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For over forty years The ECG Made Easy has been regarded as the best introductory guide to the ECG, with sales of over half a million copies as well as being translated into more than a dozen languages. Hailed by the British Medical Journal as a "medical classic", it has been a favourite of generations of medical and health care staff who require clear, basic knowledge about the ECG. This famous book encourages the reader to accept that the ECG is easy to understand and that its use is just a natural extension of taking the patient’s history and performing a physical examination. It directs users of the electrocardiogram to straightforward and accurate identification of normal and abnormal ECG patterns.

Key Features

• A practical and highly informative guide to a difficult subject.

• Provides a full understanding of the ECG in the diagnosis and management of abnormal cardiac rhythms.

• Emphasises the role of the full 12 lead ECG with realistic reproduction of recordings.

• The unique page size allows presentation of 12-lead ECGs across a single page for clarity.

Categories:
Year:
2019
Edition:
9
Publisher:
Elsevier
Language:
english
Pages:
269
ISBN 10:
0702074578
ISBN 13:
9780702075056
Series:
Made Easy
File:
PDF, 15.82 MB
Download (pdf, 15.82 MB)

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The ECG Made Easy
NINTH EDITION

John Hampton DM MA DPhil FRCP
FFPM FESC
Emeritus Professor of Cardiology, University of Nottingham, UK

Joanna Hampton MD MA BM BCh FRCP
Consultant Physician, Addenbrooke's Hospital, Cambridge, UK
EDINBURGH LONDON NEW
YORK OXFORD
PHILADELPHIA ST LOUIS SYDNEY 2019

Table of Contents
Cover image
Title Page
Copyright
How to use this book
Part 1: The ECG made very easy indeed: a beginner's guide
Part 2: The basics: the fundamentals of ECG recording, reporting
and interpretation
Part 3: Making the most of the ECG: the clinical interpretation of
individual ECGs
Part 4: Now test yourself
Quick reminders
Further reading
Preface

Part 1 The ECG made very easy indeed: a beginner's
guide

1 The ECG made very easy indeed
What is an ECG?
When do you need an ECG?
How to record an ECG?
How to interpret an ECG: the basics
Rhythms you must be able to recognize
Patterns you must be able to recognize
The normal ECG and its variants
ECG red flags

Part 2 The basics: the fundamentals of ECG
recording, reporting and interpretation
2 What the ECG is about
What to Expect from the ECG
The electricity of the heart
The different parts of the ECG
The ECG – electrical pictures
The shape of the QRS complex
Making a recording – practical points
How to report an ECG

3 Conduction and its problems
Conduction problems in the AV node and His bundle
Conduction problems in the right and left bundle branches –
bundle branch block
Conduction problems in the distal parts of the left bundle branch
What to do
4 The rhythm of the heart
The intrinsic rhythmicity of the heart
Abnormal rhythms
The bradycardias – the slow rhythms
Extrasystoles
The tachycardias – the fast rhythms
Fibrillation
Wolff-Parkinson-White syndrome
The origins of tachycardias
What to do
The Identification of Rhythm Abnormalities
5 Abnormalities of P waves, QRS complexes and T waves
Abnormalities of the P wave

Abnormalities of the QRS complex
Abnormalities of the ST segment
Abnormalities of the T wave
Other abnormalities of the ST segment and;  the T wave

Part 3 Making the most of the ECG: the clinical
interpretation of individual ECGs
6 The ECG in healthy subjects
The normal cardiac rhythm
The P wave
Conduction
The QRS complex
The ST segment
The T wave
U waves
The ECG in athletes
7 The ECG in patients with chest pain or breathlessness
The ECG in patients with constant chest pain
The ECG in patients with intermittent chest pain
The ECG in patients with breathlessness

8 The ECG in patients with palpitations or syncope
The ECG when the patient has no symptoms
The ECG when the patient has symptoms
Pacemakers
Cardiac arrest

Part 4 Now test yourself
9 ECGs you must be able to recognize
ECG descriptions and interpretations
Index
Quick Reminder Guide
When reporting an ECG, remember
What to Look for
Glossary

Copyright
© 2019 Elsevier Ltd. All rights reserved.
First edition 1973
Second edition 1980
Third edition 1986
Fourth edition 1992
Fifth edition 1997
Sixth edition 2003
Seventh edition 2008
Eighth edition 2013
Ninth edition 2019
The right of John Hampton and Joanna Hampton to be identified as
author(s) of this work has been asserted by them in accordance with
the Copyright, Designs and Patents Act 1988.
No part of this publication may be reproduced or transmitted in any
form or by any means, electronic or mechanical, including
photocopying, recording, or any information storage and retrieval
system, without permission in writing from the Publisher. Details on
how to seek permission, further information about the Publisher's
permissions policies and our arrangements with organizations such as
the Copyright Clearance Center and the Copyright Licensing Agency,
can be found at our website: www.elsevier.com/permissions.
This book and the individual contributions contained in it are
protected under copyright by the Publisher (other than as may be

noted herein).
Notices
Practitioners and researchers must always rely on their own
experience and knowledge in evaluating and using any information,
methods, compounds or experiments described herein. Because of
rapid advances in the medical sciences, in particular, independent
verification of diagnoses and drug dosages should be made. To the
fullest extent of the law, no responsibility is assumed by Elsevier,
authors, editors or contributors for any injury and/or damage to
persons or property as a matter of products liability, negligence or
otherwise, or from any use or operation of any methods, products,
instructions or ideas contained in the material herein.
ISBN 978-0-7020-7457-8
978-0-7020-7466-0
Printed in China
Last digit is the print number:

9

8

7

6

5

Content Strategist: Laurence Hunter
Content Development Specialist: Fiona Conn
Project Manager: Louisa Talbott
Design: Brian Salisbury
Illustration Manager: Karen Giacomucci
Illustrator: Helius and Gecko Ltd

4

3

2

1

How to use this book

Part 1: The ECG made very easy
indeed: a beginner's guide
This guide has been written for those who are just starting to use
ECGs in their clinical practice. It aims to reduce the facts to the bare
minimum. If you have no previous knowledge of the ECG, this
chapter is for you. Once you have understood it, the rest of the book
will amplify your knowledge, but this is the place to start when using
the ECG for patient care.

Part 2: The basics: the fundamentals of
ECG recording, reporting and
interpretation
Before you can use the ECG as an aid to diagnosis or treatment, you
have to understand the basics. Part 2 of this book explains why the
electrical activity of the heart can be recorded as an ECG, and
describes the significance of the 12 ECG ‘leads’ that make ‘pictures’ of
the electrical activity seen from different directions.
Part 2 also explains how the ECG can be used to measure the heart
rate, to assess the speed of electrical conduction through different
parts of the heart, and to determine the rhythm of the heart. The
causes of common ‘abnormal’ ECG patterns are described.

Part 3: Making the most of the ECG: the
clinical interpretation of individual
ECGs
In this part of the book, we look beyond the basics and consider how
the ECG can help in the situations in which it is most used – in the
‘screening’ of healthy subjects, and in patients with chest pain,
breathlessness, palpitations or syncope. Recalling the classic ECG
abnormalities covered in Chapters 2–5, we will look at some of the
variations that can make ECG interpretation seem more difficult,
using examples of more ECGs from real patients with common
problems.

Part 4: Now test yourself
You should now be able to recognize the common ECG patterns, and
this final chapter contains twelve 12-lead ECGs from real patients for
you to interpret.

Quick reminders
This has been placed at the back of the book after the index so you can
refer to it quickly when you need to. It lists the common abnormalities
you must be able to recognize.

Further reading
The symbol indicates cross-references to useful information in The
ECG Made Practical, 7th edition (Elsevier, 2019).

Preface
The ECG Made Easy was first published in 1973, and well over threequarters of a million copies have been sold. The book has been
translated into German, French, Spanish, Italian, Portuguese, Polish,
Czech, Indonesian, Japanese, Russian and Turkish, and into two
Chinese languages. The aims of this edition are the same as before: the
book is not intended to be a comprehensive textbook of
electrophysiology, nor even of ECG interpretation – it is designed as
an introduction to the ECG for medical students, technicians, nurses
and paramedics. It may also provide useful revision for those who
have forgotten what they learned as students.
There really is no need for the ECG to be daunting: just as most
people drive a car without knowing much about engines, and
gardeners do not need to be botanists, most people can make full use
of the ECG without becoming submerged in its complexities. This
book encourages the reader to accept that the ECG is easy to
understand and that its use is just a natural extension of taking the
patient's history and performing a physical examination.
The first edition of The ECG Made Easy (1973) was described by the
British Medical Journal as a ‘medical classic’. The book has been a
favourite of generations of medical students and nurses, and it has
changed a lot through progressive editions. This ninth edition differs
from its predecessors in that it now includes a new chapter entitled
‘The ECG made very easy indeed’. This basic guide has been written
in response to feedback from both medical students and nurses, who
wanted something even easier than previous editions of The ECG
Made Easy! The guide aims to distil the bare essentials of using an ECG
in clinical practice with minimal theory and maximum practicality.
The ECG Made Easy should help students to prepare for

examinations, but for the development of clinical competence – and
confidence – there is no substitute for reporting on large numbers of
clinical records. Two companion texts may help those who have
mastered The ECG Made Easy and want to progress further. The ECG
Made Practical (formerly The ECG in Practice) deals with the
relationship between the patient's history and physical signs and the
ECG, and also with the many variations in the ECG seen in health and
disease. 150 ECG Cases (formerly 150 ECG Problems) describes 150
clinical cases and gives their full ECGs, in a format that encourages
the reader to interpret the records and decide on treatment before
looking at the answers.
We are grateful to Laurence Hunter and Fiona Conn of Elsevier for
their continuing support.
The title of The ECG Made Easy was suggested more than 45 years
ago by the late Tony Mitchell, Foundation Professor of Medicine at the
University of Nottingham, and many more books have been
published with a ‘Made Easy’ title since then. We are grateful to him
and to the many people who have helped to refine the book over the
years, and particularly to many students for their constructive
criticisms and helpful comments, which have reinforced our belief
that the ECG really is easy to understand.
JH, JH

PA R T 1

The ECG made very easy indeed:
a beginner's guide
OUTLINE
1 The ECG made very easy indeed

1

The ECG made very easy indeed
What is an ECG? 1
When do you need an ECG? 1
How to record an ECG 2
How to interpret an ECG: the basics 2
The ECG waves and what they mean 2
Interpretation starts here! 4
Rhythms you must be able to recognize 8
Patterns you must be able to recognize 10
The normal ECG and its variants 13
ECG red flags 14

This guide has been written for those who are just starting to use
ECGs in their clinical practice. It aims to reduce the facts to the bare
minimum. If you have no previous knowledge of the ECG, this
chapter is for you. Once you have understood it, the rest of the book
will amplify your knowledge, but this is the place to start when using
the ECG for patient care.

What is an ECG?
‘ECG’ stands for electrocardiogram, or electrocardiograph. In some

countries, the abbreviation used is ‘EKG’.
The heart is a pump driven by intrinsic electrical impulses which
make the heart beat. An ECG is a paper recording of that electrical
activity. The ECG records where electrical impulses start and how
they flow through the heart. It does not measure how well the heart is
pumping.
The electrical activity of the heart starts in the ‘internal pacemaker’,
which is called the sinoatrial node. This is in the right atrium. The
normal rhythm is called ‘sinus rhythm’ (properly it should be called
sinoatrial rhythm, but it isn't). The way electrical impulses flow
through the heart is called conduction.
Abnormalities in the electrical activity of the heart can result in
abnormal conduction or rhythms where the heart may go too quickly,
too slowly, or beat irregularly.
Changes to the normal flow of electricity through the heart can be
shown on an ECG and may indicate damaged heart muscle. Heart
muscle can be damaged by many disease processes such as infarction,
hypertension and pulmonary embolism.

When do you need an ECG?
An ECG should be recorded whenever a patient has chest pain,
palpitations, breathlessness or dizziness, or if the patient has had an
episode of syncope (blackout) or an unexplained fall. In addition, a
patient with a stroke or a transient ischaemic attack (TIA) must have
an ECG as these may be due to an irregular heart rhythm.
Remember that the patient's symptoms and physical signs will
guide interpretation of the ECG.

How to record an ECG?
Electrodes are placed on the chest and limbs of the patient to record
different views of the heart's electrical activity.
Each view of the heart is described as a ‘lead’. The word ‘lead’ does
not refer to the electrodes.

The rhythm of the heart can be determined from only one view, i.e.
one lead (this requires two electrodes).
For a full picture of the heart's electrical activity, a 12-lead view is
conventional.
One electrode is attached to each limb. These four electrodes
provide six ‘limb leads’ or six different views of the heart in a vertical
plane. These are called leads I, II, III, VL, VF and VR. VL, VF and VR
used to be called AVL, AVF and AVR, respectively, but the A is
essentially meaningless and is redundant.
Six electrodes are attached to the chest, recording leads V1 to V6.
Accurate placement of these electrodes is essential for comparing later
ECGs. These leads ‘look at’ the heart from the front in a horizontal
plane (Fig. 1.1).

FIG. 1.1

Lead positions for a 12-lead ECG with 12 views of the

heart

■ Top tips for recording an ECG
1. To record a ‘3-lead ECG’ using only limb electrodes, remember
the mnemonic: “Ride Your Green Bike”. R for red and right
arm. Y for yellow, G for green and B for black. Apply the first
red electrode to the right arm and work clockwise to left arm,
left leg and finally right leg (the black electrode is the earth
electrode).
2. Placement of the limb electrodes is easy: there is no specific

position to remember.
Try to find the least hairy area: anywhere from the
shoulder or outer clavicle down to the wrist is fine
for the upper limb; anywhere from the lower
abdomen to the foot on right and left side is fine for
the lower limb electrodes.
3. Placement of the chest electrodes MUST be accurate and
standardized for every recording (see Figs 1.1 and 2.24).
4. Make sure the patient is warm and relaxed.
5. Check machine settings: standard is paper speed of
25 mm/second; the voltage calibration should be set so that
1 mV causes 1 cm of upwards deflection (for more details, see
Chapter 2).
6. Make sure the date and time are recorded and always ensure
the patient's name is on the ECG.
7. Write the patient's symptoms and BP on the ECG.
For more details, see Chapter 2, pages 28–38.

How to interpret an ECG: the basics
■ Top tip: the more ECGs you read, the better you will become.
What follows is the bare minimum of ECG physiology for ECG
interpretation.

The ECG waves and what they mean
• Think of the heart as having internal wiring. The
internal pacemaker is the sinoatrial node situated
in the right atrium (Fig. 1.2)

FIG. 1.2

Internal wiring of the heart

• In a normal heart, the sinoatrial node fires
regularly and the electrical impulse spreads
through an anatomical path to the ventricles
resulting in ventricular contraction. The
ventricular contraction is felt as the pulse or the
heartbeat.
• Each heartbeat is represented by one ECG
complex.
• An ECG complex is composed of five parts (Fig.
1.3).

FIG. 1.3

ECG complex – one heartbeat

• The P wave represents electrical activation,
called depolarization, of the atrial muscle.
• The PR interval is the time taken for the

electrical impulse to spread from the atria to the
ventricles through the atrioventricular node and
the high-speed conducting pathway called the
bundle of His.
• The QRS complex records the impulse spreading
throughout the ventricles resulting in ventricular
contraction. In the normal heart, this does not take
more than 3 small squares on an ECG.
• The ST segment is the period when the
ventricles are completely activated.
• The T wave is the return (repolarization) of the
ventricular muscle to its resting electrical state.
• A normal beat is represented by one P wave
followed by one QRS complex and then one T
wave.
Interpretation starts here!
Start by looking at the patient. Take basic observations of pulse and
blood pressure before recording the ECG.
First, is the patient unwell? Are you expecting there to be an
abnormality?
■ Top tip: if the ECG does not fit your clinical expectation, check
settings and electrode placement and repeat your recording. Make
sure the ECG is recorded from the correct patient!
If you are satisfied with your recording, think: Is there anything
really obviously wrong, e.g. a very slow or fast heart rate? Complexes
that do not look like anything you have seen before? If the patient is
unwell, seek help immediately.
If the patient is stable, you have more time to try to assess the ECG
yourself.

■ Top tip: always approach the ECG the same way. Go through
the following questions in the same order every time:
Say ‘R R P W Q S T’ – it rhymes, and might help you to remember
the questions you need to answer!
R

Rate

What is the rate (measured in beats per minute [bpm])?

R

Rhythm

What is the rhythm?

P

P wave

Is there one P wave before every QRS complex?

W

Width

Is the width of the QRS complex normal (< 3 small squares)?

Q

Q wave

Are there any deep Q waves present?

S

ST segment

Is there ST segment depression or elevation?

T

T wave

Are there any abnormal inverted (upside down) T waves?

Let's now look at these questions in more detail. (Remember ‘R R P
W Q S T’.)
R

Rate: What is the rate?
The closer together the QRS complexes are, the faster the heart is beating. As a
rough guide, less than 3 large squares between each QRS complex indicates a
rate of over 100 bpm (tachycardia) (Fig. 1.4A) and more than 6 large squares
indicates a rate of less than 50 bpm (bradycardia) (Fig. 1.4B).

R

Rhythm: What is the rhythm?
Is it regular or irregular? A regular rhythm means there is the same number of
squares between each QRS complex (see Fig. 1.4A and B), and note that,
whatever the rate, the rhythm is regular.
In Fig. 1.5, there is a variable number of squares between each QRS complex,
which means it is an irregular rhythm.

P

P waves: Is it sinus rhythm?
This is the normal regular heart rhythm and means the electrical impulse starts in
the sinoatrial node and is transmitted normally from the atria to the ventricles.
This is represented by one P wave before every QRS complex.
The P wave is the key to rhythm identification.
First, can you identify the P waves? Look at all leads – the P wave may be more
visible in some leads than others.
If you cannot see a P wave, the atria are not activated normally and there must be
an abnormal rhythm (Fig. 1.6).
If there is more than one P wave before each QRS complex, then conduction to the

ventricles is abnormal. This is called heart block (Fig. 1.7).
W

Width: Is the QRS greater than 3 small squares?
If so, this means there is abnormal conduction through the ventricles.
If the QRS complex is wider than 3 small squares, the spread of electrical
activation through the ventricles must be slow. This could be because
conduction through the ventricles is abnormal, or it could be because the
electrical impulse erroneously began in the ventricular tissue rather than
coming through the bundle of His (Fig. 1.8).

Q

Q wave: Are deep Q waves present?
If the QRS complex starts with a deep downward deflection this may be a Q wave
due to an old myocardial infarction (Fig. 1.9; see Ch. 6).

S

ST segment: Are there abnormalities in the ST segment?
The ST segment should be level with the baseline, but can be elevated (Fig. 1.10)
(myocardial infarction) or depressed (Fig. 1.11) (commonly due to ischaemia).

T

T wave: Is the T wave right-way up or upside down?
It is normally upside down in VR and V1. If it is upside down in any other lead,
then the likely causes are ischaemia or ventricular hypertrophy (Fig. 1.12).

FIG. 1.4 (A) Sinus tachycardia (B) Sinus bradycardia

Irregular rhythm Variable number of squares between
each QRS complex
FIG. 1.5

FIG. 1.6

Abnormal rhythm (not sinus) No P waves

FIG. 1.7

Heart block Multiple P waves per QRS complex

FIG. 1.8

Abnormal ventricular conduction QRS ≥3 small squares

FIG. 1.9

Deep Q waves

FIG. 1.10

ST segment elevation

FIG. 1.11

ST segment depression

FIG. 1.12

T wave inversion

Rhythms you must be able to recognize
TABLE 1.1

TABLE 1.2

Patterns you must be able to recognize
The patterns you must be able to recognize, other than rhythm
disturbance, are ischaemia, infarction and normal variants. These
patterns concern the Q waves, the ST segments and the T waves.

Fig. 1.22 shows sinus rhythm with ST depression in leads V2–V6.
This change is characteristic of myocardial ischaemia and may be seen
in someone having an anginal attack. Fig. 1.23 shows sinus rhythm
with T wave inversion across all the chest leads (V1–V6). This pattern
is also typical of acute myocardial ischaemia and may be seen in
myocardial infarction.

Acute myocardial ischaemia with ST depression Sinus
rhythm with ST depression in leads V2–V6
FIG. 1.22

Acute ischaemia with T wave inversion Sinus rhythm
with T wave inversion throughout all chest leads, V1–V6
FIG. 1.23

Fig. 1.24 shows sinus rhythm with marked ST segment elevation in
leads V2–V6. This is typical of acute myocardial infarction. Myocardial

infarction with ST segment elevation is known as ‘STEMI’ (ST
segment elevation myocardial infarction). Myocardial infarction
without ST segment elevation is known as ‘NSTEMI’ (non-ST segment
elevation myocardial infarction), e.g. Fig. 1.23 which could be either
acute ischaemia or infarction.

Acute myocardial infarction with ST elevation Sinus
rhythm with ST elevation in leads V2–V6
FIG. 1.24

The normal ECG and its variants
A big problem with ECG interpretation is the number of normal
variants. ECGs from normal healthy people vary, just as normal
healthy people vary!
When you start looking at ECGs, try and spot the major
abnormalities first.
In Fig. 1.25, the T waves are normally inverted in VR and V1, but
inversion in lead III is normal provided that the T wave is upright in
VF. Other examples of normal variants are discussed in Chapter 6,
The ECG in healthy subjects.

FIG. 1.25

Normal ECG T wave inversion in III but normal T wave in

lead VF

ECG red flags
The following ECG abnormalities could be clinically important, but
always consider the patients' clinical state first. Any of these changes
could present as chest pain, breathlessness, palpitations or collapse.

• Ventricular rate above 120 bpm or below 45 bpm
• Atrial fibrillation
• Complete heart block
• ST segment elevation or depression
• Abnormal T wave inversion
• Wide QRS width
There are 12-lead examples of all these ‘red flag’ ECGs in Chapter 9.
Table 1.3
ECG Red Flags in an Unwell Patient – What to Look Out For
ECG abnormality

Consider

Ventricular rate above 120 bpm or below 45
bpm

Ischaemia, hypotension, sepsis

Atrial fibrillation

Valve disease, alcoholism, ischaemia,
infection

Complete heart block

Any heart disease

ST segment elevation or depression

Infarction, ischaemia

Abnormal T wave inversion

Infarction, ischaemia, pulmonary embolism

Wide QRS width

Any heart disease

■ TOP TIP: DON'T PANIC – THE ECG REALLY IS VERY EASY!
Now you are ready to read the remainder of the book.

PA R T 2

The basics: the fundamentals of
ECG recording, reporting and
interpretation
OUTLINE
2 What the ECG is about
3 Conduction and its problems
4 The rhythm of the heart
5 Abnormalities of P waves, QRS complexes and T waves

2

What the ECG is about
What to expect from the ECG 15
The electricity of the heart 16
The wiring diagram of the heart 16
The rhythm of the heart 16
The different parts of the ECG 16
Times and speeds 17
Calibration 20
The ECG – electrical pictures 20
The 12-lead ECG 20
The shape of the QRS complex 23
The QRS complex in the limb leads 23
The cardiac axis 23
Why worry about the cardiac axis? 26
The QRS complex in the V leads 26
Why worry about the transition point? 26
Making a recording – practical points 28
How to report an ECG 39

‘ECG’ stands for electrocardiogram, or electrocardiograph. In some
countries, the abbreviation used is ‘EKG’. Remember:

• By the time you have finished this book, you
should be able to say and mean ‘The ECG is easy
to understand’.
• Most abnormalities of the ECG are amenable to
reason.

What to Expect from the ECG
Clinical diagnosis depends mainly on a patient's history and, to a
lesser extent, on the physical examination. The ECG can provide
evidence to support a diagnosis, and in some cases it is crucial for
patient management. It is, however, important to see the ECG as a
tool, and not as an end in itself.
The ECG is essential for the diagnosis, and therefore the
management, of abnormal cardiac rhythms. It helps with the
diagnosis of the cause of chest pain, and the proper use of early
intervention in myocardial infarction depends upon it. It can help
with the diagnosis of the cause of dizziness, syncope and
breathlessness.
With practice, interpreting the ECG is a matter of pattern
recognition. However, the ECG can be analysed from first principles if
a few simple rules and basic facts are remembered. This chapter is
about these rules and facts.

The electricity of the heart
The contraction of any muscle is associated with electrical changes
called ‘depolarization’, and these changes can be detected by
electrodes attached to the surface of the body. Since all muscular
contraction will be detected, the electrical changes associated with
contraction of the heart muscle will only be clear if the patient is fully
relaxed and no skeletal muscles are contracting.
Although the heart has four chambers, from the electrical point of

view it can be thought of as having only two, because the two atria
contract together, and then the two ventricles contract together.

The wiring diagram of the heart
The electrical discharge for each cardiac cycle normally starts in a
special area of the right atrium called the ‘sinoatrial (SA) node’ (Fig.
2.1). Depolarization then spreads through the atrial muscle fibres.
There is a delay while depolarization spreads through another special
area in the atrium, the ‘atrioventricular node’ (also called the ‘AV
node’, or sometimes just ‘the node’). Thereafter, the depolarization
wave travels very rapidly down specialized conduction tissue, the
‘bundle of His’, which divides in the septum between the ventricles
into right and left bundle branches. The left bundle branch itself
divides into two. Within the mass of ventricular muscle, conduction
spreads somewhat more slowly, through specialized tissue called
‘Purkinje fibres’.

FIG. 2.1

The wiring diagram of the heart

The rhythm of the heart
As we shall see later, electrical activation of the heart can sometimes
begin in places other than the SA node. The word ‘rhythm’ is used to
refer to the part of the heart which is controlling the activation

sequence. The normal heart rhythm, with electrical activation
beginning in the SA node, is called ‘sinus rhythm’.

The different parts of the ECG
The muscle mass of the atria is small compared with that of the
ventricles, and so the electrical change accompanying the contraction
of the atria is small. Depolarization of the atria is associated with the
ECG wave called ‘P’ (Fig. 2.2). The ventricular mass is large, and so
there is a large deflection of the ECG when the ventricles are
depolarized: this is called the ‘QRS’ complex. The ‘T’ wave of the ECG
is associated with the return of the ventricular mass to its resting
electrical state (‘repolarization’).

FIG. 2.2

Shape of the normal ECG, including a U wave

The letters P, Q, R, S and T were selected in the early days of ECG
history, and were chosen arbitrarily. The P Q, R, S and T deflections
are all called waves; the Q, R and S waves together make up a
complex; and the interval between the S wave and the beginning of
the T wave is called the ST ‘segment’.
In some ECGs an extra wave can be seen on the end of the T wave,
and this is called a U wave. Its origin is uncertain, though it may
represent repolarization of the papillary muscles. If a U wave follows
a normally shaped T wave, it can be assumed to be normal. If it
follows a flattened T wave, it may be pathological (see Ch. 5).
The different parts of the QRS complex are labelled as shown in Fig.

2.3. If the first deflection is downward, it is called a Q wave (Fig. 2.3a).
An upward deflection is called an R wave, regardless of whether or
not it is preceded by a Q wave (Figs 2.3b and 2.3c). Any deflection
below the baseline following an R wave is called an S wave, regardless
of whether there is a preceding Q wave (Figs 2.3d and 2.3e).

Parts of the QRS complex (a) Q wave. (b, c) R waves. (d,
e) S waves
FIG. 2.3

Times and speeds
ECG machines record changes in electrical activity by drawing a trace
on a moving paper strip. ECG machines run at a standard rate of
25 mm/s and use paper with standard-sized squares. Each large
square (5 mm) represents 0.2 second (s), i.e. 200 milliseconds (ms) (Fig.
2.4). Therefore, there are 5 large squares per second, and 300 per
minute. So an ECG event, such as a QRS complex, occurring once per
large square is occurring at a rate of 300 bpm. The heart rate can be
calculated rapidly by remembering the sequence in Table 2.1.

Relationship between the squares on ECG paper and
time. Here there is one QRS complex per second, so the heart
rate is 60 beats/min
FIG. 2.4

TABLE 2.1
Relationship Between the Number of Large Squares Between Successive R Waves and
the Heart Rate
R–R interval (large squares)

Heart rate (beats/min)

1

300

2

150

3

100

4

75

5

60

6

50

Just as the length of paper between R waves gives the heart rate, so
the distance between the different parts of the P–QRS–T complex
shows the time taken for conduction of the electrical discharge to
spread through the different parts of the heart.
The PR interval is measured from the beginning of the P wave to
the beginning of the QRS complex, and it is the time taken for
excitation to spread from the SA node, through the atrial muscle and
the AV node, down the bundle of His and into the ventricular muscle.

Logically, it should be called the PQ interval, but common usage is
‘PR interval’ (Fig. 2.5).

FIG. 2.5

The components of the ECG complex

The normal PR interval is 120–200 ms, represented by 3–5 small
squares. Most of this time is taken up by delay in the AV node (Fig.
2.6).

FIG. 2.6

Normal PR interval and QRS complex

If the PR interval is very short, either the atria have been
depolarized from close to the AV node, or there is abnormally fast
conduction from the atria to the ventricles.
The duration of the QRS complex shows how long excitation takes
to spread through the ventricles. The QRS complex duration is
normally 120 ms (represented by 3 small squares) or less, but any
abnormality of conduction takes longer, and causes widened QRS

complexes (Fig. 2.7). Remember that the QRS complex represents
depolarization, not contraction, of the ventricles – contraction is
proceeding during the ECG's ST segment.

FIG. 2.7

Normal PR interval and prolonged QRS complex

The QT interval varies with the heart rate. It is prolonged in patients
with some electrolyte abnormalities, and, more important, it is
prolonged by some drugs. A prolonged QT interval (greater than
approximately 480 ms) may lead to ventricular tachycardia.

Calibration
A limited amount of information is given by the height of the P
waves, QRS complexes and T waves, provided the machine is
properly calibrated. A standard signal of 1 millivolt (mV) should
move the stylus vertically 1 cm (2 large squares) (Fig. 2.8), and this
‘calibration’ signal should be included with every record.

FIG. 2.8

Calibration of the ECG recording

The ECG – electrical pictures
The word ‘lead’ sometimes causes confusion. Sometimes it is used to
mean the pieces of wire that connect the patient to the ECG recorder.
Properly, a lead is an electrical picture of the heart.
The electrical signal from the heart is detected at the surface of the
body through electrodes, which are joined to the ECG recorder by
wires. One electrode is attached to each limb, and six to the front of
the chest.
The ECG recorder compares the electrical activity detected in the
different electrodes, and the electrical picture so obtained is called a
‘lead’. The different comparisons ‘look at’ the heart from different
directions. For example, when the recorder is set to ‘lead I’, it is
comparing the electrical events detected by the electrodes attached to
the right and left arms. Each lead gives a different view of the
electrical activity of the heart, and so a different ECG pattern. Strictly,
each ECG pattern should be called ‘lead…’, but often the word ‘lead’
is omitted.
The ECG is made up of 12 characteristic views of the heart, six
obtained from the ‘limb’ leads (I, II, III, VR, VL, VF) and six from the
‘chest’ leads (V1–V6). It is not necessary to remember how the leads (or
views of the heart) are derived by the recorder, but for those who like
to know how it works, see Table 2.2. The electrode attached to the
right leg is used as an earth, and does not contribute to any lead.
TABLE 2.2
ECG Leads
Lead

Comparison of electrical activity

I

LA and RA

II

LL and RA

III

LL and LA

VR

RA and average of (LA + LL)

VL

LA and average of (RA + LL)

VF

LL and average of (LA + RA)

V1

V1 and average of (LA + RA + LL)

V2

V2 and average of (LA + RA + LL)

V3

V3 and average of (LA + RA + LL)

V4

V4 and average of (LA + RA + LL)

V5

V5 and average of (LA + RA + LL)

V6

V6 and average of (LA + RA + LL)

Key: LA, left arm; RA, right arm; LL, left leg.

The 12-lead ECG
ECG interpretation is easy if you remember the directions from which
the various leads look at the heart. The six ‘standard’ leads, which are
recorded from the electrodes attached to the limbs, can be thought of
as looking at the heart in a vertical plane (i.e. from the sides or the
feet) (Fig. 2.9).

FIG. 2.9

The ECG patterns recorded by the six ‘standard’ leads

Leads I, II and VL look at the left lateral surface of the heart, leads
III and VF at the inferior surface, and lead VR looks at the right
atrium.
The six V leads (V1–V6) look at the heart in a horizontal plane, from
the front and the left side. Thus, leads V1 and V2 look at the right
ventricle, V3 and V4 look at the septum between the ventricles and the
anterior wall of the left ventricle, and V5 and V6 look at the anterior
and lateral walls of the left ventricle (Fig. 2.10).

FIG. 2.10

The relationship between the six chest leads and the

heart

As with the limb leads, the chest leads each show a different ECG
pattern (Figs 1.1 and 2.11). In each lead the pattern is characteristic,
being similar in individuals who have normal hearts.

FIG. 2.11

The ECG patterns recorded by the chest leads

The cardiac rhythm is identified from whichever lead shows the P
wave most clearly – usually lead II. When a single lead is recorded

simply to show the rhythm, it is called a ‘rhythm strip’, but it is
important not to make any diagnosis from a single lead, other than
identifying the cardiac rhythm.

The shape of the QRS complex
We now need to consider why the ECG has a characteristic
appearance in each lead.

The QRS complex in the limb leads
The ECG machine is arranged so that when a depolarization wave
spreads towards a lead the stylus moves upwards, and when it
spreads away from the lead the stylus moves downwards.
Depolarization spreads through the heart in many directions at
once, but the shape of the QRS complex shows the average direction
in which the wave of depolarization is spreading through the
ventricles (Fig. 2.12).

Depolarization and the shape of the QRS complex
Depolarization (a) moving towards the lead, causing a
predominantly upward QRS complex; (b) moving away from the
lead, causing a predominantly downward QRS complex; and (c)
at right angles to the lead, generating equal R and S waves
FIG. 2.12

If the QRS complex is predominantly upward, or positive (i.e. the R
wave is greater than the S wave), the depolarization is moving
towards that lead (Fig. 2.12a). If predominantly downward, or
negative (the S wave is greater than the R wave), the depolarization is

moving away from that lead (Fig. 2.12b). When the depolarization
wave is moving at right angles to the lead, the R and S waves are of
equal size (Fig. 2.12c). Q waves, when present, have a special
significance, which we shall discuss later.

The cardiac axis
Leads VR and II look at the heart from opposite directions. When seen
from the front, the depolarization wave normally spreads through the
ventricles from 11 o'clock to 5 o'clock, so the deflections in lead VR are
normally mainly downward (negative) and in lead II mainly upward
(positive) (Fig. 2.13).

FIG. 2.13

The cardiac axis

The average direction of spread of the depolarization wave through
the ventricles as seen from the front is called the ‘cardiac axis’. It is
useful to decide whether this axis is in a normal direction or not. The
direction of the axis can be derived most easily from the QRS complex
in leads I, II and III.
A normal 11 o'clock–5 o'clock axis means that the depolarizing
wave is spreading towards leads I, II and III, and is therefore

associated with a predominantly upward deflection in all these leads;
the deflection will be greater in lead II than in I or III (Fig. 2.14).

FIG. 2.14

The normal axis

When the R and S waves of the QRS complex are equal, the cardiac
axis is at right angles to that lead.
If the right ventricle becomes hypertrophied, it has more effect on
the QRS complex than the left ventricle, and the average
depolarization wave – the axis – will swing towards the right. The
deflection in lead I becomes negative (predominantly downward)
because depolarization is spreading away from it, and the deflection
in lead III becomes more positive (predominantly upward) because
depolarization is spreading towards it (Fig. 2.15). This is called ‘right
axis deviation’. It is associated mainly with pulmonary conditions that
put a strain on the right side of the heart, and with congenital heart
disorders.

FIG. 2.15

Right axis deviation

When the left ventricle becomes hypertrophied, it exerts more
influence on the QRS complex than the right ventricle. Hence, the axis
may swing to the left, and the QRS complex becomes predominantly
negative in lead III (Fig. 2.16). ‘Left axis deviation’ is not significant
until the QRS complex deflection is also predominantly negative in
lead II. Although left axis deviation can be due to excess influence of
an enlarged left ventricle, in fact this axis change is usually due to a
conduction defect rather than to increased bulk of the left ventricular
muscle (see Ch. 3).

FIG. 2.16

Left axis deviation

The cardiac axis is sometimes measured in degrees (Fig. 2.17),
though this is not clinically particularly useful. Lead I is taken as
looking at the heart from 0°; lead II from +60°; lead VF from +90°; and
lead III from +120°. Leads VL and VR look from –30° and –150°,
respectively.

FIG. 2.17

The cardiac axis and lead angles

The normal cardiac axis is in the range –30° to +90°. If in lead II the S
wave is greater than the R wave, the axis must be more than 90° away
from lead II. In other words, it must be at a greater angle than –30°,
and closer to the vertical (see Figs 2.16 and 2.17), and left axis
deviation is present. Similarly, if the size of the R wave equals that of
the S wave in lead I, the axis is at right angles to lead I or at +90°. This
is the limit of normality towards the ‘right’. If the S wave is greater
than the R wave in lead I, the axis is at an angle of greater than +90°,
and right axis deviation is present (Fig. 2.15).

Why worry about the cardiac axis?
Right and left axis deviation in themselves are seldom significant –
minor degrees occur in tall, thin individuals and in short, obese
individuals, respectively. However, the presence of axis deviation
should alert you to look for other signs of right and left ventricular
hypertrophy (see Ch. 5). A change in axis to the right may suggest a
pulmonary embolus, and a change to the left indicates a conduction
defect.

The QRS complex in the V leads
The shape of the QRS complex in the chest (V) leads is determined by
two things:

• The septum between the ventricles is
depolarized before the walls of the ventricles, and
the depolarization wave spreads across the
septum from left to right.
• In the normal heart there is more muscle in the
wall of the left ventricle than in that of the right
ventricle, and so the left ventricle exerts more
influence on the ECG pattern than does the right
ventricle.
Leads V1 and V2 look at the right ventricle; leads V3 and V4 look at
the septum; and leads V5 and V6 at the left ventricle (Fig. 2.10).
In a right ventricular lead the deflection is first upwards (R wave) as
the septum is depolarized. In a left ventricular lead the opposite
pattern is seen: there is a small downward deflection (‘septal’ Q wave)
(Fig. 2.18).

FIG. 2.18

Shape of the QRS complex: first stage

In a right ventricular lead there is then a downward deflection (S
wave) as the main muscle mass is depolarized – the electrical effects in
the bigger left ventricle (in which depolarization is spreading away
from a right ventricular lead) outweighing those in the smaller right
ventricle. In a left ventricular lead there is an upward deflection (R
wave) as the ventricular muscle is depolarized (Fig. 2.19).

FIG. 2.19

Shape of the QRS complex: second stage

When the whole of the myocardium is depolarized, the ECG trace
returns to the baseline (Fig. 2.20).

FIG. 2.20

Shape of the QRS complex: third stage

The QRS complex in the chest leads shows a progression from lead
V1, where it is predominantly downward, to lead V6, where it is
predominantly upward (Fig. 2.21). The ‘transition point’, where the R
and S waves are equal, indicates the position of the interventricular
septum.

FIG. 2.21

The ECG patterns recorded by the chest leads

Why worry about the transition point?
If the right ventricle is enlarged, and occupies more of the precordium
than is normal, the transition point will move from its normal position
of leads V3/V4 to leads V4/V5 or sometimes leads V5/V6. Seen from
below, the heart can be thought of as having rotated in a clockwise
direction. ‘Clockwise rotation’ in the ECG is characteristic of chronic
lung disease.

Making a recording – practical points
Now that you know what an ECG should look like, and why it looks
the way it does, we need to think about the practical side of making a
recording. Some, but not all, ECG recorders produce a ‘rhythm strip’,
which is a continuous record, usually of lead II. This is particularly
useful when the rhythm is not normal. The next series of ECGs were
all recorded from a healthy subject whose ‘ideal’ ECG is shown in Fig.
2.22.

FIG. 2.22
Note

A good record of a normal ECG

• The upper three traces show the six limb leads (I, II, III, VR,
VL, VF) and then the six chest leads
• The bottom trace is a ‘rhythm strip’, entirely recorded from

lead II (i.e. no lead changes)
• The trace is clear, with P waves, QRS complexes and T
waves visible in all leads

It is really important to make sure that the electrode marked LA is
indeed attached to the left arm, RA to the right arm and so on. If the
limb electrodes are wrongly attached, the 12-lead ECG will look very
odd (Fig. 2.23). It is possible to interpret the ECG, but it is easier to
recognize that there has been a mistake, and to repeat the recording.

The effect of reversing the electrodes attached to the
left and right arms
FIG. 2.23
Note

• Compare with Fig. 2.22, correctly recorded from the same
patient
• Inverted P waves in lead I
• Abnormal QRS complexes and T waves in lead I
• Upright T waves in lead VR are most unusual

Reversal of the leg electrodes does not make much difference to the
ECG.
The chest electrodes need to be accurately positioned, so that
abnormal patterns in the V leads can be identified, and so that records
taken on different occasions can be compared. Identify the second rib
interspace by feeling for the sternal angle – this is the point where the
manubrium and the body of the sternum meet, and there is usually a
palpable ridge where the body of the sternum begins, angling
downwards in comparison to the manubrium. The second rib is

attached to the sternum at the angle, and the second rib space is just
below this. Having identified the second space, feel downwards for
the third and then the fourth rib spaces, over which the electrodes for
V1 and V2 are attached, to the right and left of the sternum,
respectively. The other electrodes are then placed as shown in Figs 1.1
and 2.24, with V4 in the midclavicular line (the imaginary vertical line
starting from the midpoint of the clavicle); V5 in the anterior axillary
line (the line starting from the fold of skin that marks the front of the
armpit); and V6 in the midaxillary line.

The positions of the chest leads: note the fourth and
fifth rib spaces
FIG. 2.24

Good electrical contact between the electrodes and the skin is
essential. The effects on the ECG of poor skin contact are shown in
Fig. 2.25. The skin must be clean and dry – in any patient using creams
or moisturizers (such as patients with skin disorders) it should be
cleaned with alcohol; the alcohol must be wiped off before the

electrodes are applied. Abrasion of the skin is essential; in most
patients all that is needed is a rub with a paper towel. In exercise
testing, when the patient is likely to become sweaty, abrasive pads
may be used – for these tests it is worth spending time to ensure good
contact, because in many cases the ECG becomes almost unreadable
towards the end of the test. Hair is a poor conductor of the electrical
signal and prevents the electrodes from sticking to the skin. Shaving
may be preferable, but patients may not like this – if the hair can be
parted and firm contact made with the electrodes, this is acceptable.
After shaving, the skin will need to be cleaned with alcohol or a soapy
wipe.

FIG. 2.25
Note

The effect of poor electrode contact

• Bizarre ECG patterns
• In the rhythm strip (lead II), the patterns vary

Even with the best of ECG recorders, electrical interference can
cause regular oscillation in the ECG trace, at first sight giving the
impression of a thickened baseline (Fig. 2.26). It can be extremely
difficult to work out where electrical interference may be coming
from, but think about electric lights, and electric motors on beds and
mattresses.

FIG. 2.26
Note

The effect of electrical interference

• Regular sharp high-frequency spikes, giving the
appearance of a thick baseline

ECG recorders are normally calibrated so that 1 mV of signal causes
a deflection of 1 cm on the ECG paper, and a calibration signal usually
appears at the beginning (and often also at the end) of a record. If the
calibration setting is wrong, the ECG complexes will look too large or
too small (Figs 2.27 and 2.28). Large complexes may be confused with
left ventricular hypertrophy (see Ch. 5), and small complexes might
suggest that there is something like a pericardial effusion reducing the
electrical signal from the heart. So, check the calibration.

FIG. 2.27
Note

The effect of over-calibration

• The calibration signal (1 mV) at the left-hand end of each
line causes a deflection of 2 cm
• All the complexes are large compared with an ECG
recorded with the correct calibration (e.g. Fig. 2.22, in which
1 mV causes a deflection of 1 cm)

FIG. 2.28
Note

The effect of under-calibration

• The calibration signal (1 mV) causes a deflection of 0.5 cm
• All the complexes are small

ECG recorders are normally set to run at a paper speed of 25 mm/s,
but they can be altered to run at slower speeds (which make the
complexes appear spiky and bunched together) or to 50 mm/s (Figs
2.29 and 2.30). The faster speed is used regularly in some European
countries, and makes the ECG look ‘spread out’. In theory this can
make the P wave easier to see, but in fact flattening out the P wave
tends to hide it, and so this fast speed is seldom useful.

FIG. 2.29
Note

Normal ECG recorded with a paper speed of 50 mm/s

• A paper speed of 50 mm/s is faster than normal
• Long interval between QRS complexes gives the
impression of a slow heart rate
• Widened QRS complexes
• Apparently very long QT interval

FIG. 2.30
Note

A normal ECG recorded with a paper speed of 12.5 mm/s

• A paper speed of 12.5 mm/s is slower than normal
• QRS complexes are close together, giving the impression
of a rapid heart rate
• P waves, QRS complexes and T waves are all narrow and
‘spiky’

ECG recorders are ‘tuned’ to the electrical frequency generated by
heart muscle, but they will also detect the contraction of skeletal
muscle. It is therefore essential that a patient is relaxed, warm and
lying comfortably – if they are moving or shivering, or have
involuntary movements such as those of Parkinson's disease, the
recorder will pick up a lot of muscular activity, which in extreme cases
can mask the ECG (Figs 2.31 and 2.32).

FIG. 2.31
Note

An ECG from a subject who is not relaxed

• Same subject as in Figs 2.22–2.30
• The baseline is no longer clear, and is replaced by a series
of sharp irregular spikes – particularly marked in the limb
leads

FIG. 2.32
Note

The effect of shivering

• The spikes are more exaggerated than when a patient is
not relaxed
• The sharp spikes are also more synchronized, because
the skeletal muscle groups are contracting together
• The effects of skeletal muscle contraction almost
obliterate those of cardiac muscle contraction in leads I, II
and III

So, the ECG recorder will do most of the work for you – but
remember to:

• attach the electrodes to the correct limbs
• ensure good electrical contact
• check the calibration and speed settings
• make the patient comfortable and relaxed.
Then just press the button, and the recorder will automatically

provide a beautiful 12-lead ECG.

How to report an ECG
Many ECG recorders automatically provide a report, and in these
reports the heart rate and the conducting intervals are usually
accurately measured. However, the description of the rhythm and of
the QRS and T patterns should be regarded with suspicion. Recorders
tend to ‘over-report’, and to describe abnormalities where none exist:
it is much better to be confident in your own reporting.
You now know enough about the ECG to understand the basis of a
report. This should take the form of a description followed by an
interpretation.
The description should always be given in the same sequence:
1. rhythm
2. conduction intervals
3. cardiac axis
4. a description of the QRS complexes
5. a description of the ST segments and T waves.
Reporting a series of totally normal findings is possibly pedantic,
and in real life this is frequently not done. However, you must think
about all the findings every time you interpret an ECG.
The interpretation of an ECG indicates whether the record is normal
or abnormal: if abnormal, the underlying pathology needs to be
identified. One of the main problems of ECG reporting is that there is
quite a lot of variation in the normal ECG. Figs 2.33 and 2.34 are
examples of 12-lead ECGs showing normal variants.

FIG. 2.33
Note

Variant of a normal ECG

• Sinus rhythm, rate 50 bpm
• Normal PR interval (100 ms)
• Normal QRS complex duration (120 ms)
• Normal cardiac axis
• Normal QRS complexes
• Normal T waves (an inverted T wave in lead VR is normal)
• Prominent (normal) U waves in leads V2–V4
Interpretation

• Normal ECG

FIG. 2.34
Note

Variant of a normal ECG

• Sinus rhythm, rate 75 bpm
• Normal PR interval (200 ms)
• Normal QRS complex duration (120 ms)
• Right axis deviation (prominent S wave in lead I)
• Normal QRS complexes
• Normal ST segments and T waves
Interpretation

• Normal ECG – apart from right axis deviation, which could
be normal in a tall, thin person

Reminders
Basic Principles
• The ECG results from electrical changes associated with
activation (depolarization) first of the atria and then of the
ventricles.
• Atrial depolarization causes the P wave.
• Ventricular depolarization causes the QRS complex. If the first
deflection is downward, it is a Q wave. Any upward deflection
is an R wave. A downward deflection after an R wave is an S

wave.

• When the depolarization wave spreads towards a lead, the
deflection is predominantly upward. When the wave spreads
away from a lead, the deflection is predominantly downward.
• The six limb leads (I, II, III, VR, VL and VF) look at the heart
from the sides and the feet in a vertical plane.
• The cardiac axis is the average direction of spread of
depolarization as seen from the front, and is estimated from
leads I, II and III.
• The chest or V leads look at the heart from the front and the left
side in a horizontal plane. Lead V1 is positioned over the right
ventricle, and lead V6 over the left ventricle.
• The septum is depolarized from the left side to the right.
• In a normal heart the left ventricle exerts more influence on the
ECG than the right ventricle.
• Unfortunately, there are a lot of minor variations in ECGs
which are consistent with perfectly normal hearts. Recognizing
the limits of normality is one of the main difficulties of ECG
interpretation.

For more on QT interval abnormalities, see ECG Made Practical, 7th
edition, Chapter 2
For more on ECGs in healthy people, see ECG Made Practical, 7th
edition, Chapter 1

3

Conduction and its problems
Conduction problems in the AV node and His
bundle 45
First degree heart block 46
Second degree heart block 46
Third degree heart block 48
Conduction problems in the right and left bundle
branches – bundle branch block 50
Right bundle branch block 50
Left bundle branch block 53
Conduction problems in the distal parts of the left
bundle branch 55
What to do 59

We have already seen that electrical depolarization normally begins in
the sinoatrial (SA) node, and that a wave of depolarization spreads
outwards through the atrial muscle to the atrioventricular (AV) node,
and thence down the His bundle and its branches to the ventricles.
The conduction of this wave front can be delayed or blocked at any
point. Conduction problems are simple to analyse, provided you keep
the wiring diagram of the heart constantly in mind (Fig. 3.1).

FIG. 3.1

The wiring diagram of the heart

We can think of conduction problems in the order in which the
depolarization wave normally spreads: SA node → AV node → His
bundle → bundle branches. Remember in all that follows that we are
assuming depolarization begins in the normal way in the SA node.
The rhythm of the heart is best interpreted from whichever ECG
lead shows the P wave most clearly. This is usually, but not always,
lead II or lead V1. You can assume that all the ‘rhythm strips’ in this
book were recorded from one of these leads.

Conduction problems in the AV node
and His bundle
The time taken for the spread of depolarization from the SA node to
the ventricular muscle is shown by the PR interval (see Ch. 2) and is
not normally greater than 200 ms (5 small squares).
Interference with the conduction process causes the phenomenon
called ‘heart block’.

First degree heart block
If each wave of depolarization that originates in the SA node is
conducted to the ventricles, but there is delay somewhere along the
conduction pathway, then the PR interval is prolonged. This is called
‘first degree heart block’ (Fig. 3.2).

FIG. 3.2
Note

First degree heart block

• One P wave per QRS complex
• PR interval 360 ms

First degree heart block is not in itself important, but it may be a
sign of coronary artery disease, acute rheumatic carditis, digoxin
toxicity or electrolyte disturbances.

Second degree heart block
Sometimes excitation completely fails to pass through the AV node or
the bundle of His. When this occurs intermittently, ‘second degree
heart block’ is said to exist. There are three variations of this:
1. There may be progressive lengthening of the PR interval and
then failure of conduction of an atrial beat, followed by a
conducted beat with a shorter PR interval and then a repetition
of this cycle. This is the ‘Wenckebach’ or ‘Mobitz type 1’
phenomenon (Fig. 3.3).

FIG. 3.3
Note

Second degree heart block [Wenckebach (Mobitz type 1)]

• Progressive lengthening of the PR interval
• One nonconducted P wave
• Next conducted beat has a shorter PR interval than the
preceding conducted beat
• As with any other rhythm, a P wave may only show itself as a
distortion of a T wave

2. Most beats are conducted with a constant PR interval, but
occasionally there is atrial depolarization without a
subsequent ventricular depolarization. This is called the
‘Mobitz type 2’ phenomenon (Fig. 3.4).

FIG. 3.4
Note

Second degree heart block (Mobitz type 2)

• PR interval of the conducted beats is constant
• One P wave is not followed by a QRS complex

3. There may be alternate conducted and nonconducted atrial
beats (or one conducted atrial beat and then two or three
nonconducted beats), giving twice (or three or four times) as
many P waves as QRS complexes. This is called ‘2 : 1’ (‘two to
one’), ‘3 : 1’ (‘three to one’) or ‘4 : 1’ (‘four to one’) conduction
(Fig. 3.5).

FIG. 3.5
Note

Second degree heart block (2 : 1 type)

• Two P waves per QRS complex
• Normal, and constant, PR interval in the conducted beats

It is important to remember that, as with any other rhythm, a P
wave may only show itself as a distortion of a T wave (Fig. 3.6).

FIG. 3.6
Note

Second degree heart block (2 : 1 type)

• P wave in the T wave can be identified because of its
regularity

The underlying causes of second degree heart block are the same as
those of first degree block. The Wenckebach phenomenon is usually
benign, but Mobitz type 2 block and 2 : 1, 3 : 1 or 4 : 1 block may herald
‘complete’, or ‘third degree’, heart block.

Third degree heart block
Complete heart block (third degree block) is said to occur when atrial
contraction is normal but no beats are conducted to the ventricles (Fig.
3.7). When this occurs the ventricles are excited by a slow ‘escape
mechanism’ (see Ch. 4), from a depolarizing focus within the
ventricular muscle.

FIG. 3.7

Third degree heart block

Note

• P wave rate 90 bpm
• No relationship between P waves and QRS complexes
• QRS complex rate 36 bpm
• Abnormally shaped QRS complexes, because of abnormal
spread of depolarization from a ventricular focus

Complete block is not always immediately obvious in a 12-lead
ECG without a rhythm strip, where there may be only a few QRS
complexes per lead. Interpreting the ECG in Fig. 3.8 would have been
much easier with a rhythm strip, but without one, you have to look at
the PR interval in all the leads to see that there is no consistency.

FIG. 3.8
Note

Complete heart block

• Sinus rhythm, but no P waves are conducted
• Right axis deviation
• Broad QRS complexes (duration 160 ms)
• Right bundle branch block pattern
• In this case the cause of the block could not be
determined, though in most patients it results from fibrosis
of the bundle of His

Complete heart block may occur as an acute phenomenon in
patients with myocardial infarction (when it is usually transient) or it

may be chronic, usually due to fibrosis around the bundle of His. It
may also be caused by the block of both bundle branches.

Conduction problems in the right and
left bundle branches – bundle branch
block
If the depolarization wave reaches the interventricular septum
normally, the interval between the beginning of the P wave and the
first deflection in the QRS complex (the PR interval) will be normal.
However, if there is abnormal conduction through either the right or
left bundle branches (‘bundle branch block’), there will be a delay in
the depolarization of part of the ventricular muscle. The extra time
taken for depolarization of the whole of the ventricular muscle causes
widening of the QRS complex.
In the normal heart, the time taken for the depolarization wave to
spread from the interventricular septum to the furthest part of the
ventricles is less than 120 ms, represented by 3 small squares of ECG
paper. If the QRS complex duration is greater than 120 ms, then
conduction within the ventricles must have occurred via an abnormal,
and therefore slower, pathway.
A wide QRS complex can therefore indicate bundle branch block,
but widening also occurs if depolarization begins within the
ventricular muscle itself (see Ch. 4). However, remember that in sinus
rhythm with bundle branch block, normal P waves are present with a
constant PR interval. We shall see that this is not the case with
rhythms beginning in the ventricles.
Block of both bundle branches has the same effect as block of the
His bundle, and causes complete (third degree) heart block.
Right bundle branch block (RBBB) often indicates problems in the
right side of the heart, but RBBB patterns with a QRS complex of
normal duration are quite common in healthy people.
Left bundle branch block (LBBB) is always an indication of heart
disease, usually of the left ventricle.

It is important to recognize when bundle branch block is present,
because LBBB prevents any further interpretation of the cardiogram,
and RBBB can make interpretation difficult.
The mechanism underlying the ECG patterns of RBBB and LBBB
can be worked out from first principles. Remember (see Ch. 2):

• The septum is normally depolarized from left to
right.
• The left ventricle, having the greater muscle
mass, exerts more influence on the ECG than does
the right ventricle.
• Excitation spreading towards a lead causes an
upward deflection within the ECG.
Right bundle branch block
In RBBB, no conduction occurs down the right bundle branch but the
septum is depolarized from the left side as usual, causing an R wave
in a right ventricular lead (V1) and a small Q wave in a left ventricular
lead (V6) (Fig. 3.9).

FIG. 3.9

Conduction in right bundle branch block: first stage

Excitation then spreads to the left ventricle, causing an S wave in
lead V1 and an R wave in lead V6 (Fig. 3.10).

FIG. 3.10

Conduction in right bundle branch block: second stage

It takes longer than in a normal heart for excitation to reach the
right ventricle because of the failure of the normal conducting
pathway. The right ventricle therefore depolarizes after the left. This
causes a second R wave (R1) in lead V1, and a wide and deep S wave,
and consequently a wide QRS complex, in lead V6 (Fig. 3.11). For a 12lead ECG showing RBBB see Fig. 3.12. An easy way of remembering
the RBBB pattern is with the mnemonic ‘MaRRoW’. ‘M’ for the pattern
in V1; ‘W’ for the pattern in V6 and an R in the middle of ‘MaRRoW’
for Right BBB.

FIG. 3.11

Conduction in right bundle branch block: third stage

FIG. 3.12
Note

Sinus rhythm with right bundle branch block

• Sinus rhythm, rate 60 bpm
• Normal PR interval
• Normal cardiac axis
• Wide QRS complexes (160 ms)
• RSR1 pattern in lead V1 and deep, wide S waves in lead V6
• Normal ST segments and T waves

An ‘RSR1’ pattern, with a QRS complex of normal width (less than
120 ms), is sometimes called ‘partial right bundle branch block’. It is
seldom of significance, and can be considered a normal variant.

Left bundle branch block
If conduction down the left bundle branch fails, the septum becomes
depolarized from right to left, causing a small Q wave in lead V1 and
an R wave in lead V6 (Fig. 3.13).

FIG. 3.13

Conduction in left bundle branch block: first stage

The right ventricle is depolarized before the left, so despite the
smaller muscle mass there is an R wave in lead V1 and an S wave
(often appearing only as a notch) in lead V6 (Fig. 3.14). Remember that
any upward deflection, however small, is an R wave, and any
downward deflection, however small, following an R wave is called
an S wave.

FIG. 3.14

Conduction in left bundle branch block: second stage

Subsequent depolarization of the left ventricle causes an S wave in
lead V1 and another R wave in lead V6 (Fig. 3.15). This is sometimes
called a ‘W’ pattern in V1 and an ‘M’ pattern in V6. The ‘W’ pattern
may not always be present in LBBB (see Fig. 3.16). An easy way of
remembering the LBBB pattern is with the mnemonic ‘WiLLiaM’. ‘W’
for the pattern in V1, ‘M’ for the pattern in V6 and an L in the middle
of ‘WiLLiaM’ for left BBB.

FIG. 3.15

Conduction in left bundle branch block: third stage

FIG. 3.16
Note

Sinus rhythm with left bundle branch block

• Sinus rhythm, rate 100 bpm
• Normal PR interval
• Normal cardiac axis
• Wide QRS complexes (160 ms)
• M pattern in the QRS complexes, best seen in leads I, VL,
V5 and V6
• Inverted T waves in leads I, II, VL

LBBB is associated with T wave inversion in the lateral leads (I, VL
and V5–V6), though not necessarily in all of these.

Conduction problems in the distal parts
of the left bundle branch
At this point, it is worth considering in a little more detail the
anatomy of the branches of the His bundle. The right bundle branch
has no main divisions, but the left bundle branch has two – the
anterior and posterior ‘fascicles’. The depolarization wave therefore
spreads into the ventricles by three pathways (Fig. 3.17).

FIG. 3.17

The three pathways of the depolarization wave

The cardiac axis (see Ch. 2) depends on the average direction of
depolarization of the ventricles. Because the left ventricle contains
more muscle than the right, it has more influence on the cardiac axis
(Fig. 3.18).

FIG. 3.18

Effect of normal conduction on the cardiac axis

If the anterior fascicle of the left bundle branch fails to conduct, the
left ventricle has to be depolarized through the posterior fascicle, and
so the cardiac axis rotates upwards (Fig. 3.19).

FIG. 3.19

Effect of left anterior fascicular block on the cardiac axis

Left axis deviation is therefore due to left anterior fascicular block,
or ‘left anterior hemiblock’ (Fig. 3.20).

FIG. 3.20
Note

Sinus rhythm with left axis deviation (otherwise normal)

• Sinus rhythm, rate 80 bpm
• Left axis deviation: QRS complex upright in lead I, but
downward (dominant S wave) in leads II and III
• Normal QRS complexes, ST segments and T waves

The posterior fascicle of the left bundle is more often selectively
blocked, in ‘left posterior hemiblock’, but if this does occur the ECG
shows right axis deviation.
When the right bundle branch is blocked, the cardiac axis usually
remains normal, because there is normal depolarization of the left
ventricle with its large muscle mass (Fig. 3.21).

Lack of effect of right bundle branch block on the
cardiac axis
FIG. 3.21

However, if both the right bundle branch and the left anterior
fascicle are blocked, the ECG shows RBBB and left axis deviation (Fig.
3.22). This is sometimes called ‘bifascicular block’, and this ECG
pattern obviously indicates widespread damage to the conducting
system (Fig. 3.23).

Effect of right bundle branch block and left anterior
hemiblock on the cardiac axis
FIG. 3.22

FIG. 3.23
Note

Bifascicular block

• Sinus rhythm, rate 90 bpm
• Left axis deviation (dominant S wave in leads II and III)
• Right bundle branch block (RSR1 pattern in lead V1, and
deep, wide S wave in lead V6)

If the right bundle branch and both fascicles of the left bundle
branch are blocked, complete heart block occurs just as if the main His
bundle had failed to conduct.

What to do
Always remember that it is the patient who should be treated, not the
ECG. Relief of symptoms always comes first. However, some general
points can be made about the action that might be taken if the ECG
shows conduction abnormalities.

First degree block
• Often seen in normal people.
• Think about acute myocardial infarction and
acute rheumatic fever as possible causes.
• No specific action needed.

Second degree block
• Usually indicates heart disease; often seen in
acute myocardial infarction.
• Mobitz type 2 and Wenckebach block do not
need specific treatment.
• 2 : 1, 3 : 1 or 4 : 1 block may indicate a need for
temporary or permanent pacing, especially if the
ventricular rate is slow.
Third degree block
• Always indicates conducting tissue disease –
more often fibrosis than ischaemic.
• Consider a temporary or permanent pacemaker.
Right bundle branch block
• Think about an atrial septal defect.
• No specific treatment.
Left bundle branch block
• Think about aortic stenosis and ischaemic
disease.
• If the patient is asymptomatic, no action is
needed.
• If the patient has recently had severe chest pain,

LBBB may indicate an acute myocardial infarction,
and intervention should be considered.
Left axis deviation
• Think about left ventricular hypertrophy and its
causes.
• No action needed.
Left axis deviation and right bundle branch block
• Indicates severe conducting tissue disease.
• No specific treatment needed.
• Pacemaker required if the patient has symptoms
suggestive of intermittent complete heart block.
Reminders
Conduction and Its Effects on the ECG
• Depolarization normally begins in the SA node, and spreads to
the ventricles via the AV node, the His bundle, the right and
left branches of the His bundle, and the anterior and posterior
fascicles of the left bundle branch.
• A conduction abnormality can develop at any of these points.
• Conduction problems in the AV node and His bundle may be
partial (first and second degree block) or complete (third degree
block).
• If conduction is normal through the AV node, the His bundle
and one of its branches, but is abnormal in the other branch,
bundle branch block exists and the QRS complex is wide.

• The ECG pattern of RBBB and LBBB can be worked out if you
remember that:
– the septum is depolarized first from left to right
– lead V1 looks at the right ventricle and lead V6 at the
left ventricle
– when depolarization spreads towards an electrode, the
stylus moves upwards.
• The easiest way to remember the patterns of RBBB and LBBB
are with the mnemonics ‘MaRRoW’ and ‘WiLLiaM’. In RBBB,
use ‘MaRRoW’: an M pattern in V1 and a W pattern in V6, and
the letter R for RBBB in MaRRoW. In LBBB use ‘WiLLiaM’: a W
pattern in V1 and an M pattern in V6 and the letter L for LBBB
in ‘WiLLiaM’.
• Block of the anterior division or fascicle of the left bundle
branch causes left axis deviation.

For more on conduction problems and pacemakers, see ECG Made
Practical, 7th edition, Chapter 5

4

The rhythm of the heart
The intrinsic rhythmicity of the heart 62
Abnormal rhythms 62
The bradycardias – the slow rhythms 64
Atrial escape 64
Nodal (junctional) escape 64
Ventricular escape 64
Extrasystoles 67
The tachycardias – the fast rhythms 70
Supraventricular tachycardias 70
Ventricular tachycardias 74
How to distinguish between ventricular
tachycardia and supraventricular tachycardia
with bundle branch block 75
Fibrillation 77
Atrial fibrillation 78
Ventricular fibrillation 78
Wolff-Parkinson-White syndrome 80
The origins of tachycardias 80
What to do 82
The identification of rhythm abnormalities 84

So far, we have only considered the spread of depolarization that
follows the normal activation of the sinoatrial (SA) node. When
depolarization begins in the SA node the heart is said to be in sinus
rhythm. Depolarization can, however, begin in other places. Then the
rhythm is named after the part of the heart where the depolarization
sequence originates, and an ‘arrhythmia’ is said to be present.
When attempting to analyse a cardiac rhythm remember:

• Atrial contraction is associated with the P wave
of the ECG.
• Ventricular contraction is associated with the
QRS complex.
• Atrial contraction normally precedes ventricular
contraction, and there is normally one atrial
contraction per ventricular contraction (i.e. there
should be as many P waves as there are QRS
complexes).
The keys to rhythm abnormalities are:

• The P waves – can you find them? Look for the
lead in which they are most obvious.
• The relationship between the P waves and the
QRS complexes – there should be one P wave per
QRS complex.
• The width of the QRS complexes (should be
120 ms or less, i.e. 3 small squares).
• Because an arrhythmia should be identified
from the lead in which the P waves can be seen
most easily, full 12-lead ECGs are better than

rhythm strips.

The intrinsic rhythmicity of the heart
Most parts of the heart can depolarize spontaneously and
rhythmically, and the rate of contraction of the ventricles will be
controlled by the part of the heart that is depolarizing most
frequently.
The SA node normally has the highest frequency of discharge.
Therefore the rate of contraction of the ventricles will equal the rate of
discharge of the SA node. The rate of discharge of the SA node is
influenced by the vagus nerves, and also by reflexes originating in the
lungs. Changes in heart rate associated with respiration are normally
seen in young people, and this is called ‘sinus arrhythmia’ (Fig. 4.1).

FIG. 4.1
Note

Sinus arrhythmia

• One P wave per QRS complex
• Constant PR interval
• Progressive beat-to-beat change in the R–R interval

A slow sinus rhythm (‘sinus bradycardia’) can be associated with
athletic training, fainting attacks, hypothermia or myxoedema, and is
also often seen immediately after a heart attack. A fast sinus rhythm

(‘sinus tachycardia’) can be associated with exercise, fear, pain,
haemorrhage or thyrotoxicosis. There is no particular rate that is
called ‘bradycardia’ or ‘tachycardia’ – these are merely descriptive
terms. The stars in the figures in this chapter indicate the part of the
heart where the activation sequence began.

Abnormal rhythms
Abnormal cardiac rhythms can begin in one of three places (Fig. 4.2):
the atrial muscle; the region around the atrioventricular (AV) node
(this is called ‘nodal’ or, more properly, ‘junctional’); or the ventricular
muscle. Although Fig. 4.2 suggests that electrical activation might
begin at specific points within the atrial and ventricular muscles,
abnormal rhythms can begin anywhere within the atria or ventricles.

FIG. 4.2

Points where cardiac rhythms can begin

Sinus rhythm, atrial rhythm and junctional rhythm together
constitute the ‘supraventricular’ rhythms (Fig. 4.3). In
supraventricular rhythms, the depolarization wave spreads to the
ventricles in the normal way via the His bundle and its branches (Fig.
4.4). The QRS complex is therefore normal, and is the same whether
depolarization was initiated by the SA node, the atrial muscle or the
junctional region.

Division of abnormal rhythms into supraventricular and
ventricular
FIG. 4.3

Spread of the depolarization wave in supraventricular
rhythms
FIG. 4.4

In ventricular rhythms, on the other hand, the depolarization wave
spreads through the ventricles by an abnormal and slower pathway,
via the Purkinje fibres (Fig. 4.5). The QRS complex is therefore wide
and is abnormally shaped. Repolarization is also abnormal, so the T
wave is also of abnormal shape.

FIG. 4.5

Remember:

Spread of the depolarization wave in ventricular rhythm

• Supraventricular rhythms have narrow QRS
complexes.
• Ventricular rhythms have wide QRS complexes.
• The only exception to this rule occurs when
there is a supraventricular rhythm with right or
left bundle branch block, or the Wolff–Parkinson–
White (WPW) syndrome, when the QRS complex
will be wide (see p. 80).
Abnormal rhythms arising in the atrial muscle, the junctional region
or the ventricular muscle can be categorized as:

• bradycardias – slow and sustained
• extrasystoles – occur as early single beats
• tachycardias – fast and sustained
• fibrillation – activation of the atria or ventricles
is totally disorganized.

The bradycardias – the slow rhythms
It is clearly advantageous if different parts of the heart are able to
initiate the depolarization sequence, because this gives the heart a
series of fail-safe mechanisms that will keep it going if the SA node
fails to depolarize, or if conduction of the depolarization wave is
blocked. However, the protective mechanisms must normally be
inactive if competition between normal and abnormal sites of
spontaneous depolarization is to be avoided. This is achieved by the
secondary sites having a lower intrinsic frequency of depolarization
than the SA node.
The heart is controlled by whichever site is spontaneously
depolarizing most frequently: normally this is the SA node, and it

gives a normal heart rate of about 70/min. If the SA node fails to
depolarize, control will be assumed by a focus either in the atrial
muscle or in the region around the AV node (the junctional region),
both of which have spontaneous depolarization frequencies of about
50 bpm. If these fail, or if conduction through the His bundle is
blocked, a ventricular focus will take over and give a ventricular rate
of about 30 bpm.
These slow and protective rhythms are called ‘escape rhythms’,
because they occur when secondary sites for initiating depolarization
escape from their normal inhibition by the more active SA node.
Escape rhythms are not primary disorders, but are the response to
problems higher in the conducting pathway. They are commonly seen
in the acute phase of a heart attack, when they may be associated with
sinus bradycardia. It is important not to try to suppress an escape
rhythm, because without it the heart might stop altogether.

Atrial escape
If the rate of depolarization of the SA node slows down and a
different focus in the atrium takes over control of the heart, the
rhythm is described as ‘atrial escape’. Atrial escape beats can occur
singly (Fig. 4.6).

FIG. 4.6
Note

Atrial escape

• After one sinus beat the SA node fails to depolarize
• After a delay, an abnormal P wave is seen because
excitation of the atrium has begun somewhere other than
the SA node
• The abnormal P wave is followed by a normal QRS
complex, because excitation has spread normally down the
His bundle
• The remaining beats show a return to sinus arrhythmia

Nodal (junctional) escape
If the region around the AV node takes over as the focus of
depolarization, the rhythm is called ‘nodal’, or more properly,
‘junctional’ escape (Fig. 4.7).

FIG. 4.7
Note

Nodal (junctional) escape

• Sinus rhythm, rate 100 bpm
• Junctional escape rhythm (following the arrow), rate
75 bpm
• No P waves in junctional beats (indicates either no atrial
contraction or P wave lost in QRS complex)
• Normal QRS complexes

Ventricular escape

‘Ventricular escape’ is most commonly seen when conduction
between the atria and ventricles is interrupted by complete heart
block (Fig. 4.8).

FIG. 4.8
Note

Complete heart block

• Regular P waves (normal atrial depolarization)
• P wave rate 145 bpm
• QRS complexes highly abnormal because of abnormal
conduction through ventricular muscle
• QRS complex (ventricular escape) rate 15 bpm
• No relationship between P waves and QRS complexes

Ventricular escape rhythms can occur without complete heart block,
and ventricular escape beats can be single (Fig. 4.9).

FIG. 4.9
Note

Ventricular escape

• After three sinus beats, the SA node fails to discharge
• No atrial or nodal escape occurs
• After a pause there is a single wide and abnormal QRS
complex (arrowed), with an abnormal T wave
• A ventricular focus controls the heart for one beat, and
sinus rhythm is then restored

The rhythm of the heart can occasionally be controlled by a
ventricular focus with an intrinsic frequency of discharge faster than
that seen in complete heart block. This rhythm is called ‘accelerated
idioventricular rhythm’ (Fig. 4.10), and is often associated with acute
myocardial infarction. Although the appearance of the ECG is similar
to that of ventricular tachycardia (described later), accelerated
idioventricular rhythm is benign and should not be treated.
Ventricular tachycardia should not be diagnosed unless the heart rate
exceeds 120 bpm.

FIG. 4.10
Note

Accelerated idioventricular rhythm

• After three sinus beats, the SA node fails to depolarize
• An escape focus in the ventricle takes over, causing a
regular rhythm of 75 bpm with wide QRS complexes and
abnormal T waves

Extrasystoles
Any part of the heart can depolarize earlier than it should, and the
accompanying heartbeat is called an extrasystole. The term ‘ectopic’ is
sometimes used to indicate that depolarization originated in an
abnormal location, and the term ‘premature contraction’ means the
same thing.
The ECG appearance of an extrasystole arising in the atrial muscle,
the junctional or nodal region, or the ventricular muscle, is the same
as that of the corresponding escape beat – the difference is that an
extrasystole comes early and an escape beat comes late.
Atrial extrasystoles have abnormal P waves (Fig. 4.11). In a
junctional extrasystole there is no P wave at all, or the P wave appears
immediately before or immediately after the QRS complex (Fig. 4.11).
The QRS complexes of atrial and junctional extrasystoles are, of
course, the same as those of sinus rhythm.

FIG. 4.11
Note

Atrial and junctional (nodal) extrasystoles

• This record shows sinus rhythm with junctional and atrial
extrasystoles
• A junctional extrasystole has no P wave
• An atrial extrasystole has an abnormally shaped P wave

• Sinus, junctional and atrial beats have identical QRS
complexes – conduction in and beyond the His bundle is
normal

Ventricular extrasystoles, however, have abnormal QRS complexes,
which are typically wide and can be of almost any shape (Fig. 4.12).
Ventricular extrasystoles are common, and are usually of no
importance. However, when they occur early in the T wave of a
preceding beat they can induce ventricular fibrillation (see p. 78), and
are thus potentially dangerous.

FIG. 4.12
Note

Ventricular extrasystole

• The upper trace shows five sinus beats, then an early beat
with a wide QRS complex and an abnormal T wave: this is a
ventricular extrasystole (arrowed)
• In the lower trace, the ventricular extrasystoles occur
(arrowed) at the peak of the T waves of the preceding sinus
beats: this is the ‘R on T’ phenomenon

It may, however, not be as easy as this, particularly if a beat of
supraventricular origin is conducted abnormally to the ventricles
(bundle branch block, see Ch. 3). It is advisable to get into the habit of
asking five questions every time an ECG is being analysed:
1. Does an early QRS complex follow an early P wave? If so, it
must be an atrial extrasystole.
2. Can a P wave be seen anywhere? A junctional extrasystole may
cause the appearance of a P wave very close to, and even after,
the QRS complex because excitation is conducted both to the
atria and to the ventricles.
3. Is the QRS complex the same shape throughout (i.e. has it the
same initial direction of deflection as the normal beat, and has
it the same duration)? Supraventricular beats look the same as
each other; ventricular beats may look different from each
other.
4. Is the T wave the same way up as in the normal beat? In
supraventricular beats, it is the same way up; in ventricular
beats, it is inverted.
5. Does the next P wave after the extrasystole appear at an
expected time? In both supraventricular and ventricular
extrasystoles there is a (‘compensatory’) pause before the next
heartbeat, but a supraventricular extrasystole usually upsets
the normal periodicity of the SA node, so that the next SA
node discharge (and P wave) comes late.
The effects of supraventricular and ventricular extrasystoles on the
following P wave are:

• A supraventricular extrasystole resets the P
wave cycle (Fig. 4.13).

FIG. 4.13
Note

Supraventricular extrasystole

• Three sinus beats are followed by a junctional
extrasystole
• No P wave is seen at the expected time, and the next
P wave is late

• A ventricular extrasystole does not affect the SA
node, so the next P wave appears at the predicted
time (Fig. 4.14).

FIG. 4.14
Note

Ventricular extrasystole

• Three sinus beats are followed by a ventricular
extrasystole
• No P wave is seen after this beat, but the next P
wave arrives on time

The tachycardias – the fast rhythms
Foci in the atria, the junctional (AV nodal) region, and the ventricles

may depolarize repeatedly, causing a sustained tachycardia. The
criteria already described can be used to decide the origin of the
arrhythmia, and as before the most important thing is to try to
identify a P wave. When a tachycardia occurs intermittently, it is
called ‘paroxysmal’: this is a clinical description, and is not related to
any specific ECG pattern.

Supraventricular tachycardias
Atrial tachycardia (abnormal focus in the atrium)
In atrial tachycardia, the atria depolarize faster than 150 bpm (Fig.
4.15).

FIG. 4.15
Note

Atrial tachycardia

• After three sinus beats, atrial tachycardia develops at a
rate of 150 bpm
• P waves can be seen superimposed on the T waves of the
preceding beats
• The QRS complexes have the same shape as those of the
sinus beats

The AV node cannot conduct atrial rates of discharge greater than
about 200 bpm. If the atrial rate is faster than this, ‘atrioventricular
block’ occurs, with some P waves not followed by QRS complexes.

The difference between this sort of atrioventricular block and second
degree heart block is that in atrioventricular block associated with
tachycardia the AV node is functioning properly – it is preventing the
ventricles from being activated at a fast (and therefore inefficient) rate.
In first, second or third degree block associated with sinus rhythm, the
AV node and/or the His bundle are not conducting normally.

Atrial flutter
When the atrial rate is greater than 250 bpm, and there is no flat
baseline between the P waves, ‘atrial flutter’ is present (Fig. 4.16).

FIG. 4.16
Note

Atrial flutter

• P waves can be seen at a rate of 300 bpm, giving a
‘sawtooth’ appearance
• There are four P waves per QRS complex (arrowed)
• Ventricular activation is perfectly regular at 75 bpm

When atrial tachycardia or atrial flutter is associated with 2 : 1 block,
you need to look carefully to recognize the extra P waves (Fig. 4.17). A
narrow complex tachycardia with a ventricular rate of about 125–
150 bpm should always alert you to the possibility of atrial flutter with
2 : 1 block.

FIG. 4.17
Note

Atrial flutter with 2 : 1 block

• Atrial flutter with an atrial rate of 250 bpm is present, and
there is 2 : 1 block, giving a ventricular rate of 125 bpm
• The first of the two P waves associated with each QRS
complex can be mistaken for the T wave of the preceding
beat, but P waves can be identified by their regularity
• In this trace, T waves cannot be clearly identified

Any arrhythmia should be identified from the lead in which P
waves can most easily be seen. In the record in Fig. 4.18, atrial flutter
is most easily seen in lead II, but it is also obvious in leads VR and VF.

FIG. 4.18

Atrial flutter with 2 : 1 block

Note

• P waves at just over 300 bpm (most easily seen in leads II
and VR)
• Regular QRS complexes, rate 160 bpm
• Narrow QRS complexes of normal shape
• Normal T waves (best seen in the V leads; in the limb
leads it is difficult to distinguish between T and P waves)

Junctional (nodal) tachycardia
If the area around the AV node depolarizes frequently, the P waves
may be seen very close to the QRS complexes, or may not be seen at
all (Fig. 4.19). The QRS complex is of normal shape because, as with
the other supraventricular arrhythmias, the ventricles are activated
via the His bundle in the normal way.

FIG. 4.19
Note

Junctional (nodal) tachycardia

• In the upper trace there are no P waves, and the QRS
complexes are completely regular
• The lower trace is from the same patient, in sinus rhythm.
The QRS complexes have essentially the same shape as
those of the junctional tachycardia

The 12-lead ECG in Fig. 4.20 shows that in junctional tachycardia no
P waves can be seen in any lead.

FIG. 4.20
Note

Junctional tachycardia

• No P waves
• Regular QRS complexes, rate 200 bpm
• Narrow QRS complexes of normal shape
• Normal T waves

Carotid sinus massage
Carotid sinus massage (CSM) is performed by rubbing along one
carotid artery at the point of maximal pulsation. Pressure is applied to
the neck for between 5 and 10 s. CSM is always worth trying because
it may make the nature of the arrhythmia more obvious (Fig. 4.21). In
addition, CSM may have a useful therapeutic effect on
supraventricular tachycardias. CSM activates a reflex that leads to

vagal stimulation of the SA and AV nodes. This causes a reduction in
the frequency of discharge of the SA node, and an increase in the
delay of conduction in the AV node. It is the latter which is important
in the diagnosis and treatment of arrhythmias. CSM completely
abolishes some supraventricular arrhythmias, and slows the
ventricular rate in others, but it has no effect on ventricular
arrhythmias. CSM should not be attempted on patients with known
carotid artery stenosis or in those with recent transient ischaemic
attacks (TIAs) or strokes because of the risk of dislodging emboli.

FIG. 4.21
Note

Atrial flutter with carotid sinus massage (CSM)

• In this case, carotid sinus massage (applied during the
period indicated by the arrows) has increased the block
between the atria and the ventricles, and has made it
obvious that the underlying rhythm is atrial flutter

Ventricular tachycardias
If a focus in the ventricular muscle depolarizes with a high frequency
(causing, in effect, rapidly repeated ventricular extrasystoles), the
rhythm is called ‘ventricular tachycardia’ (Fig. 4.22).

FIG. 4.22
Note

Ventricular tachycardia

• After two sinus beats, the rate increases to 200 bpm
• The QRS complexes become broad, and the T waves are
difficult to identify
• The final beat shows a return to sinus rhythm

Excitation has to spread by an abnormal path through the
ventricular muscle, and the QRS complex is therefore wide and
abnormal. Wide and abnormal complexes are seen in all 12 leads of
the standard ECG (Fig. 4.23).

FIG. 4.23
Note

Ventricular tachycardia

• No P waves
• Regular QRS complexes, rate 200 bpm
• Broad QRS complexes, duration 280 ms, with a very
abnormal shape
• No identifiable T waves

Remember that wide and abnormal complexes are also seen with
bundle branch block (Fig. 4.24).

FIG. 4.24
Note

Sinus rhythm with left bundle branch block

• Sinus rhythm: each QRS complex is preceded by a P
wave, with a constant PR interval
• The QRS complexes are wide and the T waves are inverted
• This trace was recorded from lead V6, and the M pattern
and inverted T wave characteristic of left bundle branch
block are easily identifiable (remember ‘WiLLiaM’: an ‘M’
shape in V6 and the ‘L’ in the middle for left bundle branch
block)

How to distinguish between ventricular
tachycardia and supraventricular tachycardia with
bundle branch block
It is essential to remember that the patient's clinical state – whether
good or bad – does not help to differentiate between the two possible

causes of a tachycardia with broad QRS complexes. If a patient with
an acute myocardial infarction has broad complex tachycardia, it will
almost always be ventricular tachycardia. However, a patient with
episodes of broad complex tachycardia but without an infarction
could have ventricular tachycardia, or supraventricular tachycardia
with bundle branch block or the WPW syndrome (see p. 80). Under
such circumstances, the following points may be helpful:
1. Finding P waves and seeing how they relate to the QRS
complexes is always the key to identifying arrhythmias.
Always look carefully at a full 12-lead ECG.
2. If possible, compare the QRS complex during the tachycardia
with that during sinus rhythm. If the patient has bundle
branch block when in sinus rhythm, the QRS complex during
the tachycardia will have the same shape as during normal
rhythm.
3. If the QRS complex is wider than 4 small squares (160 ms), the
rhythm will probably be ventricular in origin.
4. Left axis deviation during the tachycardia usually indicates a
ventricular origin, as does any change of axis compared with a
record taken during sinus rhythm.
5. If during the tachycardia the QRS complex is very irregular,
the rhythm is probably atrial fibrillation with bundle branch
block or atrial fibrillation with WPW syndrome (see below).

Fibrillation
All the arrhythmias discussed so far have involved the synchronous
contraction of all the muscle fibres of the atria or of the ventricles,
albeit at abnormal speeds. When individual muscle fibres contract
independently, they are said to be ‘fibrillating’. Fibrillation can occur
in the atrial or ventricular muscle.

Atrial fibrillation

When the atrial muscle fibres contract independently there are no P
waves on the ECG, only an irregular line (Fig. 4.25). At times there
may be flutter-like waves for 2–3 s. The AV node is continuously
bombarded with depolarization waves of varying strength, and
depolarization spreads at irregular intervals down the His bundle.
The AV node conducts in an ‘all or none’ fashion, so that the
depolarization waves passing into the His bundle are of constant
intensity. However, these waves are irregular, and the ventricles
therefore contract irregularly. Because conduction into and through
the ventricles is by the normal route, each QRS complex is of normal
shape.

FIG. 4.25
Note

Atrial fibrillation

• No P waves, and an irregular baseline
• Irregular QRS complexes
• Normally shaped QRS complexes
• In lead V1, waves can be seen with some resemblance to
those seen in atrial flutter – this is common in atrial

fibrillation

In a 12-lead record, fibrillation waves can often be seen much better
in some leads than in others (Fig. 4.26).

FIG. 4.26
Note

Atrial fibrillation

• No P waves
• Irregular baseline
• Irregular QRS complexes, rate varying between 75 bpm
and 190 bpm
• Narrow QRS complexes of normal shape
• Depressed ST segments in leads V5–V6 (digoxin effect –
see p. 99)
• Normal T waves

Ventricular fibrillation
When the ventricular muscle fibres contract independently, no QRS
complex can be identified, and the ECG is totally disorganized (Fig.
4.27).

FIG. 4.27

Ventricular fibrillation

As the patient will usually have lost consciousness by the time you
have realized that the change in the ECG pattern is not just due to a
loose connection, the diagnosis is easy.

Wolff-Parkinson-White syndrome
The only normal electrical connection between the atria and ventricles
is the His bundle. Some people, however, have an extra or ‘accessory’
conducting bundle, a condition known as Wolff-Parkinson-White
(WPW) syndrome. The accessory bundle forms a direct connection
between the atrium and the ventricle, usually on the left side of the
heart, and in this bundle there is no AV node to delay conduction. A
depolarization wave therefore reaches the ventricle early, and ‘preexcitation’ occurs. The PR interval is short, and the QRS complex
shows an early slurred upstroke called a ‘delta wave’ (Fig. 4.28). The
second part of the QRS complex is normal, as conduction through the
His bundle catches up with the pre-excitation. The effects of the WPW
syndrome on the ECG are considered in more detail in Chapter 8.

FIG. 4.28
Note

The Wolff–Parkinson–White syndrome

• Sinus rhythm, rate 125 bpm
• Right axis deviation
• Short PR interval
• Slurred upstroke of the QRS complex, best seen in leads
V3 and V4. Wide QRS complex due to this ‘delta’ wave
• Dominant R wave in lead V1

The only clinical importance of this anatomical abnormality is that it
can cause paroxysmal tachycardia. Depolarization can spread down
the His bundle and back up the accessory pathway, and so reactivate
the atrium. A ‘re-entry’ circuit is thus set up, and a sustained
tachycardia occurs (Fig. 4.29).

Sustained tachycardia in the Wolff–Parkinson–White
syndrome
FIG. 4.29
Note

• During re-entry tachycardia, no P waves can be seen

The origins of tachycardias
We have considered the tachycardias up to now as if all were due to
an increased spontaneous frequency of depolarization of some part of
the heart. While such an ‘enhanced automaticity’ certainly accounts
for some tachycardias, others are due to re-entry circuits within the
heart muscle. The tachycardias that we have described as ‘junctional’
are usually due to re-entry circuits around the AV node, and are
therefore properly called ‘atrioventricular nodal re-entry tachycardias’
(AVNRTs). It is not possible to distinguish enhanced automaticity
from re-entry tachycardia on standard ECGs, but fortunately this
differentiation has no practical importance.

What to do
Accurate interpretation of the ECG is an essential part of arrhythmia
management. Although this book is not intended to discuss therapy in
detail, some simple approaches to patient management that logically
follow interpretation of an ECG recording are:

1. For fast or slow sinus rhythm, treat the underlying cause, not
the rhythm itself.
2. Extrasystoles rarely need treatment.
3. In patients with acute heart failure or low blood pressure due
to tachycardia, direct current (DC) cardioversion should be
considered early on.
4. Patients with any bradycardia that is affecting the circulation
can be treated with atropine, but if this is ineffective they will
need temporary or permanent pacing (Fig. 4.30).

FIG. 4.30
Note

Pacemaker

• Occasional P waves are visible, but are not related to the QRS
complexes
• The QRS complexes are preceded by a brief spike,
representing the pacemaker stimulus
• The QRS complexes are broad, because pacemakers stimulate
the right ventricle and cause ‘ventricular’ beats

5. Vagal manoeuvres such as carotid sinus massage (CSM),
Valsalva or eyeball compression may help to diagnose an
abnormal narrow tachycardia. This should be performed with
the ECG running, and may help make the diagnosis:
• sinus tachycardia: CSM causes temporary slowing of
the heart rate
• atrial and junctional tachycardia: CSM may
terminate the arrhythmia or may have no effect
• atrial flutter: CSM usually causes a temporary
increase in block (e.g. from 2 : 1 to 3 : 1)
• atrial fibrillation and ventricular tachycardia: CSM
has no effect.
For up-to-date information on how to manage acute arrhythmias,

see current resuscitation council guidelines https://www.resus.org.uk.

Reminders
Abnormal Cardiac Rhythms
• Most parts of the heart are capable of spontaneous
depolarization.
• Abnormal rhythms can arise in the atrial muscle, the region
around the AV node (the junctional region) and in the
ventricular muscle.
• Escape rhythms are slow and are protective.
• Occasional early depolarization of any part of the heart causes
an extrasystole.
• Frequent depolarization of any part of the heart causes
tachycardia.
• Asynchronous contraction of muscle fibres in the atria or
ventricles is called fibrillation.
• Apart from the rate, the ECG patterns of an escape rhythm, an
extrasystole and a tachycardia arising in any one part of the
heart are the same.
• All supraventricular rhythms have normal QRS complexes,
provided there is no bundle branch block or pre-excitation
(WPW) syndrome.
• Ventricular rhythms cause wide and abnormal QRS complexes,
and abnormal T waves.

The Identification of Rhythm
Abnormalities
Recognizing ECG abnormalities is, to a large extent, like recognizing

an elephant – once seen, never forgotten. However, in cases of
difficulty it is helpful to ask the following questions, referring to Table
4.1:
TABLE 4.1

1. Is the abnormality occasional or sustained?
2. Are there any P waves?
3. Are there as many QRS complexes as P waves?
4. Are the ventricles contracting regularly or irregularly?
5. Is the QRS complex of normal shape?
6. What is the ventricular rate?
For more on extrasystoles, tachycardias, and the identification of
broad complex tachycardias, see ECG Made Practical, 7th edition,
Chapter 4
For more on bradycardias and pacemakers, see ECG Made
Practical, 7th edition, Chapter 5

For more on WPW, see Chapter 8 in this book and ECG Made
Practical, 7th edition, Chapter 3

5

Abnormalities of P waves, QRS
complexes and T waves
Abnormalities of the P wave 86
Abnormalities of the QRS complex 86
Abnormalities of the width of the QRS
complex 87
Increased height of the QRS complex 87
The origin of Q waves 89
Abnormalities of the ST segment 95
Abnormalities of the T wave 96
Inversion of the T wave 96
Myocardial infarction 96
Ventricular hypertrophy 99
Bundle branch block 99
Digoxin 99
Other abnormalities of the ST segment and the T
wave 99
Electrolyte abnormalities 99
Nonspecific changes 99

When interpreting an ECG, identify the rhythm first. Then ask the
following questions (remember ‘R R P W Q S T’ from Chapter 1) –
always in the same sequence:

1. Are there any abnormalities of the P wave?
2. What is the direction of the cardiac axis? (Look at the QRS
complex in leads I, II and III – and at Ch. 2 if necessary.)
3. Is the QRS complex of normal duration?
4. Are there any abnormalities in the QRS complex – particularly,
are there any abnormal Q waves?
5. Is the ST segment raised or depressed?
6. Is the T wave normal?
Remember:
1. The P wave can only be normal, unusually tall or unusually
broad.
2. The QRS complex can only have three abnormalities – it can be
too broad or too tall, and it may contain an abnormal Q wave.
3. The ST segment can only be normal, elevated or depressed.
4. The T wave can only be the right way up or the wrong way up.

Abnormalities of the P wave
Apart from alterations of the shape of the P wave associated with
rhythm changes, there are only two important abnormalities:
1. Anything that causes the right atrium to become hypertrophied
(such as tricuspid valve stenosis or pulmonary hypertension)
causes the P wave to become peaked (Fig. 5.1).

FIG. 5.1

Right atrial hypertrophy

2. Left atrial hypertrophy (usually due to mitral stenosis) causes a

broad and bifid P wave (Fig. 5.2).

FIG. 5.2

Left at