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Interpreting an ECG correctly and working out what to do next can seem like a daunting task to the non-specialist, yet it is a skill that will be invaluable to any doctor, nurse or paramedic when evaluating the condition of a patient. Making Sense of the ECG has been written specifically with this in mind, and will help the student and more experienced healthcare practitioner to identify and answer crucial questions. This popular, easy-to-read and easy-to-remember guide to the ECG as a tool for diagnosis and management has been fully updated in its fifth edition to reflect the latest guidelines.
Categories:
Year:
2019
Edition:
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Publisher:
CRC Press
Language:
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ISBN 13:
9780429199080
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Making Sense of
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of the

ECG
A hands-on guide
Andrew R Houghton

Fifth edition

Consultant Cardiologist at
United Lincolnshire Hospitals NHS Trust
and Visiting Fellow, University of Lincoln,
Lincolnshire, UK
Boca Raton London New York

CRC Press is an imprint of the
Taylor & Francis Group, an informa business

CRC Press
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© 2020 by Taylor & Francis Group, LLC
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Contents

Preface to the fifth edition
Acknowledgements
Author

vii
ix
xi

1

Anatomy and physiology
Cardiac activation
The cardiac conduction system
The cardiac cycle
Further reading

1
2
3
4
5

2

PQRST: Where the waves come from
What does the ECG actually record?
How does the ECG ‘look’ at the heart?
Where do each of the waves come from?
Further reading

7
7
8
11
18

3

Performing an ECG recording
Initial preparations
Placement of the limb electrodes
Placement of the chest (precordial) electrodes
Einthoven’s triangle
Recording the 12-lead ECG
Further reading

19
19
20
21
22
25
27

4

Reporting an ECG recording
Patient data
Technical data
ECG fundamentals
ECG details
Report summary
Further reading

29
29
29
30
30
30
31

5

Heart rate
Is the heart rate below 60/min?
Is the heart rate above 100/min?
Further reading

33
35
36
39

6

An approach to heart rhythms
Identifying the cardiac rhythm
How is the patient?
Is ventricular activity present?
What is the ventricular rate?
Is the ventricular rhythm regular or irregular?
Is the QRS complex width normal or broad?
Is atrial activity present?
How are atrial activity and ventricular activity related?

41
42
43
44
44
44
45
47
47
iii

iv    Contents

Determining the cardiac rhythm
Further reading

47
48

7

Supraventricular rhythms
Sinus rhythm
Sinus arrhythmia
Sinus bradycardia
Sinus tachycardia
Sick sinus syndrome
Atrial ectopic beats
Atrial fibrillation
Atrial flutter
Atrial tachycardia
AV re-entry tachycardia
AV nodal re-entry tachycardia
Further reading

49
49
50
50
51
52
53
54
59
61
62
67
70

8

Ventricular rhythms
Ventricular ectopic beats
Accelerated idioventricular rhythm
Monomorphic ventricular tachycardia
How do I distinguish between VT and SVT?
Polymorphic ventricular tachycardia
Fascicular ventricular tachycardia
Ventricular fibrillation
Further reading

71
71
74
75
78
80
81
81
83

9

Conduction problems
Conduction block at the SA node
Conduction block at the AV node or bundle of His
Conduction block at the bundle branches
Conduction block at the fascicles
Escape rhythms
Accelerated conduction and accessory pathways
Further reading

85
85
85
88
93
93
94
95

10

The axis
Understanding and measuring the QRS axis
Is there left axis deviation?
Is there right axis deviation?
Is there extreme right axis deviation?
Further reading

97
97
106
108
110
110

11

The P wave
Are any P waves absent?
Are any P waves inverted?
Are any P waves too tall?
Are any P waves too wide?
Further reading

111
111
114
115
116
117

12

The PR interval
Is the PR interval less than 0.12 s long?
Is the PR interval more than 0.2 s long?
Does the PR interval vary or can it not be measured?

119
120
122
123

Contents   v

Is the PR segment elevated or depressed?
Further reading

127
129

13

The Q wave
Are there any ‘pathological’ Q waves?
Further reading

131
131
136

14

The QRS complex
Are any R or S waves too big?
Are the QRS complexes too small?
Are any QRS complexes too wide?
Are any QRS complexes an abnormal shape?
Are epsilon waves present?
Further reading

137
137
142
145
148
150
152

15

The ST segment
Are the ST segments elevated?
Are the ST segments depressed?
Are J waves present?
Further reading

153
153
166
170
172

16

The T wave
Are the T waves too tall?
Are the T waves too small?
Are any of the T waves inverted?
Further reading

173
174
176
177
182

17

The QT interval
Correcting the QT interval
Is the QTc interval long?
Is the QTc interval short?
Further reading

183
184
185
188
191

18

The U wave
Do the U waves appear too prominent?
Are any of the U waves inverted?
Further reading

193
194
195
196

19

Artefacts on the ECG
Electrode misplacement
External electrical interference
Incorrect calibration
Incorrect paper speed
Patient movement
Further reading

197
197
197
198
199
199
201

20

ECG interpretation in athletes
Normal ECG findings
Abnormal ECG findings
‘Borderline’ ECG findings
Further reading

203
203
206
206
207

21

Pacemakers and implantable cardioverter-defibrillators
What do pacemakers do?
Indications for temporary pacing

209
209
210

vi    Contents

Temporary pacemaker insertion and care
Indications for permanent pacing
Selection of a permanent pacemaker
Pacing and the ECG
Pacemakers and surgery
Implantable cardioverter-defibrillators
Cardiac resynchronization therapy (biventricular pacing)
Further reading

210
210
211
212
214
214
215
215

22

Ambulatory ECG recording
24-h ambulatory ECG recording
Event recorder
ECG ‘on demand’
Bedside monitoring/telemetry (inpatient)
Insertable cardiac monitor (ICM)
External loop recorder (ELR)
Smartphone/smartwatch applications
Further reading

217
218
218
219
219
220
220
220
221

23

Exercise ECG testing
What are the indications for an exercise ECG?
What are the risks of an exercise ECG?
How do I perform an exercise ECG?
When do I stop an exercise ECG?
How do I interpret an exercise ECG?
Further reading

223
223
224
225
226
226
228

Appendix 1: Glossary

229

Appendix 2: ECG resources

233

Appendix 3: Help with the next edition

235

Index237

Preface to the fifth edition

The primary aim of this fifth edition of Making Sense of the ECG remains the same as all its predecessors –
to provide the reader with a comprehensive yet readable introduction to electrocardiogram (ECG)
interpretation, supplemented by clinical information about how to act upon your findings.
Each chapter has been revised and updated, incorporating current guidelines and research. The text has
been clarified and/or expanded where necessary, new ECGs have been included, and the references and
suggestions for further reading at the end of each chapter have been updated throughout.
A new chapter has been added on ECG interpretation in athletes, with reference to the latest guidelines in
this field. New material has been included on Brugada syndrome and on ECG findings in arrhythmogenic
right ventricular cardiomyopathy. A glossary of ECG terminology has also been added as an appendix.
Once again, I am grateful to everyone who has taken the time to comment on the text and provide ECGs
from their collections. Finally, I would like to thank all the staff at CRC Press who have contributed to the
success of the Making Sense series of books.
Andrew R Houghton
2019

vii

Acknowledgements

I would like to thank everyone who provided suggestions and constructive criticism during the preparation
of each edition of Making Sense of the ECG. I am particularly grateful to the following for their invaluable
comments on the text and for allowing me to use ECGs from their collections:
Mookhter Ajij
Richard Andrews
Khin Maung Aye
Stephanie Baker
Michael Bamber
Sophie Beech
Muneer Ahmad Bhat
Gabriella Captur
Andrea Charman
Nigel Dewey
Matthew Donnelly
Simon Dubrey
Chris Eggett
Ian Ferrer
Catherine Goult

Lawrence Green
Mahesh Harishchandra
Michael Holmes
Tim Jones
Safiy Karim
Dave Kendall
Jeffrey Khoo
Daniel Law
Diane Lunn
Iain Lyburn
Sonia Lyburn
Martin Melville
Cara Mercer
Yuji Murakawa
Francis Murgatroyd

V B S Naidu
Vicky Nelmes
Claire Poole
George B Pradhan
Jane Robinson
Alun Roebuck
Catherine Scott
Penelope R Sensky
Neville Smith
Gary Spiers
Andrew Staniforth
Andrew Stein
Robin Touquet
Upul Wijayawardhana
Bernadette Williamson

I am grateful to the Resuscitation Council (UK) for its permission to reproduce algorithms from its adult
Advanced Life Support guidelines (2015). I also wish to thank the BMJ Publishing Group Ltd, Elsevier, John
Wiley & Sons Australia Ltd and Wolters Kluwer Health Inc for granting permission to use material from
their publications.
Finally, I would like to express my gratitude to Dr David Gray for all his hard work and commitment in
co-authoring the first four editions of this textbook, and to Dr Joanna Koster and the rest of the publishing
team at CRC Press for their encouragement, guidance and support during this project.

ix

Author

Dr Andrew R Houghton studied Medicine at the University of Oxford and undertook postgraduate training
in cardiology in Nottingham and Leicester. He has also trained at Stanford University in California and at
the Mayo Clinic in Minnesota. He was appointed as a Consultant Cardiologist at the United Lincolnshire
Hospitals NHS Trust, UK, in 2002, and is also a Visiting Fellow at the University of Lincoln. His subspecialty
interest is in cardiac imaging (echocardiography and cardiac MRI). He is a Fellow of the European Society
of Cardiology and of the Royal College of Physicians (London).

xi

Chapter 1
Anatomy and physiology

The heart is a hollow muscular organ that pumps blood around the body. With each beat, it pumps, at rest,
about 70 millilitres of blood and considerably more during exercise. Over a 70-year life span and at a rate
of around 70 beats per minute, the heart will beat over 2.5 billion times.
The heart consists of four main chambers (left and right atria, and left and right ventricles) and four valves (aortic,
mitral, pulmonary and tricuspid). Venous blood returns to the right atrium via the superior and inferior vena
cavae, and leaves the right ventricle for the lungs via the pulmonary artery. Oxygenated blood from the lungs
returns to the left atrium via the four pulmonary veins, and leaves the left ventricle via the aorta (Figure 1.1).
The heart is made up of highly specialized cardiac muscle comprising myocardial cells (myocytes), which
differs markedly from skeletal muscle because heart muscle:

• Is under the control of the autonomic nervous system
• Contracts in a repetitive and rhythmic manner
Superior vena
cava

Aorta
Pulmonary
artery

Right pulmonary
arteries

Left pulmonary
arteries

Right pulmonary
veins

Left pulmonary
veins
Left atrium

Right atrium

Left ventricle

Right coronary
artery
Inferior vena
cava
Figure 1.1
Key point:

Right
ventricle

Left anterior
descending artery

Cardiac anatomy.
• The heart and major vessels.
1

2    Making Sense of the ECG

• Has a large number of mitochondria which make the myocytes resistant to fatigue
• Cannot function adequately in anaerobic (ischaemic) conditions
CARDIAC ACTIVATION
Myocytes are essentially contractile but are capable of generating and transmitting electrical activity.
Myocytes are interconnected by cytoplasmic bridges or syncytia, so once one myocyte cell membrane is
activated (depolarized), a wave of depolariza­tion spreads rapidly to adjacent cells.
Myocardial cells are capable of being:

• Pacemaker cells: These are found primarily in the sinoatrial (SA) node and produce a spontaneous
electrical discharge.

• Conducting cells: These are found in:
•

•
•
•

The atrioventricular (AV) node
The bundle of His and bundle branches
The Purkinje fibres
Contractile cells: These form the main cell type in the atria and ventricles.

All myocytes are self-excitable with their own intrinsic contractile rhythm. Cardiac cells in the SA node
located high up in the right atrium generate action potentials or impulses at a rate of about 60–100 per
minute, a slightly faster rate than cells elsewhere such as the AV node (typically 40–60 per minute) or the
ventricular con­ducting system (30–40 per minute), so the SA node becomes the heart pacemaker, dictating
the rate and timing of action potentials that trigger cardiac contraction, overriding the potential of other
cells to generate impulses. However, should the SA node fail or an impulse not reach the ventricles, cardiac
contraction may be initi­ated by these secondary sites (‘escape rhythms’).
THE CARDIAC ACTION POTENTIAL
The process of triggering cardiac cells into function is called cardiac excitation–contraction coupling.
Cells remain in a resting state until activated by changes in voltage due to the complex movement of
sodium, potassium and calcium across the cell membrane (Figure 1.2); these are similar to changes
which occur in nerve cells.
Phase 4: At rest, there is little spontaneous depolarization as the Na+/K+/ATPase pump maintains
a negative stable resting membrane potential of about –90 mV. Some cardiac cells display
automaticity or spontaneous regular action potentials, which generates action potentials in
adjacent cells linked by cytoplasmic bridges or syncytia, so once one myocyte cell membrane
is activated (depolarized), a wave of excitation spreads rapidly to adjacent cells; the SA node,
whose cells are relatively permeable to sodium resulting in a less negative resting potential of
about –55 mV, is usually the source of spontaneous action potentials.
Phase 0: There is rapid opening of sodium channels with movement of sodium into the cell, the
resulting electrochemical gradient leading to a positive resting membrane potential.
Phase 1: When membrane potential is at its most positive, the electrochemical gradient causes
potassium outflow and closure of sodium channels.
Phase 2: A plateau phase follows, with membrane potential maintained by calcium influx;
membrane potential falls towards the resting state as calcium channels gradually become
inactive and potassium channels gradually open.
Phase 3: Potassium channels fully open, and the cell becomes repolarized.
Phase 4: Calcium, sodium and potassium are gradually restored to resting levels by their
respective ATPase-dependent pumps.

Anatomy and physiology   3

Phase 1

Phase 2
Phase 3

Phase 0

Phase 4
Figure 1.2
Key point:

Phase 4

The cardiac action potential.
• The different phases of the cardiac action potential.

The SA node is susceptible to influence from:

• The parasympathetic nervous system via the vagus nerve, which slows heart rate
• The sympathetic nervous system via spinal nerves from T1 to T4 – these increase heart rate and can
increase the force of contraction
• Serum concentration of electrolytes, e.g. hyperkalaemia, which can cause severe bradycardia (note that
hypokalaemia can cause tachycardia)
• Hypoxia, which can cause severe bradycardia
Cardiac drugs can also affect cardiac rate, some acting through the SA node, others through the AV node
or directly on ventricular myocytes:

• Negative chronotropes reduce cardiac rate
•
•
•

•

Such as beta blockers and calcium channel blockers
Positive chronotropes increase cardiac rate
Such as dopamine and dobutamine
Negative inotropes decrease force of contraction
Such as beta blockers, calcium channel blockers and some anti-arrhythmic drugs such as flecainide
and disopyramide
Positive inotropes increase force of contraction
Such as dopamine and dobutamine

•
•
•

THE CARDIAC CONDUCTION SYSTEM
Each normal heartbeat begins with the discharge (‘depolarization’) of the SA node. The impulse then spreads
from the SA node to depolarize the atria. After flowing through the atria, the electrical impulse reaches the
AV node, low in the right atrium.
Once the impulse has traversed the AV node, it enters the bundle of His which then divides into left and right
bundle branches as it passes into the interventricular sep­tum (Figure 1.3). The right bundle branch conducts
the wave of depolarization to the right ventricle, whereas the left bundle branch divides into anterior and
posterior fascicles that conduct the wave to the left ventricle.
The conducting pathways end by dividing into Purkinje fibres that distribute the wave of depolarization
rapidly throughout both ventricles. Normal depolarization of the ventricles is therefore usually very fast,
occurring in less than 0.12 s.

4    Making Sense of the ECG

Sinoatrial (SA) node
Atrioventricular (AV) node

Bundle of His
Left bundle branch

Right bundle branch
Left anterior fascicle
Left posterior fascicle

Figure 1.3

The cardiac conduction system.

THE CARDIAC CYCLE
The events that occur during each heartbeat are termed the cardiac cycle, commonly represented in
diagrammatic form (Figure 1.4). The cardiac cycle has four phases:
1.
2.
3.
4.

Isovolumic contraction
Ventricular ejection
Isovolumic relaxation
Ventricular filling

These phases apply to both the left and right heart, but we will focus on the left heart here for clarity.
Phases 1–2 correspond with ventricular systole and phases 3–4 with ventricular diastole.
Isovolumic contraction begins with closure of the mitral valve, caused by the ris­ing left ventricle (LV)
pressure at the start of ventricular systole (which coincides with the QRS complex on the ECG). After the
mitral valve has closed, pressure within the LV continues to rise but the LV volume remains constant (hence
‘isovolumic’) until the point when the aortic valve opens.
Ventricular ejection commences when the aortic valve opens and blood is ejected from the LV into the aorta.
Isovolumic relaxation commences with closure of the aortic valve. Pressure within the LV falls during this
phase (but volume remains constant), until the LV pressure falls below left atrium (LA) pressure. At this point,
the pressure difference between LA and LV causes the mitral valve to open and isovolumic relaxation ends.
Ventricular filling begins as the mitral valve opens and blood flows into the LV from the LA. This phase
ends when the mitral valve closes at the start of ventricular systole. Towards the end of the ventricular
filling phase, atrial systole (contraction) occurs, coinciding with the P wave on the ECG, and this augments
ventricular filling.
As shown in Figure 1.4, the pressures within the cardiac chambers vary through­out the cardiac cycle. A
pressure difference between two chambers causes the valve between them to open or close. For example,
when LA pressure exceeds LV pressure the mitral valve opens, and when LV pressure exceeds LA pressure
the mitral valve closes.

Anatomy and physiology   5

Isovolumic
contraction

Volume (mL)

Pressure (mm Hg)

120
100

Ejection

Isovolumic
relaxation
Ra

Aortic
valve
opens

w
Diastasis

Atrial systole

Aortic valve
closes
Aortic pressure

80
60
40

AV valve
opens

AV valve
closes

20

a

v

c

0
130

Atrial pressure
Ventricular pressure
Ventricular volume

90

R

50

P
1st

2nd

3rd

Q

S

T

Electrocardiogram
Phonocardiogram

Figure 1.4 The cardiac cycle.
Key point:

• The different phases of the cardiac cycle.

Further reading
Amin AS, Tan HL, Wilde AAM. Cardiac ion channels in health and disease. Heart Rhythm 2010; 7: 117–126.
Cabrera JA, Sánchez-Quintana D. Cardiac anatomy: What the electrophysiologist needs to know. Heart 2013; 99:
417–431.
Jarvis S, Saman S. Cardiac system 1: Anatomy and physiology. Nursing Times 2018; 114: 2, 34–37.

Chapter 2
PQRST: Where the waves come from

The electrocardiogram (ECG) is one of the most widely used and useful investigations in contemporary
medicine. It is essential for the identification of disorders of the cardiac rhythm, extremely useful for the
diagnosis of abnormalities of the heart (such as myocardial infarction) and a helpful clue to the presence of
generalized disorders that affect the rest of the body too (such as electrolyte disturbances).
Each chapter in this book considers a specific feature of the ECG in turn. We begin, however, with an
overview of the ECG in which the following points are explained:

• What does the ECG actually record?
• How does the ECG ‘look’ at the heart?
• Where do each of the waves come from?

It is recommended you take some time to read through this chapter before trying to interpret ECG
abnormalities.

WHAT DOES THE ECG ACTUALLY RECORD?
ECG machines record the electrical activity of the heart. They also pick up the activity of other muscles,
such as skeletal muscle, but are designed to filter this out as much as possible. Encouraging patients to relax
during an ECG recording helps to obtain a clear trace (Figure 2.1).
By convention, the main waves on the ECG are given the names P, Q, R, S, T and U (Figure 2.2). Each wave
represents depolarization (‘electrical discharging’) or repolarization (‘electrical recharging’) of a certain
region of the heart. This is discussed in more detail in the rest of this chapter.
The voltage changes detected by ECG machines are very small, being of the order of millivolts. The size of
each wave corresponds to the amount of voltage generated by the event that created it: the greater the voltage,
the larger the wave (Figure 2.3).
The ECG also allows you to calculate how long an event lasted. The speed at which ECG paper moves
through the machine is standardized at a constant rate of 25 mm/s, so each small (1 mm) square on the ECG
represents 0.04 s, and each large (5 mm) square represents 0.2 s. This means that by measuring the width
of a wave, you can calculate the duration of the event causing it. For example, the P waves in Figure 2.4 are
2.5 mm wide, so we can calculate that atrial depolarization lasted for 2.5 × 0.04 s, or 0.10 s.

7

8    Making Sense of the ECG

II
Figure 2.1
Key points:

‘Tense’

‘Relaxed’

Skeletal muscle artefact.
• An ECG from a relaxed patient is much easier to interpret.
• Electrical interference (irregular baseline) is present when the patient is tense, but the recording is
much clearer when the patient relaxes.

R

T
P

U

Q S
Figure 2.2

Standard nomenclature of the ECG recording.

Key point:

• The waves are called P, Q, R, S, T and U.

Small voltage
for atrial depolarization

Large voltage
for ventricular depolarization

II

Figure 2.3
Key point:

The size of a wave reflects the voltage that caused it.
• P waves are small (atrial depolarization generates little voltage); QRS com­plexes are larger (ventricular
depolarization generates a higher voltage).

HOW DOES THE ECG ‘LOOK’ AT THE HEART?
To make sense of the ECG, one of the most important concepts to understand is that of the ‘lead’. This is a
term you will often see, and it does not refer to the wires that connect the patient to the ECG machine (which
we will always refer to as ‘electrodes’ to avoid confusion).
In short, ‘leads’ are different viewpoints of the heart’s electrical activity. An ECG machine uses the
information it collects via its four limb and six chest electrodes to compile a comprehensive picture of the
electrical activity in the heart as observed from 12 different viewpoints, and this set of 12 views or leads
gives the 12-lead ECG its name.

PQRST: Where the waves come from   9

1 second

II

Duration of atrial depolarization
= 0.10 seconds
1 large square =
0.2 seconds

Figure 2.4
Key points:

1 small square =
0.04 seconds

The width of a wave reflects an event’s duration.
• The P waves are 2.5 mm wide.
• At a paper speed of 25 mm/s, atrial depolarization therefore took 0.10 s.

Each lead is given a name (I, II, III, aVR, aVL, aVF, V1, V2, V3, V4, V5 and V6) and its position on a 12-lead
ECG is usually standardized to make pattern recognition easier.
So what viewpoint does each lead have of the heart? Information from the four limb electrodes is used by
the ECG machine to create the six limb leads (I, II, III, aVR, aVL and aVF). How the machine does this is
discussed in Chapter 3. For now, you just need to know that each limb lead ‘looks’ at the heart from the side
(the frontal or ‘coronal’ plane), and the view that each lead has of the heart in this plane depends on the
lead in question (Figure 2.5).

ECG LEAD NOMENCLATURE
There are several ways of categorizing the 12 ECG leads. They are often referred to as limb leads
(I, II, III, aVR, aVL, aVF) and chest leads (V1, V2, V3, V4, V5, V6). They can also be divided into bipolar
leads (I, II, III) or unipolar leads (aVR, aVL, aVF, V1, V2, V3, V4, V5, V6).
Bipolar leads are generated by measuring the voltage between two electrodes – for example,
lead I measures the voltage between the left arm electrode and the right arm electrode. Unipolar
leads measure the voltage between a single positive electrode and a ‘central’ point of reference
generated from the other electrodes – for example, lead aVR uses the right arm electrode as the
positive pole and a combination of left arm and left leg electrodes as the negative pole.

As you can see from Figure 2.5, lead aVR looks at the heart from the approxi­mate viewpoint of the patient’s
right shoulder, whereas leads I and aVL have a left lateral view of the heart, and leads II, III and aVF look at
the inferior surface of the heart.
The view that each limb lead has of the heart is more formally represented in the hexaxial diagram
(Figure 2.6), which shows the angle that each limb lead has in rela­tion to the heart. This diagram is invaluable
when performing axis calculations, and how to use the diagram is described during the discussion of the
cardiac axis in Chapter 10.

10    Making Sense of the ECG

aVR
aVL

I

III
Figure 2.5
Key point:

aVF

II

The viewpoint each limb lead has of the heart.
• The limb leads ‘look’ at the heart in the frontal (or ‘coronal’) plane, and each limb lead looks at the heart
from a different angle.

–90°
–60°

–120°

–30°
aVL

–150°
aVR

0°
I

±180°

+150°

+30°

+120°
III

Figure 2.6
Key point:

+90°
aVF

+60°
II

Hexaxial diagram.
• This shows the angle of view that each limb lead has of the heart.

The six chest leads (V1–V6) look at the heart in a horizontal (‘transverse’) plane from the front and around the
side of the chest (Figure 2.7). The region of myocardium surveyed by each lead therefore varies according to
its vantage point – leads V1–V4 have an anterior view, for example, whereas leads V5–V6 have a lateral view.
Once you know the view each lead has of the heart, you can tell whether the electri­cal impulses in the heart
are flowing towards that lead or away from it. This is simple to work out, because electrical current flowing
towards a lead produces an upward (positive) deflection on the ECG, whereas current flowing away causes
a downward (negative) deflection (Figure 2.8).

PQRST: Where the waves come from   11

V1

V2
V3
V4

V6
V5 V6

V5

V1

Figure 2.7
Key point:

V2

V3

V4

The viewpoint each chest lead has of the heart.
• Each chest lead looks at the heart from a different viewpoint in the horizontal (‘transverse’) plane.

tion

tion
Direction of current

Figure 2.8
Key point:

Po

tion

The direction of an ECG deflection depends on the direction of the current.
• Flow towards a lead produces a positive deflection, flow away from a lead produces a negative
deflection and flow perpendicular to a lead produces a positive then a negative (equipolar or isoelectric)
deflection.

The origin of each wave will be discussed shortly, but just as an example consider the P wave, which represents
atrial depolarization. The P wave is positive in lead II because atrial depolarization flows towards that lead,
but it is nega­tive in lead aVR because this lead looks at the atria from the opposite direction (Figure 2.9).
In addition to working out the direction of flow of electrical current, knowing the viewpoint of each lead
allows you to determine which regions of the heart are affected by, for example, a myocardial infarction.
Infarction of the inferior surface will produce changes in the leads looking at that region, namely leads II,
III and aVF (Figure 2.10). An anterior infarction produces changes mainly in leads V1–V4 (Figure 2.11).

WHERE DO EACH OF THE WAVES COME FROM?
As we saw in Chapter 1, each normal heartbeat begins with the discharge (‘depolarization’) of the sinoatrial
(SA) node, high up in the right atrium. This is a spontaneous event, occurring 60–100 times every minute.
Depolarization of the SA node does not cause any noticeable wave on the standard ECG (although it can
be seen on specialized intracardiac recordings). The first detectable wave appears when the impulse spreads
from the SA node to depolarize the atria (Figure 2.12). This produces the P wave.

12    Making Sense of the ECG

Lead aVR

Lead II

The orientation of the P wave depends on the lead.

Figure 2.9

• P waves are normally upright in lead II and inverted in lead aVR.

Key point:

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

II

Figure 2.10
Key points:

An inferior myocardial infarction produces changes in the inferior leads.
• Leads II, III and aVF look at the inferior surface of the heart.
• ST segment elevation is present in these leads (acute inferior myocardial infarction).
• There is also reciprocal ST segment depression in leads I and aVL.

The atria contain relatively little muscle, so the voltage generated by atrial depolarization is relatively small.
From the viewpoint of most leads, the electricity appears to flow towards them, and so the P wave will be a
positive (upward) deflection. The exception is lead aVR, where the electricity appears to flow away, and so
the P wave is negative in that lead (see Figure 2.9).
After flowing through the atria, the electrical impulse reaches the atrioventricular (AV) node, low in the
right atrium. Activation of the AV node does not produce an obvious wave on the ECG, but it does contribute
to the time interval between the P wave and the subsequent Q or R wave. It does this by delaying conduction,
and in doing so acts as a safety mechanism, preventing rapid atrial impulses (for instance during atrial
flutter or fibrillation) from spreading to the ventricles at the same rate.
The time taken for the depolarization wave to pass from its origin in the SA node, across the atria, and
through the AV node into ventricular muscle is called the PR interval. This is measured from the beginning
of the P wave to the beginning of the R wave and is normally between 0.12 s and 0.20 s, or 3 to 5 small squares
on the ECG paper (Figure 2.13).

PQRST: Where the waves come from   13

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

II

Figure 2.11
Key points:

An anterolateral myocardial infarction produces changes in the anterolateral leads.
• Leads V 3 –V6, I and aVL look at the anterolateral surface of the heart.
• ST segment elevation is present in these leads.

Atrial depolarization

P wave

Figure 2.12
Key point:

The P wave.
• The P wave corresponds to atrial depolarization.

Once the impulse has traversed the AV node, it enters the bundle of His which then divides into left and
right bundle branches as it passes into the interventricular septum (Figure 2.14). Current normally flows
between the bundle branches in the interventricular septum, from left to right, and this is responsible for
the first deflection of the QRS complex. Whether this is a downward deflection or an upward deflection
depends on which side of the septum a lead is ‘looking’ from (Figure 2.15).
By convention, if the first deflection of the QRS complex is downward, it is called a Q wave. The first upward
deflection is called an R wave, whether or not it follows a Q wave. A downward deflection after an R wave
is called an S wave. Hence, a variety of complexes is possible (Figure 2.16).

14    Making Sense of the ECG

Figure 2.13
Key point:

The PR interval.
• The PR interval is normally 0.12–0.20 s long.

Sinoatrial
node

Atrioventricular
node

Figure 2.14
Key point:

Left bundle
branch

Right bundle
branch

Anterior
fascicle

Posterior
fascicle

The right and left bundle branches.
• The bundle of His divides into the right and left bundle branches in the interventricular septum.

V1

V6

Septal
depolarization
Figure 2.15 Septal depolarization.
Key point:

• The septum normally depolarizes from left to right.

PQRST: Where the waves come from   15

R

S

Q

R

R

S

Q

S

Figure 2.16 The different varieties of QRS complex.
Key point:

• The first downward deflection is a Q wave, the first upward deflection is an R wave and a downward
defection after an R wave is an S wave.

The right bundle branch conducts the wave of depolarization to the right ventricle, whereas the left bundle
branch divides into anterior and posterior fascicles that conduct the wave to the left ventricle (Figure 2.17).
The conducting pathways end by dividing into Purkinje fibres that distribute the wave of depolarization
rapidly throughout both ventricles. The depolarization of the ventricles, represented by the QRS complex,
is normally complete within 0.12 s (Figure 2.18). QRS complexes are ‘positive’ or ‘negative’, depending on
whether the R wave or the S wave is bigger (Figure 2.19). This, in turn, will depend on the view each lead
has of the heart.
The left ventricle contains considerably more myocardium than the right, and so the voltage generated by
its depolarization will tend to dominate the shape of the QRS complex.
Leads that look at the heart from the right will see a relatively small amount of voltage moving towards
them as the right ventricle depolarizes and a larger amount moving away with depolarization of the left

Left bundle
branch

Atrioventricular
node

Right bundle
branch

Anterior
fascicle

Posterior
fascicle

Figure 2.17 Divisions of the left bundle branch.
Key point:

• The left bundle branch divides into anterior and posterior fascicles.

16    Making Sense of the ECG

Ventricular
depolarization

QRS complex
Figure 2.18
Key point:

The QRS complex.
• The QRS complex cor­responds to ventricular depolarization.

Positive
Figure 2.19
Key point:

Negative

Equipolar

Polarity of the QRS complexes.
• A dominant R wave means a positive QRS complex, a dominant S wave means a negative QRS
complex, and equal R and S waves mean an equipolar (isoelectric) QRS complex.

V1

R

V6
R
Q

S

S

Figure 2.20
Key point:

The shape of the QRS complex depends on the lead’s viewpoint.
• Right-sided leads have negative QRS complexes, and left-sided leads have positive QRS complexes.

ventricle. The QRS complex will therefore be dominated by an S wave and be negative. Conversely, leads
looking at the heart from the left will see a relatively large voltage moving towards them, and a smaller
voltage moving away, giving rise to a large R wave and only a small S wave (Figure 2.20). Therefore, there is
a gradual transition across the chest leads, from a predominantly negative QRS complex to a predominantly
positive one (Figure 2.21).

PQRST: Where the waves come from   17

V1

V4

V2

V5

V3

V6

Figure 2.21
Key point:

Transition in QRS complexes across the chest leads.
• QRS complexes are normally negative in leads V1 and V2 and positive in leads V 5 and V6.

The ST segment is the transient period in which no more electrical current can be passed through the
myocardium. It is measured from the end of the S wave to the beginning of the T wave (Figure 2.22). The ST
segment is of particular interest in the diagnosis of myocardial infarction and ischaemia (see Chapter 15).
The T wave represents repolarization (‘recharging’) of the ventricular myocardium to its resting electrical
state. The QT interval measures the total time for activation of the ventricles and recovery to the normal
resting state (Figure 2.23).

ST segment

Figure 2.22

The ST segment.

18    Making Sense of the ECG

T wave

0.39 seconds

Figure 2.23

The T wave and QT interval.

The origin of the U wave is uncertain, but it may represent repolarization of the interventricular septum or
slow repolarization of the ventricles. U waves can be difficult to identify but, when present, they are most
clearly seen in the anterior chest leads V2–V3 (see Chapter 18, Figure 18.2).
You need to be familiar with the most important electrical events that make up the cardiac cycle. These are
summarized at the end of the chapter.
SUMMARY
The waves and intervals of the ECG correspond to the following events:
ECG event
P wave
PR interval
QRS complex
ST segment
T wave
QT interval
U wave

Note:

Cardiac event
Atrial depolarization
Start of atrial depolarization to start of ventricular depolarization
Ventricular depolarization
Pause in ventricular electrical activity before repolarization
Ventricular repolarization
Total time taken by ventricular depolarization and repolarization
Uncertain – possibly:
• Interventricular septal repolarization
• Slow ventricular repolarization

Depolarizations of the SA and AV nodes are important events but do not in
­themselves produce a detectable wave on the standard ECG.

Further reading
Blakeway E, Jabbour RJ, Baksi J et al. ECGs: Colour-coding for initial training. Resuscitation 2012; 83: e115–e116.
Hurst JW. Naming of the waves in the ECG, with a brief account of their genesis. Circulation 1998; 98: 1937–1942.

Chapter 3
Performing an ECG recording

This guide to performing a standard 12-lead ECG recording is based upon the current clinical guidelines
of the Society for Cardiological Science and Technology in the United Kingdom (see ‘Further Reading’).
Anyone performing a 12-lead ECG recording should have received appropriate training and been assessed
in their skills by a competent practitioner.

INITIAL PREPARATIONS
Before making a 12-lead ECG recording, check that the ECG machine is safe to use and has been cleaned
appropriately. Before you start, ensure you have an adequate supply of:

• Recording paper
• Skin preparation equipment
• Electrodes

Introduce yourself to the patient and confirm their identity. Explain what you plan to do and why, and
ensure that they consent to undergoing the ECG recording.
The 12-lead ECG should be recorded with the patient in a semi-recumbent position (approximately 45°) on a
couch or bed in a warm environment, while ensuring that the patient is comfortable and able to relax. This is
not only important for patient dignity, but also helps to ensure a high-quality recording with minimal artefact.

Skin preparation
In order to apply the electrodes, the patient’s skin needs to be exposed across the chest, the arms and the
lower legs. Ensure that you follow your local chaperone policy, and offer the patient a gown to cover any
exposed areas once the electrodes are applied.
To optimize electrode contact with the patient’s skin and reduce ‘noise’, consider the following tips:

• Removal of chest hair
•

•

It may be necessary to remove chest hair in the areas where the electrodes are to be applied. Ensure
the patient consents to this before you start. Carry a supply of disposable razors on your ECG cart
for this purpose.
Light abrasion
Exfoliation of the skin using light abrasion can help improve electrode contact. This can be achieved
using specially manufactured abrasive tape or by using a paper towel.

•

19

20    Making Sense of the ECG

• Skin cleansing
•

•

An alcohol wipe helps to remove grease from the surface of the skin, although this may be better
avoided if patients have fragile or broken skin.
Electrode placement
Correct placement of ECG electrodes is essential to ensure that the 12-lead ECG can be interpreted
correctly. Electrode misplacement is a common occurrence, reported in 0.4% of ECGs recorded in
the cardiac outpatient clinic and 4.0% of ECGs recorded in the intensive care unit.

•

The standard 12-lead ECG consists of:

• Three bipolar limb leads (I, II and III)
• Three augmented limb leads (aVR, aVL and aVF)
• Six chest (or ‘precordial’) leads (V –V )
1

6

As we saw in Chapter 2, these 12 leads are generated using 10 ECG electrodes, 4 of which are applied to the
limbs and 6 of which are applied to the chest. The ECG electrodes are colour coded; however, two different
colour-coding systems exist internationally. In Europe, the International Electrotechnical Commission
(IEC) system uses the following colour codes:
Right arm
Left arm
Right leg
Left leg
Chest V1
Chest V2
Chest V3
Chest V4
Chest V5
Chest V6

Red
Yellow
Black
Green
White/red
White/yellow
White/green
White/brown
White/black
White/violet

To help you in placing the limb electrodes, remember the mnemonic ‘Ride Your Green Bike’. Start by
attaching the red (‘Ride’) electrode on the patient’s right arm, then move around the patient’s torso clockwise,
attaching the yellow (‘Your’) electrode on the left arm, then the green (‘Green’) electrode on the left leg, and
finally the black (‘Bike’) electrode on the right leg.
In the United States the American Heart Association (AHA) system uses a different set of colour codes:
Right arm
Left arm
Right leg
Left leg
Chest V1
Chest V2
Chest V3
Chest V4
Chest V5
Chest V6

White
Black
Green
Red
Brown/red
Brown/yellow
Brown/green
Brown/blue
Brown/orange
Brown/purple

PLACEMENT OF THE LIMB ELECTRODES
The four limb electrodes should be attached to the forearms and lower legs just proximal to the wrist and
ankle (Figure 3.1). If the electrodes have to be placed in a more proximal position on the limb (perhaps
because of leg ulcers or a previous amputation), this should be noted on the ECG recording. Placing the limb

Performing an ECG recording   21

LA

RA

RL

Figure 3.1
Key point:

LL

Placement of the limb electrodes.
• The electrodes are placed on the right arm (RA), left arm (LA), right leg (RL) and left leg (LL).

electrodes more proximally on the limbs can alter the appearance of the ECG, and it is therefore important
that the person interpreting the recording is aware that an atypical electrode position has been used.

PLACEMENT OF THE CHEST (PRECORDIAL) ELECTRODES
The six chest electrodes should be positioned on the chest wall as shown in Figure 3.2. Common errors, which
should be avoided, include placing electrodes V1 and V2 too high and V5 and V6 too low. The correct locations are:
Chest V1
Chest V2
Chest V3
Chest V4
Chest V5
Chest V6

4th intercostal space, right sternal edge
4th intercostal space, left sternal edge
Midway in between V2 and V4
5th intercostal space, mid-clavicular line
Left anterior axillary line, same horizontal level as V4
Left mid-axillary line, same horizontal level as V4 and V5

As with the limb electrodes, any variation from the standard locations should be noted on the ECG recording
to avoid misinterpretation.
The simplest way to count the rib spaces is to begin by finding the angle of Louis, the horizontal bony ridge
part way down the sternum. Run a finger down from the top of the sternum until you feel this ridge, and
then run your finger sideways and slightly downward to the patient’s right until you reach a space between
the ribs and the right-hand edge of the sternum – this is the 2nd intercostal space. Count down the rib spaces
with your fingers to the 3rd and then the 4th intercostal space, and this is where you place electrode V1. The
equivalent space at the left sternal edge is the location for electrode V2.

22    Making Sense of the ECG

Mid-clavicular line

Anterior
axillary line
1

Figure 3.2

2

3

4

5

6

Mid axillary
line

Placement of the chest (precordial) electrodes.

Next, staying to the left of the sternum, count down to the 5th intercostal space and find the mid-clavicular
line – this is the location for electrode V4. Electrode V3 can then be positioned midway between V2 and V4.
Then, move horizontally from electrode V4 to the patient’s left until you reach the anterior axillary line. This
is the location for electrode V5. It is important to ensure that you do not follow the rib space round to V5, but
stay horizontal. Finally, remaining in a horizontal line with V4, place electrode V6 in the mid-axillary line.
FEMALE PATIENTS
Placement of the chest electrodes can sometimes pose difficulties in female patients because of the
left breast. By convention, the electrodes V4 –V6 are placed underneath the left breast.

In some situations, principally when a posterior myocardial infarction is suspected, it is helpful to obtain
an ECG recording using electrodes placed around the posterior of the patient’s chest. In this case, the V4,
V5 and V6 electrodes are repositioned to become V7, V8 and V9 electrodes as follows:
Chest V7
Chest V8
Chest V9

Left posterior axillary line, same horizontal level as V4
Left mid-scapular line, same horizontal level as V4
Left spinal border, same horizontal level as V4

As always when using non-standard electrode positions, be sure to annotate the ECG so that it is clear which
lead is which.

EINTHOVEN’S TRIANGLE
Before we record the ECG, it is worth pausing for a moment to consider how the electrodes we have attached
actually make the recording. As this is a little complicated, you can, if you wish, skip this section for now
and move on to ‘Recording the 12-Lead ECG’.

Performing an ECG recording   23

Right arm
–

Left arm
+

Lead I

–

–

Lead II

Lead III

+

+

Left leg

Figure 3.3 Einthoven’s triangle, formed by the placement of the right arm (RA), left arm (LA) and left leg (LL) electrodes.

If we consider the three bipolar limb leads I, II and III to begin with, these are generated by the ECG machine
using various pairings of the left arm (LA), right arm (RA) and left leg (LL) electrodes (Figure 3.3). The three
limb leads are called ‘bipolar’ leads because they are generated from the potential difference between pairs
of these limb electrodes:

• Lead I is recorded using RA as the negative pole and LA as the positive pole.
• Lead II is recorded using RA as the negative pole and LL as the positive pole.
• Lead III is recorded using LA as the negative pole and LL as the positive pole.

If you measure the potential differences in each of these three limb leads at any one moment, they are linked
by the equation:
II = I + III
In other words, the net voltage in lead II will always equal the sum of the net voltages in leads I and III.
This is known as Einthoven’s law. You can see this in action in Figure 3.4. In this ECG:

• The R wave in lead I measures 5 mm, with no significant S wave, giving a net size of 5 mm (or 0.5 mV).
• The R wave in lead III measures 3.5 mm, with an S wave of 2.5 mm, giving a net size of 1 mm (or 0.1 mV).
Using Einthoven’s law:
II = I + III
II = 0.5 mV + 0.1 mV
II = 0.6 mV
If you look at lead II in Figure 3.4, there is an R wave of 8 mm and an S wave of 2 mm, so the net size of the
QRS complex is, as we predicted, 6 mm (or 0.6 mV).

24    Making Sense of the ECG

I

II

III

Figure 3.4 Leads I, II and III.
Key point:

• According to Einthoven’s law, the net voltage in lead II will always equal the sum of the net voltages
in leads I and III.
I

–

+
–

–

II

III

+

Figure 3.5

+

Einthoven’s triangle, simplified as an equilateral triangle.
–

–

–

+ I

+
III

Figure 3.6

+
II

Einthoven’s triangle, with all three vectors centred on the same point.

Einthoven’s triangle, as represented in Figure 3.3, can be simplified and repre­sented as in Figure 3.5. This
can be further represented as in Figure 3.6, with the vectors all centred on the same point, which makes it
clearer as to how leads I, II and III achieve their ‘view’ of the heart. Compare this to the hexaxial diagram
in Figure 2.6 (see Chapter 2), and it should now be a little easier to visualize how the limb electrodes RA,
LA and LL relate to the leads I, II and III, and how these leads’ views of the heart come about.

Performing an ECG recording   25

aVR

+

+

aVL

+
aVF
Figure 3.7 Leads aVR, aVL and aVF, represented diagrammatically.

What about the other three limb leads, aVR, aVL and aVF? These leads are generated in a similar way to
leads I, II and III. However, this time two of the electrodes are combined to form the negative pole, and the
other electrode acts as the positive pole. Hence:

• Lead aVR is recorded using LA+LL as the negative pole and RA as the positive pole.
• Lead aVL is recorded using RA+LL as the negative pole and LA as the positive pole.
• Lead aVF is recorded using RA+LA as the negative pole and LL as the positive pole.

Figure 3.7 shows how these three leads can be represented diagrammatically, with regard to their vectors
and therefore their views of the heart. Again, this corresponds to the angles shown in the hexaxial diagram
in Figure 2.6.
What about the chest leads, V1–V6? For these leads, the negative pole is generated by combining the
electrodes RA, LA and LL. This combination of all three limb electrodes – which is known as Wilson’s
central terminal – gives the average potential across the body, which approximates to zero. Each of the six
chest leads uses the relevant chest electrode as a positive pole to measure the potential difference.

THE RIGHT LEG ELECTRODE
You may have noticed that the right leg electrode (RL) hasn’t been featured so far in the discussion
about how the ECG leads are generated. So what does the RL electrode actually do? RL is used by
the ECG machine as a ‘reference’ electrode to help reduce unwanted ‘noise’ during the recording.

RECORDING THE 12-LEAD ECG
Ensure that the patient’s name and other relevant identification details (e.g. date of birth, hospital number)
have been entered into the ECG and that the machine is displaying the correct date and time. Encourage the
patient to relax while the recording is being made, and check that the patient is lying still and not clenching
their muscles.
Do not use a filter for the initial recording; however, if necessary, the recording can be repeated with the
filter switched on if the initial recording shows ‘noise’.

26    Making Sense of the ECG

ECG MACHINE FILTERS
ECG machines offer a number of types of filters to try to improve the quality of the ECG signal.
A low-frequency filter (also known as a high-pass filter) is used to filter out low-frequency signals,
typically anything less than 0.05 Hz, to reduce baseline drift. A high-frequency (or low-pass) filter is
used to filter out high-frequency signals, typically anything over 100 Hz, to reduce interference from
skeletal muscle. A ‘notch’ filter is specifically designed to filter out noise at a specific frequency and
can be used to reduce electrical alternating current ‘hum’ at 50 or 60 Hz. While filtering can improve
the appearance of the ECG, it can also introduce distortion, particularly of the ST segments, and
thus should only be used when necessary. For this reason, ECGs should always initially be recorded
with the filters off and repeated with the filters on only if needed.

Make the ECG recording at a paper speed of 25 mm/s and a gain setting of 10 mm/mV. If, however, the ECG
contains high-voltage complexes (as in left ventricular hypertrophy,), repeat the recording at a gain setting
of 5 mm/mV (ensuring that this is clearly marked on the ECG).
Once the recording has been made, check that it is of good quality and ensure that all the patient details
are correctly shown on it. If the patient was experiencing any symptoms at the time of the recording
(such as chest pain or palpitations), note this on the recording, as such information can prove very useful
diagnostically. If the patient was experiencing symptoms during the recording, or if the recording shows
any clinically urgent abnormalities, report this information to a more senior staff member as appropriate.
Once you are satisfied with the ECG recording, detach the electrodes from the patient and assist them in
getting dressed. Ensure that the materials used during the recording are disposed of safely and appropriately.
ECG RECORDINGS IN DEXTROCARDIA
In dextrocardia, the heart is located on the right side of the chest rather than on the left . Dextrocardia
is suggested by poor R wave progression across the chest leads and by P wave inversion in lead I. If a
patient has known or suspected dextrocardia, repeat the recording with the chest electrodes positioned
in a mirror image on the right side of the chest. Ensure the ECG is labelled clearly with V3R, V4R, etc. to
demonstrate that right-sided chest electrodes have been used. The limb electrodes are usually left in their
standard positions, as this helps to ‘flag up’ the apparent dextrocardia on the ECG, but if you do prefer
to reverse the limb electrodes too, then it is essential to label the reversed limb leads clearly on the ECG.
Ensure that copies of both ECGs (the standard one and the one with right-sided electrodes) are retained.

SUMMARY
To record an optimal 12-lead ECG:

•
•
•

•
•
•
•
•

Explain the procedure to the patient and obtain their consent.
Ensure the patient is comfortable.
Prepare the skin before applying the electrodes.
• Removal of chest hair
• Light abrasion
• Skin cleansing
Place the electrodes correctly.
Only use ECG filters where necessary, and note this on the ECG.
Check that the ECG recording is of good quality.
Label the ECG recording appropriately.
Ensure that any clinically urgent abnormalities are acted upon.

Performing an ECG recording   27

Further reading
Campbell B, Richley D, Ross C, Eggett CJ. Clinical guidelines by consensus: Recording a standard 12-lead
electrocardiogram. An approved method by the Society for Cardiological Science and Technology (SCST). 2017.
Available for download from www.scst.org.uk.
Kligfield P, Gettes LS, Bailey JJ et al. AHA/ACCF/HRS recommendations for the standardization and interpretation
of the electrocardiogram: Part I: The electrocardiogram and its technology. J Am Coll Cardiol 2007; 49: 1109–1127.
Macfarlane PW, Coleman EN. Resting 12 lead ECG electrode placement and associated problems. 1995. Published by
The Society for Cardiological Science and Technology. Available for download from http://www.scst.org.uk.
Rudiger A, Hellermann JP, Mukherjee R et al. Electrocardiographic artifacts due to electrode misplacement and their
frequency in different clinical settings. Am J Emerg Med 2007; 25: 174–178.

Chapter 4
Reporting an ECG recording

The reporting of an ECG recording is best done in a methodical manner to ensure that the report is
comprehensive and doesn’t overlook any potentially important details. In this chapter is a systematic
overview of how to approach a 12-lead ECG, and all of these points will be expanded upon in the chapters
that follow.
Your everyday reports may not need to be as detailed as the one presented at the end of this chapter, but it
is nonetheless good practice to have a thorough ‘mental checklist’ to work through as you review an ECG
to ensure that all the key findings are covered.

PATIENT DATA
Begin by checking key information on the ECG and/or request form relating to the patient:

• Patient name
• Date of birth
• Identification number (e.g. hospital number)
• Reason for the request
• Relevant past medical history
• Relevant medication
TECHNICAL DATA

Next, report on technical data pertaining to the recording, namely:

• Date and time of recording
• Paper speed and calibration
• Technical quality
• Any atypical settings
• Additional leads (e.g. posterior leads, right-sided chest leads)
• Physiological manoeuvres (e.g. ECG recorded during deep inspiration)
• Diagnostic or therapeutic manoeuvres (e.g. ECG recorded during carotid sinus massage)

29

30    Making Sense of the ECG

ECG FUNDAMENTALS
Next, report on the fundamental features of the ECG recording itself, namely:

• Rate
• Rhythm
•

•
•
•

Supraventricular
Ventricular
Conduction problems
Axis

ECG DETAILS
Next, review the individual features of the ECG using a step-by-step approach. Describe:

• P wave
• PR interval
• Q wave
• QRS complex
• ST segment
• T wave
• QT interval
• U wave

Don’t overlook any additional waves or deflections, such as pacing spikes, delta waves or J waves (Osborn
waves). It’s not usually necessary to describe ‘secondary’ features that are implicit in a ‘primary’ abnormality –
for instance, if you state that the ECG shows left bundle branch block, then you wouldn’t need to describe
the individual ST segment or T wave changes that normally accompany left bundle branch block.

REPORT SUMMARY
End your report with a summary of the key ECG findings, placing them where possible in the context
of the clinical information provided. Finally, your report should include your name, job title and (where
applicable) professional registration number.
Your complete report may read like this:
This 12-lead ECG was performed on Mr John Smith, born on 1 January 1950, hospital number
123456. The request form states that the patient is experiencing breathlessness and irregular
palpitations. He has a history of inferior myocardial infarction in 2011. He is currently taking aspirin,
simvastatin, bisoprolol and ramipril.
The recording was performed on 1 August 2013, using a paper speed of 25 mm/s and a calibration
of 10 mm/mV. The recording is of good quality with no artefact.
The ventricular rate is tachycardic at 114/min. The rhythm is atrial fibrillation, as evidenced by no
co-ordinated atrial activity and irregularly irregular QRS complexes. The QRS axis is normal at +64°.
The P waves are absent and so the PR interval cannot be measured. There are deep Q waves and
inverted T waves in the inferior leads. The remainder of the QRS complexes are unremarkable. The
ST segments are normal. The QT interval is normal (QTc measures 428 ms). There are no U waves
present.

Reporting an ECG recording   31

In conclusion, this 12-lead ECG shows:

•
•

Atrial fibrillation with a fast ventricular rate (114/min)
Inferior Q waves and T wave inversion, consistent with an old inferior myocardial infarction

Reported by: Dr AN Other, Consultant Cardiologist, Registration no. 123456

If you have old ECGs for comparison, you may wish to include details of any rele­vant changes in the ECG in
your report (e.g. new evidence of myocardial infarction, new conduction problems, changes in rhythm, etc.).
SUMMARY
To report a 12-lead ECG, review the following features:

•

•

•

•

Patient data
• Patient name
• Date of birth
• Identification number (e.g. hospital number)
• Reason for the request
• Relevant past medical history
• Relevant medication
Technical data
• Date and time of recording
• Paper speed and calibration
• Technical quality
• Any non-standard settings
ECG fundamentals
• Rate
• Rhythm
• Axis
ECG details
• P wave
• PR interval
• Q wave
• QRS complex
• ST segment
• T wave
• QT interval
• U wave
• Additional features (e.g. pacing spikes, delta waves, J waves)

Conclude your ECG report with a summary of the key findings and your own professional identification
details.

Further reading
Mason JW, Hancock EW, Gettes LS. AHA/ACCF/HRS recommendations for the standardization and interpretation of
the electrocardiogram: Part II: Electrocardiography diagnostic statement list. J Am Coll Cardiol 2007; 49: 1128–1135.
Richley D, Gunney H. Clinical guidelines by consensus: ECG reporting standards and guidance. An approved method
by the Society for Cardiological Science and Technology (SCST). 2019. Available for download from www.scst.org.uk.

Chapter 5
Heart rate

Measurement of the heart rate and the identification of the cardiac rhythm go hand in hand, as many
abnormalities of heart rate result from arrhythmias. The following chapters discuss in detail how to identify
the cardiac rhythm. To begin, however, ways to measure the heart rate and the abnormalities that can affect
it will be described.
When we talk of measuring the heart rate, we usually mean the ventricular rate, which corresponds to the
patient’s pulse. Depolarization of the ventricles produces the QRS complex on the ECG, and so it is the rate
of QRS complexes that needs to be measured to determine the heart rate.
Measurement of the heart rate is simple and can be done in several ways. However, before you try to measure
anything, check that the ECG has been recorded at the standard UK and US paper speed of 25 mm/s. If so,
then all you have to remember is that a 1-min ECG tracing covers 300 large squares. If the patient’s rhythm
is regular, all you have to do is count the number of large squares between two consecutive QRS complexes,
then divide it into 300.
For example, in Figure 5.1 there are approximately 4 large squares between each QRS complex. Therefore:
Heart rate =

300
= 75/min
4

An alternative, and slightly more accurate, method is to count small squares rather than big ones. For this
method, you need to remember than a 1-min ECG tracing covers 1500 small squares. Count the number
of small squares between two consecutive QRS complexes, and divide it into 1500.
Using the ECG in Figure 5.1, there are 21 small squares between each QRS complex. Therefore:
Heart rate =

1500
= 71/min
21

This method does not work so well when the rhythm is irregular, as the number of squares between each
QRS complex varies from beat to beat. So, instead, count the number of QRS complexes in 50 large squares
(Figure 5.2) – the length of the rhythm strip on a standard ECG. This is the number of QRS complexes in
10 s. To work out the rate/min, simply multiply by 6:
Number of QRS complexes in 50 large squares = 19
Therefore, number of QRS complexes in 10 s = 19
Therefore, number of QRS complexes/min = 19 × 6 = 114
33

34    Making Sense of the ECG

I

aVR

II

V5

V2

aVL

aVF

III

V4

V1

V6

V3

II

Figure 5.1 Calculating heart rate when the rhythm is regular.
• There are approximately 4 large squares between each QRS complex, corresponding to a heart rate
of approximately 75/min.
• More precisely, there are 21 small squares between each QRS complex, giving a more accurate heart
rate of 71/min.

Key points:

An ECG ruler can be helpful, but follow the instructions on it carefully. Some ECG machines will calculate
heart rate and print it on the ECG, but always check machine-derived values, as the machines do occasionally
make errors!
Whichever method you use, remember it can also be used to measure the atrial or P wave rate as well as
the ventricular or QRS rate. Normally, every P wave is followed by a QRS complex, and so the atrial and
I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

II

Figure 5.2
Key point:

Calculating heart rate when the rhythm is irregular.
• There are 19 QRS complexes in 50 large squares (10 s), corresponding to a heart rate of 114/min.

Heart rate   35

Lead II

Figure 5.3
Key point:

The P wave rate can differ from the QRS complex rate.
• This rhythm strip shows third-degree AV block, with a P wave (atrial) rate of 94/min and a QRS complex
(ventricular) rate of 33/min.

ventricular rates are the same. However, the rates can be different if, for example, some or all of the P waves
are prevented from activating the ventricles (Figure 5.3). Situations where this may happen are described
in later chapters.
Once you have measured the heart rate, you need to decide whether it is normal or abnormal. As a general
rule, a heart rate between 60 and 100/min is normal. If the rate is below 60/min, the patient is said to be
bradycardic. With a heart rate above 100/min, the patient is tachycardic. Therefore, the two questions you
need to ask about heart rate are:

• Is the heart rate below 60/min?
• Is the heart rate above 100/min?

If the answer to either question is yes, turn to the appropriate half of this chapter to find out what to do next.
If not, turn to Chapter 6 to start your identification of the cardiac rhythm.

IS THE HEART RATE BELOW 60/MIN?
Bradycardia is arbitrarily defined as a heart rate below 60/min. Identification of the cardiac rhythm and
any conduction disturbances is essential, and this is discussed in the following chapters.
Problems to consider in the bradycardic patient are:

• Sinus bradycardia
• Sick sinus syndrome
• Second-degree and third-degree atrioventricular (AV) block
• ‘Escape’ rhythms
• AV junctional escape rhythm
• Ventricular escape rhythms
• Asystole
Sinus bradycardia can be normal, for example in athletes or during sleep, but in others it may indicate an
underlying problem. The differential diagnosis and treat­ment are discussed in Chapter 7.
Sick sinus syndrome is the coexistence of sinus bradycardia with episodes of sinus arrest and sinoatrial
block. Patients may also have episodes of paroxysmal tachycardia, giving rise to tachy-brady syndrome.
In second-degree AV block some atrial impulses fail to be conducted to the ventricles, and this can lead
to bradycardia. In third-degree AV block, no atrial impulses can reach the ventricles; in response, the
ventricles usually develop an ‘escape’ rhythm (see next). It is important to remember that AV block can
coexist with any atrial rhythm.
Escape rhythms are a form of ‘safety net’ to maintain a heart beat if the normal mechanism of impulse
generation fails or is blocked. They may also appear during episodes of severe sinus bradycardia. Escape
rhythms are discussed in more detail in Chapter 9.

36    Making Sense of the ECG

Table 5.1 Common negatively chronotropic drugs
•
•
•
•

Beta blockers (do not forget eye drops)
Some calcium antagonists, e.g. verapamil, diltiazem
Digoxin
Ivabradine

Asystole implies the absence of ventricular activity, and so the heart rate is zero. Asystole is a medical
emergency and requires immediate diagnosis and treat­ment if the patient is to have any chance of
survival.
Do not forget that arrhythmias that are usually associated with normal or fast heart rates may be slowed by
certain drugs, resulting in bradycardia. For exam­ple, patients with atrial fibrillation (which if untreated may
cause a tachycardia) can develop a bradycardia when commenced on anti-arrhythmic drugs. Table 5.1 lists
drugs that commonly slow the heart rate (negatively chronotropic). A thorough review of all the patient’s
current and recent medications is therefore essential.
DRUG POINT
A complete drug history is essential in any patient with an abnormal ECG.

The first step in managing a bradycardia is to assess the urgency of the situation; in the peri-arrest situation,
use the ABCDE approach and assess the patient for adverse features. The Resuscitation Council (UK) 2015
algorithm on the immediate management of bradycardia in adults is shown in Figure 5.4. The lon­ger-term
management of specific bradycardias is discussed in the chapters which follow.

IS THE HEART RATE ABOVE 100/MIN?
Tachycardia is arbitrarily defined as a heart rate above 100/min. When a patient presents with a tachycardia,
begin by identifying the cardiac rhythm. See Chapter 6 for an approach to recognizing cardiac rhythms.
Begin the process of identification by checking whether the QRS complexes are:

• Narrow (<3 small squares)
• Broad (>3 small squares)

Narrow-complex tachycardias always arise from above the ventricles – that is, they are supraventricular
in origin. The possibilities are:

• Sinus tachycardia
• Atrial tachycardia
• Atrial flutter
• Atrial fibrillation
• AV re-entry tachycardia (AVRT)
• AV nodal re-entry tachycardia (AVNRT)

All of these are discussed in detail in Chapter 7.
Broad QRS complexes can occur if normal electrical impulses are conducted abnor­mally or ‘aberrantly’ to
the ventricles. This delays ventricular activation, widening the QRS complex. Any of the aforementioned
supraventricular tachycardias (SVTs) can also present as a broad-complex tachycardia if aberrant
conduction is present.

Heart rate   37

Assess using the ABCDE approach
Monitor SpO2 and give oxygen if hypoxic
Monitor ECG and BP, and record 12-lead ECG
Obtain IV access
Identify and treat reversible causes (e.g.
electrolyte abnormalities)

Shock
Syncope

Adverse features?
Myocardial ischaemia
Heart failure

No

Yes

Atropine 500 mcg IV

Satisfactory response?

No

Yes

Consider interim measures:
Atropine 500 mcg IV repeat to
maximum of 3 mg
OR
Transcutaneous pacing
OR
Isoprenaline 5 mcg min–1 IV
Adrenaline 2-10 mcg min–1 IV
Alternative drugs*

Seek expert help
arrange transvenous pacing

Yes

Risk of asystole?
Recent asystole
Mobitz II AV block
Complete heart block with
broad QRS
Ventricular pause >3 s

No
Continue observation

* Alternatives include:
Aminophylline
Dopamine
Glucagon (if bradycardia is caused by beta-blocker or calcium channel blocker)
Glycopyrrolate (may be used instead of atropine)

Figure 5.4 Resuscitation Council (UK) 2015 adult bradycardia algorithm. (Reproduced with the kind permission of the
Resuscitation Council [UK].)

Broad-complex tachycardia should also make you think of ventricular arrhythmias:

• Ventricular tachycardia
• Accelerated idioventricular rhythm
• Torsades de pointes

Each of these, including aberrant conduction, is discussed in Chapter 8. How to distinguish between
ventricular tachycardia and SVT with aberrant conduction also discussed in Chapter 8.

38    Making Sense of the ECG

Ventricular fibrillation (VF) is hard to categorize. The chaotic nature of the underlying ventricular activity
can give rise to a variety of ECG appearances, but all have the characteristics of being unpredictable and
chaotic. Ventricular fibrillation is a medical emergency and so it is important that you can recognize it
immediately.
Management of tachycardia depends on the underlying rhythm, and the treatment of the different
arrhythmias is detailed in the following chapters. The first step, as with managing a bradycardia, is to
assess the urgency of the situation – in the peri-arrest situation, use the ABCDE approach and assess the
patient for adverse features . The Resuscitation Council (UK) 2015 algorithm on the immediate management
of tachycardia (with a pulse) in adults is shown in Figure 5.5. The longer-term manage­ment of specific
tachycardias is discussed in the chapters which follow.
Clues to the nature of the arrhythmia may be found in the patient’s history. Ask the patient about:

• How any palpitations start and stop (sudden or gradual)
• Whether there are any situations in which they are more likely to happen (e.g. during exercise, lying
quietly in bed)
• How long they last
• Whether there are any associated symptoms (dizziness, syncope, falls, fatigue, breathlessness and chest pain)
Also ask the patient to ‘tap out’ how the palpitations feel – this will give you clues about the rate (fast or
slow) and rhythm (regular or irregular).
Also enquire about symptoms of related disorders (e.g. hyperthyroidism) and obtain a list of current
medications. Check for any drugs (e.g. salbutamol) that can increase the heart rate (positively chronotropic).
Do not forget to ask about caffeine intake (e.g. coffee, tea and energy drinks).
Assess using ABCDE approach
Monitor SpO2 and give oxygen if hypoxic
Monitor ECG and BP, and record 12-lead ECG
Obtain IV access
Identify and treat reversible causes (e.g. electrolyte abnormalities)

Yes - Unstable

Synchronised DC Shock*
Up to 3 attempts

Adverse features?
Shock
Myocardial ischaemia
Syncope
Heart failure
No - Stable

Seek expert help

Is QRS narrow (< 0.12 s) ?
Amiodarone 300 mg IV over 10–20 minutes
Repeat shock
Then give amiodarone 900 mg over 24 hours

Broad

Narrow

Broad QRS
Is QRS regular?

Narrow QRS
Is rhythm regular?

Regular

Irregular

Seek expert help

Possibilities include:
AF with bundle branch block
treat as for narrow complex
Pre-excited AF
consider amiodarone

Regular

If VT (or uncertain rhythm):
Amiodarone 300 mg IV over 20–
60 minutes then 900 mg over
24 hours
If known to be SVT with bundle
branch block:
Treat as for regular narrowcomplex tachycardia

Vagal manoeuvres
Adenosine 6 mg rapid IV bolus;
if no effect give 12 mg
if no effect give further 12 mg
Monitor/record ECG continuously

Irregular
Probable AF:
Control rate with beta-blocker or
diltiazem
If in heart failure consider digoxin or
amiodarone
Assess thromboembolic risk and
consider anticoagulation

Sinus rhythm achieved?
Yes

No

Probable re-entry paroxysmal SVT:
Record 12-lead ECG in sinus rhythm
If SVT recurs treat again and consider
anti-arrhythmic prophylaxis

Seek expert help
Possible atrial flutter:
Control rate (e.g. with beta-blocker)

Figure 5.5 Resuscitation Council (UK) 2015 adult tachycardia (with pulse) algorithm. AF – atrial fibrillation; SVT –
supraventricular tachycardia; VT – ventricular tachycardia. (Reproduced with the kind permission of the Resuscitation
Council [UK].)

Heart rate   39

A thorough examination is always important, looking for evidence of haemodynamic disturbance
(hypotension, cardiac failure and poor peripheral perfusion) and coexistent disorders (e.g. thyroid goitre).
Use the history, examination and further investigations (e.g. plasma electrolytes, thyroid function tests) to
reach a diagnosis. Ambulatory ECG recording may be helpful if circumstances permit it (see Chapter 22).

SUMMARY
To assess the heart rate, ask the following questions.
1. Is the heart rate below 60/min?
		 If yes, consider:

•
•
•
•
•

Sinus bradycardia
Sick sinus syndrome
Second-degree and third-degree AV block
Escape rhythms
• AV junctional escape rhythm
• Ventricular escape rhythms
Asystole

2. Is the heart rate above 100/min?
		 If yes, consider:

•

•

Narrow-complex tachycardia
• Sinus tachycardia
• Atrial tachycardia
• Atrial flutter
• Atrial fibrillation
• AV re-entry tachycardia
• AV nodal re-entry tachycardia
Broad-complex tachycardia
• Narrow-complex tachycardia with aberrant conduction
• Ventricular tachycardia
• Accelerated idioventricular rhythm
• Torsades de pointes

Further reading
Details of Advanced Life Support guidelines, and training courses in resuscitation, can be obtained from the
Resuscitation Council (UK) at https://www.resus.org.uk/.
Meek S, Morri F. ABC of clinical electrocardiography: Introduction. I – Leads, rate, rhythm, and cardiac axis. Br Med
J 2002; 324: 415–418.

Chapter 6
An approach to heart rhythms

In Chapters 7–9 we will be discussing the cardiac rhythms that you may encounter in everyday practice. To
begin, however, we will overview how to approach the identification of a patient’s cardiac rhythm. Following
the step-by-step approach in this chapter will give you a firm foundation for tackling the problem of rhythm
recognition.
To identify the cardiac rhythm with confidence you need to begin with a rhythm strip – a prolonged
recording of the ECG from just one lead. Most ECG machines automatically include a rhythm strip at the
bottom of a 12-lead ECG (Figure 6.1). If your machine does not, make sure you have recorded one yourself.
The machine may give you a choice about which of the 12 leads will appear as the rhythm strip – most
commonly, lead II is selected as this tends to give the clearest view of P wave activity. However, sometimes
it is necessary to select one of the other leads to gain a clearer picture of the rhythm.
The diagnosis of abnormal cardiac rhythms is not always easy, and some of the more complex arrhythmias
can tax the skills of even the most experienced cardiologist. It is appropriate, therefore, to begin this chapter
with the following warning:
SEEK HELP
If in doubt about a patient’s cardiac rhythm, do not hesitate to seek the advice of a cardiologist.

This advice is particularly important if the patient is haemodynamically compromised by the arrhythmia,
or if you are contemplating treatment of any kind.
There are many ways in which you can approach the identification of arrhythmias, and this is reflected in
the numerous ways in which they can be categorized:

• Regular versus irregular
• Bradycardias versus tachycardias
• Narrow complex versus broad complex
• Supraventricular versus ventricular

The common cardiac rhythms are listed in Table 6.1 and the following chapters con­tain a detailed
description of each rhythm and its key characteristics, together with example ECGs. Let’s begin, however,
with a systematic strategy for working towards a rhythm diagnosis.

41

42    Making Sense of the ECG

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

II

Rhythm strip (lead II)

Figure 6.1
Key point:

The rhythm strip.
• The standard lead used for the rhythm strip is lead II, but alternative leads can be selected if it helps
to clarify the cardiac rhythm.

IDENTIFYING THE CARDIAC RHYTHM
When you analyze the cardiac rhythm, always keep in mind the two primary questions that you are trying
to answer:

• Where does the impulse arise from?

•

•
•
•
•

Sinoatrial (SA) node
Atria
Atrioventricular (AV) junction
Ventricles
How is the impulse conducted?
Normal conduction
Impaired conduction
Accelerated conduction (e.g. Wolff–Parkinson–White [WPW] syndrome)

•
•
•

The following seven questions will help you to narrow down the possible diagnoses:
1.
2.
3.
4.
5.
6.
7.

How is the patient?
Is ventricular activity present?
What is the ventricular rate?
Is the ventricular rhythm regular or irregular?
Is the QRS complex width normal or broad?
Is atrial activity present?
How are atrial activity and ventricular activity related?

Each of the sections that follow represents a step in this approach to rhythm recognition.

An approach to heart rhythms   43

Table 6.1

Cardiac rhythms

• SA nodal rhythms
• Sinus rhythm
• Sinus arrhythmia
• Sinus bradycardia
• Sinus tachycardia
• Sick sinus syndrome
• Atrial rhythms
• Atrial ectopic beats
• Atrial fibrillation
• Atrial flutter
• Atrial tachycardia
• Junctional rhythms
• Junctional ectopic beats
• AV re-entry tachycardia (AVRT)
• AV nodal re-entry tachycardia (AVNRT)
• Ventricular rhythms
• Ventricular ectopic beats
• Accelerated idioventricular rhythm
• Monomorphic ventricular tachycardia (VT)
• Polymorphic ventricular tachycardia (torsades de pointes)
• Ventricular fibrillation (VF)
• Conduction problems
• SA block
• AV blocks
– First-degree AV block
– Second-degree AV block
– Mobitz type I AV block
– Mobitz type II AV block
– 2:1 AV block
– Third-degree AV block
• Bundle branch and fascicular blocks
– Right bundle branch block
– Left bundle branch block
– Left anterior fascicular block
– Left posterior fascicular block
• Escape rhythms

A similar approach to the ECG is used by the Resuscitation Council (UK) to train healthcare professionals in
rhythm recognition. Attending an Advanced Life Support (ALS) course is an excellent way to improve
your skills in cardiac rhythm recognition and, of course, in learning how to provide advanced life support.
Contact details for the Resuscitation Council (UK) are provided at the end of this chapter (see ‘Further
reading’). If you live outside the UK, approach your local pro­v ider of ALS training for advice.

HOW IS THE PATIENT?
Clinical context is all important in ECG interpretation, and so don’t attempt to interpret an ECG rhythm
without knowing the clinical context in which the ECG was recorded. Take the example of a rhythm strip
that appears to show normal sinus rhythm. If it was recorded from a patient who is unconscious and pulseless,
the diagnosis will be pulseless electrical activity (PEA), not sinus rhythm. Similarly, the presence of artefact
on an ECG can be misread as an arrhythmia unless the clinical context is known. To avoid these problems:

• If you are interpreting an ECG that someone else has recorded, always insist on knowing the clinical
details of the patient and the reason why it was recorded.
• If you are recording an ECG that someone else will interpret later, always make a note of the clinical context at

the top of the ECG to help with the interpretation (e.g. ‘Patient experiencing chest pain at time of recording’).

44    Making Sense of the ECG

The clinical context will also help you decide how urgently to deal with an arrhythmia. When assessing a
‘sick’ patient, use the ABCDE approach:

• Airway: Check for any evidence of airway obstruction
• Breathing: Assess the patient’s breathing, paying attention to respiratory rate, chest percussion and
auscultation, and oxygenation
• Circulation: Assess the patient’s circulation, including pulse rate, blood pressure and capillary refill time
• Disability: Assess level of consciousness and neurological status
• Exposure: Ensure adequate exposure to permit a full examination

As you assess a patient with an arrhythmia, be alert for ‘adverse features’ which indicate haemodynamic instability:

• Shock: As evidenced by hypotension (systolic blood pressure <90 mmHg), clamminess, sweating, pallor,
confusion or reduced conscious level
• Syncope: As a consequence of cerebral hypoperfusion
• Myocardial ischaemia: Indicated by ischaemic chest pain and/or ischaemic ECG changes (see Chapters
15 and 16)
• Heart failure: Pulmonary oedema, elevated jugular venous pressure, peripheral/sacral oedema
IS VENTRICULAR ACTIVITY PRESENT?
Look at the ECG as a whole for the presence of electrical activity. If there is none, assess:

• The patient (do they have a pulse?)
• The electrodes (has something become disconnected?)
• The gain setting (is the gain setting on the monitor too low?)

If the patient is pulseless with no electrical activity evident on the ECG, they are in asystole and appropriate
emergency action must be taken (see Chapter 8, Figure 8.8 for more details). Beware of diagnosing asystole
in the presence of a completely flat ECG trace – there should usually be some baseline drift present. A
completely flat line usually means an electrode has become disconnected – check the electrodes (and, of
course, the patient) carefully when making your diagnosis.
P waves may appear on their own (for a short time) after the onset of ventricular asystole. The presence
of ‘P waves only’ on the ECG is important to recognize, as the patient may respond to emergency pacing
manoeuvres such as percussion pacing, transcutaneous pacing or temporary transvenous pacing.
If QRS complexes are present, move on to the next question.

WHAT IS THE VENTRICULAR RATE?
Ventricular activity is represented on the ECG by QRS complexes. The methods for determining the
ventricular rate are discussed in Chapter 5. Once you have calcu­lated the ventricular rate, you will be able
to classify the rhythm as:

• Bradycardia (<60 beats/min)
• Normal (60–100 beats/min)
• Tachycardia (>100 beats/min)

IS THE VENTRICULAR RHYTHM REGULAR OR IRREGULAR?
Having determined the ventricular rate, go on to assess regularity. Look at the spacing between QRS
complexes – is it the same throughout the rhythm strip? Irregularity can be subtle, so it is useful to measure
the distance between each QRS complex. One way to do this is to place a piece of paper alongside the rhythm

An approach to heart rhythms   45

Table 6.2 Regular and irregular cardiac rhythms
• Regular rhythms
• Sinus rhythm
• Sinus bradycardia
• Sinus tachycardia
• Atrial flutter (if constant AV block, e.g. 2:1)
• Atrial tachycardia
• AV re-entry tachycardia (AVRT)
• AV nodal re-entry tachycardia (AVNRT)
• Accelerated idioventricular rhythm
• Monomorphic ventricular tachycardia (VT)
• Polymorphic ventricular tachycardia (torsades de pointes)
• Third-degree AV block (if regular escape rhythm)
• Irregular rhythms
• Sinus arrhythmia (rate varies with respiration)
• Ectopic beats (atrial, junctional, ventricular)
• Atrial fibrillation
• Atrial flutter (if variable AV block)
• Sinus arrest and SA block
• Mobitz type I second-degree AV block
• Mobitz type II second-degree AV block

strip and make a mark on it next to every QRS complex. By moving the marked paper up and down along
the rhythm strip, you can soon see if the gaps between the QRS complexes are the same or vary. Once you
have assessed the regularity, you will be able to classify the ventricular rhythm as:

• Regular (equal spacing between QRS complexes)
• Irregular (variable spacing between QRS complexes)

Table 6.2 lists the causes of regular and irregular cardiac rhythms.
If the rhythm is irregular, it is helpful to try to characterize the degree of irregularity. Atrial fibrillation, for
example, is a totally chaotic rhythm with no discernible pattern to the QRS complexes. Sinus arrhythmia,
by comparison, shows a cyclical variation in ventricular rate that is not chaotic but has a clear periodicity
to it, coinciding with the patient’s breathing movements.
In intermittent AV block, if an impulse is blocked en route to the ventricles as a result of a conduction
problem, the corresponding QRS complex will fail to appear where expected and the beat will be ‘missed’
(see Chapter 9, Figure 9.4). The degree of irregularity will depend upon the nature of the conduction
problem – the block of impulses may be predictable, in which case there will be a ‘regular irregularity’, or
unpredictable.
Similarly, ectopic beats may occur in a predictable manner or unpredictably, giving rise to regular or irregular
irregularities accordingly. In ventricular bigeminy, for example, a ventricular ectopic beat arises after each
normal QRS complex, leading to a ‘regular irregularity’ of the ventricular rhythm (see Chapter 8, Figure 8.2).

IS THE QRS COMPLEX WIDTH NORMAL OR BROAD?
The width of the QRS complex can provide valuable clues about the origin of the cardiac rhythm. By
answering this question, you will have narrowed down the ori­gin of the impulse to one half of the heart.
Ventricular rhythms are generated within the ventricular myocardium; supraventricular rhythms are
generated anywhere up to (and including) the AV junction (Figure 6.2).
Normally, the ventricles are depolarized via the His–Purkinje system, a network of rapidly conducting
fibres that run throughout the ventricular myocardium. As a result, the ventricles are normally completely
depolarized within 0.12 s, and the corresponding QRS complex on the ECG is less than 3 small squares wide.

46    Making Sense of the ECG

Supraventricular

Ventricular

Figure 6.2
Key point:

Supraventricular versus ventricular rhythms.
• Supraventricular applies to any structure above the ventricles (and electri­cally distinct from them).

However, if there is a problem with conduction within the ventricles, such as a block of part of the His–
Purkinje system (as seen in left or right bundle branch block), depolarization has to spread directly from
myocyte to myocyte instead. This takes longer, and so the QRS complex becomes wider than 3 small squares.
This is also the case if the impulse has arisen within the ventricles (instead of coming via the AV node),
as in the case of a ventricular ectopic beat or in VT. If an impulse does not pass through the AV node, it
cannot use the rapid His–Purkinje conduction system. Once again, it must travel from myocyte to myocyte,
prolonging the process of depolarization.
This allows us to use the width of the QRS complex to try to determine how the ventricles were depolarized.
If the QRS complex is narrow (<3 small squares), the ventricles must have been rapidly depolarized by an
impulse that came through the AV node – the only way into the His–Purkinje system. The patient is then
said to have a supraventricular rhythm (arising from above the ventricles).
If the QRS complex is broad (>3 small squares), there are two possible explanations:
1. The impulse may have arisen from within the ventricles and thus been unable to travel via the His–
Purkinje system (ventricular rhythm).
2. The impulse may have arisen from above the ventricles but not been able to use all the His–Purkinje
system because of a conduction problem (supraventricular rhythm with aberrant conduction).
This is summarized in Table 6.3.
Trying to distinguish between ventricular rhythms and supraventricular rhythms with aberrant conduction
can be difficult, particularly if the patient is tachycardic and there is concern that the rhythm is VT. The
distinction between VT and SVT is discussed specifically in Chapter 8, Section ‘How do I distinguish
detween VT and SVT?’.
Table 6.3 Broad-complex versus narrow-complex rhythms
Rhythm origin
Supraventricular
Supraventricular
Ventricular
Note:

Rhythm conduction
Normal
Aberrant (e.g. bundle branch block)
Myocyte to myocyte

QRS complex
Narrow
Broad
Broad

Only supraventricular rhythms with normal conduction can gain access to
the His–Purkinje system to rapidly depolarize the ventricles.

An approach to heart rhythms   47

IS ATRIAL ACTIVITY PRESENT?
Atrial electrical activity can take several forms, which can be grouped into four categories:

• P waves (atrial depolarization)
• Flutter waves (atrial flutter)
• Fibrillation waves (atrial fibrillation)
• Unclear activity

The presence of P waves indicates atrial depolarization. However, it does not mean that the depolarization
necessarily started at the SA node. P waves will appear during atrial depolarization regardless of where it
originated – it is the orientation of the P waves that tells you where the depolarization originated (Chapter 7).
Upright P waves in lead II suggest that atrial depolarization originated in or near the SA node. Inverted P
waves suggest an origin closer to, or within, the AV node (see Chapter 11, Figure 11.4).
Flutter waves are seen in atrial flutter at a rate of 300/min, creating a sawtooth baseline of atrial activity
(see Chapter 7, Figure 7.8). This can be made more readily apparent by manoeuvres that transiently block
the AV node.
Fibrillation waves are seen in AF and correspond to random, chaotic atrial impulses occurring at a rate of
400–600/min (see Chapter 7, Figure 7.7). This leads to a chaotic, low-amplitude baseline of atrial activity.
The nature of the atrial activity may be unclear. This may be because P waves are ‘hidden’ within the QRS
complexes, as is often the case during AV nodal re-entry tachycardia. In such cases atrial depolarization is
taking place, but its electri­cal ‘signature’ on the ECG cannot easily be seen because the simultaneous, larger
amplitude QRS complex hides it. Atrial activity may also be absent in, for example, sinus arrest or SA block,
in which case the atria may be electrically silent.

HOW ARE ATRIAL ACTIVITY AND VENTRICULAR ACTIVITY RELATED?
Having examined the activity of the atria and of the ventricles, the final task is to determine how the two are
related. Normally an impulse from the atria goes on to depolarize the ventricles, leading to a 1:1 relationship
between P waves and QRS complexes. However, impulses from the atria may sometimes fail to reach the
ven­tricles, or the ventricles may generate their own impulses independent of the atria.
If every QRS complex is associated with a P wave, this indicates that the atria and ventricles are being
activated by a common source. This is usually, but not necessarily, the SA node (e.g. AV junctional rhythms
will also depolarize both atria and ventricles).
If there are more P waves than QRS complexes, conduction between atria and ventricles is being either
partly blocked (with only some impulses getting through) or completely blocked (with the ventricles having
developed their own escape rhythm). Conduction problems are discussed further in Chapter 9.
More QRS complexes than P waves indicates AV dissociation, with the ventricles operating independently
of the atria and at a higher rate (see Chapter 12, Figure 12.10).
Always bear in mind that the P wave may be difficult or even impossible to discern clearly. Therefore, it can
sometimes be difficult to say conclusively that atrial activity is absent.

DETERMINING THE CARDIAC RHYTHM
Using the aforementioned seven questions, you now have a ‘toolkit’ with which to tackle the diagnosis
of cardiac rhythms. As you read about supraventricular rhythms, ventricular rhythms and conduction
problems in the next three chapters, think about these seven questions and how they relate to each of the

48    Making Sense of the ECG

rhythms described. Each rhythm has its own set of ECG characteristics, and by assessing the ECG in a
methodical manner you will quickly learn how to distinguish between them.
There are a handful of rhythms that you should learn by rote so that you can recognize them without
hesitation in an emergency – these are the cardiac arrest rhythms (ventricular fibrillation, ventricular
tachycardia, asystole and pulseless electrical activity), which are also discussed further in the following
chapters.
SUMMARY
Approach the identification of the cardiac rhythm by asking the following seven questions:
1.
2.
3.
4.
5.
6.
7.

How is the patient?
Is ventricular activity present?
What is the ventricular rate?
Is the ventricular rhythm regular or irregular?
Is the QRS complex width normal or broad?
Is atrial activity present?
How are atrial activity and ventricular activity related?

Further reading
Details of Advanced Life Support guidelines, and training courses in resuscitation, can be obtained from the
Resuscitation Council (UK) at https://www.resus.org.uk/.
Jastrzebski M, Sasaki K, Kukla P et al. The ventricular tachycardia score: A novel approach to electrocardiographic
diagnosis of ventricular tachycardia. Europace 2016; 18: 578–584.
Wellens HJJ. Ventricular tachycardia: Diagnosis of broad QRS complex tachycardia. Heart 2001; 86: 579–585.
Whinnett ZI, Sohaib SMA, Davies DW. Diagnosis and management of supraventricular tachycardia. BMJ 2012; 345:
e7769.

Chapter 7
Supraventricular rhythms

Supraventricular rhythms are those which arise above the level of the ventricles, i.e. from the sinoatrial (SA) node,
the atria or the atrioventricular (AV) node. This includes normal rhythms (sinus rhythm, sinus arrhythmia),
abnormal rhythms (e.g. atrial fibrillation, atrial flutter, etc.), and rhythms which may or may not be ‘normal’
depending upon the clinical context (e.g. sinus tachycardia). All of these are discussed in this chapter.
The supraventricular rhythms we will consider are:

• Sinus rhythm
• Sinus arrhythmia
• Sinus bradycardia
• Sinus tachycardia
• Sick sinus syndrome
• Atrial ectopic beats
• Atrial fibrillation
• Atrial flutter
• Atrial tachycardia
•
•

•
•

Focal atrial tachycardia
Multifocal atrial tachycardia
Atrioventricular re-entry tachycardia (AVRT)
Atrioventricular nodal re-entry tachycardia (AVNRT)

SINUS RHYTHM
Sinus rhythm is the normal cardiac rhythm, in which the SA node acts as the natural pacemaker, discharging
at a rate of 60–100/min (Figure 7.1). The characteristic features of sinus rhythm are:

• Heart rate is 60–100/min
• P wave morphology is normal (e.g. upright in lead II and inverted in lead aVR)
• Every P wave is followed by a QRS complex

If the patient is in sinus rhythm, move on to check whether there might be any conduction problems
(Chapter 9) and then determine the cardiac axis (Chapter 10) before assessing the rest of the ECG step-bystep (Chapters 11–18). If not, continue reading this chapter to diagnose the rhythm.
49

50    Making Sense of the ECG

Lead II

Figure 7.1
Key point:

Normal sinus rhythm.
• The heart rate is 75/min, the P waves are upright (lead II) and every P wave is followed by a QRS complex.
Inspiration

Lead II

Figure 7.2
Key point:

Physiological sinus arrhythmia.
• The heart rate increases during inspiration, the P waves are upright (lead II) and every P wave is
followed by a QRS complex.

SINUS ARRHYTHMIA
Sinus arrhythmia is the variation in heart rate that is seen during inspiration and expiration (Figure 7.2).
The characteristic features of sinus arrhythmia are:

• The heart rate varies with respiration, with the difference between the longest and shortest P–P intervals
being >0.12 s (3 small squares)
• During inspiration, the heart rate increases as a reflex response to the increased volume of blood returning
to the heart (which triggers baroreceptors that inhibit vagal tone)
• During expiration, the heart rate decreases as a reflex response to the decreased volume of blood returning
to the heart (vagal tone is no longer inhibited)
• P wave morphology is normal (e.g. upright in lead II and inverted in lead aVR)
• Every P wave is followed by a QRS complex
Sinus arrhythmia is harmless and no investigations or treatment are necessary.

SINUS BRADYCARDIA
Sinus bradycardia is sinus rhythm with a heart rate of less than 60/min (Figure 7.3). The characteristic
features of sinus bradycardia are:

• The heart rate is less than 60/min
• P wave morphology is normal (e.g. upright in lead II and inverted in lead aVR)
• Every P wave is followed by a QRS complex

It is unusual for sinus bradycardia to be slower than 40/min. Sinus bradycardia can be a normal finding,
e.g. in athletes during sleep. However, always consider the following possible causes:

• Drugs (e.g. digoxin, beta blockers – including beta blocker eye drops)
• Ischaemic heart disease and myocardial infarction

Supraventricular rhythms   51

Lead II

Figure 7.3

Sinus bradycardia.
• The heart rate is 46/min, the P waves are upright (lead II) and every P wave is followed by a QRS complex.

Key point:

• Hypothyroidism
• Hypothermia
• Electrolyte abnormalities
• Obstructive jaundice
• Uraemia
• Raised intracranial pressure
• Sick sinus syndrome

If the sinus bradycardia is severe, escape beats and escape rhythms may occur (Chapter 9). The management
of bradycardia (of any cause) is discussed in Chapter 5.

SINUS TACHYCARDIA
Sinus tachycardia is sinus rhythm with a heart rate of greater than 100/min (Figure 7.4). The characteristic
features of sinus tachycardia are:

• The heart rate is greater than 100/min
• P wave morphology is normal (e.g. upright in lead II and inverted in lead aVR)
• Every P wave is followed by a QRS complex
I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

II

Figure 7.4 Sinus tachycardia.
Key point:

• The heart rate is 136/min, the P waves have a normal orientation in each lead, and every P wave is
followed by a QRS complex.

52    Making Sense of the ECG

It is unusual for sinus tachycardia to exceed 180/min, except in fit athletes. At this heart rate, it may be
difficult to differentiate the P waves from the T waves, so the rhythm can be mistaken for an AV nodal
re-entry tachycardia.
Physiological causes of sinus tachycardia include anything that stimulates the sympathetic nervous
system – anxiety, pain, fear, fever or exercise. Always consider the following causes as well:

• Drugs, e.g. adrenaline, atropine, salbutamol (do not forget inhalers and nebulizers), caffeine and alcohol
• Ischaemic heart disease and acute myocardial infarction
• Heart failure
• Pulmonary embolism
• Fluid loss
• Anaemia
• Hyperthyroidism

The management of sinus tachycardia is that of the cause. When a patient has an appropriate tachycardia
(e.g. compensating for low blood pressure, such as in fluid loss), the tachycardia is helping to maintain the
patient’s blood pressure and so slowing it with beta blockers can lead to disastrous decompensation. It is
the underlying problem that needs addressing. However, if the sinus tachycardia is inappropriate, as in
hyperthyroidism, then the tachycardia is counterproductive and using drug treatment (e.g. beta blockers)
to slow the tachycardia may be helpful.
WARNING
In sinus tachycardia, never attempt to slow the heart rate until you have established the cause.

Persistent ‘sinus tachycardia’ should lead to suspicion that the diagnosis may be incorrect – both atrial
flutter and atrial tachycardia can, on casual inspection, be mistaken for sinus tachycardia. However,
persistent ‘inappropriate’ sinus tachycardia is recognized as a clinical entity, referring to a persistent increase
in daytime resting heart rate (>100/min) which is out of proportion to any clinical factors, and with an
excessive increase in heart rate on physical activity. On ambulatory ECG monitoring, the overall average
heart rate is typically >90/min. P wave morphology is normal. The condition is poorly understood, but it
may result from enhanced automaticity within the SA node or from autonomic dysfunction. Inappropriate
sinus tachycardia can be treated with rate-controlling drugs (such as beta blockers) or, in severe symptomatic
cases, electrophysiological modification/ablation of the S