupling intervals with the beats (sinus beat) preceding
them (whereas ordinary ectopic beats have a fixed coupling interval)
— The time intervals between each two successive parasystolic ectopic beats have a simple
arithmetical relationship to one another. So in the ECG the long inter-ectopic intervals
(measured between two successive parasystolic ectopic beats) are multiple of the shorter
ones.

Type of parasystole
| | |
Atrial parasystole Junctional or nodal parasystole Ventricular parasystole
2nd pacemaker in ectopic focus 2nd pacemaker in ectopic focus 2nd pacemaker in ventricle
in atria in AVN
Disorders Produced by Two Independent Pacemakers 141
Diagnosis of Parasystole by ECG
Diagnosis of parasystole is made by taking extra long lead and by determining the presence of two pacemakers
and note the characteristics of sinus parasystolic beat.
Demonstrate two different rhythms—one is normal sinus rhythm emanating from SAN, the other
parasystolic ectopic rhythm usually emanating from ectopic focus in ventricle.
|
| |
Features of parasystolic ectopic beat Features of SAN beat
• Shaped like ventricular premature beat • Shaped like normal sinus beat
• It follows sinus beat • It precedes parasystolic ectopic
• Occurring independently of sinus beat hence varying • Discharge rate faster than para-
coupling interval (ordinary ectopic beats have a fixed systolic ectopic
coupling time)
• Time interval between parasystolic ectopic beats
(Inter-ectopic interval) is constant or multiple of
a common denominator
• Discharge rate of parasystolic ectopic is slow
• Parasystole is usually associated with heart disease
but may occur in normal people
ILLUSTRATIVE ECG SHOWING PARASYSTOLE (Figs 32.1 and 32.2)
Fig. 32.1: Atrial parasystole: Presence of two pacemakers are indicated by two types of atrial complexes.
One “P” of sinus origin and the other “P” of ectopic origin in the atria
|
| |
Sinus pacemaker producing sinus “P” character- Ectopic pacemaker in atria producing atrial ectopic
ised by its resemblance to normal P-wave, prece- beat. It resembles atrial ectopic beat. Occurring
ding parasystolic atrial ectopic. The only uncom- independent of sinus beat hence varying coupling
mon finding is slower than parasystolic ectopic interval. Inter-ectopic interval is constant. The only
uncommon finding is fast rate of parasystolic beat
(Modified from Goldman)
Fig. 32.2: Ventricular parasystole: (a) Parasystolic ectopic “A” producing ectopic rhythm characterized by VPB like shape,
follows sinus beat(B), varying coupling intervals “C”, constant inter-ectopic intervals “D” and slower rate than sinus beats
(b) Sinus beat “B” is normal shaped, precedes parasystolic ectopic beat “A” and faster than parasystolic ectopic beats
33 Atrioventricular Dissociation
In AV dissociation, auricle and ventricle are driven by two independent pacemakers: one is SA node (or atrial
ectopic focus) driving auricle and another in AV node driving ventricle due to failure of transmission through
AV node. Transmission failure may be transient or permanent:
|
| |
Transient due to Permanent due to
Acute rheumatic fever, digitalis toxicity and Complete heart block, atrial fibrillation, atrial flutter,
hypopotassemia due to excess use of diuretics ventricular tachycardia, nodal tachycardia, recent
inferior wall infarction and digitalis toxicity
A protective mechanism may or may not be present to slower atrial rhythm from bombardment by faster
AV nodal rhythm resulting in two types of AV dissociation
|
| |
Incomplete AV dissociation Complete AV dissociation
If protective mechanism is present, higher atrial If protective mechanism is not present, interference
pacemaker is able to activate heart producing does not occur and complete AV dissociation results
normal beat and thereby interferes with more
dominant AV nodal pacemaker rhythm. This inter-
ference dissociation is also called incomplete AV
dissociation and this auricular driven normal beat is
called ventricular capture beat. Hence, incomplete
dissociation is associated with ventricular capture beat
Approach
First, find out auricular rate (P-P interval) and ventricular rate (R-R interval). In AV dissociation both rates
are different suggesting presence of two pacemakers

Next, find out P-R interval which is progressively shorter. Schanroth (1973) says, atrioventricular dissociation
should always be suspected when the P-R intervals become progressively shorter

Then find out whether AV dissociation is incomplete or complete.
|
| |
Incomplete dissociation Complete dissociation
Associated with ventricular capture beat (P-wave Not associated with ventricular capture beat
walking through and transmitted through AV node
interfering dominant nodal rhythm followed by
normal QRS)

Atrioventricular Dissociation 143

Next, find out whether auricular rate is faster or slower than ventricular rate
|
| |
Auricular rate faster, suggests complete heart Auricular rate slower, suggests AV dissociation
block with AV dissociation without CHB

Finally, find out the aetiological diagnosis
A. AV dissociation with CHB... Causes are IHD., Stokes-Adams attack
B. AV dissociation without CHB... Usually transient as in acute rheumatic fever, digoxin toxicity,
hypokalemia. May be associated with sinus bradycardia with AV escape, nodal rhythm, ventricular
premature beat, ventricular tachycardia, atrial fibrillation and flutter

Next, find out the shape of QRS
|
| |
Normal QRS Bizarre QRS
 
Suggests 2nd pacemaker in the AV node Suggests 2nd pacemaker in the ventricle with
aberrant ventricular conduction
Note
Independent atrial activity in the form of P-waves can be identified in about 20 percent cases of ventricular
tachycardia suggestive of an atrioventricular dissociation. A normal relationship of P-wave to QRS complex
denies ventricular tachycardia even QRS is wide and bizarre. |
| |
Incomplete AV dissociation Complete AV dissociation
ECG pattern ( See Fig. 33.1) ECG Pattern ( See Fig. 33.2)
a. Auricular rate is slightly slower than ventri- a. No VCB
cular rate b. R-R interval is perfectly regular without interfered
b. VCB is premature, i.e. early compared to by VCB. Hence, AV dissociation without VCB with
dominant R-R interval regular R-R interval is called complete AV dis-
c. R-R interval is regular except when VCB occurs sociation
d. Because VCB interferes dominant rhythm this c. Auricular rate faster than ventricular rate
is called interference dissociation or incomplete
AV dissociation
ILLUSTRATIVE ECG SHOWING AURICULO-VENTRICULAR DISSOCIATION

(Figs 33.1 to 33.4)
Fig. 33.1: Auriculoventricular dissociation (incomplete). Auricular rate is independent of ventricular rate except for the normally
conducted beat (ventricular capture beat) marked VCB. P follows QRS and so nodal in origin. VCB is auricular in origin which
interferes dominant rhythm (interference dissociation)
Fig. 33.2: Complete or third degree heart block (complete AV dissociation). Ventricular rate completely independent of
auricular rate. QRS complexes are wide, hence the second pacemaker is in the ventricle. P-R interval varies. Atrial rate
faster than ventricular rate
Fig. 33.3: Auriculoventricular dissociation. Auricular and ventricular rate are independent of each other points to different two
pacemakers. One pacemaker is in the sinus node and the other in the AV node. Sinus node pacemaker drives auricle and AV
node pacemaker drives ventricle. Auricular rate is slower than ventricular rate. Two independent pacemakers are due to
failure of transmission of impulses through AV junction. Failure of transmission is due to physiological depression or pathological
depression of AV node. Physiological depression is transient and associated with acute rheumatic fever, digitalis intoxication
or hypokalemia. Pathological depression is due to complete AV block. In physiological depression auricular rate is slower
than ventricular rate. In pathological depression auricular rate is faster than ventricular rate. Occasionally, sinus node impulse
reaches AV node and finds AV node not refractory and transmitted through AV node to ventricle and activates ventricle. This
is called ventricular capture beat. This P-wave is followed by normal QRS which is early compared to dominant R-R interval.
This type of AV dissociation is associated with capture beat A is a sinus beat produced by SA node pacemaker. B, C, E are
nodal beats not preceded by P-wave and produced by AV nodal pacemaker. D beat is ventricular capture beat which is
produced by SA node pacemaker
Fig. 33.4: Incomplete AV dissociation with complete AV block. Atrial rate is faster than ventricular rate. The ventricular
capture beat (VCB) appear early compared to dominant R-R interval. This is called incomplete AV dissociation because
some sinus beats get through the AV node to produce ventricular beats. Complete heart block is suggested by slower
ventricular rate than auricular rate
Hemiblock of Left Bundle Branch 145
34 Hemiblock of Left Bundle Branch
The conduction defect in one of the two main divisions of the left bundle branch is called hemiblock. The left
bundle branch divides shortly, after its origin into two divisions:
1. Anterior division supplying anterior and superior papillary muscles of left ventricle
2. Posterior division supplying inferior and posterior papillary muscles of left ventricle. Normally, impulses
spread simultaneously through both divisions. If conduction is blocked in the anterior division left anterior
hemiblock is produced and the excitatory process will spread through the posterior division and the anterior
part of left ventricle becomes stimulated later. Reverse is true if block is in the posterior division. See
below:
Bundle of His divides into two branches
|
| |
Left bundle branch divides into two branches Right bundle branch
|
| |
Anterior division Posterior division
Supplies anteriorly and superiorly: Supplies inferiorly and posteriorly:
 
Its block produces left anterior hemi- Its block produces left posterior
block (anterolateral parietal block) hemiblock
ECG Pattern
Left anterior hemiblock Left posterior hemiblock

Two types:
a. Without infarction: Left axis deviation • Right axis deviation of +120
+ Flat T in I, aVL and V5,V6 • Small r in I and aVL
b. With infarction: (Peri-infarction block) • Small q in III and aVL
i. With antero-lateral infarct: Q in I • Absence of right ventricular hypertrophy
and aVL + Left axis deviation + • Exclusion of other causes of right axis
small r in II, III, and aVF deviation
ii. With diaphragmatic infarct: Left axis
deviation + Q in II, III, and aVF + S
in I + R in III and aVF
Incidence: Common Rare
Association: Often associated with RBBB
Causes: Often due to ischaemic heart disease Commonest cause IHD
Also remember differential diagnosis of causes of left axis deviation:

Causes Remarks
Left anterior hemiblock Very high degree of left axis deviation usually of
–60 degree, small q in I, a small r in III. QRS
duration normal
Coronary artery disease ST depressing, T-wave inversion
Left ventricular hypertrophy Increased voltage R in V5, V6. ST and T changes of
left ventricular strain pattern
Left bundle branch block Wide R (M-shaped complex) in V5,V6
Pulmonary emphysema Low voltage of QRS
Normal In 10 percent cases
Other types of bundle branch block:
Monofascicular block ________→ Left anterior hemiblock or Left posterior hemiblock
Intraventricular block ________→ QRS prolonged 0.12 second or more in all the chest leads
Bifascicular block:
_____
Implies right bundle branch → RBBB + Left anterior hemiblock
_____
block plus a block either in → RBBB + Left posterior hemiblock
the anterior or the posterior
division of left bundle branch
Trifascicular block: __________→ RBBB + Left anterior hemiblock + Left posterior hemiblock or
Implies RBBB plus a block Bifascicular block + prolonged P-R or
in both the anterior and the LBBB + Prolonged P-R or
posterior divisions of the left Alternating RBBB and LBBB
bundle branch
ILLUSTRATIVE ECG SHOWING LEFT ANTERIOR HEMIBLOCK (Figs 34.1 and 34.2)
Fig. 34.1: Left anterior hemiblock: Left axis deviation. Small q in I and aVL small r in II, III, aVF.
Associated with anterior myocardial infarction
Hemiblock of Left Bundle Branch 147
Fig. 34.2: Left anterior hemiblock: Left axis deviation. Small “r” in II, III and aVF. Small “r” in II, III and
aVF. Small “q” in I and aVL. Right bundle branch block. Inverted T in V4, V5 and V6
35 Bundle Branch Block
Classification of Bundle Branch Block
1. Right bundle branch block:

a. Complete
b. Incomplete
2. Left bundle branch block:
a. Complete
b. Incomplete
3. Left anterior hemiblock
4. Left posterior hemiblock
RIGHT BUNDLE BRANCH BLOCK
Mechanism
Conduction blocked in right main branch of bundle of His


Sequence of depolarisation Effect seen in V1 and V6 leads

First septal depolarisation from left  First arm of M-shaped complex
to right (arrow 1), Figure 35.1A (arrow 1), Figure 35.1A

Next left ventricular depolarisation  Notch of M complex (arrow 2),
from right to left (arrow 2), Figure 35.1A
Figure 35.1A

Right ventricular depolarisation  Second arm of M complex (arrow 3)
delayed from left to right (arrow 3) figure 35.1A. In V6 broad and slurred
figure 35.1A because blocked right S-wave due to delayed and left right
bundle branch right ventricle ventricular depolarisation
activates by the stimulus from left
bundle arriving below the block.
Bundle Branch Block 149
Fig. 35.1A: Right bundle branch block
Right Bundle Branch Block (Fig. 35.1B)
Fig. 35.1B: Right bundle branch block: In V1-V2 leads: rR widened; widened QRS interval 0.12 second or more:
S-T depression and T inversion and no Q-wave. In V5-6 lead: Slurred broad S-wave
Approach
First, ascertain the minimum diagnostic criteria
• rsR’ complex in V1, V2 and V3R, QRS interval greater than 0.12 second in V1, V2 and V3R
• Wide S in lead I, V5, and V6

Next, look for other supportive evidences:
A. Chest leads:
• S-T depression and T inversion V1, V2 and V3.
B. Limb leads:
• Wide rSr or QR in aVR

• Then, proceed for differential diagnosis

Differential diagnosis of right bundle branch block and right ventricular hypertrophy. It is not easy to diagnose
right ventricular hypertrophy if associated with right bundle branch block. Differential points are as follows:
RBBB Right VH
QRS interval: 0.12 second or more Less than 0.12 second
rsR, qR, rR or R in V1: rSR’ complex present in V1 R-wave, qR or rR complex seen
VAT in V1 0.06 second or more .03 to 0.05 second

Also remember a Q-wave in V1, V2 rules out right bundle branch block, except in septal infarction and
marked clockwise rotation.

Lastly, find out the aetiology of right bundle branch block
A. Transitory right bundle branch block:
• Acute pulmonary embolism
• Acute exacerbation of chronic bronchitis with emphysema.
B. Permanent right bundle branch block:
• Coronary artery disease
• Hypertensive heart disease
• Causes of right ventricular hypertrophy and dilation
• Atrial septal defect (95% cases)
• Myocarditis (rheumatic, diphtheritic)
• Valvular heart disease, i.e. mitral stenosis.
Incomplete Right Bundle Branch Block

Incomplete right bundle branch block is due to functional or organic defect in the right bundle which slows
but does not interrupt transmission of the impulses to the ventricles.
ECG Pattern of Incomplete Right Bundle Branch Block

• Broad S in lead I and V6
• M-complex in V1, V2, V3r and V4r
• QRS 0.8 to less than 0.12 second
Aetiology
• Normal
• Right or left ventricular hypertrophy
• Transient block in right ventricular strain due to pulmonary embolism, acute myocardial infarction
• Atrial septal defect.
LEFT BUNDLE BRANCH BLOCK

Mechanism
Conduction blocked in left main branch of bundle of HIS (Fig. 35.2A)
Fig. 35.2A: Left bundle branch block
Sequence of depolarisation ECG pattern as seen in left ventricular

and right ventricular leads
First septal depolarisation from right to left 1. Left ventricular leads (V5, V6) will show widened
QRS or M complex with secondary T inversion

and S-T depression
Next, right ventricular depolarisation 2. Right ventricular leads show a broadened

from left to right and notched QS

Finally, left ventricular depolarisation
from right to left. Left bundle branch
stimulates below the block by stimulus
reaching it from right side of septum
ECG Patterns: Approach (Fig. 35.2B)
First ascertain minimum diagnostic criteria:

• rsr or M complex in V5 and V6 and lead I without Q-wave
• QRS interval greater than 0.12 second.

Next look for other associated evidence:
A. Chest leads
• S-T depression and T inversion in V5 and V6.
B. Limb Leads
• M-shaped complex in aVL if heart is horizontal
• M-shaped complex in aVF if heart is vertical.
C. Standard Leads
• Wide R or rsR complex, absent Q-wave, S-T depression or T inversion in lead I.

Find out the aetiology:
1. Ischaemic heart disease.
2. Hypertensive heart disease.
3. Causes of left ventricular hypertrophy.
4. Non-rheumatic myocarditis
5. Congenital heart disease involving septum.

Differential diagnosis of left bundle branch block and left ventricular hypertrophy:
Left bundle branch block Left Ventricular Hypertrophy
• Q absent in V5, V6. Presence of • Q-wave frequently present in V5, V6
Q excludes
• Left bundle branch block or indicates
associated infarction.
• M-shaped complex present in V5, V6 • Absent M complex in V5, V6
• QRS interval equal to or greater than • QRS interval less than 0.12 seconds.
0.12 seconds.
Occasionally, additional leads such as V7 and V8 are taken which show V5 and V6 pattern.
Fig. 35.2B: V4 to V6: rsR or RsR complex; QRS interval 0.12 second or more; no Q-wave;
S-T depression and T inversion. In V1-2 leads: Slurred and broad S-wave
36 Accelerated Conduction or
Pre-excitation Syndrome or Wolff-
Parkinson-White Syndrome
Impulse arising in SA node travels through an accessory pathway of specialized conduction tissue bypassing
the AV node. The pathway starts from atrial muscle and communicates with intraventricular conduction
system resulting in early (premature) activation of a portion of ventricular myocardium and the remaining
myocardium is activated latter via normal AV conduction system:
Impulse originates in SA node travels through two pathways
|
| |
Accessory pathway bypassing Normal pathway through AV node
 
Resulting in premature excitation of a portion Resulting in late excitation of remaining
of myocardium devoid of inherent delay unlike portion of myocardium due to normal
normal delay in AV node and bundle of His delay in AV node and bundle of His

Producing the following ECG pattern
1. WPW syndrome
2. Isolated accelerated conduction
3. Accelerated conduction associated with atrial arrhythmia
Patients with the above arrhythmias are prone to paroxysmal atrial tachycardia, atrial flutter and fibrillation.
Except atrial arrhythmias, WPW syndrome and isolated accelerated conduction may be found in normal
individuals and does not alter the normal life expectancy. Occasionally, accelerated conduction may be
associated with Ebstein disease and idiopathic hypertrophic subaortic stenosis

Basis of ECG patterns
|
| |
Due to absence of delay in the accessory Due to double activation of ventricle early through
pathway it is termed “Accelerated conduction” accessory pathway and late through normal pathway
 
Results in short P-R interval (Fig 36.1) Results in wide QRS. Initial or ascending portion of
QRS has slurred appearance due to premature excita-
tion of small portion of ventricular myocardium.

Frequently S-T segment and T-wave are opposite
to deflection of QRS resembling bundle branch
block
Accelerated Conduction or Pre-excitation Syndrome or Wolff-Parkinson-White Syndrome 155
Fig. 36.1: Wolff-Parkinson-White syndrome (group B): Note short P-R interval, widened QRS, and slurring of the ascending
limb of QRS in lead V5 and V6 and of the descending limb in V1 and V2. In type A QRS deflection is mainly upright in V1 and
V2 (Resembling right bundle branch block)
ECG Pattern
WPW Syndrome
A. Short P-R interval (0.11 to 0.14 second).

B. Broad and slurred QRS complex.
C. A short and thickened deflection marking the onset and upward stroke of QRS complex called delta wave.
D. With or without S-T segment and T-wave opposite to deflection of QRS.
Two types of WPW syndrome are described by Rosenbaum et al (1970)
|
| |
Type A Type B
QRS deflection mainly upright in V1 and V2 QRS deflection mainly negative in V1 and V2
resembling right bundle branch block or

Differential diagnosis of WPW syndrome
1. Short P-R interval with normal QRS occurs in Lown-
Ganong-Levine syndrome and paroxysmal atrial
tachycardia.
2. Normal P-R interval with slurring of initial portion
of R-wave a normal variant

Look for delta waves which occur in most cases of WPW syndrome. Carotid sinus
pressure and exercise may cause WPW syndrome to disappear and thus the diagnosis
is confirmed.
37 Sick Sinus Syndrome
History and Mechanism
This is characterized by deficient function of the sinoatrial node. It was first described by Lown. This syndrome
consists of sino-atrial block associated with bursts of sinus arrest characterized by bradyarrhythmia and also
accompanied by atrial fibrillation and atrial tachycardia manifested by tachyarrhythmia. Hence, the name
“Tachybradycardia” syndrome. The sinoatrial node is so depressed that it does not resume its function as
expected. It is intermittent, more in females and commonest in the 7th decade but can occur in any age.
It is clinically manifested by symptoms of cerebral ischaemia with faintness, syncope or even sudden
death.
ECG Pattern
a. Sinus bradycardia, this may be intermittent or constant and is usually the first sign of the disorder.
Occasionally, rate is normal but it may fail to rise after exercise, fever or congestive cardiac failure.
b. Pause due to sino-atrial block or sinus arrest.
c. Tachycardia due to atrial fibrillation or atrial tachycardia.
d. Nodal rhythm
ILLUSTRATIVE ECG OF SICK SINUS SYNDROME (Figs 37.1 to 37.4)
Fig. 37.1: Sick sinus syndrome—Key: APB or AP = Atrial premature beat. JE = Junctional escape
Sick Sinus Syndrome 157
Fig. 37.2: Sick sinus syndrome: Sequence: 1, 2, 3, 4, sinus in origin—5 nodal ectopic—6 sinus—long pause of SA block—7
nodal escape beat—8 sinus beat—9 sinus beat—10, 13 supraventricular tachycardia with aberrant ventricular conduction—
14, 15, 17, 18, of sinus origin—16 atrial premature beat with compensatory pause
Fig. 37.3: Sick sinus syndrome: 1 = Sinus beat. 2 = Sinus beat. 3 = Sinus beat. 4 = Pause. 5 = Ventricular escape beat (not
preceded by P-wave, QRS shape bizarre). 6 = Nodal escape beat (not preceded by P-wave QRS normal shape)
7 = Sinus beat
Fig. 37.4: Sick sinus syndrome: Sequence: Sinus (S1) beat-Pause-Junctional escape
beat (J)—Fusion beat and the sequence is repeated
38 How to Read the ECG of Arrhythmias
First, find out whether it is tachyarrhythmia or bradyarrhythmia or any other arrhythmias.

Next, note the characteristics of PQRST, P-wave, QRS complex, P-R interval, P-P interval and R-R
interval.
Bradyarrhythmias
A. PQRST Abnormalities
|
| |
Normal PQRST PQRST dropped producing pause
P, P-R interval and QRS complex
normal. T and P distinct 1. Sinoatrial block
 2. Sinus arrest
Sinus bradycardia 
Measure R-R interval
|
| |
R-R of pause double the R-R of the pause more than
R-R between normal beats double the R-R of normal beats
 
SA block Sinus arrest

Then find out whether pause is
followed by escape beats (QRS
without P). Also note the shape
of QRS |
| |
QRS normal shaped Wide QRS
 
Nodal escape Ventricular escape
B. P-wave Abnormalities
Deformed P-wave with high AV block.
1. Fibrillary waves—Auricular fibrillation
with high AV block
2. Flutter waves—Auricular flutter with high
AV block
High AV block produces slow ventricular
rate.
How to Read the ECG of Arrhythmias 159
C. P and QRS Abnormalities

1. P not allowed by QRS (QRS dropped)
due to interruption of impulse at AVN
due to AV block

Note the P-R interval
|
| |
Progressive lengthening Constant P-R
|
of P-R till a beat dropped | |
 R-R constant with regular R-R varies with irregular
2nd degree AV block (Mobitz dropping of beats dropping of beats
type I) + Wenckebach  
2nd AV block with regular Mobitz II
dropping of beats (Mobitz II)

2. P independent of QRS
Atrial and ventricular rate vary
R-R constant
P-P constant
P-R varies

Suggests complete heart block
3. Position of P as related to QRS
Inverted P precedes QRS
Inverted P or upright P follows QRS
P absent, only QRS (P merged with QRS)

Suggests nodal rhythm which is slow 40-60/minute
Tachyarrhythmias
Note the Rate
• Rate greater than 100/minute and below 150/minute suggests sinus tachycardia
• Rate above 150/minute suggests PAT or VT
Note Rhythm
Regular Slightly irregular Irregular

• Sinus tachycardia • Ventricular tachycardia • Multiple ectopic (atrial, nodal,
• Paroxysmal: ventricular)
i. Atrial tachycardia • Ventricular fibrillation
ii. AV nodal tachycardia • Ventricular flutter
Characteristics of P-wave
P normal Absent or P deformed P premature Abnormal relation

indistinct P with QRS
• Sinus tachy- • VT • Fast auricular Multiple ectopics • P independent of
cardia • PAT (P merged with T) fibrillation (fibril- QRS → VT
• PAT • Nodal tachycardia lary waves) • Inverted P precedes
• Nodal tachy- • Ventricular fibrillation • Auricular flutter or follows QRS or P
cardia • Ventricular flutter (flutter waves) merged with QRS →
Nodal tachycardia
Characteristics of QRS
Narrow and normal QRS Wide and bizarre QRS

• Sinus tachycardia • Ventricular tachycardia (VT)
• PAT • Multiple ventricular premature beat
• Nodal tachycardia • Ventricular fibrillation
• PAT with AV block • Ventricular flutter
• Auricular fibrillation • PAT with bundle branch block
• Auricular flutter • PAT with ventricular aberrant conduction
• Multiple atrial premature beats
Effect of Carotid Sinus Pressure
Effective Not effective

• PAT • Ventricular tachycardia
• Sinus tachycardia (Temporarily slowing) • Some cases of PAT
• Atrial flutter (increases AV block, more
flutter waves revealed)
• PAT with AV block (more P-waves revealed)
III. Arrhythmias other than tachyarrhythmias and bradyarrhythmias.

Some of these arrhythmias are described under tachyarrhythmias and bradyarrhythmias also.
Rhythm P-wave QRS complex Relation Other findings

of P with QRS
Auricular Irregular Replaced by Normal F-waves at 300 to 600/ Best seen
fibrillation fibrillary waves minute with rapid in V1, V2
ventricular response
Auricular Regular (fixed Replaced by Normal F-waves 250-350/ Best seen in
flutter AV block); flutter waves minute with 2:1, 3:1 II, III, aVR,
irregular (varying (saw-toothed) or 4:1 AV block aVF and V1
AV block)
Sinus Irregular: increases Normal Normal Normal
arrhythmia during inspiration,
decreases during
expiration
Contd...
How to Read the ECG of Arrhythmias 161
Contd...

of P with QRS
Atrial Irregular Normal or Normal Premature P with com- Bigemini
ectopic deformed pensatory pause (not
fully compensatory)
Ventricular Irregular P may or may Wide bizarre Premature QRS with Bigemini or cou-
ectopic not be found full compensatory pled rhythm,
pause interpolated
Nodal Irregular Inverted or Normal Inverted P precedes or
ectopic absent P follows QRS, upright
P follows QRS, P may
be merged with QRS
(absent P)
Nodal Irregular P absent QRS normal Occurs after a pause
escape beat as in SA block or
sinus arrest
Ventricular Irregular P absent Wide and — do —
escape beat bizarre
Parasystole • Varying coup- P normal Shaped like
ling interval ventricular
• Inter-ectopic ectopic
interval slight
variation
• Occasional
fusion beat
• Discharge rate
slow
Wandering Variation in rhythm Changing shape
pacemaker of P with vary-
ing P-R
WPW Regular Short P-R Wide QRS
syndrome with slurring
of ascending
limb of QRS
Left anterior Left axis deviation
hemiblock small r in II, III and
Interventricular aVF, deep S in II, III,
aVF. No evidence of
inferior wall infarc-
tion
Interventri- Regular Normal Wide Normal
cular conduc-
tion defect
Left posterior Regular Normal Normal Normal • Right axis deviation
hemiblock
Contd...
Contd...

of P with QRS
• Small q in II, III, aVF
• No evidence of right
ventricular hyper-
trophy
• Exclude other causes
of right axis devia-
tion
Monofasci- Left anterior or left
cular block posterior hemiblock
Bifascicular block (Two branches out of three branches blocked) i. Right bundle branch
block + Left anterior
hemiblock
ii. Right bundle branch
block + Left poste-
rior hemiblock
Trifascicular block (All the three branches blocked) i. Bifascicular block
+ P-R prolonged
ii. Left bundle branch
block + prolonged
P-R
iii. Alternating right
bundle branch block
and left bundle
branch block
Peri-infarction block (Infarction + interruption in the conduction i. Abnormal Q as evi-
through one of the divisions of left bundle) dence of infarction
ii. QRS interval not
prolonged
iii. Left axis deviation
Electrographic Patterns in Acquired Heart Disease 163
Other Abnormal ECG Patterns
39 Electrocardiographic Patterns in
Acquired Heart Disease
ECG Findings in Acquired Valvular Disease

Normal Right ventri- Left atrial right Left ventri- Bi-ventri- Axis-bundle Arrhythmia Other Findings
cular hyper- atrial enlarge- cular hyper- cular hy- branch block
trophy ment trophy strain pertrophy
Aortic Normal LVH and LAD Left Left anterior
stenosis strain BBB hemiblock
Aortic LVH and Prolonged P-R
regurgitation strain aortic root
disease
Mitral Normal RVH a. Left atrial Right axis. Auricular
stenosis enlargement Incomplete fibrillation
suggested by right BBB
wide or bifid P
in II, III, aVF
or only in II
b. Associated
right atrial
enlargement
(tall peaked P)
suggests Mitral
plus tricuspid
stenosis
Mitral Left atrial LVH Auricular
regurgition enlargement (see fibrillation in
Mitral stenosis) late stage
Mitral valve Auricular and T inverted in
prolapse ventricular inferolateral
premature chest leads
beat
Tricuspid No RVH Right atrial Tall tented P
stenosis hypertrophy in II, III, aVF
Tricuspid RVH Auricular
regurgitation fibrillation
Pulmonary RVH Incomplete Inverted T in
stenosis right BBB chest leads
Pulmonary Normal
regurgitation
40 Electrocardiographic Patterns in
Congenital Heart Disease
The surgery in congenital heart disease has progressed much in recent years. Now the emphasis is on corrective
procedure than on palliative measures. Preoperative diagnosis is more important and many non-invasive and
invasive diagnostic aids have sprung up. The electrocardiogram in congenital heart disease is not diagnostic
but suggestive. It should be remembered that the ECG in the newborn and in the infant normaly shows right
ventricular hypertrophy and it is very difficult to differentiate from pathological right ventricular hypertrophy
due to congenital heart disease. Multiple congenital cardiac lesions alters the electrocardiogram. Postoperative
follow-up electrocardiogram also may help. In the electrocardiogram specially note normalcy, left ventricular
hypertrophy, right ventricular hypertrophy, bundle branch block, axis deviation and bi-ventricular hypertrophy.
See the flow diagram.
ECG Findings in Congenital Heart Disease
ECG
|
| | | | | |
Normal LVH RVH With RBBB With Axis Bi-ventricular
↓ ↓ ↓ ↓ deviation hypertrophy
1. Coarctation of 1. Coarctation of 1. Lutembacher 1. ASD (Primum ↓
aorta in a child aorta in adult syndrome defect) 1. VSD (large
2. PDA (small defect) 2. PDA (large (Fig.40.1) 2. TOF in elderly defect)
4. VSD (small defect) defect) 2. VSD (large) 3. Anomalous 2. Eisenmenger
5. Truncus arterio- 3. VSD (large 3. Eisenmenger drainage of syndrome
sus stenosis (lesser defect) syndrome pulmonary 3. Truncus
degree of stenosis) 4. Truncus arterio- 4. Severe pulmo- veins 4. Single ventricle
6. Idiopathic dilation sus (left axis) nary stenosis 5. ASD (septum
of pulmonary 5. Congenital aor- (Fig. 40.6) primum)
artery tic stenosis (left 5. Truncus arterio- | |
BBB) sus (Fig. 40.2) RAD LAD
6. Single ventricle 6. Transposition 1. ASD with Excludes ASD
7. Tricuspid atresia of great vessels secondum with secondum
8. Endocardial (with tall not- defect (Fig. 40.4) defect
fibroelastosis ched P-wave) 2. Tetralogy of
7. Pseudotruncus Fallot (Fig. 40.3
(with prominent and 40.5)
P-wave)
Contd...
Electrocardiographic Patterns in Congenital Heart Disease 165
8. Single ventricle
PDA plus RVH
points to reversed
shunt due to pulmo-
nary hypertension
9. In VSD, RVH points
to greater operative
risk due to pulmonary
hypertension
ILLUSTRATIVE ECG SHOWING ABNORMALITIES IN CONGENITAL HEART DISEASE
Fig. 40.1: Lutembacher syndrome: Right ventricular hypertrophy; Right axis deviation; Marked clockwise rotation (QR in
aVR, R-S in V4-V5-V6). Prominent R with depressed S-T segment and inverted T in V1 to V4. Deep S without S-T and T-wave
changes in V5 and V6
Fig. 40.2: Persistent truncus arteriosus: Very prominent and peaked P-waves in II,
aVF and V1 to V6. Right ventricular hypertrophy. Inverted T in V1 to V6
Fig. 40.3: Tetralogy of Fallot: Right ventricular hypertrophy (Tall R in V1). Ischaemic type inverted T in V1 to V5
Fig. 40.4: Interatrial septal defect—ostium secondam type. Right ventricular hypertrophy;
Incomplete right bundle branch block
Fig. 40.5: Tetralogy of Fallot. Right ventricular hypertrophy. Peaked P-wave in V1, V2 and V3
Electrocardiographic Patterns in Congenital Heart Disease 167
Fig. 40.6: Pure pulmonary valvular stenosis: Right ventricular hypertrophy.

Marked inverted T-waves in chest leads, II, III and aVF
41 Other Abnormal
Electrocardiographic Patterns
There are some specific clinical conditions which have special ECG patterns:
1. Ventricular aneurysm
2. Pulmonary embolism
3. Drug toxicity:
a. Digitalis
b. Quinidine
c. Emetine
4. Myocarditis
5. Endocarditis
6. Pericarditis
7. Electrolyte effect:
a. Potassium effect
b. Calcium effect
8. Hyperventilation syndrome.
Waves S-T segment QT interval Axis deviation Arrhythmias
P-R interval position, rotation
bundle branch
Ventricular Tall R in aVR Persistent eleva-
aneurysm: tion in infarcted
leads even acute
infarct is over
(Figs 41.1A and B)
Pulmonary • Tall and sharp P Depressed in right Vertical lie mar- Sinus tachycardia
embolism: • Inverted T in chest leads ked clockwise
right chest leads rotation transient
(Fig. 41.2) right bundle branch
block (complete or
incomplete)
Digitalis: T inversion Depression Short QT AV block, ecto-
shaped like pics, coupled rhy-
correction mark thm nodal rhythm,
or sag like or AV dissociation
scooped or PAT, Auricular
hammock shaped fibrillation, VT,
(Fig. 41.3) rarely ventricular
fibrillation
Contd...
Other Abnormal Electrocardiographic -Patterns 169
Contd...
Waves S-T segment QT interval Axis deviation Arrhythmias
P-R interval position, rotation
bundle branch
Quinidine: S-T depression Prolonged QT AV block, ventri-
cular fibrillation,
cardiac standstill
Emetine: —Do— P-R prolonged
Myocarditis: Inverted T-waves Depression or Prolonged QT, Bundle branch Partial heart block
(Fig. 41.4) elevation of P-R (Fig. 41.6) block
S-T segment
Pericarditis: Low voltage Widespread
(Fig. 41.5) QRS in all leads S-T elevation
Hypokalemia: T low U S-T depressed Prolonged QT
prominent
Hyperkalemia: Absent P (Auri- S-T depressed
cular arrest low
R tall T Pro-
longed QRS
(Fig. 41.7)
High calcium: Shortened QT
Low calcium: Prolonged QT
ILLUSTRATIVE ECG
Fig. 41.1A: Ventricular aneurysm: Persistently elevated S-T segment in V4, V5 and V6.
Aneurysm over lateral surface of heart
Fig. 41.1B: Acute diffuse pericarditis: Elevated S-T segment is not pronounced and persists for shorter period
Fig. 41.2: Acute pulmonary embolism: Deeply inverted T-waves in V3R and from V1 and V4. Clockwise rotation.
Prominent R in aVR. rr in V1 (Incomplete right bundle branch block). S in I, V4, V5 and V6
Fig. 41.3: Shape of S-T segment
Fig. 41.4: Myocarditis: Inverted T-waves in II, III, aVF, V4, V5 and V6
Fig. 41.5: S-T segment concave elevation (Convex elevation in myocardial infarction), without Q-wave (Q in myocardial
infarction) without T-wave inversion. Reciprocal depression of S-T segment as seen in myocardial infarction is not seen.
S-T elevation only for a short period. The lower figure shows acute myocardial infarction. The upper figure shows pericardial
infarction
Other Abnormal Electrocardiographic -Patterns 171
Fig. 41.6: Hypokalemia
Fig. 41.7: Hyperkalemia

42 ECG Report
Rate
Atrial Ventricular Atrioventricular ratio—A : V

Effect of : Carotid sinus pressure Respiration Exercise
Rhythm
a. Regular:
Sinoatrial Nodal Idioventricular
b. Irregular:
SAN Atria AVN Ventricle
Impulse formation:
Impulse conduction:
Pause
PQRST QRS P Compensatory
absent absent absent pause
Position Axis Rotation
Vertical Right axis Clockwise
Horizontal Left axis Anti-clockwise
Intermediate Normal axis Normal
Auricular activity: P-wave

Shape : Tall Peaked Wide and bifid Varying
Direction : Inverted Diaphasic
Absent : Replaced by Burried in Dropped
Relation with QRS : Premature P P with absent QRS P independent of QRS
Ventricular activity
Q-wave (Maximum height ¼ of R; Maximum width 0.04 second)
Depth
R-wave (Maximum voltage 13 mm in aVL, 20 mm in aVF and 27 mm in V6)
Voltage : High Low
Width : (RR pattern)
ECG Report 173
S-wave
Depth
R and S-wave
R:S R+S (Tallest R + Deepest S)
QRS complex (Width maximum 0.10 second)

Width : Narrow Wide Bizarre Normal
Voltage : High Low Varying Normal
T-wave (Height maximum 1/3rd of R; Minimum 1/8th of R)

Upright Inverted Flat
Symmetrical :
Asymmetrical :
S-T segment
Isoelectric :
Elevation :
Concave Convex Horizontal
Depression :
Concave Convex Horizontal
Intervals
P-R : Prolonged Shortened Varying Normal

Q-T : Prolonged Shortened Normal
R-R : Prolonged Shortened Irregular
P-P : Prolonged Shortened Irregular
J point (Maximum 2 mm deviation)

VAT (Range of intrinsicoid deflection in V1 0.015-0.035 and in V5 or V6 0.035-0.055 second)
Other waves
U-wave : Prominent Inverted
Delta-wave :
Index PB
Index
A B
Abnormal waves, segments and intervals in Bradyarrhythmias

different ECG leads 62 significance of . 62 approach 99
Accelerated conduction 154 causes of 100
Angina differential diagnosis of 100
diagnosis of 48 heart block 101
Arrhythmia based on ECG patterns idioventricular 103
premature beats 84 nodal 104
with P-wave changes 85 illustrative ECG of 100
with PQRST change 84 sinus 100
Arrhythmias 86, 105, 124 Branches of coronary artery and sites of infarction 68
Bundle branch block 148
atrial 105
aetiology 151
junctional or nodal 105, 124
left 151
diagnosis 124
mechanism 151
mechanism of 86
approach 150
sequence of events 86
classification of 148
miscellaneous 105 mechanism 148
ventricular 105 right 148
Atrial fibrillation ECG pattern of 150
ECG pattern 119 Bundle of his 145
approach 119
mechanism 119 C
AVnode 119 Cardiac arrhythmias 80,82
atrium 119 classification of 82
ventricle 119 arising from conduction system 82
Atrial premature beat 108 arising from ectopic focus 82
ECG illustrations of 109 Cardiac muscle 2
atrial and junctional 111 depolarisation and repolarisation of 2
atrial bigemini 111 sequence of 4
blocked 109 electrical activity in 2
with aberrant ventricular conduction 110 E
ECG pattern 108 ECG
Atrioventricular dissociation complex 9
approach 142 heart position in 11
complete 142 rotation of heart 11
incomplete 142 pattern 11
illustrative ECG 143 waves 9
Auricular flutter amplitude 9
ECG pattern 120 direction 9
mechanism 120 duration 9
AV node 120 mechanism 9
atrium 120 ECG of arrhythmias
ventricle 120 how to read 158
Axis deviation left 15 bradyarrhythmias 158
right 15 tachyarrhythmias 159
ECG report 172 Parasystole 140

Electrocardiographic patterns diagnosis of 141
illustrative ECG 169 illustrative ECG 141
specific clinical conditions 168 type of 140
H Paroxysmal atrial tachycardia (PAT)
approach to 114
Heart block
classification 135 ECG pattern 114
illustrative ECG 136 illustrative ECG 115
complete AV block 138 focus of stimulation of APB 118
first degree AV block 136 with APB 118
second degree AV block 137 with AV block 117
mechanism 135 with manifest P-wave 116
Heart disease with narrow QRS complex 116
acquired 163 with wide QRS 115
ECG findings in 163 Pre-excitation syndrome 154
congenital 164 Premature beats
ECG findings in 164 different types of 113
Heart rate 80 Q
Hemiblock 145
Q-T interval
L causes 60
clinical notes 60
Leads Q-wave
bipolar or standard 6 approach 25
electrocardiographic 8 mechanism 25
unipolar 6 pathological 25
Left bundle branch 145 causes of 25
M QRS complex
abnormal 33
Myocardial infarct abnormal voltage of QRS 34
age of infarct 66 wide bizarre QRS 34
clinical notes 73 wide QRS 33
ECG changes in 66
S
N
S-T segment 45
Nodal escape 125 approach 46
Normal heart 79 causes of abnormalities 456
types of 46
P concave S-T elevation 47
P-R interval convex S-T elevation 46
approach 57 Sick sinus syndrome
prolonged 57 ECG pattern 156
shortened 58 history and mechanism 156
varying 58 illustrative ECG of 156
causes of abnormalities 57 Sinoatrial block 19
P-wave Specialised conducting tissues
abnormal 16 anatomy of 1
causes of 16 physiology of 1
absent 16 T
causes of 16
approach 18 T-wave 40
Pacemakers 140 approach 41
Index 177
causes 40 V
deep inversion 40 Ventricular hypertrophy
flattened 40 left 74
tall peaked 41 clinical approach to 75
Tachyarrhythmia differential diagnosis 76
approach 90 mechanism 75
right 77
causes of 90
approach to 78
flow diagram for 91 ECG pattern 77
illustrative ECG of 93 mechanism 77
atrial 95 Ventricular premature beat
fast atrial fibrillation 97 ECG pattern 127
nodal 97 illustrative ECG 128
sinus 93 Ventricular tachycardia
ventricular 95 approach to 132
ECG pattern 132
U illustrative ECg 133
U-wave W
approach 44 Wolff-Parkinson-White syndrome 154

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Bedside Approach

Gami NK MRCP(Edin) FRCP(Edin)

Bedside Approach to Electrocardiography

First Edition 2002

Publishing Director: RK Yadav

Typeset at JPBMP typesetting unit

NP Mishra MD FRCP (Edin)

This book is a bedside approach to the electrocardiography. Despite of astonishing advances in

1. Impulse Generation in the Heart ..... .... ..... 1

Waves, Intervals and Segments

6. P-Wave .... ..... ..... .... ..... 16

14. ECG Changes in Myocardial Infarct ..... .... ..... 66

15. Left Ventricular Hypertrophy .. ..... .... ..... 74

17. Cardiac Arrhythmia ..... ..... .... ..... 80

24. Approach to Atrial Premature Beats ..... .... ..... 108

Other Abnormal ECG Patterns

39. Electrographic Patterns in Aquired Heart Disease .... ..... 163

Index .... ..... ..... .... ..... 175

Table 1.2: Physiology of specialised conducting tissues

Rate of activation Remarks

Electrical Activity in Cardiac Muscle

Fig. 1.1: Electrical activity in cardiac muscle

Depolarisation and Repolarisation of Cardiac Muscles

Fig. 1.6: Right ventricular complex

ECG Waves Cardiac Cycle Heart Sounds

QRS interval First heart sound occurs during QRS

2 Leads of the Clinical

Bipolar or Standard Leads

Fig. 2.1: Unipolar electrode connection without augmentation

NE ______ G ______ EE aVL

Table 2.1: Electrocardiographic leads

THE NORMAL WAVES, COMPLEXES, AND INTERVALS

Fig. 3.1: Nomenclature

HEART POSITION IN ECG

Rotation of heart on the following three axis:

ECG PATTERN (Fig. 4.1)

Left ventricular complex Right ventricular complex Other changes

aVL aVF aVL aVF

HORIZONTAL HEART POSITION VERTICAL HEART POSITION

Diagrammatic representation of clockwise rotation of Diagrammatic representation of anti-clockwise rotation of

Fig. 4.2: Marked clockwise rotation:

Fig. 4.4: Counterclockwise rotation:

Fig. 4.5: Extreme clockwise rotation

There are two types of axis deviation (Fig. 5.1).

LEAD I LEAD II LEAD III LEAD I LEAD II LEAD III

A. LEFT AXIS DEVIATION B. RIGHT AXIS DEVIATION

Causes of Abnormal P-Waves

P-wave may be revealed or not revealed (absent P-wave).

I. Causes of absent P-waves

Sinoatrial Block (SA Block)

Suppression of SA node is SA block. It is characterised by a prolonged pause (due to dropping of a

Illustrative ECG Showing Absent or Modified P-wave (Figs 6.1 to 6.5)

Fig. 6.4: Hyperpotassemia: P-wave absent

Fig. 6.5: Nodal premature beat (N). P buried in QRS

Illustrative ECG Showing Inverted P-wave (Figs 6.6 and 6.7)

Illustrative ECG Showing Abnormal Shapes of P-wave (Figs 6.8 to 6.10)

Fig. 6.10: AB + BC = greater than CD + DE i.e. compensatory pause incomplete

Illustrative ECG Showing Multiple or Isolated

Fig. 6.11: Supraventricular tachycardia with 2:1 AV block.

Fig. 6.12: Complete heart block. Multiple P-waves

Fig. 6.14: Wenckebach phenomenon (Mobitz type I AV block): Multiple P-waves.

A Few More ECG Showing Abnormalities of P-wave (Figs 6.16 to 6.21)

Fig. 6.18: Right atrial hypertrophy. Prominent P, P-Pulmonale

NE G EE aVL