Making Sense of the ECG

MAKING SENSE OF
the ECG
Reading an ECG correctly and working out what to do next is an invaluable skill for any doctor, nurse or
paramedic when evaluating the condition of a patient.
Making Sense of the ECG: Cases for Self Assessment helps students and more experienced healthcare
practitioners to consolidate their knowledge of ECG interpretation through real-life scenarios. The patients’
history, examination and initial investigations are presented along with questions on the ECG interpretation,
allowing readers to assess their ability to interpret ECGs accurately, perform differential diagnosis and decide
upon the most appropriate clinical management in each situation. Detailed explanatory answers respond to
the questions posed, as well as providing practical clinical guidance and essential revision support.
Used alongside the popular textbook Making Sense of the ECG: A Hands-on Guide 6E, or independently,
as a vital tool to consolidate knowledge and prepare for clinical practice, this latest edition has been fully
updated in line with the latest management guidelines and features a new appendix listing the key diagnosis
in each ECG, making it easier to locate topics for revision.
Making Sense . . .
About the Series
The Making Sense of series covers a variety of medical topics and subjects allied to medicine. Some of
them are practical and technique-based, some provide professional advice, and some relate to professional
development. All titles are easy to navigate for quick reference and include plenty of features such as
‘summary boxes’, ‘pearls of wisdom’, and ‘clinical considerations’. Easy to understand, written in a jargon-
free style, and convenient for carrying around, the Making Sense series provides hands-on guidance to be
referred to often in both clinical and reference contexts.
Making Sense of the Chest X-Ray: A Hands-on Guide

Paul Jenkins
Making Sense of Clinical Teaching: A Hands-on Guide to Success

Edited By Samy A. Azer
Making Sense of Fluids and Electrolytes: A Hands-on Guide

Zoja Milovanovic, Abisola Adeleye
Making Sense of Lung Function Tests: A Hands-on Guide, 2E

Jonathan Dakin, Mark Mottershaw, Elena Kourteli
Making Sense of Exercise Testing

Robert B. Schoene, H. Thomas Robertson
Making Sense of Sleep Medicine: A Hands-on Guide

Edited by Karuna Datta and Deepak Shrivastava
Making Sense of the EEG: From Basic Principles to Clinical Applications

Udaya Seneviratne
Making Sense of the Pediatric EEG

Edited by Maria Augusta Montenegro
Making Sense of the ECG: A Hands-on Guide, 6E

Andrew R Houghton
Making Sense of the ECG: Cases for Self Assessment, 3E

Andrew R Houghton
For more information about this series please visit: www.routledge.com/Making-Sense-of/book-series/

CRCMAKISENS
MAKING SENSE OF
the ECG
Cases for Self Assessment
THIRD EDITION
Andrew R Houghton
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ISBN: 978-1-032-75057-6 (hbk)

ISBN: 978-1-032-73554-2 (pbk)
ISBN: 978-1-003-47218-6 (ebk)
DOI: 10.1201/9781003472186
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by Apex CoVantage, LLC
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Contents
Preface to the Third Edition xi

Acknowledgementsxiii
Authorxv
Normal Values xvii
Case 1 1
Case 2 5
Case 3 7
Case 4 9
Case 5 11
Case 6 13
Case 7 17
Case 8 19
Case 9 21
Case 10 23
Case 11 25
Case 12 29
Case 13 31
Case 14 35
Case 15 37
Case 16 39
Case 17 41
Case 18 43
Case 19 45
Case 20 47
Case 21 49
Case 22 51
Case 23 53
Case 24 55
Case 25 57
Case 26 59
viii Contents
Case 27 61
Case 28 63
Case 29 65
Case 30 69
Case 31 71
Case 32 73
Case 33 75
Case 34 77
Case 35 79
Case 36 83
Case 37 87
Case 38 89
Case 39 91
Case 40 93
Case 41 95
Case 42 97
Case 43 99
Case 44 101
Case 45 105
Case 46 109
Case 47 111
Case 48 115
Case 49 117
Case 50 119
Case 51 121
Case 52 125
Case 53 127
Case 54 129
Case 55 131
Case 56 133
Case 57 135
Case 58 139
Case 59 143
Contents ix
Case 60 145

Case 61 149
Case 62 151
Case 63 153
Case 64 155
Case 65 159
Case 66 161
Case 67 163
Case 68 165
Case 69 169
Case 70 171
Appendix 1: List of Cases 173
Index177
Preface to the Third Edition
If you have already read Making Sense of the ECG: A Hands-on Guide, Sixth Edition, you may now be
keen to put your knowledge to the test. In this companion volume, Making Sense of the ECG: Cases for Self
Assessment, Third Edition, you can test your skills in ECG interpretation with 70 individual clinical cases.
This book is simple to use. Each of the cases begins with an ECG, an illustrative clinical scenario (to place
the ECG in an appropriate context) and a number of questions. On turning the page, you will find the
answers to the questions together with a detailed analysis of the ECG. This is followed by a general com-
mentary on the ECG and the clinical case, as well as suggestions for further reading. The ECG cases are
presented in order of increasing difficulty and so, whatever your experience in ECG interpretation, you will
find cases to challenge your skills.
The text has been fully updated for this new edition with reference to the latest guidelines and suggestions
for further reading. All the cross-references to the new companion volume, Making Sense of the ECG: A
Hands-on Guide, Sixth Edition, have been updated. There is also the new addition of a list of cases as an
appendix, which will facilitate finding specific ECGs for revision.
Once again, I am grateful to everyone who has taken the time to comment on the text and to provide ECGs
from their collections. Finally, I would like to thank all the staff at CRC Press/Taylor & Francis who have
contributed to the success of the Making Sense of series of books.
Andrew R Houghton
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 invalu-
able comments on the text and for allowing me to use ECGs from their collections:
Mookhter Ajij Lawrence Green V B S Naidu

Richard Andrews Mahesh Harishchandra Vicky Nelmes
Khin Maung Aye Michael Holmes Claire Poole
Stephanie Baker Tim Jones George B Pradhan
Michael Bamber Safiy Karim Jane Robinson
Sophie Beech Dave Kendall Alun Roebuck
Muneer Ahmad Bhat Jeffrey Khoo Catherine Scott
Gabriella Captur Daniel Law Penelope R Sensky
Andrea Charman Diane Lunn Neville Smith
Nigel Dewey Iain Lyburn Gary Spiers
Matthew Donnelly Sonia Lyburn Andrew Staniforth
Simon Dubrey Martin Melville Andrew Stein
Chris Eggett Cara Mercer Robin Touquet
Ian Ferrer Yuji Murakawa Upul Wijayawardhana
Catherine Goult Francis Murgatroyd Bernadette Williamson
I would also like to express my gratitude to Dr David Gray for all his hard work and commitment in co-
authoring the first edition of this textbook, and to Dr Joanna Koster and the rest of the publishing team at
CRC Press/Taylor & Francis for their encouragement, guidance and support during this project.
Author
Dr Andrew R Houghton studied medicine at the University of Oxford and undertook postgraduate train-
ing 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. His subspecialty interest is in cardiac imaging (echocardiography and
cardiovascular MRI). He is a fellow of the Royal College of Physicians (London). He has published several
textbooks in cardiology, including Making Sense of the ECG (winner of the Royal Society of Medicine’s
Richard Asher Prize and the BMA’s Student Textbook Award), Making Sene of the ECG: Cases for Self
Assessment and Making Sense of Echocardiography (Highly Commended at the BMA’s Medical Book
Awards).
Normal Values
The following adult reference ranges apply to the cases presented in this textbook. Please note that the refer-
ence ranges in your clinical practice may differ depending upon the laboratory.
Full Blood Count (FBC)

Hb 130–180 g/L (male)
115–165 g/L (female)
White cell count (WCC) 3.6–11.0 × 109/L
Platelets 140–400 × 109/L
Urea and Electrolytes (U&E)

Na 133–146 mmol/L
K 3.5–5.3 mmol/L
Urea 2.5–7.8 mmol/L
Creatinine 59–104 mmol/L (male)
45–84 mmol/L (female)
CASE 1
CLINICAL SCENARIO
Male, aged 28 years. Examination
Athletic build.
Presenting complaint Pulse: 50/min, regular.
Asymptomatic fitness instructor. This screen- Blood pressure: 128/80.
ing ECG was performed at a ‘well man’ medical JVP: not elevated.
check-up. Heart sounds: normal.
Chest auscultation: unremarkable.
History of presenting complaint No peripheral oedema.
Nil – the patient is asymptomatic. Old appendicectomy scar noted in right iliac fossa.
Past medical history Investigations

Appendicectomy (aged 17 years). FBC: Hb 148, WCC 6.2, platelets 229.
U&E: Na 140, K 4.4, urea 3.7, creatinine 78.
Thyroid function: normal.
Chest X-ray: normal heart size, clear lung fields.
QUESTIONS
1. What does this ECG show?
2. How did you calculate the heart rate?
3. Is the heart rate normal?
4. Is any further action required?
DOI: 10.1201/9781003472186-1
2 Making Sense of the ECG: Cases for Self Assessment
ECG ANALYSIS You can therefore count the number of QRS

complexes in 50 large squares, and then mul-
Rate 50/min tiply this number by 6 to give the number of
Rhythm Sinus bradycardia QRS complexes per minute.
3. Generally speaking, bradycardia is defined as a
QRS axis Normal (+42°)
heart rate below 60/min. However, it is always
P waves Normal important to assess clinical data in the context of
PR interval Normal (160 ms)
the patient. This is a young patient with an ath-
letic background, and so a relatively slow resting
QRS duration Normal (76 ms) heart rate is not unusual. In this clinical context,
T waves Normal the mild sinus bradycardia is not of concern.
QTc interval Normal (407 ms) 4. No – the patient can be reassured that the ECG is
normal.
Additional comments COMMENTARY

There is a very slight variation in heart rate on the
ECG – the distance between consecutive QRS com- • One of the most important principles of ECG
plexes (the R-R interval) varies slightly. This is not interpretation, and indeed in interpreting any
unusual and results from a slight variation in heart test result, is to place things in their clinical
rate with respiration. context. Although the ‘normal range’ for the
heart rate in sinus rhythm is 60–100/min, a rate
that is 50–60/min is seldom of any significance
ANSWERS or clinical consequence. If a patient is athletic,
it is not unusual to have a mild resting brady-
1. This ECG shows mild sinus bradycardia but is cardia and it is important not to diagnose this as
otherwise normal. pathological.
2. There are several ways to calculate heart rate: • Whenever you interpret an ECG, it is impor-
• At a standard paper speed of 25 mm/s, there tant to begin by asking ‘How is the patient?’ This
will be 300 large squares for every minute of will give you the clinical context you require
ECG recording. You can therefore count the to make a correct assessment. Similarly, if you
number of large squares between two consec- make an ECG recording, it is good practice to
utive QRS complexes – in this example, there make a note of the clinical context at the top of
are 6 – and then divide this number into 300 the ECG, along with the patient’s identification
(i.e. 300/6). This gives a heart rate of 50/min. details and the date/time of the recording.
• An alternative, and slightly more accurate, This can take the form of a brief sentence to
method is to count small squares rather say ‘Patient complaining of palpitations’, or
than big ones. For this method, you need to ‘Patient experiencing severe chest tightness’ or
remember than a 1 min ECG recording cov- just ‘Patient asymptomatic’. This makes it much
ers 1500 small squares. Count the number of easier for you – and for others – to interpret the
small squares between two consecutive QRS ECG when it is reviewed later on.
complexes, and divide it into 1500. • A mild sinus bradycardia can also be the result
• The mentioned methods are best used when of drug treatment (particularly beta-blockers,
the rhythm is regular. If the rhythm is digoxin, ivabradine or rate-limiting calcium
irregular (e.g. atrial fibrillation) it is better channel blockers, such as verapamil). Don’t for-
to count the total number of QRS complexes get about beta-blocking eye drops, which can
along a strip 50 large squares in length. have systemic effects.
A strip of 50 large squares is equivalent to 10 s • The T wave inversion seen in lead aVR and in
of recording (at a paper speed of 25 mm/s). lead V1 is a normal finding.
Case 1 3
Further Reading
Making Sense of the ECG 6th edition: Heart rate, p 37; Sinus Meek S et al. ABC of clinical electrocardiography:
rhythm, p 163; Sinus bradycardia, p 164. Introduction. I – Leads, rate, rhythm, and cardiac axis.
British Medical Journal (2002). PMID 11850377.
CASE 2
CLINICAL SCENARIO
Male, aged 27 years. Past medical history
Nil of note.
Presenting complaint
No cardiac symptoms but aware he has an Examination
‘abnormal ECG’. Pulse: 60/min, slightly irregular.
Blood pressure: 126/88.
History of presenting complaint JVP: not elevated.
Patient had been scheduled for knee surgery Heart sounds: normal.
and was seen by a nurse in the surgical preop- Chest auscultation: unremarkable.
erative assessment clinic. The nurse reported a No peripheral oedema.
slightly irregular pulse and requested an ECG.
Subsequently, the patient was referred to the Investigations
cardiology clinic for a preoperative cardiac FBC: Hb 165, WCC 4.3, platelets 353.
opinion. U&E: Na 140, K 4.5, urea 4.4, creatinine 98.
QUESTIONS
2. What is the mechanism of this?
3. What is the likely cause?
4. What are the key issues in managing this patient?
DOI: 10.1201/9781003472186-2
ECG ANALYSIS the medulla oblongata. One centre, the nucleus

ambiguus, provides parasympathetic input
Rate 60/min to the heart via the vagus nerve, affecting the
Rhythm Sinus arrhythmia sinoatrial node. Inspiration signals the nucleus
accumbens to inhibit the vagus nerve, increas-
ing heart rate, while expiration increases vagal
P waves Normal activity and reduces heart rate.)
4. No action is needed. Reassure the patient (and
the pre-assessment clinic staff) that sinus
QRS duration Normal (100 ms) arrhythmia is a normal finding.
T waves Normal
QTc interval Normal (400 ms) COMMENTARY
ANSWERS • Sinus arrhythmia is of no pathological

consequence.
1. Every P wave is followed by a normal QRS com- • Sinus arrhythmia is usually only seen in indi-
viduals below the age of 30 years.
plex, but the heart rate varies. Observation of the
patient confirms that this coincides with respira- • Normally, the heart rate in sinus rhythm changes
tion, with the heart rate increasing on inspira- very little at rest. In sinus arrhythmia, the slight
tion and decreasing on expiration. This is sinus variation in cycling usually exceeds 120 ms
arrhythmia. between the longest and the shortest cycle (cycle
length is equal to the interval between successive
2. There is variation in the heart rate in response
R waves, the RR interval).
to respiration, increasing reflexly during inspi-
ration (due to increased venous return to the • Sinus arrhythmia may be aggravated by any fac-
heart) and decreasing during expiration. tor that increases vagal tone.
3. This is a normal physiological response. The
exact mechanism of sinus arrhythmia has been Further Reading
the subject of investigation and debate for many
Making Sense of the ECG 6th edition: Sinus arrhythmia,
years. There is some evidence that the respi- p 164; Is the ventricular rhythm regular or irregular?
ratory variation in heart rate is mediated via p 51.
carotid baroreceptors and/or cardiopulmonary Piepoli M et al. Origin of respiratory sinus arrhythmia in con-
receptors. Others suggest a central mechanism. scious humans. An important role for arterial carotid
(Heart rate is normally controlled by centres in baroreceptors. Circulation (1997). PMID 9107168.
CASE 3
CLINICAL SCENARIO
Female, aged 36 years. Examination
Pulse: 72/min, regular with occasional prema-
Presenting complaint ture beat.
Palpitations. Blood pressure: 118/76.
JVP: not elevated.
History of presenting complaint Heart sounds: normal.
Six-month history of ‘missed beats’ occurring Chest auscultation: unremarkable.
at rest, particularly when lying quietly in bed. No peripheral oedema.
Symptoms are more troublesome after drinking
coffee. Investigations
FBC: Hb 138, WCC 5.7, platelets 240.
Past medical history U&E: Na 141, K 4.3, urea 2.8, creatinine 68.
Nil. Thyroid function: normal.
QUESTIONS
2. What advice would you offer?
3. Is any drug treatment required?
DOI: 10.1201/9781003472186-3
ECG ANALYSIS atrial premature beats (APBs) or premature

atrial contractions (PACs). Atrial ectopic beats
Rate 72/min occur earlier than expected (in contrast with
Rhythm Sinus rhythm with an atrial ectopic beat escape beats, which occur later than expected).
• Atrial ectopic beats can arise from any part of
the atria, and the shape of the P wave depends
P waves Present upon where in the atria the ectopic has arisen
from. In this patient’s ECG, the P wave of the
atrial ectopic beat has a shape very similar to
QRS duration Normal (70 ms) the P wave of a normal sinus beat, suggesting
T waves Normal an ectopic focus near to the sinoatrial node. In
QTc interval Normal (416 ms)
contrast, atrial ectopic beats that arise from low
down in the atria, near the atrioventricular node,
will have P waves that are inverted in the inferior
Additional comments leads but upright in lead aVR. This is because the
The P wave associated with the atrial ectopic beat is wave of depolarization will predominantly move
visible just towards the end of the preceding T wave. upwards in the atria, rather than downwards
from the sinoatrial node. The P wave may also
ANSWERS appear very close to, or overlap with, the QRS
complex, as a focus of depolarization near the
1. This ECG shows normal sinus rhythm with a atrioventricular node will reach the ventricles
single atrial ectopic beat (the seventh beat along more quickly than one that has to travel from the
the rhythm strip). sinoatrial node.
2. The caffeine in coffee and in some cola drinks • Avoidance of triggers such as caffeine, alco-
can be a trigger for atrial ectopic beats, and so hol and nicotine is often sufficient to reduce
advise the patient to switch to decaffeinated the frequency of atrial ectopic beats. They are
alternatives. Other cardiac stimulants (such as generally benign, and so drug treatment is not
alcohol and nicotine) can also act as triggers and usually needed unless the associated sensation
should be moderated or avoided as appropriate. of palpitations is very frequent and trouble-
3. Drug treatment is seldom required unless the some. If treatment is required, beta-blockers
atrial ectopic beats cause particularly trouble- can be effective in suppressing atrial ectopic
some symptoms. activity.
COMMENTARY Further Reading

• Atrial ectopic beats are also known as atrial extra- Making Sense of the ECG 6th edition: Atrial ectopic beats,
systoles, atrial premature complexes (APCs), p 167.
CASE 4
CLINICAL SCENARIO
Pulse: 66/min, regular.
Presenting complaint Blood pressure: 152/98.
Asymptomatic. JVP: not elevated.
Heart sounds: normal.
History of presenting complaint Chest auscultation: unremarkable.
Patient had recently moved house. She saw her No peripheral oedema.
new family doctor for a routine health check
which included an ECG. Automated print-out Investigations
reported ‘abnormal ECG’. FBC: Hb 124, WCC 6.7, platelets 296.
Past medical history Chest X-ray: normal heart size, clear lung fields.
Mild hypertension. Echocardiogram: trivial mitral regurgitation into
Diet-controlled diabetes mellitus. a nondilated left atrium. Normal left ventricular
Osteoarthritis and bilateral hip replacements. function.
QUESTIONS
3. What are the likely causes?
DOI: 10.1201/9781003472186-4
ECG ANALYSIS 60 years and around 6% of those over 60 years.

It is a common feature of vagally induced brady-
Rate 66/min cardia, particularly in athletic individuals, as an
Rhythm Sinus rhythm increase in vagal tone decreases atrioventricular
nodal conduction.
4. First-degree atrioventricular block can also be a
P waves Normal feature of conduction system fibrosis, ischaemic
PR interval Prolonged (240 ms)
heart disease, electrolyte abnormalities (e.g. hypo-
kalaemia), acute rheumatic myocarditis, Lyme
QRS duration Normal (100 ms) disease and drugs such as beta-blockers, rate-lim-
T waves Normal iting calcium channel blockers and digoxin.
COMMENTARY
ANSWERS • First-degree atrioventricular block is asymp-
tomatic and no action is indicated. It rarely
1. The PR interval (which is measured from the
progresses to second- or third-degree atrioven-
start of the P wave to the start of the QRS com-
tricular block. It should, however, raise the possi-
plex) is greater than 200 ms, so conduction
bility of one of the diagnoses listed earlier (which
through the atrioventricular node is delayed;
may require treatment in its own right).
this delay is constant for each cardiac cycle. This
is first-degree atrioventricular block (‘first- • First-degree atrioventricular block is not an indi-
cation for pacing.
degree heart block’).
2. First-degree atrioventricular block is caused by
delayed conduction of the atrial impulse to the Further Reading
ventricles through the atrioventricular node. Making Sense of the ECG 6th edition: First-degree atrioven-
3. First-degree atrioventricular block is present tricular block, p 202; Is the PR interval more than
in around 1% of individuals below the age of 0.2s long? p 82.
CASE 5
CLINICAL SCENARIO
Fatigue. JVP: not elevated.
The patient has a history of resistant hyperten- No peripheral oedema.
sion and his medication was amended 6 weeks
ago. Since that time he has felt tired and has Investigations
noticed a reduction in his exercise capacity. FBC: Hb 138, WCC 7.6, platelets 313.
Past medical history
Hypertension, treated with ramipril, indapamide,
amlodipine and, for the last six weeks, atenolol.
QUESTIONS
1. What rhythm is seen on this ECG?
2. What investigations would be appropriate?
3. What treatment is needed?
4. Is a pacemaker required?
DOI: 10.1201/9781003472186-5
ECG ANALYSIS COMMENTARY

Rate 42/min • Sinus bradycardia can be a normal finding in
Rhythm Sinus bradycardia athletic individuals and also in most people dur-
ing sleep.
• Always looks for correctable causes such as drug
P waves Normal treatment (particularly beta-blockers, digoxin,
ivabradine, or rate-limiting calcium channel
blockers, such as verapamil). Do not forget about
QRS duration Normal (100 ms) beta-blocking eye drops, which can have sys-
T waves Normal temic effects.
QTc interval Normal (368 ms) • Other causes include hypothyroidism, hypo-
thermia, myocardial ischaemia and infarction,
raised intracranial pressure (look for the combi-
nation of falling pulse and rising blood pressure),
ANSWERS
uraemia, obstructive jaundice, electrolyte abnor-
1. Sinus bradycardia, with a heart rate of 42/min. malities and sick sinus syndrome.
2. In addition to the FBC and U&E listed, it • Permanent pacing is a treatment for symptomatic
would be appropriate to do thyroid function bradycardia, but it is essential to make sure that
tests (to exclude hypothyroidism). An echo- other correctable causes are identified and treated
cardiogram would determine whether left first – in this case, withdrawal of any negatively
ventricular dysfunction is contributing to the chronotropic drugs (those that slow the heart).
patient’s fatigue. Sometimes temporary transvenous pacing is
3. A reduction in the dose of the beta-blocker, and required to support the patient, if they are severely
possibly its complete withdrawal. Any reduc- symptomatic from their bradycardia, while any
tions in beta-blocker dose must be undertaken correctible causes are identified and treated.
gradually to reduce the risk of ‘rebound’ tachy-
cardia or hypertension. Further Reading
4. A pacemaker is unlikely to be necessary –
Making Sense of the ECG 6th edition: Sinus bradycardia,
the clinical history makes it likely that
p 164; Indications for temporary pacing, p 224;
the fatigue and bradycardia resulted from Indications for permanent pacing, p 225.
the recent introduction of a beta-blocker, so the NICE clinical guideline NG136 – Hypertension in adults:
patient’s fatigue should resolve on withdrawal Diagnosis and management. 2023. Downloadable
of this. from www.nice.org.uk/guidance/ng136.
CASE 6
CLINICAL SCENARIO
Pulse: 132/min, irregularly irregular.
Presenting complaint Blood pressure: 120/70 approximately.
Palpitations and breathlessness. JVP: not seen (obese).
History of presenting complaint Chest auscultation: fine basal crackles.
The patient had been well until 3 days ago. She No peripheral oedema.
noticed her heart beating faster when walking.
She had also started to struggle when doing Investigations
housework. FBC: Hb 117, WCC 5.6, platelets 310.
Past medical history Thyroid function: normal.
Ischaemic heart disease for 10 years. When she Troponin I: negative.
recently moved house and changed doctor, her Chest X-ray: mild cardiomegaly.
usual beta-blocker was omitted in error from the Echocardiogram: mild mitral regurgitation into
repeat prescription. nondilated left atrium. Left ventricular systolic
function impaired (ejection fraction 43%).
QUESTIONS
DOI: 10.1201/9781003472186-6
ECG ANALYSIS screen for structural heart disease. Risk stratify

the patient with regard to thromboembolic (and
Rate 132/min bleeding) risk and anticoagulate as appropri-
Rhythm Atrial fibrillation ate. Decide whether attempting to restore (and
maintain) sinus rhythm would be appropriate,
QRS axis Normal (−4°)
or whether to accept AF and pursue a rate con-
P waves Absent trol strategy. Where appropriate, investigations
for coronary artery disease may also be required.
PR interval N/A
Where necessary, ventricular rate control can be
QRS duration Prolonged (140 ms) achieved with beta-blockers, rate-limiting cal-
T waves Inverted (leads V1–V4) cium channel blockers, digoxin, or if other alter-
natives cannot be used, amiodarone.
QTc interval Mildly prolonged (474 ms)
COMMENTARY
Additional comments
There is a right bundle branch block (RBBB), which • AF is common (the commonest sustained
accounts for the T wave inversion. arrhythmia) and its prevalence increases with
age.
ANSWERS
• AF may be:
• First diagnosed – namely, patients present-
ing in atrial fibrillation for the first time
1. The irregularly irregular rhythm with no dis-
cernible P waves means that this is atrial fibril- • Paroxysmal – self-terminating episodes, typ-
ically lasting <48 h, although they can last up
lation (AF) with a fast ventricular response.
to 7 days
There is also RBBB.
2. The basis of AF is rapid, chaotic depolarization • Persistent – an episode of continuous atrial
fibrillation lasting >7 days or requiring
occurring throughout the atria as a consequence
cardioversion
of multiple ‘wavelets’ of activation. No P waves
are seen and the ECG baseline consists of low- • Long-standing persistent – where AF has
amplitude oscillations (fibrillation or ‘f’ waves). been present for at least one year, but there is
Although around 400–600 impulses reach the still an aim to restore sinus rhythm
AV node every minute, only some will be trans- • Permanent – continuous AF where the
mitted to the ventricles. The ventricular rate is arrhythmia is ‘accepted’, and there is no plan
typically fast (100–180/min), although the rate to restore sinus rhythm.
can be normal or even slow. Transmission of the • AF may be asymptomatic but can be accompa-
atrial impulses through the AV node is erratic, nied by awareness of an irregular heartbeat, dys-
making the ventricular (QRS complex) rhythm pnoea, fatigue, dizziness and syncope.
‘irregularly irregular’. • The presence of AF increases a patient’s stroke
3. There are many possible causes of AF. These risk fivefold, and one in five strokes occurs as a
include hypertension, ischaemic heart disease, result of AF. Strokes that occur in AF are more
valvular heart disease, cardiomyopathies, myo- likely to be disabling or fatal.
carditis, atrial septal defect and other congenital • For patients with prosthetic mechanical heart
heart disease, hyperthyroidism, alcohol, pulmo- valves or moderate-severe mitral stenosis, anti-
nary embolism, pneumonia and cardiac surgery. coagulation with warfarin is recommended for
4. Patients with AF require a careful assessment to all, unless there are contraindications.
identify (and treat) the underlying cause. This • For all other patients, decisions on anticoagula-
includes a thorough history and examination, tion should be based upon the CHA2DS2-VASc
12-lead ECG and blood tests to check electrolytes scoring system together with an assessment for
and renal function, thyroid function tests and a potential bleeding risk using the HAS-BLED
full blood count. Echocardiography is used to scoring system.
Case 6 15
Further Reading
Making Sense of the ECG 6th edition: Atrial fibrillation, p Hindricks G et al. 2020 ESC guidelines for the diagnosis
168; Is the ventricular rhythm regular or irregular? and management of atrial fibrillation developed
p 51. in collaboration with the European association for
cardio-thoracic surgery (EACTS). European Heart
Journal (2021). PMID 32860505.
CASE 7
CLINICAL SCENARIO
Clammy, in pain.
Crushing central chest pain. Blood pressure: 148/82.
JVP: not elevated.
Two-hour history of crushing central chest pain, Chest auscultation: unremarkable.
which awoke the patient at 4:00 a.m. The pain No peripheral oedema.
radiates to the left arm and is associated with
breathlessness, nausea and sweating. Investigations
Angina diagnosed 1 year ago. Troponin I: elevated.
Hypertension diagnosed 6 years ago. Chest X-ray: normal heart size, clear lung fields.
Active cigarette smoker (48 pack-year smoking Echocardiogram: akinesia of inferior wall of left
history). ventricle, overall ejection fraction 50%.
QUESTIONS
2. What other type of ECG recording should be performed? Why should this be done?
3. What treatment is indicated?
4. Should this ECG be repeated? When should it be repeated and why?
DOI: 10.1201/9781003472186-7

Rate 85/min • An urgent ECG is required in any patient pre-
Rhythm Sinus rhythm senting with cardiac-sounding chest pain. The
presence of ST segment elevation signifies acute
QRS axis Normal (+10°) occlusion of a coronary artery and indicates a
P waves Present need for urgent restoration of coronary blood
flow (reperfusion), usually with primary PCI.
Time is of the essence – the longer reperfusion
QRS duration Normal (92 ms) is delayed, the more myocardial necrosis will
T waves Lateral T inversion occur.
• The right ventricle is involved in 10–50% of infe-
rior ST segment elevation myocardial infarctions.
It can be diagnosed by performing an ECG using
Additional comments right-sided chest leads (V1R–V6R) and looking for
There is ST segment elevation in the inferior leads ST segment elevation in V4R. Right ventricular
(II, III, aVF) with reciprocal ST/T wave changes in infarction is important to recognize because it can
the lateral leads (I, aVL, V5–V6). have significant haemodynamic consequences.
It may lead to signs of right heart failure (raised
jugular venous pressure and peripheral oedema).
ANSWERS If these patients develop hypotension, this may be
because of failure of the right ventricle to pump
1. This ECG shows an acute inferior ST segment
sufficient blood to the left ventricle. Thus, despite
elevation myocardial infarction (STEMI).
the signs of right heart failure, it may be necessary
2. Another ECG should be performed immediately
to give intravenous fluids to maintain left heart
using right-sided chest leads (V1R–V6R) to look
filling pressures. This is one situation in which
for evidence of right ventricular involvement in
haemodynamic monitoring with a pulmonary
the inferior myocardial infarction.
artery catheter can prove helpful.
3. Having diagnosed STEMI, the key priority is
urgent coronary revascularization, which is usually
• The differential diagnosis of ST segment elevation
includes acute myocardial infarction, left ventric-
undertaken with primary percutaneous coronary
ular aneurysm, Prinzmetal’s (vasospastic) angina,
intervention (PCI). Primary PCI is usually per-
pericarditis, high take-off left bundle branch
formed in patients with acute STEMI presenting
block and Brugada syndrome.
within 12 h of the onset of symptoms. If primary
PCI is unavailable, then intravenous administra-
tion of a thrombolytic agent may be considered.
4. Yes – if thrombolysis is used, the ECG must be Further Reading
repeated 90 min after the start of thrombolysis to
Making Sense of the ECG 6th edition: Are the ST segments
determine whether coronary reperfusion has suc- elevated? p 113; ST segment elevation myocardial
cessfully been achieved. This is shown by resolution infarction, p 114; Why is right ventricular infarction
of the ST segment elevation by ≥50%. In addition, important? p 119.
whether primary PCI or thrombolysis is used, the Byrne RA et al. 2023 ESC guidelines for the manage-
ECG must be monitored throughout coronary ment of acute coronary syndromes. European Heart
reperfusion because of the risk of arrhythmias. Journal (2023). PMID 37622654.
CASE 8
CLINICAL SCENARIO
Pulse: 84/min.
Exertional chest pain, usually when walking JVP: not elevated.
uphill in cold and windy weather. Heart sounds: normal.
Had been referred to hospital a few years ago
with symptoms of exertional chest pain and Investigations
diagnosed with angina. FBC: Hb 127, WCC 6.4, platelets 400.
Past medical history Chest X-ray: mild cardiomegaly, early pulmonary
Hypertension – well controlled. congestion.
Mild chronic airways disease. Echocardiogram: impaired left ventricular sys-
Type 2 diabetes mellitus. tolic function (ejection fraction 42%).
Is scheduled for prostatectomy – this ECG was
recorded at preoperative assessment clinic.
QUESTIONS
2. What is the underlying mechanism?
DOI: 10.1201/9781003472186-8
ECG ANALYSIS more commonly causes right bundle branch

block).
Rate 84/min 3. The causes of LBBB include ischaemic heart
Rhythm Sinus rhythm disease, cardiomyopathy, left ventricular hyper-
trophy (secondary to hypertension or aortic ste-
QRS axis Left axis deviation (−51°)
nosis) and fibrosis of the conduction system.
P waves Normal 4. The presence of LBBB is almost invariably path-
PR interval Normal (160 ms) ological. Investigations are appropriate in the
clinical context of chest pain, breathlessness and
QRS duration Prolonged (125 ms)
palpitations and also when LBBB is an inciden-
T waves Inverted in leads I, aVL, V6 tal finding preoperatively. Echocardiography is
useful in looking for cardiomyopathy, left ven-
tricular hypertrophy and valve disease. Options
to investigate for evidence of ischaemic heart
ANSWERS disease include functional imaging (stress echo-
cardiography, stress cardiac MRI, or nuclear
1. This ECG shows sinus rhythm with broadened myocardial perfusion imaging) or anatomical
and notched QRS complexes (QRS duration >120 imaging (CT or invasive coronary angiography).
ms), QS in lead V1 and a broad-notched R wave
in V6: this is left bundle branch block (LBBB).
2. LBBB results from a failure of conduction in the COMMENTARY
left bundle branch. The left ventricle must be
activated indirectly via the right bundle branch,
• LBBB is commonly seen in the elderly. In the
absence of symptoms or when perioperative risk
so the right ventricle is activated before the left
assessment is not warranted, no investigations
ventricle. This lengthens the overall duration of
are necessary.
ventricular depolarization and therefore broad-
ens the QRS complexes (greater than 120 ms) and
also distorts the QRS complexes. Repolarization Further Reading
is also abnormal, and ST segment depression and Making Sense of the ECG 6th edition: Bundle branch block,
T wave inversion are frequently seen. LBBB may p 106; Left bundle branch block, p 205.
also be intermittent – especially in acute myocar- Francia P et al. Left bundle-branch block – Pathophysiology,
dial ischaemia. It may also occur with tachycar- prognosis, and clinical management. Clinical
dia (although rate-related bundle branch block Cardiology (2007). PMID 17385703.
CASE 9
CLINICAL SCENARIO
Pulse: 60/min, occasional irregularity.
Palpitations. JVP: not elevated.
Six-month history of intermittent palpita- No peripheral oedema.
tions, feeling like ‘missed beats’, particularly at
rest. Otherwise asymptomatic. No chest pain, Investigations
breathlessness, pre-syncope, or syncope. No FBC: Hb 147, WCC 6.3, platelets 365.
prolonged episodes of palpitation. U&E: Na 141, K 4.5, urea 4.8, creatinine 89.
Nil.
QUESTIONS
1. What rhythm is seen on this ECG?
2. What investigations might be appropriate?
3. What treatment options are available?
DOI: 10.1201/9781003472186-9
ECG ANALYSIS ventricular contractions (PVCs), are a common

finding and are often asymptomatic. They can,
Rate 60/min however, cause troublesome palpitations and
Rhythm Sinus rhythm with a single sometimes herald a risk of dangerous arrhyth-
ventricular ectopic beat mias. Patients with VEBs therefore require
appropriate clinical assessment.
QRS axis
P waves
Normal (+6°)
Present
• VEBs cause broad QRS complexes and occur
earlier than the next normal beat would have
PR interval Normal (140 ms) occurred. VEBs may be followed by inverted
P waves if the atria are activated by retrograde
QRS duration Normal (80 ms)
conduction. If retrograde conduction does not
T waves Normal occur, there will usually be a full compensatory
QTc interval Normal (380 ms) pause before the next normal beat because the
sinoatrial node will not be ‘reset’.
ANSWERS
• Two consecutive VEBs are termed a couplet;
three or more are termed ventricular tachycardia
(VT).
1. This ECG shows sinus rhythm with a single ven-
tricular ectopic beat (VEB). • Multiple VEBs which share the same QRS com-
plex morphology originate from a single focus
2. VEBs are often benign, but some patients may
within the ventricles and are therefore called
be at risk of dangerous ventricular arrhythmias.
unifocal. Where VEBs have two or more differ-
Assessment should include a full history and
ent morphologies, they arise from different foci
examination and needs to be particularly thor-
and are called multifocal.
ough in those with structural heart disease or
risk factors for sudden cardiac death (e.g. fam- • Causes of VEBs include myocardial ischaemia/
ily history). Investigations may need to include a infarction, electrolyte disturbance (e.g. hypoka-
check of serum electrolytes, 12-lead ECG, echo- laemia, hypomagnesaemia), myocarditis, cardio-
cardiography, ambulatory ECG monitoring (to myopathy, caffeine, alcohol, sympathomimetic
quantify the frequency of VEBs and to screen drugs and digoxin toxicity.
for ventricular tachycardia) and imaging inves- • If VEBs are infrequent, and if structural heart
tigations to look for evidence of coronary artery disease and documented VT are absent, the
disease. prognosis is generally good.
3. Identify and address any underlying causes • Beta-blockers can be useful in those with trou-
(e.g. high caffeine intake, electrolyte abnor- blesome symptoms but otherwise benign VEBs,
malities, myocardial ischaemia, cardio- although reassurance alone may suffice in this
myopathy). Benign VEBs may require just patient group. Where feasible, catheter ablation
reassurance, although beta-blockers may help can be considered where symptoms are trouble-
if symptoms are troublesome. Patients at risk some or there is a risk of malignant arrhythmias.
of dangerous arrhythmias may require cath- An implantable cardioverter defibrillator is also
eter ablation or an implantable cardioverter an option to provide protection from dangerous
defibrillator. arrhythmias.

Making Sense of the ECG 6th edition: Ventricular ectopic
• VEBs, also known as ventricular extrasystoles, beats, p 187.
ventricular premature complexes (VPCs), ven- Ng GA. Treating patients with ventricular ectopic beats.
tricular premature beats (VPBs), or premature Heart (2006). PMID 17041126.
CASE 10
CLINICAL SCENARIO
Pulse: 120/min.
Direct questioning reveals that the patient is No peripheral oedema.
aware of an episodic fast heartbeat, particularly
at times of stress and anxiety. Recently started Investigations
studying at a local college and has been finding FBC: Hb 129, WCC 6.5, platelets 356.
the coursework stressful. U&E: Na 141, K 4.1, urea 3.8, creatinine 86.
Nil of note. Echocardiogram: normal valves and normal left
ventricular function (ejection fraction 67%).
QUESTIONS
DOI: 10.1201/9781003472186-10
ECG ANALYSIS to slow an ‘appropriate’ sinus tachycardia can

lead to haemodynamic decompensation.
Rate 120/min
Rhythm Sinus tachycardia COMMENTARY
QRS axis
P waves
Normal (+35°)
Normal
• Clinical examination is essential. Request thy-
roid function tests. Catecholamine levels may be
PR interval Normal (136 ms) abnormal (phaeochromocytoma) – check espe-
cially if there is a history of hypertension.
QRS duration
T waves
Normal (98 ms)
Normal
• Palpitations can be documented using:

• 12-lead ECG – most useful if the patient com-
plains of palpitations during the recording
• 24 h (or longer) ambulatory ECG recording –
if palpitations are infrequent, the patient will
ANSWERS have nothing to record
1. There is a normally shaped P wave before every • Cardiomemo – this patient-activated device
QRS complex. This is sinus tachycardia (sinus may be carried for several weeks until an epi-
rhythm with a heart rate greater than 100/min). sode of palpitations occurs
2. Sinus tachycardia is usually a normal physi- • Implantable ECG loop recorder – this is particu-
ological response to physical or emotional larly useful if palpitations are infrequent but a
stress. There are numerous potential causes, serious arrhythmia is still suspected. The device
including pain, anaemia, fever, drugs (e.g. is implanted subcutaneously and records the
adrenaline, atropine, salbutamol [do not forget ECG continuously, storing periods that show
inhalers and nebulizers], caffeine and alcohol), arrhythmias or coincide with symptoms
ischaemic heart disease and acute myocardial • Symptoms sometimes give a clue as to the under-
infarction, heart failure, pulmonary embo- lying rhythm disturbance:
lism, fluid loss and hyperthyroidism. Rarely, it
can be the result of a primary sinoatrial node
• Heart ‘ jumping’ or ‘missing a beat’– ectopics
(atrial or ventricular)
abnormality.
3. First, it is important to establish that a tachycar-
• Intermittent rapid erratic heartbeat – parox-
ysmal atrial fibrillation
dia is indeed sinus tachycardia, as atrial tachy-
cardia and atrial flutter can both resemble sinus
• Sustained rapid regular palpitations with
abrupt onset and termination – atrioventricu-
tachycardia if the ECG is not inspected carefully lar re-entry tachycardia or atrioventricular
enough. Second, a careful assessment of the nodal re-entry tachycardia
patient is required to establish the cause of the
sinus tachycardia and whether or not it is hae-
modynamically ‘appropriate’ (compensating for Further Reading
low blood pressure such as fluid loss or anaemia) Making Sense of the ECG 6th edition: Sinus tachycardia,
or ‘inappropriate’ (e.g. anxiety, thyrotoxicosis). p 165; Ambulatory ECG recording, p 233.
Third, although beta-blockers are effective at Olshansky B et al. Inappropriate sinus tachycardia.
slowing sinus tachycardia, using a beta-blocker Europace (2019). PMID 23265330.
CASE 11
CLINICAL SCENARIO
Male, aged 66 years. JVP: not elevated.
Heart sounds: 3/6 pan-systolic murmur at apex,
Presenting complaint radiating to axilla.
Progressive exertional breathlessness. Chest auscultation: bilateral inspiratory crackles
at both lung bases.
No peripheral oedema.
History of presenting complaint
Normally active, he had noticed a gradual fall in
Investigations
his exercise capacity over a 2-week period prior to
presentation. The main limiting factor in his exer- FBC: Hb 139, WCC 8.1, platelets 233.
cise was breathlessness. He had not experienced U&E: Na 137, K 4.2, urea 5.3, creatinine 88.
any orthopnoea or paroxysmal nocturnal dys- Thyroid function: normal.
pnoea, and did not have any peripheral oedema. Troponin I: negative.
Chest X-ray: mild cardiomegaly, early pulmonary
congestion.
Echocardiogram: anterior mitral valve leaflet
Mitral valve prolapse with moderate mitral prolapse with posteriorly directed jet of mod-
regurgitation. erate mitral regurgitation into a moderately
dilated left atrium. Left ventricular systolic func-
Examination tion impaired (ejection fraction 47%).
QUESTIONS
1. What rhythm does this ECG show?
2. What is the mechanism of this arrhythmia?
3. How can the atrial rhythm be demonstrated more clearly?
4. What are the key issues in managing this arrhythmia?
DOI: 10.1201/9781003472186-11
ECG ANALYSIS • There is a thromboembolic risk, and so con-

sider the patient for antithrombotic therapy
Rate 75/min in the same way as for atrial fibrillation.
Rhythm Atrial flutter • Electrical cardioversion can be very effective
QRS axis Normal (+68°) in restoring sinus rhythm and, as a general
rule, atrial flutter is easier to cardiovert than
P waves Absent – atrial flutter waves are present
atrial fibrillation.
PR interval Not applicable • Electrophysiological intervention with radio
frequency ablation of the atrial flutter re-entry
circuit is an effective procedure with a success
T waves Normal rate >95%.

The ‘sawtooth’ pattern of atrial flutter is clearly evi-
dent, particularly in the inferior leads (II, III and
• Atrial flutter is often considered to be a subtype
of atrial tachycardia and is characterized by a
aVF) and in chest lead V1. There is one QRS com- macro re-entry circuit, typically within the right
plex for every 4 flutter waves (note that one flutter atrium and involving the cavotricuspid isthmus
wave is masked by each QRS complex), indicating (CTI-dependent or Type I flutter). Less com-
4:1 atrioventricular block. monly, other forms of flutter are seen that do not
involve the CTI (non-CTI-dependent or Type II
ANSWERS flutter). These usually occur in relation to an area
of scar tissue in the atria, often in the context of
1. Atrial flutter with 4:1 atrioventricular block. prior cardiac surgery.
2. Atrial flutter usually results from a macro re- • Although the atria depolarize around 300 times/
entry circuit within the right atrium (although min in atrial flutter, the atrioventricular node
other variants are recognized). The atria typi- (fortunately) cannot conduct impulses to the ven-
cally depolarize 300 times/min, giving rise to tricles that quickly, so after conducting an impulse
300 flutter waves/min. However, depending on the node will remain refractory for the next one,
the type of atrial flutter, flutter rates can vary two or even more impulses until it is ready to
between 250/min and 350/min. conduct again. In this example, the node is con-
3. Flutter waves are best seen in the inferior leads ducting every fourth flutter wave to the ventricles,
and in lead V1. They can be difficult to see when giving rise to 4:1 atrioventricular block.
the ventricular rate is higher (e.g. with 2:1 or 3:1 • The heart rate will vary according to the degree of
block) as the flutter waves are masked by the atrioventricular block – ventricular rates often run
overlying QRS complexes. Temporary blocking at 150/min (2:1 block), 100/min (3:1 block) or 75/
of the atrioventricular node with carotid sinus min (4:1 block). The block can be variable, with a
massage or adenosine (except where contra- varying heart rate and an irregular pulse.
indicated) can block the QRS complexes for a • Atrial flutter with 2:1 block is particularly com-
few seconds, revealing the atrial activity more mon. In cases of 2:1 block the ventricular rate is
clearly. around 150/min. Always consider a diagnosis of
4. There are four key aspects to the treatment of atrial flutter whenever someone presents with a
atrial flutter: regular narrow-complex tachycardia and a ven-
• Ventricular rate control – the drugs used tricular rate of 150/min.
for ventricular rate control are the same as • The differential diagnosis of atrial flutter includes:
those for atrial fibrillation (beta-blockers or • Atrial tachycardia – The atrial rate is usually
rate-limiting calcium channel blockers [e.g. lower, and the atrial activity is marked by abnor-
verapamil, diltiazem] and/or digoxin). mally shaped P waves rather than flutter waves.
Case 11 27
Further Reading
• Atrial fibrillation – Can be mistaken for atrial Making Sense of the ECG 6th edition: Atrial flutter,
flutter with variable block. Atrial activity in p 173.
atrial fibrillation is less well defined on the Brugada J et al. 2019 ESC guidelines for the manage-
ECG than the sawtooth pattern seen in atrial ment of patients with supraventricular tachycardia.
flutter. European Heart Journal (2020). PMID 31504425.
CASE 12
CLINICAL SCENARIO
Severe ‘crushing’ central chest pain. JVP: not elevated.
Chest pain on exertion for 3 months but put it No peripheral oedema.
down to indigestion. Tried over-the-counter ant-
acids and pain eventually got better. However, Investigations
he was then woken from sleep with severe chest FBC: Hb 155, WCC 6.9, platelets 198.
pain. Started to have difficulty breathing. U&E: Na 139, K 5.1, urea 4.4, creatinine 96.
Past medical history Troponin I: normal (at 3 h).
Hypertension for 10 years. Chest X-ray: no cardiomegaly, mild pulmonary
Smoker of 30 cigarettes per day for 40 years. congestion.
Echocardiogram: normal valves. Mild concentric
left ventricular hypertrophy. Left ventricular sys-
tolic function impaired (ejection fraction 46%).
QUESTIONS
DOI: 10.1201/9781003472186-12

Rate 90/min • Cardiac-sounding chest pain may be due to an
Rhythm Sinus rhythm acute coronary syndrome, classified on the basis
of the ECG as:
• ST segment elevation myocardial infarc-
P waves Normal tion (STEMI): the ECG shows ST segment
elevation and the primary aim of treatment is
reopening of the coronary artery and reper-
QRS duration Normal (90 ms) fusion of the myocardium via urgent primary
T waves Normal PCI (or thrombolysis depending on local
availability).
• Non-ST segment elevation acute coronary
syndrome (NSTEACS): the ECG may be nor-
Additional comments mal or may show ST segment depression or
There is ST segment depression in leads V2–V6 and T wave inversion. The primary aim of treat-
aVL. ment is urgent antiplatelet, antithrombotic,
and anti-ischaemic drug treatment, followed
ANSWERS by coronary angiography and revasculariza-
tion as appropriate.
1. The ECG shows sinus rhythm. There is ST seg- • In the case of NSTEACS, cases are subsequently
ment depression in leads V2–V6 and aVL, indi- divided into non-ST segment elevation myocar-
cating myocardial ischaemia in the territory of dial infarction (NSTEMI) or unstable angina
the left anterior descending coronary artery. (UA) once the high-sensitivity troponin (I or
As the high-sensitivity troponin level remained T) results become available. The subgroup of
normal at 3 h, this represents unstable angina. patients with an elevated troponin level is clas-
2. The mechanism of this ischaemia is likely to be sified as having had a NSTEMI; those whose
a reduction in blood flow to the myocardium troponin level remains normal are classified as
because of a degree of obstruction to flow down having UA.
the left anterior descending coronary artery. In • As well as providing a diagnostic label, high-sen-
view of the clinical presentation (acute coronary sitivity troponin results are helpful in allowing
syndrome), it is likely that a previously stable cor- risk stratification – the degree of troponin eleva-
onary endothelial plaque has ruptured, exposing tion predicts a higher risk of future cardiovascu-
the lipid-rich core. Platelets adhere, change shape lar events.
and secrete adenosine diphosphate (ADP) and
other pro-aggregants; this may ‘seal’ and stabilize
the plaque, but the lumen may be at least partially Further Reading
obstructed, reducing blood flow. Making Sense of the ECG 6th edition: Are the ST segments
3. Admit the patient to a monitored area. Give pain depressed? p 126; Myocardial ischaemia, p 127.
relief with opiates with or without intravenous Byrne RA et al. 2023 ESC guidelines for the manage-
nitrates; beta-blockers with or without calcium ment of acute coronary syndromes. European Heart
Journal (2023). PMID 37622654.
channel blockers; and antiplatelets and anti-
NICE clinical guideline NG185 – Acute coronary syn-
thrombotics per local protocols. Check high-
dromes. 2020. Downloadable from www.nice.org.
sensitivity troponin levels to aid diagnosis and uk/guidance/ng185.
help formulate management. Arrange coronary Wagner GS et al. AHA/ACCF/HRS recommendations for
angiography to define coronary anatomy and, as the standardization and interpretation of the elec-
appropriate, to plan coronary revascularization trocardiogram: Part VI: Acute ischaemia/infarction.
with percutaneous coronary intervention (PCI) Journal of the American College of Cardiology (2009).
or coronary artery bypass grafting. PMID 19281933.
CASE 13
CLINICAL SCENARIO
Angina.
Presenting complaint Type 2 diabetes mellitus.
Six-month history of worsening exertional chest Hypertension.
pain.
Examination
History of presenting complaint Patient supine in cardiac catheter department,
Listed for urgent coronary angiography to inves- undergoing coronary angiography. Appears
tigate his chest pain. This ECG was recorded dur- pale and clammy.
ing his coronary angiogram, which had revealed Blood pressure: 158/88, falling rapidly to
a severe left main stem coronary stenosis. The become unrecordable while this ECG was
ECG shown earlier was recorded just after the recorded. Patient became unresponsive during
first injection of contrast into the left coronary this ECG recording.
artery. The patient complained of chest pain
and then became unresponsive. Investigations
Glucose: 8.3 (known diabetes).
QUESTIONS
2. What immediate action should be taken?
3. What medium-term action should be taken?
DOI: 10.1201/9781003472186-13
ECG ANALYSIS peripheral perfusion, cardiac rhythm, neurolog-

ical status (including Glasgow Coma Scale score)
Rate 52/min (during sinus rhythm), then and urine output and fluid balance. In addition,
unmeasurable check arterial blood gases, blood urea and elec-
Rhythm Sinus rhythm with ventricular ectopics, trolytes (including potassium, magnesium and
followed by ventricular tachycardia (VT) calcium), chest X-ray and blood glucose, 12-lead
which rapidly degenerates into ECG and full blood count. In view of the critical
ventricular fibrillation (VF) nature of the patient’s coronary disease, arrange
QRS axis Left axis deviation (the axis moves urgent revascularization.
increasingly leftward during the four
sinus beats)
COMMENTARY
P waves Present for the sinus beats, then
absent during VT/VF • VF is characterized by its chaotic waveform with
PR interval Normal during sinus beats (160 ms)
no discernible organized ventricular activity, in
the context of a patient who is pulseless. A pre-
QRS duration Normal during sinus beats (110 ms) cordial thump is seldom successful in restoring
T waves Normal during sinus beats sinus rhythm, but it is worth a single attempt at a
precordial thump if the arrest was witnessed and
QTc interval Normal during sinus beats (392 ms)
monitored, and DC cardioversion is not immedi-
ately available. Lose no time, however, in obtaining
a defibrillator and administering a shock.
Additional comments
The ventricular tachycardia (VT) is triggered by a
• VEBs that fall on the T wave (R on T ventricular
ectopics) occur during ventricular repolariza-
ventricular ectopic beat (VEB) occurring during the
tion, which is a vulnerable time for ventricular
T wave of the fourth sinus beat (R on T ectopic).
arrhythmias. As the ventricles repolarize, they do
so in a ‘patchy’ fashion, meaning that some areas
ANSWERS of the myocardium repolarize more quickly than
others. This leads to islands of refractory myo-
1. The ECG shows a ventricular ectopic, followed cardium, surrounded by myocardium that has
by four normal sinus beats. Another VEB then repolarized. A ventricular ectopic arising at this
occurs during the T wave of the fourth sinus beat time can establish a re-entry circuit around one
(R on T ectopic), triggering pulseless VT which of these refractory islands, causing VT, which can
then rapidly degenerates into VF. then degenerate into VF.
2. The patient has sustained a cardiac arrest (pulse- • The VEBs and consequent pulseless VT/VF were,
less VT/VF). As this was a witnessed and moni- in this case, related to the patient’s critical coro-
tored arrest, a precordial thump can be given nary disease. The left main stem is a critically
followed, if unsuccessful, by defibrillation. In important part of the coronary arteries and isch-
this case, the patient did not respond to a pre- aemia or infarction arising from a left main stem
cordial thump but sinus rhythm was restored stenosis will affect a large proportion of the left
following a single biphasic shock of 150 J. The ventricle.
patient should then be reassessed with regards • Although arrhythmias account for 35% of all
to their airway, breathing and circulation. complications during coronary angiography,
3. Following successful resuscitation, transfer the they account for only 12% of deaths, reflecting
patient to a coronary or intensive care unit for the careful monitoring of patients in the cardiac
monitoring of airway and breathing (including catheter department and the high level of exper-
pulse oximetry), vital signs (pulse, blood pressure tise of staff in Advanced Life Support.
[preferably via an arterial line] and temperature),
Case 13 33
Further Reading
Making Sense of the ECG 6th edition: Ventricular fibrilla- Details of Advanced Life Support guidelines, and train-
tion, p 197; Ventricular ectopic beats, p 187. ing courses in resuscitation, can be obtained from
the Resuscitation Council UK. Downloadable from
www.resus.org.uk/.
CASE 14
CLINICAL SCENARIO
No significant medical history.
Sensation of ‘missed heartbeats’. Examination
Pulse: 57/min, irregular (occasional ‘missed beats’).
History of presenting complaint Blood pressure: 144/94.
After retiring and adopting a more sedentary life- JVP: not elevated.
style, the patient first became aware of something Heart sounds: normal.
wrong when he was sitting quietly, reading the Chest auscultation: unremarkable.
newspaper. He noticed that every now and then, No peripheral oedema.
his heart appeared to ‘miss a beat’. Although he
still enjoyed his normal weekend walking and Investigations
badminton, he was anxious in case the missed FBC: Hb 143, WCC 7.5, platelets 278.
beats were a sign of heart disease, as his mother U&E: Na 139, K 5.0, urea 5.1, creatinine 96.
had recently died of a ‘massive heart attack’. He Chest X-ray: normal heart size, clear lung fields.
reported his concerns to his family doctor. Echocardiogram: normal.
QUESTIONS
3. What is the prognosis?
DOI: 10.1201/9781003472186-14
ECG ANALYSIS there is a stronger indication for pacing, even if

patients are asymptomatic.
Rate 57/min
Rhythm Sinus rhythm with second-degree COMMENTARY
atrioventricular block (Mobitz
type I) • ‘Palpitations’ can be difficult to document, espe-
QRS axis Unable to assess (rhythm strip) cially if they are infrequent, of short duration or
associated with sudden collapse. Options are:
P waves Normal
• Prolonged (or repeated) Holter recording
PR interval Variable – gradually lengthens for 24, 48 or 72 h duration – this will record
before ‘resetting’ after a every heartbeat for a set period and will help
non-conducted P wave determine whether the patient’s perceived
QRS duration Normal (110 ms) ‘palpitation’ is related to a cardiac problem. It
is especially useful when symptoms occur on
T waves Normal
most days.
QTc interval Normal (400 ms) • If there are no events to record, the patient
may be given a patient-activated Cardiomemo
device – this can be carried for much longer
ANSWERS periods (weeks if necessary) until the patient
reports that a ‘palpitation’ has occurred.
1. The PR interval gradually increases after each • In a few patients, symptoms may still be suspected
successive P wave until one P wave is not con- to be due to a cardiac arrhythmia but are not fre-
ducted at all, resulting in a ‘missed beat’. After quent enough for short ambulatory recordings to
this, conduction reverts to normal and the cycle be practical. An insertable cardiac monitor (ICM)
starts over again. This is an example of second- may help. About the size and shape of a small
degree atrioventricular block of the Mobitz type computer ‘memory stick’, an ICM is implanted
I (Wenckebach phenomenon) subtype. under local anaesthesia, just below the skin of the
2. One can imagine Mobitz type I atrioventricu- left chest wall. Although the device records con-
lar block as the atrioventricular node becoming tinuously, the patient is taught how to electroni-
increasingly ‘tired’ as it conducts each P wave – cally document when an event occurred so that
as a result, the node takes longer and longer to the timing of the event can be checked against the
conduct each subsequent P wave until it totally cardiac rhythm at that time. The device can also
‘gives up’ and fails to conduct a P wave at all. automatically store rhythm strips when it detects
This, however, gives the atrioventricular node a a suspected rhythm disturbance.
chance to ‘rest’, and by the time the next P wave
arrives, it is ready to conduct normally before Further Reading
the cycle repeats itself.
Making Sense of the ECG 6th edition: Second-degree atrio-
3. When Mobitz type I AV block occurs at the
ventricular block, p 203; Mobitz type I atrioventric-
level of the AV node, it is generally regarded as ular block, p 203; Indications for permanent pacing,
‘benign’, and a permanent pacemaker is gen- p 225.
erally not required unless the frequency of Glikson M et al. 2021 ESC guidelines on cardiac pacing
‘dropped’ ventricular beats causes a symptom- and cardiac resynchronization therapy. European
atic bradycardia. When the block is infranodal Heart Journal (2021). PMID 34455430.
(as identified by electrophysiological testing),
CASE 15
CLINICAL SCENARIO
Patient appears dehydrated and unwell.
Fatigue and feeling generally unwell. Blood pressure: 88/44.
JVP: low.
Known chronic renal impairment. One-week his- Chest auscultation: unremarkable.
tory of diarrhoea and vomiting, with very poor No peripheral oedema.
fluid intake. Presented with fatigue and feeling No urine output following urinary catheterization.
generally unwell.
Investigations
Past medical history FBC: Hb 108, WCC 22.1, platelets 211.
Chronic renal impairment. U&E: Na 130, K 8.2, urea 32.7, creatinine 642.
QUESTIONS
2. What is the cause?
DOI: 10.1201/9781003472186-15
ECG ANALYSIS • At higher potassium levels, the QRS com-

plexes become broad and there is lengthening
Rate 66/min of the PR interval (with flattening or even loss
Rhythm Either sinus rhythm (with undetectable of the P wave).
P waves) or junctional rhythm • Sinoatrial and atrioventricular block can
develop.
QRS axis Unable to assess in view of bizarre
QRS complex morphology • At very high potassium levels, the QRS com-
plexes become increasingly bizarre and merge
P waves Not visible with the T waves to resemble a sine wave.
PR interval Not applicable • Arrhythmias (including ventricular fibrilla-
tion and asystole) can occur at any point.
•
QRS duration Broad, bizarre complexes
There is considerable variation in the ECG
T waves Large, broad appearances between individuals with hyperka-
QTc interval Prolonged (>500 ms) laemia. Some patients will develop quite marked
ECG abnormalities with fairly modest hyper-
ANSWERS kalaemia, while others can have minor ECG
changes despite severe hyperkalaemia.
1. This ECG shows absent P waves and broad, • Because of the risk of life-threatening arrhyth-
bizarre QRS complexes. With increasing potas- mias, patients with hyperkalaemia need continu-
sium levels, the P waves become smaller in size ous ECG monitoring.
before disappearing altogether. Patients can also • If the diagnosis of hyperkalaemia is confirmed
develop sinoatrial and atrioventricular block. by an elevated plasma potassium level, assess the
The rhythm here may therefore be sinus rhythm patient for symptoms and signs of an underly-
with such small P waves that they are no longer ing cause (e.g. renal failure, as in this case). In
evident, or a junctional rhythm (although junc- particular, review their treatment chart for inap-
tional rhythms are usually slower). propriate potassium supplements and potas-
2. The cause of these ECG appearances is severe hyper- sium-sparing diuretics.
kalaemia – the patient’s potassium level is mark- • Hyperkalaemia needs urgent treatment if it is
edly elevated at 8.2 mmol/L. This has developed as causing ECG abnormalities or the plasma potas-
a result of acute-on-chronic renal failure, which is sium level is above 6.5 mmol/L.
likely to have been precipitated by dehydration.
Further Reading
COMMENTARY Making Sense of the ECG 6th edition: Hyperkalaemia, p
• In general, hyperkalaemia causes a sequence of 134.

Montague BT et al. Retrospective review of the frequency
ECG changes at different potassium levels: of ECG changes in hyperkalemia. Clinical Journal of
• Early ECG changes include tall ‘tented’ T the American Society of Nephrology (2008). PMID
waves, shortening of the QT interval and ST 18235147.
segment depression.
CASE 16
CLINICAL SCENARIO
Asymptomatic. JVP: normal.
Incidental finding when attending for private No peripheral oedema.
insurance medical.
Investigations
Nil of note. U&E: Na 141, K 4.9, urea 5.5, creatinine 90.
Echocardiogram: normal.
QUESTIONS
3. What are the possible causes?
DOI: 10.1201/9781003472186-16
ECG ANALYSIS atrial activity, as the refractory period of the

AV node places an upper limit on how rapidly
Rate 66/min atrial impulses can be transmitted to the ventri-
Rhythm Sinus rhythm cles. Incomplete separation leaves an accessory
pathway, most often located in the left free wall
or postero-septal wall, bypassing the AV node.
P waves Normal Occasionally multiple pathways exist.
PR interval Short (90 ms)
4. Patients may remain asymptomatic. Some patients
with a WPW ECG pattern experience episodes of
QRS duration Lengthened (160 ms) atrioventricular re-entry tachycardia (AVRT), in
T waves Normal which case they are said to have WPW syndrome.
This can be treated pharmacologically or with
ablation of the accessory pathway.

A delta wave is present (an initial slurred upstroke
on the QRS complexes). • Symptoms of AVRT are very variable. Patients
complain of ‘palpitations’, usually of sudden
onset and abrupt termination. The palpitations
ANSWERS vary greatly in duration and severity, and may be
accompanied by chest pain, dizziness or syncope.
1. A P wave precedes every QRS complex so the
rhythm is sinus rhythm. However, the PR interval • With anterograde conduction via the AV node and
retrograde conduction via the accessory pathway,
is short, and there is slurring of the initial part of
an orthodromic AVRT is said to occur. This is the
the QRS complex producing a delta wave, clearly
commoner type of AVRT and during the tachy-
visible in leads I, aVL and V1–V6. This is the Wolff–
cardia, the delta wave is lost. An AVRT taking the
Parkinson–White (WPW) ECG pattern.
opposite route (down the accessory pathway and
2. Conduction from atria to ventricles is usu-
up the AV node) is said to be antidromic. This is
ally through a single connection involving the
rarer, and when it does occur, only delta waves are
atrioventricular (AV) node and bundle of His.
seen as the whole of the ventricular mass is acti-
In patients with WPW ECG pattern, a second
vated via the accessory pathway.
or ‘accessory’ pathway (the bundle of Kent)
coexists and conducts an electrical signal from • Some patients do not have any rhythm distur-
bance, and the finding of a WPW ECG pattern is
the atria to the ventricles at a faster rate than
made incidentally when an ECG is recorded for
through the AV node, which means that the PR
an unrelated problem. Patients who are asymp-
interval is shorter than normal. As a result, the
tomatic should nonetheless be seen by a cardiac
ventricles are activated by the accessory pathway
electrophysiologist to assess their risk of poten-
before the impulse has (simultaneously) been
tially hazardous arrhythmias (e.g. rapidly con-
transmitted through the AV node – known as
ducted atrial fibrillation) in the future.
ventricular pre-excitation. It causes the delta-
shaped upstroke of the R wave. Eventually, the
impulse via the AV node catches up and fuses Further Reading
with the impulse depolarizing the ventricles via
Making Sense of the ECG 6th edition: Wolff–Parkinson–
the accessory pathway, so that the remainder of White syndrome, p 80; Atrioventricular re-entry
ventricular depolarization occurs normally. tachycardia, p 176.
3. During fetal development, the atria and ven- Keating L et al. Electrocardiographic features of Wolff–
tricles are separated electrically, with a single Parkinson–White syndrome. Emergency Medicine
connection through the AV node and bundle Journal (2003). PMID 12954704.
of His. This protects the ventricles from rapid
CASE 17
CLINICAL SCENARIO
Severe central chest pain. JVP: not elevated.
Four-hour history of heavy central chest pain, No peripheral oedema.
radiating to the left arm and associated with
breathlessness and sweating. Chest pain Investigations
resolved after administration of opiates on FBC: Hb 153, WCC 9.8, platelets 271.
arrival in hospital. This ECG was performed 24 h U&E: Na 139, K 4.0, urea 5.8, creatinine 81.
after presentation. Chest X-ray: normal heart size, clear lung fields.
Troponin I: elevated.
Past medical history Echocardiogram: hypokinesia of inferolateral
Hypertension diagnosed 2 years ago. walls of left ventricle, overall ejection fraction
Ex-smoker (15 pack-year smoking history). 50%.
QUESTIONS
1. What abnormalities does this ECG show?
2. What is the diagnosis?
DOI: 10.1201/9781003472186-17
ECG ANALYSIS ST segment elevation myocardial infarction

(STEMI) and non-ST segment elevation ACS
Rate 60/min (NSTEACS) on the basis of the ECG appear-
Rhythm Sinus rhythm ances. The ECG of a patient with NSTEACS may
show ST segment depression, T wave inversion
or may be normal.
P waves Normal • The differential diagnosis of T wave inversion
includes:
• Myocardial ischaemia
• Myocardial infarction
T waves T wave inversion in leads II, III, aVF, V5–V6 • Ventricular hypertrophy with ‘strain’
and a biphasic T wave in lead V4 • Digoxin effect
QTc interval Normal (420 ms) • T wave inversion is normal in leads aVR and V1,
and in some patients can be a variant of normal
ANSWERS in leads V2, V3 and III. An inverted T wave is also
normal in lead aVL if it follows a negative QRS
1. This ECG shows inferolateral T wave inversion complex.
(leads II, III, aVF, V5–V6, with a biphasic T wave • The location of ischaemic changes on an ECG is
in lead V4). an indicator of the myocardial territory affected:
2. The ECG indicates an inferolateral non-ST ele-
vation acute coronary syndrome (NSTEACS).
The elevated troponin levels confirm myocardial Leads containing ST segment Location of event
elevation
damage, and therefore, a diagnosis of infero-
lateral non-ST segment elevation myocardial V1–V2 Septal
infarction (NSTEMI) can be made. In patients V3–V4 Anterior
in whom a high-sensitivity troponin is not
I, aVL, V5–V6 Lateral
elevated 3 h after the onset of chest pain, myo-
cardial infarction can be ruled out, and the diag- V1–V4 Anteroseptal
nosis would be one of unstable angina. I, aVL, V3–V6 Anterolateral
3. The initial treatment of NSTEACS includes
II, III, aVF Inferior
antiplatelet, antithrombotic and anti-ischaemic
drugs as appropriate. Urgent coronary angiog- I, aVL, V5–V6, II, III, aVF Inferolateral
raphy should be undertaken as indicated with
a view to coronary revascularization with per- Further Reading
cutaneous coronary intervention (PCI) or coro-
nary artery bypass grafting as appropriate. Making Sense of the ECG 6th edition: Are any of the T waves
inverted? p 137.
Byrne RA et al. 2023 ESC guidelines for the manage-
COMMENTARY ment of acute coronary syndromes. European Heart
Journal (2023). PMID 37622654.
• An urgent ECG is required in any patient pre- NICE clinical guideline NG185 – Acute coronary syn-
senting with cardiac-sounding chest pain. Acute dromes. 2020. Downloadable from www.nice.org.uk/
coronary syndromes (ACS) can be divided into guidance/ng185.
CASE 18
CLINICAL SCENARIO
Awaiting minor surgery. Attended hospital for JVP: normal.
preoperative assessment. Heart sounds: normal.
Asymptomatic; incidental finding.
Investigations
Fit and well – keen tennis player. U&E: Na 140, K 4.7, urea 4.5, creatinine 94.
No significant medical history. Chest X-ray: normal heart size, clear lung fields.
QUESTIONS
DOI: 10.1201/9781003472186-18
ECG ANALYSIS cardiomyopathy, atrial septal defect, Ebstein’s

anomaly, Fallot’s tetralogy and pulmonary
Rate 66/min embolism (usually massive). It can also occur
Rhythm Sinus rhythm at fast heart rates in supraventricular tachycar-
dia – this may lead to an incorrect diagnosis of
ventricular tachycardia. Incomplete RBBB is
P waves Normal found in 2–3% of normal individuals and is usu-
ally of no clinical significance.
4. RBBB does not cause symptoms and does not
QRS duration Prolonged (140 ms) require treatment. However, it is a prompt to look
T waves Normal for an underlying cause. Investigations should
be appropriate for the clinical presentation.
COMMENTARY
Additional comments
The QRS complexes have a right bundle branch • RBBB may be intermittent, occurring during
block morphology. episodes of tachycardia (when the heart rate
exceeds the refractory period of the right bun-
dle). Although both right and left bundle branch
ANSWERS block can be ‘rate-related’ in this way, the right
bundle is more likely to be affected.
1. The QRS complexes are broad (140 ms) and the
QRS complex in lead V1 has a rSR´ (‘M’ shape) • An RBBB morphology is seen in Brugada syn-
drome, in association with persistent ST segment
morphology. This is right bundle branch block
elevation in leads V1–V3. Brugada syndrome is
(RBBB).
an important diagnosis to make as it predisposes
2. In RBBB the interventricular septum depolar-
individuals to syncope and sudden death due to
izes normally from left to right. The electrical
ventricular arrhythmias. It probably accounts
impulse then passes down the left bundle so the
for 50% of cases of sudden cardiac death with an
left ventricle depolarizes normally, but depolar-
apparently ‘normal’ heart. Although the ECG has
ization of the right ventricle is delayed because
an RBBB morphology in Brugada syndrome, this
the depolarization has to occur via the left ven-
is not due to RBBB as such but rather is due to
tricle, travelling from myocyte to myocyte,
abnormal ventricular repolarization.
rather than directly via the Purkinje fibres. This
leads to a broad QRS complex with the charac-
teristic rSR´ morphology in lead V1. Further Reading
3. RBBB is a relatively common finding in nor- Making Sense of the ECG 6th edition: Bundle branch block,
mal hearts but can be a marker of underly- p 106; Right bundle branch block, p 205; Brugada
ing disease including ischaemic heart disease, syndrome, p 124.
CASE 19
CLINICAL SCENARIO
Rapid regular palpitations. JVP: normal.
Heart sounds: normal (tachycardic).
Normally fit and well with no prior history of pal-
pitations. The patient presented with a 3 h his- Investigations
tory of rapid regular palpitation. FBC: Hb 155, WCC 6.2, platelets 347.
Wolff–Parkinson–White syndrome diagnosed at Chest X-ray: normal heart size, clear lung fields.
age 21 on a routine ECG at an insurance medical.
QUESTIONS
2. What is the underlying pathophysiological mechanism?
3. What initial treatment would be appropriate?
4. What treatment might be appropriate in the longer term?
DOI: 10.1201/9781003472186-19
ECG ANALYSIS options for orthodromic AVRT include beta-

blockers or non-dihydropyridine calcium chan-
Rate 204/min nel blockers.
Rhythm Atrioventricular re-entry
tachycardia (AVRT) COMMENTARY
QRS axis Unable to assess (single lead)
P waves Inverted P waves after each

• Patients with a WPW pattern on their ECG have
an accessory pathway (the bundle of Kent) that
QRS complex (distorting the
provides an anatomical substrate for the devel-
ST segment/T wave)
opment of AVRT – once an episode of AVRT
PR interval Not applicable occurs, the patient is said to have WPW syn-
QRS duration Normal (80 ms) drome. Not all patients with a WPW ECG pat-
tern will experience AVRT, however, and some
T waves Distorted by inverted P waves can live out their full life without ever experienc-
QTc interval Normal (406 ms) ing an episode of AVRT.
• Where WPW patients do get episodes of AVRT,
this is usually orthodromic. Orthodromic AVRT
ANSWERS is characterized by a narrow-complex tachy-
cardia in which the delta wave is absent during
1. Atrioventricular re-entry tachycardia (AVRT). the tachycardia (even though it is present dur-
2. A re-entry circuit involving an accessory ing normal sinus rhythm) and the P waves are
pathway – in this case, the bundle of Kent in seen after the QRS complexes, and are inverted
Wolff–Parkinson–White (WPW) syndrome. in the inferior leads. In the ECG presented here,
The re-entry circuit travels from atria to inverted P waves can be seen at the junction of
ventricles down through the AV node, per the ST segment and the T wave.
normal, but then travels back up to the atria
retrogradely via the accessory pathway. This is
• AVRT is around 10 times less common than AV
nodal re-entry tachycardia (AVNRT), which is
known as an orthodromic AVRT (in contrast caused by a micro re-entry circuit within the
to an antidromic AVRT, in which the re-entry AV node. P waves are usually easier to discern
circuit travels in the opposite direction, down in AVRT than in AVNRT, and the ECG in sinus
the accessory pathway and back up the AV rhythm in patients with a history of AVNRT
node). is usually normal, but in those with a history
3. Transiently blocking the AV node can terminate of AVRT, it may reveal a short PR interval or
the AVRT. Methods to achieve this include: delta wave. The distinction between AVRT and
• Valsalva manoeuvre AVNRT can be difficult, however, and may
• Carotid sinus massage require electrophysiological studies.
• Intravenous adenosine
• Intravenous verapamil
Further Reading
4. The patient can be taught the Valsalva manoeu-
vre to try to terminate episodes. Catheter abla- Making Sense of the ECG 6th edition: Atrioventricular re-
entry tachycardia, p 176; Wolff–Parkinson–White
tion of the accessory pathway is curative in a
syndrome, p 80.
very high proportion of cases (initial success rate
Brugada J et al. 2019 ESC guidelines for the manage-
92%, with a recurrence rate of 8%), at relatively ment of patients with supraventricular tachycardia.
low risk, and so should be considered a first-line European Heart Journal (2020). PMID 31504425.
therapy in symptomatic patients with WPW Kotadia ID et al. Supraventricular tachycardia: An over-
syndrome. If catheter ablation is not feasible view of diagnosis and management. Clinical
or desirable, then long-term pharmacological Medicine (2020). PMID 31941731.
CASE 20
CLINICAL SCENARIO
Pulse: 75/min, regular with occasional ‘dropped
Presenting complaint beat’.
Syncope. Blood pressure: 156/96.
JVP: normal.
Brought to emergency department feeling Chest auscultation: unremarkable.
unwell after an episode of collapse with loss No peripheral oedema.
of consciousness. Reported several episodes
of dizziness in past few months. Quickly back Investigations
to normal within minutes but episodes tend to FBC: Hb 139, WCC 8.1, platelets 233.
reoccur. U&E: Na 137, K 4.2, urea 5.3, creatinine 88.
Past medical history Troponin I: negative.
Osteoarthritis. Chest X-ray: normal.
QUESTIONS
DOI: 10.1201/9781003472186-20
ECG ANALYSIS sinus node dysfunction should be withdrawn).

Permanent pacing is appropriate for symptom-
Rate 75/min atic patients (as in this example).
Rhythm Sinus rhythm with intermittent
sinoatrial block COMMENTARY
QRS axis Unable to assess (rhythm strip)
P waves Normal (when present)

• Sinoatrial block should be distinguished from
sinus arrest. In sinoatrial block there is a pause
PR interval Normal (172 ms) with one or more absent P waves, and then the
next P wave appears exactly where predicted – in
other words, the sinoatrial node continues to
T waves Normal ‘keep time’, but its impulses are not transmit-
QTc interval Normal (440 ms) ted beyond the node to the atria. In sinus node
arrest, the node itself stops firing for a variable
time period, so the next P wave occurs after a
ANSWERS variable interval.
• Sinoatrial block and sinus arrest can both be fea-
1. The underlying rhythm is normal sinus rhythm tures of sick sinus syndrome. Other features of
but then a P wave fails to appear; the next P wave sick sinus syndrome can include sinus bradycar-
appears after a pause of 2.4 s. The R-R interval dia, brady-tachy syndrome and atrial fibrillation.
is 0.8 s, so the P wave has arrived ‘on schedule’, • Offer appropriate advice to patients who drive a
three complete cycle lengths after the last P wave. vehicle and who suffer from presyncope or syn-
This is sinoatrial block, one of several types of cope – very often, they will be barred from driv-
sinus node dysfunction. ing until the problem has been diagnosed and/or
2. Sinoatrial node exit block may result from idio- corrected as appropriate. Driving regulations vary
pathic fibrosis of the sinus node. Other causes between countries. In the UK, information on the
include ischaemic heart disease, myocarditis, medical aspects of fitness to drive can be found
cardiomyopathy, cardiac surgery (especially on the website of the Driver and Vehicle Licensing
atrial septal defect repair), drugs (such as beta- Agency (www. dvla.gov.uk).
blockers and rate-limiting calcium channel
blockers) and digoxin toxicity, excessive vagal Further Reading
tone, and many inflammatory and infiltrative Making Sense of the ECG 6th edition: Sinoatrial block,
disorders. p 201.
3. Asymptomatic sinus node dysfunction does Glikson M et al. 2021 ESC guidelines on cardiac pacing
not require treatment, but address any under- and cardiac resynchronization therapy. European
lying causes (e.g. drugs that can contribute to Heart Journal (2021). PMID 34455430.
CASE 21
CLINICAL SCENARIO
Exertional breathlessness and fatigue. JVP: elevated by 2 cm.
Heart sounds: loud first heart sound (S1) with an
History of presenting complaint opening snap. Low-pitched 2/6 mid-diastolic
One-year history of gradual onset exertional murmur with pre-systolic accentuation heard at
breathlessness and fatigue, with steady fall in apex. Loud pulmonary component to second
exercise capacity. heart sound (P2).
Mild peripheral oedema.
Rheumatic fever aged 12 years.
Investigations
Chest X-ray: large left atrium.
QUESTIONS
3. What would be the most helpful investigation?
4. What treatment is available?
DOI: 10.1201/9781003472186-1

Rate 84/min • P mitrale results from enlargement of the left
Rhythm Sinus rhythm atrium. The enlarged atrium takes longer to depo-
larize, and thus the P wave becomes broader.
QRS axis Normal (+87°) Although P mitrale does not require treatment
P waves Broad, bifid in its own right, its presence should alert you to
look for left atrial enlargement. This often results
from mitral valve disease but can also result from
QRS duration Normal (100 ms) left ventricular hypertrophy (the elevated filling
T waves Normal pressures of the ‘stiff’ left ventricle causes gradual
enlargement of the left atrium).
• Decisions about which operative intervention to
use in mitral stenosis depend primarily on the
ANSWERS morphology of the mitral valve and its associated
structures. Clear imaging of the valve is there-
1. The P waves are broad and bifid (‘P mitrale’). fore essential, and most patients will require a
2. In the clinical context, the most likely cause is transoesophageal echocardiogram to examine
left atrial enlargement secondary to rheumatic the valve in detail.
mitral stenosis. The clinical features are in keep- • Patients with severe mitral stenosis often develop
ing with severe mitral stenosis and associated atrial fibrillation. The consequent loss of P waves
pulmonary hypertension. means that the ECG evidence of left atrial
3. An echocardiogram would allow direct visu- enlargement is lost.
alization of the mitral valve, measurement of
left atrial size and an estimation of pulmonary Further Reading
artery pressure. Making Sense of the ECG 6th edition: Are any P waves too
4. Correction of the mitral stenosis is indicated, wide? p 76.
using percutaneous balloon mitral valvulo- Platonov PG. P-wave morphology: Underlying mecha-
plasty, surgical mitral valvotomy or mitral valve nisms and clinical implications. Annals of Noninvasive
replacement. Electrocardiology (2012). PMID 22816534.
CASE 22
CLINICAL SCENARIO
Pulse: 66/min, regular with frequent ‘dropped’
Presenting complaint beats.
Episodes of irregular heartbeat; occasionally Blood pressure: 106/56.
feeling faint. JVP: not elevated.
For several weeks the patient had been afraid No peripheral oedema.
to leave his house due to frequent periods of
feeling dizzy. Collapsed on two occasions, wak- Investigations
ing to find himself on the floor. Back to normal FBC: Hb 122, WCC 8.4, platelets 342.
in minutes. Eventually sought advice of a doctor U&E: Na 137, K 4.2, urea 5.3, creatinine 88.
when he collapsed in the toilet and hit his head Thyroid function: normal.
on the door. Troponin I: negative.
Past medical history Echocardiogram: structurally normal valves. Left
Angina. ventricular systolic function impaired (ejection
Hypertension. fraction 44%).
QUESTIONS
2. Does the patient require a pacemaker?
DOI: 10.1201/9781003472186-22
ECG ANALYSIS 2. A pacemaker is not indicated. This is atrial tri-

geminy, not second-degree atrioventricular
Rate 66/min block.
Rhythm Sinus rhythm with atrial ectopic
beats (atrial trigeminy) COMMENTARY
P waves Normal
• Atrial ectopic beats are also known as atrial extra-
systoles, atrial premature complexes (APCs),
PR interval 140 ms (when P wave is atrial premature beats (APBs) or premature
followed by a QRS complex) atrial contractions (PACs). Atrial ectopic beats
occur earlier than expected (in contrast with
escape beats, which occur later than expected).
T waves Normal
• Atrial ectopic beats can arise from any part of the
QTc interval Normal (420 ms) atria, and the shape of the P wave depends upon
where in the atria the ectopic has arisen from.
• Avoidance of triggers, such as caffeine, alcohol
ANSWERS and nicotine, is often sufficient to reduce the
frequency of atrial ectopic beats. They are gener-
1. At first glance, this ECG might look like second- ally benign, and so drug treatment is not usually
degree atrioventricular block, with intermittent needed unless the associated sensation of palpi-
non-conduction of P waves. However, on closer tations is very frequent and troublesome. If treat-
inspection, it can be seen that the non-conducted ment is required, beta-blockers can be effective
P waves occur slightly earlier than expected and in suppressing atrial ectopic activity.
have a different morphology to the conducted
P waves. This is because the non-conducted P
• This patient’s episodes of dizziness and syncope
were unrelated to his arrhythmia, and were
waves are atrial ectopic beats. Indeed, every third instead due to overtreatment of his hyperten-
P wave is an atrial ectopic beat (atrial trigeminy). sion, causing episodes of medication-induced
Their different morphology occurs because the hypotension.
atrial ectopic beats arise from a different region
of the atria to the normal sinus beats. Moreover,
because the atrial ectopic beats are early, they Further Reading
occur while the ventricles are still repolarizing, Making Sense of the ECG 6th edition: Atrial ectopic beats,
so they are not followed by a QRS complex. p 167.
CASE 23
CLINICAL SCENARIO
Patient walks with a stick.
Presenting complaint Comfortable at rest.
Asymptomatic – routine ECG performed Pulse: 86/min, regular.
prior to orthopaedic surgery (right total hip Blood pressure: 136/78.
replacement). JVP: not elevated.
No cardiac history as asymptomatic. No peripheral oedema.

Osteoarthritis of the right hip. No prior cardiac FBC: Hb 128, WCC 6.7, platelets 178.
history. U&E: Na 138, K 3.8, urea 5.7, creatinine 91.
QUESTIONS
2. What can cause this?
3. Is any treatment necessary?
DOI: 10.1201/9781003472186-23
ECG ANALYSIS • If the QRS complex is positive in leads I and

II, then the axis is normal.
Rate 86/min • If the QRS complex is positive in lead I and
Rhythm Sinus rhythm negative in lead II, then there is left axis
deviation.
QRS axis Left axis deviation (−51°)
• If the QRS complex is negative in lead I and
P waves Normal positive in lead II, then there is right axis
PR interval Normal (160 ms) deviation.

• Negative QRS complexes in both leads I and II
represent extreme axis deviation – this most
T waves Normal commonly indicates incorrect positioning of the
QTc interval Normal (450 ms) limb electrodes but can also be seen in ventricu-
lar tachycardia (with extreme axis shift) and in
ventricular pacing.
ANSWERS • The left bundle branch divides into two sub-
branches or fascicles – the left anterior fascicle
1. Left axis deviation (QRS axis –51°).
and the left posterior fascicle. Block of the left
2. Left axis deviation can occur in normal individ-
anterior fascicle (left anterior fascicular block,
uals, and also as a result of:
also known as left anterior hemiblock) can
• Left anterior fascicular block
occur as a result of fibrosis of the conduct-
• Wolff–Parkinson–White (WPW) syndrome ing system (of any cause) or from myocardial
• Inferior myocardial infarction infarction.
• Primum atrial septal defect • On its own, left anterior fascicular block is
• Ventricular tachycardia not thought to carry any prognostic signifi-
3. Left axis deviation does not require treatment in cance and no specific treatment is required.
its own right. The isolated presence of left axis deviation
should not be a bar to this patient’s orthopae-
dic surgery.
COMMENTARY
• The normal QRS axis lies between –30° and +90° Further Reading
(although some cardiologists accept anything up
to +120° as normal). Left axis deviation is con- Making Sense of the ECG 6th edition: The axis, p 55; Is there
left axis deviation? p 64.
ventionally diagnosed when the axis lies more
Seko Y et al. Clinical impact of left and right axis deviations
leftward (negative) than –30°.
• A quick way to assess QRS axis is to look at leads
with narrow QRS complex on 3-year outcomes in a
hospital-based population in Japan. Scientific Reports
I and II: (2021). PMID 33903653.
CASE 24
CLINICAL SCENARIO
Nausea and vomiting. JVP: not elevated.
Heart sounds: loud first heart sound; mid-dia-
History of presenting complaint stolic rumble and pan-systolic murmur.
Patient has had atrial fibrillation for several Chest auscultation: unremarkable.
years – not previously problematic. A week ago, Trace of ankle oedema.
felt generally unwell with mild fever and cough
productive of green sputum. Family doctor pre- Investigations
scribed antibiotics for a presumed respiratory FBC: Hb 139, WCC 8.1, platelets 233.
tract infection. Although her symptoms were U&E: Na 132, K 3.1, urea 8.9, creatinine 286.
resolving, she stopped eating and drinking as Thyroid function: normal.
she felt nauseous. Troponin I: negative.
Chest X-ray: mild cardiomegaly.
Past medical history Echocardiogram: thickened mitral leaflets with
Rheumatic fever as child. Mixed mitral valve restricted movement; moderate mitral regurgi-
disease but symptoms not severe enough to tation into a moderately dilated left atrium. Left
warrant valve surgery. Under regular follow-up ventricular systolic function impaired (ejection
with a cardiologist. fraction 43%).
QUESTIONS
2. Is this a sign of drug toxicity?
3. What mechanisms are involved?
4. What are the common ECG findings of digoxin toxicity?
DOI: 10.1201/9781003472186-24
ECG ANALYSIS concomitant prescribing with verapamil or amio-

darone, dehydration and hypokalaemia. The half-
Rate 72/min life of digoxin with normal renal function is 36–48
Rhythm Atrial fibrillation h, so in toxicity simply stopping the drug and
supportive measures may be enough. It may be as
long as 5 days in renal impairment. Digoxin is not
P waves Absent removed by dialysis – if toxicity causes arrhyth-
mias or malignant hyperkalaemia (due to para-
PR interval N/A
lysed cell membrane-bound ATPase-dependent
QRS duration Normal (110 ms) Na/K pumps), antibody fragments that bind with
T waves Inverted in most leads digoxin (Digibind) provide a specific antidote.
COMMENTARY
Additional comments • As well as digoxin effect, other causes of ST
There is downsloping ‘reverse tick’ ST segment segment depression include myocardial isch-
depression in the inferior and anterolateral leads. aemia, acute posterior myocardial infarction,
reciprocal changes in acute ST segment eleva-
tion myocardial infarction, and left ventricular
ANSWERS hypertrophy with ‘strain’.
1. The rhythm is irregularly irregular with no dis- • Always be careful to distinguish between ECG
cernible P waves (atrial fibrillation). The QRS features seen with normal digoxin levels and those
complexes are normal but the ST segments are indicative of digoxin toxicity. Digoxin levels can
downward-sloping with a ‘reverse tick’ morphol- be measured and guide clinical decision-making.
ogy: this is typical (although not diagnostic) of • Symptoms of digoxin toxicity are non-specific:
digitalis (digoxin) effect. blurred vision, impaired colour perception (yel-
2. It is important to distinguish between the effects low or green vision was first reported by William
of digoxin on the ECG at normal therapeutic Withering in 1785), confusion, anorexia, nau-
levels, and the effects of digoxin toxicity. ST seg- sea, vomiting and diarrhoea.
ment depression is a normal finding in patients • The risk of digoxin toxicity depends on the dose
on digoxin, as is a reduction in T wave size and of digoxin, physical size of the patient, renal
shortening of the QT interval. At toxic levels of function and potassium level. Levels do not need
digoxin, T wave inversion can occur, as can vir- to be routinely monitored but they are helpful if
tually any arrhythmia (but classically paroxysmal toxicity is suspected.
atrial tachycardia with atrioventricular block). • Caution – always interpret digoxin levels in the
3. The effects of digoxin on the ECG are complex. light of clinical and chemical data.
It has a direct action by inducing electrical
and mechanical effects by inhibiting sodium Further Reading
ion (and secondarily potassium ion) transport
Making Sense of the ECG 6th edition: Atrial fibrillation,
across myocardial and pacemaker cells and an
p 168; Are the ST segments depressed? p 126.
indirect effect by increasing vagal tone. Rautaharju PM et al. AHA/ACCF/HRS recommendations
4. The most common ECG findings of digoxin for the standardization and interpretation of the elec-
toxicity are: heart block, bradycardia, junc- trocardiogram: Part IV: The ST segment, T and U
tional tachycardia and atrial fibrillation. Risk of waves, and the QT interval. Journal of the American
digoxin toxicity increases with renal impairment, College of Cardiology (2009). PMID 19281931.
CASE 25
CLINICAL SCENARIO
Patient breathless at rest. In discomfort.
Sudden onset breathlessness and pleuritic Blood pressure: 116/84.
chest pain. JVP: elevated by 3 cm.
Heart sounds: gallop rhythm.
History of presenting complaint Chest auscultation: pleural rub heard in right
Patient underwent left total knee replacement midzone.
2 days ago. Developed sudden onset breath- No peripheral oedema.
lessness and right-sided pleuritic chest pain.
Investigations
Left knee osteoarthritis. U&E: Na 141, K 4.3, urea 5.4, creatinine 95.
QUESTIONS
2. What is the likely cause of this ECG appearance?
3. What investigations would be appropriate?
4. What are the treatment options?
DOI: 10.1201/9781003472186-25
ECG ANALYSIS embolism and/or are haemodynamically unsta-

ble. Administer oxygen therapy for hypoxia.
Rate 128/min
Rhythm Sinus tachycardia COMMENTARY
QRS axis
P waves
Normal (+16°)
Normal
• Sinus tachycardia is the commonest ECG abnor-
mality found in pulmonary embolism.
PR interval Normal (160 ms) • ECG indicators of right heart strain (pressure
and/or volume overload) include the S1Q3T3
pattern, also referred to as the McGinn–White
T waves Inverted in leads III, aVF, sign (after Sylvester McGinn and Paul White, who
V1–V4 first described the pattern in 1935). However,
QTc interval Mildly prolonged (467 ms) although the S1Q3T3 pattern is often described
as an indicator of pulmonary embolism, it is rela-
tively insensitive and non-specific – it is only evi-
Additional comments dent in around half of patients, and can occur in
There is an S1Q3T3 pattern and anterior T wave any condition that causes acute right heart strain
inversion. (e.g. bronchospasm, pneumothorax).
• In those patients already suspected of having a
ANSWERS pulmonary embolism, the presence of anterior
T wave inversion has a sensitivity and specific-
1. This ECG shows: ity of >80% for diagnosing massive pulmonary
• Sinus tachycardia embolism.
• An S wave in lead I, and a Q wave and an • Other ECG abnormalities seen in pulmonary
inverted T wave in lead III (S1Q3T3) embolism can include incomplete right bundle
• Anterior T wave inversion branch block, P pulmonale (right atrial enlarge-
2. Acute pulmonary embolism. ment), non-specific ST segment changes and
3. Appropriate investigations for suspected acute atrial fibrillation/flutter.
pulmonary embolism include: • A normal ECG does not exclude a diagnosis of
• Arterial blood gases pulmonary embolism.
• D-dimers
• Chest X-ray (usually normal initially) Further Reading
• Imaging studies: computed tomography (CT)
Making Sense of the ECG 6th edition: Sinus tachycardia,
pulmonary angiography or nuclear scintigra-
p 165; S1Q3T3 pattern, p 93.
phy lung ventilation – perfusion (V/Q) scan Ferrari E et al. The ECG in pulmonary embolism.
4. The treatment of pulmonary embolism includes Predictive value of negative T waves in precor-
anticoagulation, although consider thromboly- dial leads – 80 case reports. Chest (1997). PMID
sis in patients who have massive pulmonary 9118684.
CASE 26
CLINICAL SCENARIO
Breathless, especially going up stairs. JVP: elevated by 2 cm.
Heart sounds: loud first sound, mitral regurgi-
History of presenting complaint tation easily heard.
Was fairly well until 3 months ago when a new Chest auscultation: unremarkable.
family doctor changed her medication. Mild pitting ankle oedema.

Rheumatic fever. FBC: Hb 126, WCC 5.9, platelets 345.
Mitral regurgitation. U&E: Na 133, K 4.1, urea 6.7, creatinine 168.
Chest X-ray: mild cardiomegaly, early pulmonary
congestion.
Echocardiogram: thickened mitral leaflets,
moderate mitral regurgitation into a moder-
ately dilated left atrium. Left ventricular systolic
function impaired (ejection fraction 45%).
QUESTIONS
DOI: 10.1201/9781003472186-26
ECG ANALYSIS • Initiation of other medication – some may

increase digoxin levels (amiodarone, dil-
Rate 54/min tiazem, verapamil, spironolactone); some
Rhythm Atrial fibrillation with a slow may reduce levels (antacids, sulphasalazine,
ventricular response metoclopramide, domperidone)
In this case, the cause of the ‘slow’ atrial fibrillation
was a change in digoxin dose from 125 mcg to 250
P waves Absent mcg daily, despite the impaired renal function.
PR interval N/A

COMMENTARY
T waves Normal
QTc interval Normal (402 ms) • Always ensure that the rhythm has been diag-
nosed correctly before giving treatment – an
inaccurate diagnosis means incorrect treatment
ANSWERS that may cause symptoms to get worse.
1. This ECG shows an irregularly irregular rhythm
• ‘Slow’ atrial fibrillation may not be easy to diag-
nose as the ECG baseline does not always show
with absent P waves and a slow ventricular rate:
fibrillation waves and QRS complexes may look
this is atrial fibrillation with a slow ventricu-
remarkably regular.
lar response.
2. Atrial fibrillation with a slow ventricular response
• Digoxin is renally excreted and has a half-life
of 36–48 h. It has a narrow therapeutic ‘win-
is commonly due to an inappropriately high dose
dow’ and so caution must be taken in mak-
of a rate-limiting drug (such as a beta-blocker,
ing dose adjustments in patients with renal
rate-limiting calcium channel blocker or digoxin),
impairment.
although sometimes atrial fibrillation itself can
occur with a relatively slow ventricular rate. • The signs of digoxin toxicity include:
3. Many patients with atrial fibrillation are stable
for years on their rate-controlling medication
• Cardiovascular – bradycardia (<60/min), atrio-
ventricular conduction block, supraventricular
regimen but their ventricular rate control may tachycardia, ventricular extrasystoles
be affected by:
• Central nervous system – dizziness, confu-
sion, nightmares, hallucinations
• Intercurrent illness – this may cause an increased
• Visual – yellowing of vision, halo effect
heart rate, e.g. respiratory infection
• Drug compliance – failure to take as prescribed • Gastrointestinal – anorexia, nausea, vomiting,
diarrhoea, abdominal pain
may cause inappropriately high or low drug
levels
• Changing renal function with age – this affects
Further Reading
the levels of drugs that are renally excreted
• Gastrointestinal symptoms – these may make Making Sense of the ECG 6th edition: Atrial fibrillation,
absorption unpredictable p 168.
CASE 27
CLINICAL SCENARIO
Patient had been resting at home following a
Presenting complaint right leg injury 3 weeks earlier.
Sudden collapse.
Examination
History of presenting complaint Unresponsive – Glasgow Coma Scale score 3/15.
Patient admitted for investigation of right calf Pulse: unrecordable – pulses not palpable.
tenderness and swelling. Collapsed suddenly Blood pressure: unrecordable.
in the X-ray department immediately after JVP: neck veins distended.
he arrived for a leg ultrasound Doppler. This No respiratory movements.
rhythm strip was recorded on arrival of the car- Right calf red and swollen.
diac arrest team.
Investigations
QUESTIONS
1. What does this ECG rhythm strip show?
2. What is the clinical diagnosis, and the likely underlying cause?
3. What action should be taken?
DOI: 10.1201/9781003472186-27
ECG ANALYSIS • It is important to remember that PEA can be seen

in conjunction with any cardiac rhythm that
Rate 108/min would normally sustain a circulation. The diag-
Rhythm Sinus tachycardia nosis of PEA is therefore not an ECG diagnosis
per se (the ECG can look entirely normal) but is
QRS axis Unable to assess (single lead)
based upon the clinical context of a patient with
P waves Normal no cardiac output despite a heart that appears to
be working electrically.
• Causes of PEA include:
• Hypoxia
T waves Normal • Hypovolaemia
QTc interval Mildly prolonged (456 ms) • Hyperkalaemia, hypokalaemia, hypocalcae-
mia, acidaemia and other metabolic disorders
• Hypothermia
ANSWERS • Tension pneumothorax
• Tamponade
1. This ECG rhythm strips shows sinus tachycardia, • Toxic substances
108/min. • Thromboembolism (pulmonary embolus/
2. The patient has collapsed and is unconscious coronary thrombosis)
(Glasgow Coma Scale score 3/15) with no detect-
able cardiac output. This is therefore a cardiac
• PEA is managed according to the non-shockable
rhythms (PEA and asystole) treatment algo-
arrest with pulseless electrical activity (PEA), rithm of the Resuscitation Council (UK).
sometimes also called electromechanical dissoci-
ation (EMD). The likely cause in this clinical con-
text is massive pulmonary embolism, secondary Further Reading
to a deep vein thrombosis of the right leg. Making Sense of the ECG 6th edition: How is the patient?
3. Follow standard basic and Advanced Life Support p 49.
algorithms. PEA is a non-shockable rhythm, Details of Advanced Life Support guidelines, and train-
and it is particularly important to look for an ing courses in resuscitation, can be obtained from
underlying treatable cause. the Resuscitation Council UK. Downloadable from
www.resus.org.uk/.
COMMENTARY
• PEA occurs when the heart is still working elec-
trically but is failing to produce an output.
CASE 28
CLINICAL SCENARIO
Woken from sleep with severe chest pain. JVP: not elevated.
Heart sounds: soft pan-systolic murmur at apex
History of presenting complaint (mitral regurgitation).
Had angina on exertion for over 4 years. Similar Chest auscultation: bilateral basal crackles.
pain to usual angina but much worse. Never had No peripheral oedema.
pain at rest or at night before – felt like there
was ‘someone sitting on my chest’. The pain Investigations
radiated to the left arm and was associated with FBC: Hb 115, WCC 5.2, platelets 401.
breathlessness. She was afraid she might die. U&E: Na 132, K 4.5, urea 7.0, creatinine 131.
Troponin I: elevated.
Past medical history Chest X-ray: mild cardiomegaly, early pulmo-
Hypertension – well controlled on amlodipine. nary congestion.
Diabetes mellitus. Echocardiogram: mild mitral regurgitation. Left
Hypercholesterolaemia. ventricular systolic function impaired (ejection
Ex-smoker. Strong family history of coronary fraction 47%).
artery disease.
QUESTIONS
DOI: 10.1201/9781003472186-28
ECG ANALYSIS patients will require longer-term treatment

with dual antiplatelet therapy (aspirin plus a
Rate 66/min P2Y12 inhibitor, such as ticagrelor or clopido-
Rhythm Sinus rhythm grel), usually for 12 months, and then aspirin
long term, together with lipid-lowering ther-
apy. Consideration should also be given, where
P waves Normal indicated, to treatment with a beta-blocker, an
angiotensin-converting enzyme inhibitor and a
mineralocorticoid receptor antagonist.
T waves Merged with ST segment COMMENTARY

• An urgent ECG is required in any patient pre-
senting with cardiac-sounding chest pain. The
Additional comments presence of ST segment elevation signifies acute
There is ST segment elevation in the lateral leads occlusion of a coronary artery and indicates a
(I, aVL, V4–V6). need for urgent restoration of coronary blood
flow (reperfusion). Time is of the essence – the
ANSWERS longer reperfusion is delayed, the more myocar-
dial necrosis will occur.
1. There is ST segment elevation in limb leads • The differential diagnosis of ST segment elevation
I and aVL and chest leads V4–V6. This is an includes STEMI, Takotsubo cardiomyopathy, left
acute lateral ST segment elevation myocardial ventricular aneurysm, vasospastic (Prinzmetal)
infarction (STEMI). angina, pericarditis, left bundle branch block,
2. Acute occlusion of the circumflex coronary Brugada syndrome and high take-off.
artery. • In STEMI, the ECG changes gradually ‘evolve’.
3. A previously stable coronary endothelial plaque The earliest change is ST segment elevation
has ruptured, exposing the lipid-rich core. accompanied, or even preceded, by tall ‘hyper-
Platelets adhere, change shape and secrete adenos- acute’ T waves. Over the next few hours or days,
ine diphosphate (ADP) and other pro-aggregants. Q waves appear, the ST segments return to nor-
These seal and stabilize the plaque but at the cost mal and the T waves become inverted. It is usual
of narrowing of the coronary artery lumen. This for some permanent abnormality of the ECG to
is often totally, or almost totally, occluded. persist following STEMI – usually ‘pathologi-
4. Having diagnosed STEMI, the key priority is cal’ Q waves, although the T waves may remain
urgent coronary revascularization, which is inverted permanently too.
usually undertaken with primary percutane-
ous coronary intervention (PCI). Primary PCI Further Reading
is usually performed in patients with acute
Making Sense of the ECG 6th edition: Are the ST segments
STEMI presenting within 12 h of the onset of
elevated? p 113; ST segment elevation myocardial
symptoms. If primary PCI is unavailable, then infarction, p 114.
intravenous administration of a thrombolytic Rautaharju PM et al. AHA/ACCF/HRS recommendations
agent may be considered. The initial treatment for the standardization and interpretation of the elec-
of STEMI also includes pain relief (an opioid trocardiogram: Part IV: The ST segment, T and U
intravenously and an anti-emetic) and oxygen waves, and the QT interval. Journal of the American
if hypoxic (SaO2 <90%). Following STEMI, College of Cardiology (2009). PMID 19281931.
CASE 29
CLINICAL SCENARIO
Female, aged 23 years. Past medical history
Nil.
Rapid regular palpitations. Examination
History of presenting complaint Blood pressure: 112/72.
Two-year history of episodic rapid regular pal- JVP: normal.
pitations, normally lasting only a few minutes, Heart sounds: normal (tachycardic).
with a sudden onset and termination. The Chest auscultation: unremarkable.
current episode started suddenly 2 h prior to
presentation. Investigations
QUESTIONS
2. What is the underlying pathophysiological mechanism?
3. What initial treatment would be appropriate?
4. What treatment might be appropriate in the longer term?
DOI: 10.1201/9781003472186-29
ECG ANALYSIS include a non-dihydropyridine calcium chan-

nel blocker or a beta-blocker.
Rate 180/min
Rhythm Atrioventricular nodal re-entry COMMENTARY
tachycardia
QRS axis Normal (+22°) • In patients with a dual atrioventricular nodal

pathway, an impulse arriving at the atrioven-
P waves Visible as a small negative
tricular node will normally split and travel down
deflection at the end of the QRS
both pathways at the same time, but the impulse
complex in the inferior leads
travelling via the fast pathway arrives at the bun-
PR interval Not applicable dle of His first and depolarizes the ventricles. By
QRS duration Normal (60 ms) the time the impulse travelling down the slow
pathway arrives at the bundle of His, the bundle
T waves Normal is refractory and so this impulse goes no further.
QTc interval Normal (450 ms) • However, if a supraventricular ectopic beat hap-
pens to occur during the refractory period of
the fast pathway, this ectopic will travel down
ANSWERS the slow pathway and, by the time it reaches the
end of the slow pathway, the fast pathway may
1. Atrioventricular nodal re-entry tachycardia
have repolarized. If so, this impulse will then
(AVNRT).
travel back up along the fast pathway and then
2. A re-entry circuit involving a dual atrioventric-
back down the slow pathway, ad infinitum. In the
ular nodal pathway – one of the atrioventricular
common form of AVNRT, this slow-fast re-entry
nodal pathways conducts impulses quickly (the
circuit gives rise to the arrhythmia. Fast-slow
‘fast’ pathway) but has a long refractory period,
and slow-slow re-entry circuits are also possible.
the other pathway conducts impulses more
slowly (the ‘slow’ pathway) but has a shorter • In AVNRT, P waves are often hard or even impos-
sible to discern. In around a quarter of cases,
refractory period (see Commentary).
they are hidden within the QRS complexes. In
3. Transiently blocking the atrioventricular node
another two-thirds of cases, they can be seen as
can terminate the AVNRT. Methods to achieve
a small negative deflection at the end of the QRS
this include:
complexes in the inferior leads, and/or as a small
• Valsalva manoeuvre
positive deflection at the end of the QRS complex
• Carotid sinus massage in lead V1. In a small number of cases, the P wave
• Intravenous adenosine can be found just before the QRS complex.
• Intravenous non-dihydropyridine calcium • AVNRT is around 10 times commoner than atrio-
channel blocker ventricular re-entry tachycardia (AVRT – the
• Intravenous beta-blocker result of an atrioventricular accessory pathway
4. The patient can be taught the Valsalva manoeu- as seen in Wolff–Parkinson–White [WPW] syn-
vre to try to terminate episodes. In the lon- drome). The ECG performed during sinus rhythm
ger term, catheter ablation is the treatment of in a patient prone to AVNRT is usually normal, but
choice for symptomatic patients. Long-term in those prone to AVRT, an ECG in sinus rhythm
drug therapy is often ineffective at preventing may reveal a short PR interval or delta wave, sug-
AVNRT episodes (although it may reduce their gesting WPW syndrome. The distinction between
frequency and duration), but if patients prefer AVRT and AVNRT can be difficult, however, and
to avoid catheter ablation, then drug options may require electrophysiological studies.
Case 29 67
Further Reading
Making Sense of the ECG 6th edition: Atrioventricular Katritsis DG et al. Atrioventricular nodal reentrant tachy-
nodal re-entry tachycardia, p 181. cardia. Circulation (2010). PMID 20733110.
ment of patients with supraventricular tachycardia.
European Heart Journal (2020). PMID 31504425.
CASE 30
CLINICAL SCENARIO
Pulse: 42/min, irregular.
Increasing exertional breathlessness. JVP: normal.
Had been fairly well until developed chest No peripheral oedema.
infection. Breathlessness has got progressively
worse since. Investigations
Previous rheumatic fever. Thyroid function: normal.
Troponin I: negative.
QUESTIONS
DOI: 10.1201/9781003472186-30
ECG ANALYSIS 3. The presence of ‘reverse tick’ lateral ST segment

depression suggests that the patient is taking
Rate 42/min digoxin, and indeed this arrhythmia proved to
Rhythm Atrial tachycardia with variable be the result of digoxin toxicity.
atrioventricular block 4. Temporary (and occasionally permanent)
withdrawal of digoxin treatment. Supportive
measures until digoxin levels have fallen to ther-
P waves Present but abnormal morphology apeutic levels. An alternative anti-arrhythmic
PR interval N/A drug may be required.
T waves Abnormal COMMENTARY
• In atrial tachycardia, the ventricular rate depends
upon the degree of atrioventricular block. With
Additional comments 1:1 conduction, the ventricular rate may be rapid.
The P waves are abnormally shaped, indicating • Atrial tachycardia may occur in tachy-brady syn-
an atrial focus away from the sinoatrial node, drome, rheumatic and ischaemic heart disease,
and the P wave rate is 156/min (but most P waves chronic airways disease and cardiomyopathy.
are not conducted to the ventricles). There is also • Digoxin affects the heart in various ways:
a partial RBBB pattern and lateral ST segment • An inotropic effect through inhibition of the
depression. sodium/potassium/ATPase pump
• Increased automaticity of Purkinje fibres
ANSWERS
• Slowing of conduction through the atrioven-
tricular node due to increased vagal activity
1. This ECG shows regular P waves at a rate of 156/ • With digoxin toxicity, increased automaticity
min. The P waves have an abnormal morphol- results in an increased atrial rate and slowing of
ogy, indicating a focus away from the sinoatrial conduction induces atrioventricular block and
node. Only some of the P waves are followed by subsequent slowing of the ventricular rate.
QRS complexes, and the QRS rate is variable. • Toxicity can occur with digoxin levels within
This is atrial tachycardia with variable atrio- the therapeutic range if there is severe hypoka-
ventricular block. laemia (often due to diuretic therapy) or renal
2. Atrial tachycardia differs from sinus tachycar- impairment.
dia in that the impulses are generated by an • Although paroxysmal atrial tachycardia with
ectopic focus somewhere within the atrial myo- variable block is considered the ‘hallmark’ of
cardium rather than the sinus node, as a result digoxin toxicity, in clinical practice the arrhyth-
of increased automaticity, triggered activity or a mia is often sustained. In addition, digoxin can
re-entry circuit. Atrial tachycardia can be focal cause almost any cardiac arrhythmia.
(arising from one discrete focus in the atria) or
multifocal (arising from multiple foci, with at Further Reading
least three different P wave morphologies on the Making Sense of the ECG 6th edition: Atrial tachycardia,
ECG), and it can be paroxysmal or sustained. p 175.
The variable atrioventricular block is due to Brugada J et al. 2019 ESC guidelines for the manage-
depressed conduction through the atrioventric- ment of patients with supraventricular tachycardia.
ular node. European Heart Journal (2020). PMID 31504425.
CASE 31
CLINICAL SCENARIO
Pulse: 66/min, regular with infrequent ectopics.
Episodic palpitations. JVP: not elevated.
A 2-year history of rapid regular palpitations, No peripheral oedema.
occurring once a week on average and lasting
for between 10 and 60 min. Prolonged episodes Investigations
are associated with dizziness. FBC: Hb 145, WCC 5.7, platelets 286.
Nil. Chest X-ray: normal heart size, clear lung fields.
QUESTIONS
2. What is the likely cause of the patient’s palpitations?
3. What further investigations would be appropriate?
DOI: 10.1201/9781003472186-31
ECG ANALYSIS • The ‘classical’ view of LGL syndrome is that

patients have an accessory pathway (some-
Rate 66/min times called the bundle of James) which
Rhythm Sinus rhythm with a single bypasses the AV node. However, unlike the
supraventricular ectopic beat bundle of Kent in Wolff–Parkinson–White
syndrome, the accessory pathway in LGL syn-
drome does not activate the ventricular muscle
P waves Normal directly. Instead, it simply connects the atria
PR interval Short (100 ms) to the bundle of His. As a result, the AV node is
bypassed (so the PR interval is short), but there
QRS duration Normal (76 ms) is no ventricular pre-excitation (and therefore
T waves Normal there is no delta wave).
QTc interval Normal (450 ms) • A short PR interval (in the absence of a delta
wave) is a relatively common finding and the
contemporary view is that a short PR interval
Additional comments alone is not sufficient reason to diagnose LGL
The PR interval is short at 100 ms. syndrome. Instead, LGL syndrome is diagnosed
when patients with a short PR interval (and no
ANSWERS delta wave) present with re-entry tachycardias.
Those who do not experience re-entry tachy-
1. The ECG shows a short PR interval, measuring cardias are instead considered to have a normal
100 ms (2.5 small squares). In the context of epi- variant of AV conduction known as enhanced
sodic palpitations, this is suggestive of a diagno- AV nodal conduction.
sis of Lown–Ganong–Levine (LGL) syndrome. • Many electrophysiologists have questioned the
The diagnosis can be confirmed by demonstrat- pathophysiological basis of LGL syndrome alto-
ing the occurrence of episodes of atrioventricu- gether, as a variety of fibre abnormalities have
lar re-entry tachycardia (AVRT). been identified quite distinct from the original
2. The occurrence of episodic regular palpitations description of James fibres, and the functional
in the setting of a short PR interval makes it significance of many of these anomalies remains
likely that the underlying cause of the palpita- unclear. Indeed, most patients with a short PR
tions is an AVRT. interval and paroxysmal tachycardias are found
3. The patient’s ECG should be recorded during an to have a ‘conventional’ substrate for their tachy-
episode of palpitation in order to make a diag- cardia (such as atrioventricular nodal re-entry
nosis of AVRT and thus to confirm LGL syn- tachycardia) on electrophysiological testing,
drome. Ambulatory ECG recording can be used. and it may be the case that the short PR interval
As the patient’s symptoms are occurring once a simply represented an incidental variant of AV
week on average, a 7-day ECG event recorder or node conduction in such cases.
a Cardiomemo would be the most effective ways
of trying to capture an event.
Further Reading
COMMENTARY Making Sense of the ECG 6th edition: Lown–Ganong–
Levine syndrome, p 81.
• The diagnosis of LGL syndrome requires the pres- Lown B et al. The syndrome of short P-R interval, normal
ence of a short PR interval (<120 ms), a normal QRS complex and paroxysmal rapid heart action.
QRS complex duration and episodes of AVRT. Circulation (1952). PMID 14926053.
CASE 32
CLINICAL SCENARIO
Pulse: 120/min, regular with occasional ectopic beats.
Presenting complaint JVP: not elevated.
Admitted to hospital with chest pain and breath- Heart sounds: soft ejection systolic murmur in
lessness on exertion. aortic area, radiating to neck.
Symptom-free until 3 months ago. Developed
chest pain on exertion, especially if walking Investigations
uphill, in cold weather or when wind blowing. FBC: Hb 129, WCC 6.5, platelets 342.
History of hypertension and hypercholesterol- Chest X-ray: mild cardiomegaly, early pulmonary
aemia. Acute myocardial infarction 3 years ago. congestion.
Chronic bronchitis on home nebulizers. Echocardiogram: mild aortic stenosis, with pres-
sure drop of 20 mmHg across valve, mild mitral
regurgitation into a non-dilated left atrium. Left
ventricular systolic function impaired (ejection
fraction 43%) with anterior wall akinesia.
QUESTIONS
2. What is the cause?
DOI: 10.1201/9781003472186-32

Rate 120/min • This patient clearly has a history of coronary
Rhythm Sinus tachycardia with artery disease, in view of the previous myocar-
occasional atrial ectopic beats dial infarction, and presents with a clinical his-
tory consistent with angina (ischaemic-sounding
chest pain).
P waves Normal • A patient referred for ‘routine’ surgery may report
PR interval Normal (180 ms) a previous myocardial infarction or an ECG may
show evidence of an ‘old’ (previously undiag-
QRS duration Normal (80 ms) nosed) myocardial infarction. The risk of an
T waves Normal adverse perioperative event is increased with:
QTc interval Normal (440 ms) • Known coronary disease, especially within 3
months of a myocardial infarction
• Previously unidentified coronary disease
Additional comments • Valvular heart disease, especially aortic stenosis
Anterior Q waves (leads V1–V3). • Cardiac arrhythmia
• Heart failure/cardiogenic shock
ANSWERS • Coronary risk factors indicating high risk of
coronary disease
1. There are Q waves in the anterior chest leads • Renal impairment
V1–V3, indicative of a previous anterior myo- • Abnormal liver function
cardial infarction. Q waves are considered
‘pathological’ if they exceed two small squares
• Previous stroke or transient ischaemic attack
(TIA)
in depth, or are greater than 25% of the size of
• Poor exercise tolerance
the following R wave, and/or are greater than 1
small square wide. • Guidelines are available to assess perioperative
risk (see ‘Further Reading’).
2. Previous acute occlusion of the left anterior
descending coronary artery.
3. Investigate for evidence of myocardial ischaemia Further Reading
– consider, as appropriate, functional imaging
for ischaemia (stress echocardiogram, stress car- Making Sense of the ECG 6th edition: The Q wave, p 91.
Halvorsen S et al. 2022 ESC guidelines on cardiovascular
diac MRI scan or nuclear myocardial perfusion
assessment and management of patients undergoing
scan) and/or anatomical imaging for coronary non-cardiac surgery. European Heart Journal (2022).
atheroma (CT or invasive coronary angiogra- PMID 36017553.
phy). Ensure the patient is receiving appropri- Leivo J et al. The prognostic significance of Q waves and
ate secondary prevention in view of his previous T wave inversions in the ECG of patients with
history of myocardial infarction and left ventric- STEMI: A substudy of the TOTAL trial. Journal of
ular systolic dysfunction. Electrocardiology (2023). PMID 37295167.
CASE 33
CLINICAL SCENARIO
Dizziness and syncope, breathlessness. JVP: elevated by 2 cm, intermittent cannon
waves.
History of presenting complaint Heart sounds: variable intensity of second heart
Four-day history of increasing breathlessness sound.
and dizziness, culminating in an episode of syn- Chest auscultation: few bi-basal inspiratory
cope in which the patient suddenly fell to the crackles.
floor with little warning. Mild peripheral oedema.

Myocardial infarction 2 months earlier. FBC: Hb 121, WCC 6.3, platelets 206.
Type 2 diabetes mellitus. U&E: Na 136, K 4.2, urea 4.8, creatinine 81.
Chest X-ray: cardiomegaly, pulmonary vascular
congestion.
QUESTIONS
2. What are the possible causes?
3. What treatment is required?
DOI: 10.1201/9781003472186-33

Rate Atrial – 90/min • In third-degree AV block (‘complete heart block’),
Ventricular – 32/min there is complete interruption of conduction between
Rhythm Third-degree atrioventricular atria and ventricles so that the two are working inde-
block (‘complete heart block’) pendently. The atrial (P wave) rate is faster than the
ventricular (QRS complex) rate, and the P waves
QRS axis Can’t be measured (single lead)
bear no relationship to the QRS complexes.
P waves Present • QRS complexes usually arise as the result of a
PR interval Variable – no apparent ventricular escape rhythm. The QRS complexes
connection between P waves are usually broad due to a subsidiary pacemaker
and QRS complexes (‘escape rhythm’) arising in the left or right bundle
branches. However, if the AV block occurs high
up in the conduction system (at the level of the AV
T waves Inverted in leads III, aVF, V1–V4 node) and a subsidiary pacemaker arises in the
QTc interval Prolonged (475 ms) bundle of His, the QRS complexes may be narrow.
• Any atrial rhythm can coexist with third-degree
AV block, and so the P waves may be abnormal
ANSWERS or even absent.
• In a patient with a recent onset of third-degree
1. Third-degree atrioventricular (AV) block (‘com- AV block, always consider the possibility of Lyme
plete heart block’). disease. This is transmitted by the spirochaete
2. Third-degree AV block can result from: Borrelia burgdorferi and, in the second stage of the
• Drug toxicity (e.g. anti-arrhythmics) illness, can lead to first-degree, second-degree or
• Fibrosis/calcification of the conduction third-degree AV block. The AV block can resolve
system entirely in response to antibiotics, although the
• Myocardial ischaemia/infarction patient may require support with a temporary
• Infection (e.g. Lyme disease) pacemaker during treatment.
• Myocardial infiltration (e.g. amyloid, sarcoid) • In congenital third-degree AV block, which is
uncommon, the block is usually at the level of the
• Neuromuscular diseases (e.g. myotonic mus-
AV node and is often associated with maternal
cular dystrophy)
anti-Ro or anti-La antibodies.
• Metabolic disorders (e.g. hypothyroidism)
• Cardiac procedures (e.g. ablation procedures,
aortic valve surgery) Further Reading
• Congenital complete heart block Making Sense of the ECG 6th edition: Third-degree atrio-
3. In most cases, acquired third-degree AV block ventricular block, p 203; Cardiac implantable elec-
requires a permanent pacemaker. An excep- tronic devices, p 223.
tion to this is if there is a reversible cause (such Glikson M et al. 2021 ESC guidelines on cardiac pacing
and cardiac resynchronization therapy. European
as drug toxicity, e.g. beta-blockers, or infec-
Heart Journal (2021). PMID 34455430.
tion, such as Lyme disease), in which case the
Kusumoto FM et al. 2018 ACC/AHA/HRS guideline
patient may only require supportive treatment on the evaluation and management of patients
(which may include temporary pacing) until with bradycardia and cardiac conduction delay:
the cause has been treated and the AV block Executive summary. Journal of the American College
has resolved. of Cardiology (2019). PMID 30412710.
CASE 34
CLINICAL SCENARIO
Feeling generally weak and lethargic. Also had JVP: normal.
frequent palpitations. Heart sounds: normal.
Fit and well until about 3 months ago when
diagnosed with hypertension and commenced Investigations
on a thiazide-like diuretic. FBC: Hb 147, WCC 5.6, platelets 168.
Hypertension. Chest X-ray: normal heart size, clear lung fields.
Echocardiogram: normal valves. Concentric left
ventricular hypertrophy.
QUESTIONS
DOI: 10.1201/9781003472186-34
ECG ANALYSIS a common cause). Mild hypokalaemia can be cor-

rected with dietary or oral supplements. Severe
Rate 84/min hypokalaemia is a medical emergency and should
Rhythm Sinus rhythm be corrected with slow intravenous infusion of
appropriately diluted potassium chloride – fast or
QRS axis Borderline left axis deviation (–30°)
concentrated infusions may predispose to ventric-
P waves Small but normal morphology ular arrhythmias.
QRS duration Normal (80 ms) COMMENTARY

T waves Normal • Mild hypokalaemia may occur without symptoms.
QTc interval Normal (390 ms) Moderate hypokalaemia may cause muscle weak-
ness, cramps and constipation. With more severe
hypokalaemia, flaccid paralysis, hyporeflexia, respi-
ANSWERS ratory depression and tetany may be seen.
1. This ECG shows first-degree atrioventricular • Hypokalaemia is much more common than
block (long PR interval), small T waves and there hyperkalaemia and can produce the following
are U waves evident. These findings are second- ECG changes:
ary to hypokalaemia. • First-degree atrioventricular block
2. Depolarization of myocardial cells is dependent on • Depression of the ST segment
the movement of ions across the cell membrane, • Small T waves
the most important being potassium. The resting • Prolongation of the QT interval
transmembrane potential is determined largely • Prominent U waves
by the ratio of the intracellular (140 mmol/L) to
extracellular (3.5 to 5 mmol/L) potassium ion con-
• Resulting instability of cell membranes causes an
increased risk of cardiac arrhythmia, especially
centration, and the absolute level of extracellular atrial and ventricular ectopic beats, atrial and
potassium ion concentration is the most impor- ventricular tachycardia, various heart blocks and
tant factor affecting the cell membrane. ventricular fibrillation.
3. The hypokalaemia is likely secondary to the
patient’s diuretic therapy. Other causes of
• Hypomagnesaemia is common with hypokalae-
mia; alone, it causes similar ECG abnormalities.
hypokalaemia include vomiting and diarrhoea, Hypokalaemia is often difficult to correct until
excessive perspiration, rectal villous adenoma, the magnesium level is normal.
intestinal fistula, Cushing’s and Conn’s syn-
dromes, alkalosis, purgative and laxative misuse,
• Caution – digoxin toxicity is more likely with
hypokalaemia.
renal tubular failure, hypomagnesaemia (usually
evident when K+ remains low after potassium
• Although distinct ECG changes may be observed
in hypokalaemia, the ECG is not a reliable indica-
supplementation). Rare causes include Bartter’s tor of the serum potassium level.
syndrome (hereditary defect of muscular ion
channels) and hypokalaemic periodic paralysis.
4. If hypokalaemia is suspected, assess the patient for Further Reading
symptoms (such as muscle weakness and cramps) Making Sense of the ECG 6th edition: Hypokalaemia, p 136;
and enquire about prescribed drugs (diuretics are Do the U waves appear too prominent? p 154.
CASE 35
CLINICAL SCENARIO
Patient comfortable at rest.
Asymptomatic – routine ECG performed during Blood pressure: 168/104.
hypertension follow-up visit. JVP: not elevated.
Precordium: left parasternal heave.
History of presenting complaint Heart sounds: loud aortic component of second
Six-year history of hypertension, treated with an heart sound (A 2).
angiotensin-converting enzyme (ACE) inhibitor. Chest auscultation: unremarkable.
Six-year history of hypertension.
Investigations
QUESTIONS
2. What investigation would help to confirm this?
3. What can cause these appearances? What is the likely cause here?
DOI: 10.1201/9781003472186-35
ECG ANALYSIS appropriate treatment is that of the underlying

cause – in this case, hypertension. The aim in
Rate 66/min most patients is to control the blood pressure to
Rhythm Sinus rhythm a level below 140/90.
P waves Normal
COMMENTARY
PR interval Normal (167 ms) • There are many criteria for the ECG diag-
nosis of left ventricular hypertrophy, with
varying sensitivity and specificity. Generally,
T waves Normal the diagnostic criteria are quite specific (if
QTc interval Normal (420 ms) the criteria are present, the likelihood of the
patient having left ventricular hypertrophy
is >90%) but not very sensitive (the criteria
Additional comments will fail to detect 40–80% of patients with left
In the chest leads there are deep S waves (up to 15 ventricular hypertrophy). The diagnostic cri-
mm in lead V2) and tall R waves (up to 39 mm) in teria include:
lead V4. • In the limb leads:
– R wave >11 mm in lead aVL
ANSWERS – R wave >20 mm in lead aVF
– S wave >14 mm in lead aVR
1. This ECG shows deep S waves (up to 15 mm in – Sum of R wave in lead I and S wave in lead
lead V2) and tall R waves (up to 39 mm) in lead V4 III >25 mm
in the chest leads. These appearances are indica-
tive of left ventricular hypertrophy. The diagnos-
• In the chest leads:
– R wave of ≥25 mm in the left chest leads
tic criteria in this case include:
– S wave of ≥25 mm in the right chest leads
• R wave in lead V4 measuring 39 mm
– Sum of S wave in lead V1 and R wave in
• S wave in lead V1 plus R wave in lead V5 total-
lead V5 or V6 >35 mm (Sokolow–Lyon
ling 41 mm
criterion)
• Tallest R wave and deepest S wave in chest
– Sum of tallest R wave and deepest S wave
leads totalling 54 mm
in the chest leads >45 mm
2. An echocardiogram (or cardiac magnetic reso-
nance scan) would allow direct visualization of
• The Cornell criteria involve measuring the S
wave in lead V3 and the R wave in lead aVL. Left
the left ventricle, assessment of the extent of left
ventricular hypertrophy is indicated by a sum of
ventricular hypertrophy, assessment of left ven-
>28 mm in males and >20 mm in females.
tricular systolic (and diastolic) function and also
assessment of the heart valves. • The Romhilt–Estes scoring system allocates
points for the presence of certain criteria. A score
3. Left ventricular hypertrophy can result from:
of 5 indicates left ventricular hypertrophy and
• Hypertension
a score of 4 indicates probable left ventricular
• Aortic stenosis hypertrophy. Points are allocated as follows:
• Coarctation of the aorta • 3 points – for (a) R or S wave in limb leads
• Hypertrophic cardiomyopathy of ≥20 mm, (b) S wave in right chest leads of
The clinical findings indicate that poorly con- ≥25 mm or (c) R wave in left chest leads of
trolled hypertension is the most likely cause of ≥25 mm
left ventricular hypertrophy in this case. • 3 points – for ST segment and T wave changes
4. Where left ventricular hypertrophy is second- (‘typical strain’) in a patient not taking digi-
ary to pressure overload of the left ventricle, the talis (1 point with digitalis)
Case 35 81
Further Reading
• 3 points – for P-terminal force in V1 >1 mm Making Sense of the ECG 6th edition: Left ventricular
deep with a duration >0.04 s hypertrophy, p 98.
• 2 points – for left axis deviation (beyond –15°) Peguero JG et al. Electrocardiographic criteria for the
• 1 point – for QRS complex duration >0.09 s diagnosis of left ventricular hypertrophy. Journal of
the American College of Cardiology (2017). PMID
• 1 point – for intrinsicoid deflection (the inter- 28359515.
val from the start of the QRS complex to the
peak of the R wave) in V5 or V6 >0.05 s
CASE 36
CLINICAL SCENARIO
Breathlessness on exertion. JVP: elevated by 2 cm.
Heart sounds: systolic murmur 3/6 in mitral area.
Patient has had episodes of syncope and breath- Mild pitting ankle oedema.
lessness for months. The syncope resolved fol-
lowing treatment but her breathlessness never Investigations
improved back to normal. She now has episodes FBC: Hb 116, WCC 4.2, platelets 176.
of paroxysmal nocturnal dyspnoea. As she U&E: Na 133, K 4.3, urea 8.5, creatinine 234.
attends the hospital regularly, she reported her Chest X-ray: marked cardiomegaly, fluid in hori-
persistent symptoms to the cardiac physiologist. zontal fissure.
Echocardiogram: moderate mitral regurgita-
Past medical history tion into a moderately dilated left atrium. Left
Congestive cardiac failure – unsure of medica- ventricular function severely impaired (ejection
tion but been on escalating doses of several fraction 24%).
drugs since she developed breathlessness.
QUESTIONS
DOI: 10.1201/9781003472186-36
ECG ANALYSIS systole may produce a wave of blood to flow

retrogradely into the cerebral veins. Generally
Rate 72/min speaking, in an active individual, physiological
pacing with a dual-chamber or DDD pacemaker
Rhythm Ventricular pacing
will harness atrial contractility and timing to
QRS axis Left axis deviation (−48°) optimize cardiac function.
P waves Occasionally visible
PR interval N/A COMMENTARY

• Pacemakers are described by pacing codes:
T waves Abnormal • The first letter of the code identifies the
QTc interval Prolonged (540 ms)
chambers that can be paced (A – atrium,
V – ventricle, D – dual)
• The second letter of the code identifies the
chambers that can be sensed (A – atrium,
ANSWERS V – ventricle, D – dual)
1. There are occasional P waves visible between • The third letter of the code identifies what the
pacemaker does if it detects intrinsic activity
some (but not all) of the QRS complexes and
(I – inhibited, T – triggered, D – dual)
occasional P waves can be seen deforming the
ST segment. There is, however, no association • The fourth letter denotes whether rate respon-
between P waves and QRS complexes, indicat- siveness (R) is present
ing complete heart block. In addition, the QRS • The fifth letter identifies anti-tachycardia
complexes are broad and preceded by a distinct functions, if present (P – pacing, S – shock
‘spike’ – this is ventricular pacing. The patient delivered, D – dual)
has had a VVI permanent pacemaker implanted • The most commonly encountered pacemakers are:
for a diagnosis of complete heart block. • VVI – a single lead pacemaker that senses
2. The ‘spike’ is an electrical discharge from a pace- ventricular activity; if no activity is detected,
maker, either temporary or permanent. In this the pacemaker will take over cardiac rhythm
case, a permanent single-chamber or VVI (see by pacing the ventricle
the following coding schema) pacemaker has • AAI – the pacemaker has a single lead, this
been implanted to relieve symptoms of syncope. time sensing atrial activity; if no activity is
This paces the ventricle at a preset rate, in this detected, the pacemaker paces the atrium
case 72/min. If a ventricular depolarization is • DDD – there are pacemaker leads in both
sensed, the pacemaker is ‘inhibited’ – all the atrium and ventricle, and so it senses activ-
beats on this ECG are ‘paced’ beats. ity in both chambers. It can pace atrium, ven-
3. The pacemaker has been implanted because tricle or both sequentially
of complete heart block. The rate of the escape • AAIR, VVIR and DDDR are rate-responsive
rhythm of the ventricles of approximately 15–40/ varieties of those previously mentioned. The
min is inadequate for most activities and causes pacemaker adjusts its pacing rate according to
fatigue, dizziness and syncope. the patient’s level of activity to mimic physio-
4. The pacemaker to be implanted must be chosen logical response to exercise. Several parameters
with care. Insertion of a VVI pacemaker when can be monitored by pacemakers to determine
there are P waves may cause symptoms due to the patient’s level of activity, including move-
‘pacemaker syndrome’, when an atrial contrac- ment (using an accelerometer) and respiratory
tion against a closed tricuspid valve during rate (using a transthoracic impedance sensor).
Case 36 85
Further Reading
Making Sense of the ECG 6th edition: Cardiac implantable Kusumoto FM et al. 2018 ACC/AHA/HRS guideline on
electronic devices, p 223. the evaluation and management of patients with
Glikson M et al. 2021 ESC guidelines on cardiac pacing bradycardia and cardiac conduction delay. Journal
and cardiac resynchronization therapy. European of the American College of Cardiology (2018). PMID
Heart Journal (2021). PMID 34455430. 30412710.
CASE 37
CLINICAL SCENARIO
Rapid regular palpitations. JVP: normal.
Heart sounds: normal (tachycardic).
Six-month history of episodic rapid regular pal-
pitations. The current episode started suddenly Investigations
2 h prior to presentation. FBC: Hb 154, WCC 6.3, platelets 317.
Past medical history Chest X-ray: normal heart size, clear lung
Nil. fields.
QUESTIONS
1. What arrhythmia is seen in the initial part of this recording?
2. What intervention is likely to have been made at the point the rhythm changes?
3. What other interventions could have produced a similar result?
DOI: 10.1201/9781003472186-37

Rate 158/min (during AVNRT) • The mechanism of AVNRT is discussed in Case
29.
Rhythm Initially AVNRT, followed by
sinus rhythm • Vagal manoeuvres such as carotid sinus mas-
sage or the Valsalva manoeuvre are often effec-
QRS axis Unable to assess (single tive in terminating episodes of AVNRT (and also
lead) AVRT). The Valsalva manoeuvre describes the
P waves Buried within QRS action of forced expiration against a closed glot-
complexes during AVNRT tis. To perform it, patients are asked to breathe in
(normal during sinus and then to strain for 15 s with their breath held.
rhythm) Alternatively, they can be given a 10 mL plastic
PR interval Normal (180 ms) during syringe and asked to ‘blow’ into the hole to try to
sinus rhythm push out the plunger from the opposite end. This
is virtually impossible to achieve, but in trying to
QRS duration Normal (100 ms) during
do so the patient effectively performs a Valsalva
AVNRT
manoeuvre.
T waves Normal • The modified Valsalva manoeuvre also requires
QTc interval Normal (438 ms) during the patient to strain for 15 s, but immediately at
sinus rhythm the end of the strain, the patient is laid flat and
their legs are raised to an angle of 45° by a staff
member for a further 15 s. The patient is then
ANSWERS returned to a semi-recumbent position for a fur-
ther 45 s before reassessment of cardiac rhythm.
1. The first part of the recording shows a regular
In the REVERT trial it was found that the modi-
narrow-complex tachycardia (158/min) with P
fied Valsalva manoeuvre restores sinus rhythm
waves buried within the QRS complexes (note
in 43% of patients, versus only 17% for the stan-
the slight difference in shape of the QRS com-
dard Valsalva manoeuvre.
plexes during the tachycardia compared to those
during sinus rhythm). This is atrioventricular • Do not use the old-fashioned vagal manoeuvre of
applying eyeball pressure, as this can cause eye-
nodal re-entry tachycardia (AVNRT). Other
ball trauma.
possibilities include:
• Atrioventricular re-entry tachycardia (AVRT), • Do not use carotid sinus massage in individuals
although in AVRT inverted P waves are often with known or suspected carotid or cerebrovas-
seen halfway between QRS complexes cular disease, including those with carotid bruits.
• Atrial flutter with 2:1 atrioventricular block,
although one would normally expect to see Further Reading
evidence of flutter waves Making Sense of the ECG 6th edition: Atrioventricular
2. The intervention performed is carotid sinus nodal re-entry tachycardia, p 181.
massage, which briefly blocks the atrioventric- Appelboam A et al. Postural modiﬁcation to the standard
ular node and terminates the arrhythmia. This Valsalva manoeuvre for emergency treatment of
rules out atrial flutter (carotid sinus massage supraventricular tachycardias (REVERT): A ran-
domised controlled trial. Lancet (2015). PMID
would help reveal flutter waves but would not
26314489.
terminate atrial flutter).
3. Other interventions that can briefly block the ment of patients with supraventricular tachycardia.
atrioventricular node, terminating AVNRT, European Heart Journal (2020). PMID 31504425.
include the Valsalva manoeuvre or the adminis- Katritsis DG et al. Atrioventricular nodal reentrant tachy-
tration of intravenous adenosine. cardia. Circulation (2010). PMID 20733110.
CASE 38
CLINICAL SCENARIO
Pulse: 45/min with long pauses.
Felt unwell while driving. JVP: not elevated.
Occasional episodes of dizziness. One episode No peripheral oedema.
of collapse and unconsciousness while driving
resulted in admission following a road traffic Investigations
accident. FBC: Hb 139, WCC 6.6, platelets 203.
Nil of note. Echocardiogram: structurally normal valves,
normal left ventricular function.
QUESTIONS
DOI: 10.1201/9781003472186-38
ECG ANALYSIS function should be withdrawn. Symptoms

include sudden onset of confusion, breathless-
Rate 45/min, followed by a 5.2 s ness, syncope, chest pain, fatigue, or, if the event
pause occurs at night, disturbed sleep. Symptoms can
Rhythm Sinus bradycardia followed
be relieved by implanting a permanent pace-
by sinus arrest, then a maker. An atrial (AAI) pacemaker monitors and
junctional escape beat paces the atrium. Some patients also demon-
strate atrioventricular conduction problems and
QRS axis Unable to assess
a dual-chamber (DDD) pacemaker is necessary
P waves Normal (when present) to restore atrioventricular sequential pacing.
PR interval Borderline prolonged (200
ms)
COMMENTARY
T waves Normal
• Sinus arrest should be distinguished from sino-
atrial block. In sinus arrest, the sinoatrial node
QTc interval Normal (420 ms) stops firing for a variable time period, so the next P
wave occurs after a variable interval. In sinoatrial
block there is a pause with one or more absent P
ANSWERS waves, and then the next P wave appears exactly
where predicted – in other words, the sinoatrial
1. This ECG rhythm strip shows two leads. There node continues to ‘keep time’, but its impulses are
are two sinus beats, with a bradycardic heart rate not transmitted beyond the node to the atria.
of 45/min. There is then a pause of 5.2 s, during
which no P waves are present. This is followed
• Sinus arrest and sinoatrial block can both be
features of sick sinus syndrome. Other features
by a junctional escape beat. This is an episode of sick sinus syndrome can include sinus brady-
of sinus arrest. The preceding sinus bradycardia cardia (as seen here), tachy-brady syndrome and
is suggestive of underlying sinus node dysfunc- atrial fibrillation.
tion (SND).
2. The sinus node fails to discharge reliably and ‘on
• Offer appropriate advice to patients who drive a
vehicle and who suffer from presyncope or syn-
time’ – there is cessation of P wave activity for a cope – very often, they will be barred from driv-
variable and unpredictable time period (compare ing until the problem has been diagnosed and/
this with sinoatrial block – Case 20). It can also or corrected as appropriate. Driving regulations
be caused by excessive vagal inhibition, infarc- vary between countries. In the UK, information
tion, fibrosis, acute myocarditis, cardiomyopa- on the medical aspects of fitness to drive can be
thy, drugs (digoxin, procainamide, quinidine) found on the website of the Driver and Vehicle
or amyloidosis. A slower subsidiary pacemaker Licensing Agency.
further down the conduction pathway will some-
times take over – in this case, the atrioventricular
junction (as evidenced by a beat with a narrow Further Reading
QRS complex but no preceding P wave). Making Sense of the ECG 6th edition: Sinus bradycardia,
3. If asymptomatic, no treatment is required, p 164; Sinus arrest, p 167; P waves are intermittently
although drugs that can disrupt sinus node absent, p 74.
CASE 39
CLINICAL SCENARIO
Routine ECG for insurance medical. JVP: not elevated.
No history – normally fit and well. No peripheral oedema.

No prior medical history. FBC: Hb 138, WCC 5.1, platelets 345.
QUESTIONS
2. What is the cause of these ECG appearances?
3. What should you do next?
DOI: 10.1201/9781003472186-39

Rate 66/min • It is thought that errors in electrode placement
are made in up to 4% of ECG recordings. When
Rhythm Sinus rhythm
recording an ECG it is essential to check the
QRS axis Right axis deviation (+152°) electrode positioning carefully, as electrode mis-
P waves Inverted in leads I and aVL, placement can cause significant changes in the
biphasic in lead aVR ECG’s appearance and therefore lead to diagno-
sis (and treatment) errors.
• Any permutation of the limb and chest elec-
QRS duration Normal (70 ms) trodes is theoretically possible, but the common-
T waves Inverted in leads I and aVL,
est electrode placement errors involve switching
upright in lead aVR two of the limb electrodes or two of the chest
electrodes.
• Always assess ECGs in the patient’s clinical con-
text, and ECG abnormalities that are unexpected
ANSWERS or ‘don’t make sense’ should always prompt
a check of whether the ECG was recorded
1. This ECG has an unusual appearance: correctly.
• There is extreme right axis deviation (+152°),
and a positive QRS complex in lead aVR.
• When an electrode placement error is recog-
nized, repeat the ECG (with correct electrode
• The QRS complexes in leads I and aVL are placement) at the earliest opportunity.
negative, and there is P wave and T wave
inversion in these leads too.
2. These appearances are difficult to account for Further Reading
clinically – although similar appearances are Making Sense of the ECG 6th edition: Performing an
seen in the limb leads in dextrocardia, we would ECG recording, p 21; Electrode placement, p 22;
also expect to find abnormalities in the chest Electrode misplacement, p 157.
leads in dextrocardia (whereas in this patient the Campbell B et al. Clinical guidelines by consensus:
chest leads are normal). Moreover, the patient’s Recording a standard 12-lead electrocardio-
clinical examination and chest X-ray have not gram. An approved method by the Society for
shown dextrocardia. This patient’s ECG appear- Cardiological Science and Technology (SCST).
ances are therefore due to misplacement of the 2017. Downloadable from www.scst.org.uk.
Rajaganeshan R et al. Accuracy in ECG lead placement
right and left arm electrodes.
among technicians, nurses, general physicians
3. Check the ECG electrode positioning and reposition and cardiologists. International Journal of Clinical
the right and left arm electrodes on the appropriate Practice (2008). PMID 17764456.
limb, so that the ECG can be repeated with all the Rudiger A et al. Electrocardiographic artifacts due
electrodes in the correct place. When this patient’s to electrode misplacement and their frequency
ECG was repeated, with the arm electrodes posi- in different clinical settings. American Journal of
tioned correctly, it was found to be normal. Emergency Medicine (2007). PMID 17276807.
CASE 40
CLINICAL SCENARIO
Pulse: 108/min, regular with occasional ectopic
Presenting complaint beats.
Severe central chest pain. Blood pressure: 108/76.
JVP: not elevated.
Patient was walking to local shops. Experienced Chest auscultation: unremarkable.
rapid onset of severe central crushing chest No peripheral oedema.
pain, associated with breathlessness and nau-
sea. Similar to (but much worse than) her usual Investigations
angina. FBC: Hb 121, WCC 4.7, platelets 390.
Past medical history Troponin I: elevated.
Exertional angina for many years. Chest X-ray: mild cardiomegaly.
Mild hypertension. Echocardiogram: left ventricular systolic func-
Type 2 diabetes mellitus. tion borderline low (ejection fraction 52%), with
posterior wall hypokinesia.
QUESTIONS
3. What treatment would be appropriate in this patient?
DOI: 10.1201/9781003472186-40
ECG ANALYSIS <90%). Following STEMI, patients will require

longer-term treatment with dual antiplatelet
Rate 108/min therapy (aspirin plus a P2Y12 inhibitor, such as
ticagrelor or clopidogrel), usually for 12 months,
Rhythm Sinus rhythm with
occasional ventricular
and then aspirin long-term, together with lipid-
ectopic beats lowering therapy. Consideration should also
be given, where indicated, to treatment with a
QRS axis Left axis deviation (+36°) beta-blocker, an angiotensin-converting enzyme
P waves Normal inhibitor and a mineralocorticoid receptor
antagonist.
QRS duration Upper limit of normal

(120 ms)
COMMENTARY
T waves Limb leads – normal • On a conventional ECG, the usual STEMI
Chest leads – merged with appearances of pathological Q waves, ST seg-
ST segment ment elevation and inverted T waves will, in a
posterior STEMI, be seen as reciprocal changes
in the anterior leads V1–V3, i.e. R waves (instead
of Q waves), ST segment depression (instead of
Additional comments elevation) and upright T waves (rather than
inverted) when viewed from leads V1–V3.
There are tall dominant R waves in leads V1–V4 with
ST segment depression. • The hallmark ST segment elevation of an acute
STEMI is not seen in an acute posterior myocar-
dial infarction unless an ECG is recorded using
ANSWERS posterior leads, V7–V9, on the back of the chest.
Posterior myocardial infarctions are therefore
1. This ECG shows tall dominant R waves in leads commonly overlooked, or misdiagnosed as ante-
with ST segment depression in the anterior chest rior wall ischaemia. Using posterior leads helps
leads. This is an acute posterior ST segment to distinguish between the two diagnoses.
elevation myocardial infarction (STEMI).
2. Posterior STEMI results from occlusion of the
• In the clinical context of acute chest pain with ST
segment depression in the anterior or anterosep-
coronary artery supplying the posterior wall of tal leads, always consider the possibility of poste-
the heart – in 70% of cases, the right coronary rior myocardial infarction.
artery (and in the remainder the circumflex
artery).
• Posterior myocardial infarction is one cause of a
‘dominant’ R wave in lead V1. Other causes are:
3. Having diagnosed STEMI, the key priority is
urgent coronary revascularization, which is
• Right ventricular hypertrophy
usually undertaken with primary percutane-

• Wolff–Parkinson–White syndrome with a
left-sided accessory pathway
ous coronary intervention (PCI). Primary PCI is
usually performed in patients with acute STEMI
presenting within 12 h of the onset of symptoms. Further Reading
If primary PCI is unavailable, then intravenous Making Sense of the ECG 6th edition: Acute posterior myo-
administration of a thrombolytic agent may be cardial infarction, p 128.
considered. The initial treatment of STEMI also Byrne RA et al. 2023 ESC guidelines for the manage-
includes pain relief (an opioid intravenously and ment of acute coronary syndromes. European Heart
an anti-emetic) and oxygen if hypoxic (SaO2 Journal (2023). PMID 37622654.
CASE 41
CLINICAL SCENARIO
Reduced conscious level (Glasgow Coma Scale
Presenting complaint score 11/15).
Found collapsed at home. Right leg shortened and externally rotated.
Temperature: 30.8°C.
History of presenting complaint Pulse: 96/min, irregularly irregular.
Patient found lying on the floor of her home by a Blood pressure: 98/54.
neighbour. She had slipped and fallen the previ- JVP: not elevated.
ous evening when preparing to go to bed, and Heart sounds: normal.
was found 11 h later having been on the floor all Chest auscultation: unremarkable.
night. She had fractured her right hip and was No peripheral oedema.
unable to stand.
Investigations
Stroke 4 years earlier (full recovery). U&E: Na 134, K 5.1, urea 11.7, creatinine 148.
Creatine kinase: elevated at 1565.
QUESTIONS
2. What is the cause of these ECG appearances?
3. What other ECG findings may be seen in this condition?
DOI: 10.1201/9781003472186-41
ECG ANALYSIS rewarming is suitable for most patients with

mild hypothermia; consider active rewarming
Rate 96/min for those with moderate or severe hypothermia.
Rhythm Atrial fibrillation Manage comorbidities (e.g. sepsis or, in this case,
a hip fracture) as appropriate.
QRS axis Right axis deviation (+98°)
P waves Absent (atrial fibrillation) COMMENTARY

PR interval
QRS duration
Not applicable
Normal (90 ms)

• J waves, also known as Osborn waves, are char-
acterized by a dome- or hump-shaped deflection
T waves Normal of the ECG at the junction of the QRS complex
and the ST segment (the J point). J waves have
been reported to be present in around 80% of
ECGs in hypothermic patients (below 33°C), but
Additional comments they are also sometimes seen in patients with a
J waves (also known as ‘Osborn waves’) are visible normal body temperature and are therefore not
in lead V4. completely specific for hypothermia.
• A variety of arrhythmias can be seen in hypo-
thermia. Sinus tachycardia is the earliest abnor-
ANSWERS mality, followed (as core temperature falls) by
sinus bradycardia, then atrial ectopics and atrial
1. This ECG shows atrial fibrillation with J waves, fibrillation (often with a slow ventricular rate).
also known as Osborn waves. The J wave is a As the temperature falls further, the QRS com-
small positive deflection seen at the junction plexes become increasingly broad and the risk of
between the QRS complex and the ST segment ventricular fibrillation increases. Finally, asys-
and is usually best seen in the inferior limb leads tole occurs.
and the lateral chest leads (in this case the J • Ventricular fibrillation can be refractory to defi-
waves are most clearly seen in lead V4). The cor- brillation in the severely hypothermic patient.
rected QT interval is prolonged at 472 ms. In patients with a core temperature below 30°C,
2. Hypothermia (the patient’s temperature is 30.8°C). the onset of ventricular tachycardia or fibril-
3. J waves, atrial fibrillation and prolongation of lation should be treated with an attempt at
the QT interval are all features of hypothermia. defibrillation – if this is ineffective, defer further
In addition, the ECG in hypothermia may also attempts until the patient’s core temperature is
show broadening of the QRS complexes, length- above 30°C.
ening of the PR interval, atrioventricular block,
ventricular arrhythmias and asystole. Further Reading
4. The treatment of hypothermia includes grad- Making Sense of the ECG 6th edition: Are J waves present?
ual rewarming and the administration, where p 131.
appropriate, of warm intravenous fluids and Mattu A et al. Electrocardiographic manifestations of
warm humidified oxygen. Careful monitoring hypothermia. American Journal of Emergency
of vital signs and of the ECG is required. Passive Medicine (2002). PMID 12098179.
CASE 42
CLINICAL SCENARIO
Breathlessness on exertion, but no chest pain. JVP: not elevated.
History of presenting complaint Chest auscultation: bilateral inspiratory crackles.
Patient had a heart attack 6 months previously. No peripheral oedema.
Never returned to previous activity levels. In
past few weeks, noticed more breathlessness Investigations
than usual – had to avoid stairs as much as pos- FBC: Hb 127, WCC 8.0, platelets 284.
sible, and steep paths were now impossible. U&E: Na 139, K 4.6, urea 4.8, creatinine 124.
Occasional paroxysmal nocturnal dyspnoea. Troponin I: negative.
Chest X-ray: enlarged left ventricle. Pulmonary
Past medical history oedema.
No history of lung disease.
QUESTIONS
2. What would be the most useful investigation?
DOI: 10.1201/9781003472186-42
ECG ANALYSIS with heart failure, an embolic event, intractable

arrhythmias or chest pain. Treatment of heart
Rate 96/min failure, rhythm abnormalities and anticoagula-
Rhythm Sinus rhythm tion are required as appropriate. Surgical resec-
tion of the aneurysm (aneurysmectomy) may
improve symptoms.
P waves Normal
PR interval Normal (160 ms) COMMENTARY

• Coronary artery disease and acute myocardial
T waves Normal infarction are the most common causes of a
QTc interval Mildly prolonged (455 ms) left ventricular aneurysm. Rarer causes include
trauma, Chagas disease and sarcoidosis.
Additional comments
• Left ventricular aneurysm is a late complication
of myocardial infarction, seen in around 10% of
There are deep anterior Q waves with persistent ST survivors.
segment elevation. • Left ventricular aneurysm may present as:
• Breathlessness – aneurysmal tissue is non-
ANSWERS contractile, so an extensive aneurysm may
cause loss of a large proportion of left ventric-
1. Deep Q waves with persistent ST segment eleva- ular function and lead to symptoms and signs
tion in leads V1–V4, 6 months after a previous of heart failure
myocardial infarction, is suggestive of a left ven- • Ventricular arrhythmia – the ischaemic bor-
tricular aneurysm. der zone is a substrate for ventricular ectopic
2. An echocardiogram would confirm the presence beats and ventricular tachycardia
of a left ventricular aneurysm and allow assess- • Sudden death – this may be due to ventricular
ment of left ventricular function and any valvu- arrhythmias or to spontaneous rupture of the
lar dysfunction. A cardiac magnetic resonance aneurysmal segment
scan is also useful for delineating the extent of • Chest pain – the border zone between infarcted
any aneurysmal segment, assessing myocardial aneurysmal tissue and healthy, non-infarcted
viability and screening for any intraventricular myocardium can become ischaemic
thrombus. • Embolism – thrombus may form in a ventricu-
3. Although the ST segment elevation on the lar aneurysm, due to the relative stasis of blood,
admission ECG may suggest a new infarction, and embolize
the history (progressive breathlessness without
chest pain) is not compatible with this diagnosis.
A chest X-ray may show an abnormal cardiac sil- Further Reading
houette and the high-sensitivity troponin levels Making Sense of the ECG 6th edition: Are the ST segments
will be in the normal range. Patients may present elevated? p 113; Left ventricular aneurysm, p 120.
CASE 43
CLINICAL SCENARIO
Pulse: 66/min, regularly irregular.
Heart sounds: regularly irregular.
Patient attended for preoperative screening for No peripheral oedema.
a right inguinal hernia repair. His pulse was noted
to be irregular, and this ECG was performed. Investigations
Right inguinal hernia. No prior cardiovascular Thyroid function: normal.
history. Chest X-ray: normal heart size, clear lung fields.
Echocardiogram: normal cardiac structure and
function.
QUESTIONS
1. What arrhythmia does this ECG show?
2. Where in the heart has this arrhythmia originated?
DOI: 10.1201/9781003472186-43
ECG ANALYSIS • VEBs cause broad QRS complexes (unlike supra-

ventricular ectopics, which usually cause narrow
Rate 66/min QRS complexes). The VEB, having arisen within
Rhythm Ventricular bigeminy the ventricular myocardium, has to conduct from
myocyte to myocyte in order to depolarize the
QRS axis Normal (+80°) for sinus beats, inferior
ventricles – this is slower than conduction via
axis for ventricular ectopic beats
the His-Purkinje system, and hence ventricular
P waves Present for sinus beats depolarization takes longer than it would with a
PR interval 160 ms normal sinus beat.
QRS duration Normal (80 ms) for sinus beats, broad

• VEBs arising from the right ventricle have a left
bundle branch block morphology, and those
(140 ms) for ventricular ectopic
arising from the left ventricle have a right bundle
beats
branch block morphology.
T waves Normal for sinus beats, inverted for
ventricular ectopic beats
• On checking the radial pulse of a patient with
bigeminy, the VEBs usually feel weaker than
QTc interval Normal (440 ms) the normal sinus beats (because the ventricle
has not filled fully by the time systole occurs).
As a result, VEBs may sometimes be missed on
ANSWERS
palpation of the radial pulse. Patients with ven-
1. In this ECG every normal sinus beat is followed tricular bigeminy are therefore sometimes mis-
by a broad and abnormally shaped QRS com- takenly diagnosed as being bradycardic when
plex, a ventricular ectopic beat (VEB). This 1:1 their pulse is taken at the wrist, if only the sinus
coupling between sinus beats and VEBs is called beats are counted. Even automated monitoring
ventricular bigeminy. equipment (e.g. blood pressure monitors, pulse
2. As the name suggests, VEBs arise within the oximeters) can sometimes underestimate the
ventricles. In this case the VEBs have a left bun- heart rate by ‘missing’ the VEBs. Careful inspec-
dle branch block morphology in the chest leads, tion of an ECG will reveal the correct heart rate.
indicating an origin in the right ventricle. The • The normal sinus beat after the VEB can also
VEBs also have an inferior axis in the limb leads feel stronger than usual, as there will have been
(positive complexes in leads II, III and aVF) indi- a slightly longer period for ventricular filling due
cating an origin in the basal part of the ventricle. to the compensatory pause after the VEB (‘extra-
Taken together, these features suggest the most systolic potentiation’).
likely origin of the VEBs is in the basal right ven- • For more information on the investigation and
tricle, most probably the right ventricular out- management of VEBs, see ‘Commentary’ in Case
flow tract. 9.

Making Sense of the ECG 6th edition: Ventricular ectopic
• An ectopic beat arises earlier than the next nor- beats, p 187.
mal (sinus) beat would have occurred (in contrast Ng GA. Treating patients with ventricular ectopic beats.
to escape beats, which arise later than expected). Heart (2006). PMID 17041126.
CASE 44
CLINICAL SCENARIO
Breathlessness. Persistent nocturnal cough. JVP: elevated by 4 cm.
Dizziness. Heart sounds: normal.
Chest auscultation: bi-basal crackles.
History of presenting complaint Pitting peripheral oedema to mid-calf.
Had been fit and well until 2 months ago when
he had a viral infection. Never really regained Investigations
fitness afterwards. Had had several courses of FBC: Hb 122, WCC 8.1, platelets 346.
antibiotics from family doctor but his symp- U&E: Na 136, K 4.9, urea 7.8, creatinine 124.
toms persisted. Frequent nocturnal waking with Thyroid function: normal.
breathlessness. Became worried when he found Troponin I: negative.
he was breathless walking around his flat and he Chest X-ray: enlarged left ventricle. Pulmonary
noticed his pulse was very erratic. oedema.
Echocardiogram: dilated left ventricle with poor
Past medical history function. Mildly impaired right ventricular func-
Nil else of note. tion. Functional mitral regurgitation.
Smokes 10 cigarettes per day.
Drinks 12 units alcohol per week.
No family history of heart disease.
QUESTIONS
DOI: 10.1201/9781003472186-44

Rate 108/min overall, but very variable • Broad-complex tachycardia is due to VT, or to
Rhythm Underlying sinus rhythm with supraventricular tachycardia (SVT) with aber-
frequent bursts of non-sustained rant conduction (such as bundle branch block or
ventricular tachycardia ventricular pre-excitation). Where there is doubt
about the diagnosis, it should be assumed to be
QRS axis Normal (+45°) in sinus rhythm,
VT until proven otherwise.
P waves
extreme axis deviation in VT
Normal
• Most cases (80%) of broad-complex tachycardia
are due to VT, and the likelihood of VT (rather
PR interval Normal (172 ms) than SVT with aberrant conduction) is even
higher when structural heart disease is present.
QRS duration Normal (90 ms) in sinus rhythm, broad
Haemodynamic stability is not a reliable guide in
complexes in ventricular tachycardia
distinguishing between VT and SVT with aber-
T waves Normal morphology where seen rant conduction, as VT can be remarkably well
QTc interval Difficult to assess tolerated by some patients.
• A very reliable ECG indicator of VT is the presence
of atrioventricular dissociation, where the atria
and ventricles are seen to be working independently.
ANSWERS
Atrioventricular dissociation is indicated by:
1. Underlying sinus rhythm is seen with normal • Independent P wave activity
axis. There are frequent runs of non-sustained • Fusion beats
broad-complex tachycardia with a marked • Capture beats
change in axis. These are bursts of ventricular • Other ECG features can also provide clues to the
tachycardia (VT). diagnosis. Most patients with SVT and aberrant
2. The underlying diagnosis is most likely to be conduction will have a QRS complex morphology
a dilated cardiomyopathy secondary to viral that looks like a typical LBBB or RBBB pattern.
myocarditis. Patients with VT will often (but not always) have
3. Treatment is aimed at controlling the signs and more unusual-looking QRS complexes which
symptoms of congestive cardiac failure until don’t fit a typical bundle branch block pattern.
resolution occurs – this may take weeks or • Many other ECG features suggest (but do not
months (if at all). Patients usually respond to a prove) a diagnosis of VT rather than SVT with
combination of loop diuretic, together with the aberrant conduction, including:
‘four pillars’ of heart failure drug therapy (an • Very broad QRS complexes (>160 ms)
angiotensin-converting enzyme inhibitor or an • Extreme QRS axis deviation
angiotensin receptor blocker or an angiotensin • Concordance (same QRS direction) in leads
receptor – neprilysin inhibitor, a beta-blocker, V1–V6
a mineralocorticoid receptor antagonist and • An interval >100 ms from the start of the R
a sodium-glucose cotransporter 2 inhibitor). wave to the deepest point of the S wave (this is
Anti-arrhythmic drugs may be needed for ven- called Brugada’s sign) in one chest lead
tricular tachyarrhythmias, and device therapy • A notch in the downstroke of the S wave (this
(cardiac resynchronization therapy and/or an is called Josephson’s sign)
implantable cardioverter defibrillator) may be
required. Surgical options include a left ventric-
ular assist device (LVAD) to support the function Further Reading
of the failing heart, and cardiac transplantation Making Sense of the ECG 6th edition: Ventricular tachycar-
for those with severe heart failure that fails to dia, p 191; How do I distinguish between VT and
improve. SVT? p 194.
Case 44 103
Alzand BSN et al. Diagnostic criteria of broad QRS com- Zeppenfeld K et al. 2022 ESC guidelines for the manage-
plex tachycardia: Decades of evolution. Europace ment of patients with ventricular arrhythmias and
(2011). PMID 21131372. the prevention of sudden cardiac death. European
Jastrzebski M et al. Comparison of five electrocardio- Heart Journal (2022). PMID 36017572.
graphic methods for differentiation of wide QRS-
complex tachycardias. Europace (2012). PMID
22333239.
CASE 45
CLINICAL SCENARIO
Patient in discomfort and sitting upright.
Presenting complaint Temperature: 38.1°C.
Central chest pain, exacerbated by lying supine Pulse: 110/min, regular.
and on deep inspiration. Blood pressure: 128/80.
JVP: not elevated.
History of presenting complaint Heart sounds: soft pericardial friction rub.
Viral symptoms for 1 week, with chest pain for Chest auscultation: unremarkable.
3 days. No peripheral oedema.

Nil. FBC: Hb 152, WCC 9.2, platelets 364.
ESR and CRP: elevated.
QUESTIONS
2. What other tests would be appropriate?
3. What can cause this condition?
DOI: 10.1201/9781003472186-45
ECG ANALYSIS • Radiotherapy

• Traumatic
Rate 110/min
• Drug-induced
Rhythm Sinus rhythm 4. Direct treatment of the underlying cause
QRS axis Normal (+65°) should be carried out where possible. Anti-
inflammatory agents (e.g. aspirin, ibuprofen) are
P waves Normal
often effective and are used in combination with
PR interval Normal (160 ms) colchicine as a first-line treatment.
COMMENTARY
T waves Normal
QTc interval Normal (433 ms) • The ST segment elevation of pericarditis has four
characteristics that, while not pathognomonic,
help to distinguish it from STEMI:
Additional comments • The ST segment elevation is typically wide-
There is widespread ST segment elevation (concave spread, affecting all of those leads (anterolat-
upward or ‘saddle-shaped’) in leads I, II, III, aVF eral and inferior) that ‘look at’ the inflamed
and V2–V6, with reciprocal ST segment depression epicardium. Leads aVR and V1 usually show
in lead aVR. reciprocal ST segment depression
• The ST segment elevation is characteristically
‘saddle shaped’ (concave upward)
ANSWERS • T wave inversion occurs only after the ST seg-
ments have returned to baseline
1. This ECG shows widespread ST segment eleva-
tion (concave upward or ‘saddle-shaped’) in leads • Q waves do not develop
I, II, III, aVF and V2–V6, with reciprocal ST seg- • Pericarditis can also cause depression of the PR
ment depression in lead aVR. In the clinical con- segment, which is thought to be caused by atrial
text, these findings are consistent with a diagnosis involvement in the inflammatory process. PR
of pericarditis. segment depression is a specific ECG feature of
2. In addition to those listed, other appropriate pericarditis and may be seen in any leads except
tests would include: aVR and V1 (where there may be PR segment
• Cardiac markers (high-sensitivity troponin) elevation).
• Echocardiography • Patients with pericarditis and ST segment eleva-
tion will often have an elevation in their cardiac
• Viral serology with or without other microbi-
markers (high-sensitivity troponin) as a result of
ology as indicated
a degree of coexistent myocarditis. It is important
• Autoantibody screen, complement levels,
not to misdiagnose acute myocardial infarction,
immunoglobulins
and a coronary angiogram may be required to
3. Pericarditis has many causes, including: clarify the diagnosis.
• Idiopathic
• Echocardiography is important to monitor for
• Infective (viral, bacterial, tuberculous, fungal, the appearance of a pericardial effusion (not
parasitic) always present, but may develop as a complica-
• Myocardial infarction (first few days) tion). This can cause cardiac tamponade.
• Dressler’s syndrome (1 month or more post- • The differential diagnosis of ST segment elevation
myocardial infarction) includes STEMI, Takotsubo cardiomyopathy, left
• Uraemia ventricular aneurysm, vasospastic (Prinzmetal)
• Malignancy angina, pericarditis, left bundle branch block,
• Connective tissue disease Brugada syndrome and high take-off.
Case 45 107
Further Reading
Making Sense of the ECG 6th edition: Are the ST segments Chiabrando JG et al. Management of acute and recurrent
elevated? p 113; Pericarditis, p 122; Is the PR seg- pericarditis: JACC state-of-the-art review. Journal
ment elevated or depressed? p 87. of the American College of Cardiology (2020). PMID
31918837.
CASE 46
CLINICAL SCENARIO
Exertional breathlessness. JVP: not elevated.
Heart sounds: normal (but irregular rhythm).
History of presenting complaint Chest auscultation: bi-basal inspiratory crackles.
Six-week history of exertional breathlessness. Mild peripheral oedema.
Also aware of an irregular heartbeat.
Investigations
Hypertension. U&E: Na 139, K 4.8, urea 9.4, creatinine 147.
Chest X-ray: normal heart size, mild pulmonary
congestion.
Echocardiogram: normal valves. Mild left ven-
tricular hypertrophy with mildly impaired systolic
function (ejection fraction 48%).
QUESTIONS
1. What rhythm does this ECG show?
DOI: 10.1201/9781003472186-46
ECG ANALYSIS • Electrophysiological intervention with radio-

frequency ablation of the atrial flutter re-entry
Rate 51/min circuit is an effective procedure with a success
Rhythm Atrial flutter rate of 95%.
P waves Not visible (flutter waves are present)

COMMENTARY
PR interval N/A • Atrial flutter is often considered to be a subtype
of atrial tachycardia and is characterized by a
macro re-entry circuit, typically within the right
T waves Inverted in leads I, aVL, V5, V6 atrium and involving the cavotricuspid isthmus
QTc interval Normal (318 ms) (CTI-dependent, or Type I, flutter). Less com-
monly, other forms of flutter are seen that do not
involve the CTI (non-CTI-dependent, or Type II,
ANSWERS
flutter). These usually occur in relation to an area
1. There are low amplitude flutter waves at around of scar tissue in the atria, often in the context of
300/min which give a ‘sawtooth’ baseline: this prior cardiac surgery.
is atrial flutter. There is variable atrioventricu- • In atrial flutter the atrial rate is usually 250–330/
lar block, giving rise to an irregularly irregu- min and often almost exactly 300/min. The AV
lar rhythm with a ventricular rate of around node cannot normally keep up with such a high
51/min. atrial rate, and AV block occurs. This is most
2. There are four key aspects to the treatment of commonly 2:1 block, where only alternate atrial
atrial flutter: impulses get through the AV node to initiate
• Ventricular rate control – in this case, there a QRS complex, although 3:1, 4:1 or variable
degrees of block are also seen.
is a high (and variable) degree of atrioven-
tricular block and so the ventricular rate is • Rate-controlling medication is not always neces-
relatively slow. Rate-controlling medication sary in atrial flutter (or in atrial fibrillation), as
is therefore not required in this case, unless some cases have a normal (or even a slow) ven-
there is a marked increase in atrioventricular tricular rate. However, assessing ventricular rate
conduction (and therefore in ventricular rate) only at rest can underestimate how much the rate
on exertion. rises during periods of activity. It is therefore a
• There is a thromboembolic risk in atrial flut- good idea to assess ventricular rate not just at rest
but also after a short period of exertion.
ter, and so consider the patient for antico-
agulant therapy in the same way as for atrial
fibrillation. Further Reading
• Electrical cardioversion can be very effective Making Sense of the ECG 6th edition: Atrial flutter, p 173.
in restoring sinus rhythm and, as a general Brugada J et al. 2019 ESC guidelines for the manage-
rule, atrial flutter is easier to cardiovert than ment of patients with supraventricular tachycardia.
atrial fibrillation. European Heart Journal (2020). PMID 31504425.
CASE 47
CLINICAL SCENARIO
Asymptomatic – routine ECG performed at fol- JVP: not elevated.
low-up visit to cardiology outpatient clinic. Heart sounds: normal.
Nil – patient currently asymptomatic.
Investigations
Treated for sick sinus syndrome 2 years ago. U&E: Na 141, K 4.3, urea 2.8, creatinine 68.
QUESTIONS
2. What device did this patient receive 2 years ago to treat their sick sinus syndrome?
3. Does this device have one electrode or two? How might you find out?
4. What do you understand by the term AAIR?
DOI: 10.1201/9781003472186-47

Rate 70/min • Permanent pacemakers can be single-chamber
Rhythm Atrial pacing (a single electrode pacing/sensing either the
right atrium or the right ventricle) or dual-
QRS axis –
chamber (two electrodes, one to pace/sense the
P waves Present following atrial pacing spike right atrium and another to pace/sense the right
ventricle).
PR interval
QRS duration
Short
Normal (80 ms)

• For sick sinus syndrome, a single-chamber atrial
pacemaker is usually appropriate unless there
T waves Biphasic (initially positive but with are any problems (or potential problems) with
negative terminal deflection) atrioventricular node conduction, in which case
a dual-chamber pacemaker is a better option.
•
Pacemakers can be identified on the ECG by
their pacing spikes. The presence of a pacing
Additional comments spike followed by a P wave indicates atrial pac-
Pacing spikes are evident prior to each P wave. ing. A pacing spike followed by a QRS complex
indicates ventricular pacing.
ANSWERS • Pacemakers are described by pacing codes:
• The first letter of the code identifies the
1. There are sharp downward vertical deflections chambers that can be paced (A – atrium,
prior to each P wave. These represent pacing V – ventricle, D – dual)
spikes. The position of these prior to the P wave • The second letter of the code identifies the
indicates atrial pacing. chambers that can be sensed (A – atrium,
2. The patient has had a pacemaker implanted two V – ventricle, D – dual)
years ago to treat their sick sinus syndrome. • The third letter of the code identifies what the
3. It is not possible to say. The pacemaker is cer- pacemaker does if it detects intrinsic activity
tainly capable of pacing the atria, as evidenced (I – inhibited, T – triggered, D – dual)
by pacing spikes followed by P waves, and an • The fourth letter denotes whether rate respon-
atrial pacing electrode must therefore be pres- siveness (R) is present
ent. However, the absence of ventricular pacing • The fifth letter identifies anti-tachycardia
does not rule out the possibility that a ventricu- functions, if present (P – pacing, S – shock
lar electrode is also present – if it is a dual-cham- delivered, D – dual)
ber pacemaker, the ventricular lead may simply
be monitoring ventricular activity but not sup-
• Thus an AAIR pacemaker can pace the atrium.
However, if it senses intrinsic atrial activity (nor-
plying any pacing spikes at present. If in doubt, mal P waves), it will be inhibited and stop pac-
most patients with pacemakers will carry a pace- ing. The R indicates that it is rate responsive
maker identity card. Failing that, a chest X-ray and can therefore increase its pacing rate (and
will reveal the number of pacing electrodes. thus the patient’s heart rate) if it detects that the
This patient actually had a single-chamber pace- patient is undertaking physical exertion. Several
maker (AAIR). parameters can be monitored by pacemakers to
4. The term AAIR is a pacing code and describes determine the patient’s level of activity, including
a pacemaker that paces the atrium, senses the movement (using an accelerometer) and respi-
atrium, is inhibited by intrinsic atrial activity ratory rate (using a transthoracic impedance
and is rate-responsive. sensor).
Case 47 113
Further Reading
Making Sense of the ECG 6th edition: Cardiac implantable Kusumoto FM et al. 2018 ACC/AHA/HRS guideline on
electronic devices, p 223. the evaluation and management of patients with
Glikson M et al. 2021 ESC guidelines on cardiac pacing bradycardia and cardiac conduction delay. Journal
and cardiac resynchronization therapy. European of the American College of Cardiology (2018). PMID
Heart Journal (2021). PMID 34455430. 30412710.
CASE 48
CLINICAL SCENARIO
Asymptomatic. JVP: cannon waves visible.
Asymptomatic (routine ECG performed for No peripheral oedema.
hypertension assessment).
Investigations
Hypertension. U&E: Na 140, K 3.9, urea 6.6, creatinine 105.
QUESTIONS
DOI: 10.1201/9781003472186-48
ECG ANALYSIS (seen here at 54/min) in which each P wave is fol-

lowed by a QRS complex, and a separate parasys-
Rate Atrial – 104/min tolic rhythm (at a rate of 50/min) with P waves that
Ventricular – 54/min are taller than the normal P waves. Because the two
rates are slightly different, the parasystolic P waves
Rhythm Sinus rhythm with atrial parasystole
can be seen to gradually ‘march through’ the nor-
QRS axis Unable to assess (rhythm strip) mal sinus rhythm P waves.
P waves Two morphologies – normal and
abnormal COMMENTARY
PR interval There is a normal PR interval for the
‘sinus rhythm’ P waves. The atrial
• Parasystole is very rare. It can occur in the atria
(atrial parasystole) or in the ventricles (ven-
parasystole P waves are
non-conducted and so these do
tricular parasystole). Ventricular parasystole is
not have a PR interval commoner.

• The ectopic focus in parasystole is surrounded
by a region of myocardium that causes ‘entrance
T waves Normal block’, protecting the ectopic focus from being
QTc interval Normal (399 ms) depolarized by the normal beats. The ectopic
focus is therefore able to function independently
of the underlying rhythm.
ANSWERS
• Parasystole can be continuous or intermittent.
• Occasional fusion beats (between a normal beat
1. This ECG shows atrial parasystole. and a parasystolic beat) may be seen.
2. Atrial parasystole occurs when there is a second-
ary pacemaker within the atria that fires in parallel Further Reading
with the sinoatrial node. Thus, there are two simul- Friedberg HD et al. Atrial parasystole. British Heart
taneous atrial rhythms – normal sinus rhythm Journal (1970). PMID 5440513.
CASE 49
CLINICAL SCENARIO
Hypertension. JVP: not elevated.
Patient noted to be hypertensive (152/94) dur- No peripheral oedema.
ing routine check-up. This ECG was performed
as part of his cardiovascular assessment. Investigations
Recently diagnosed hypertension – not on Chest X-ray: normal heart size, clear lung fields.
medication.
QUESTIONS
2. What would you do next?
DOI: 10.1201/9781003472186-49

Rate 64/min • ECGs are normally recorded at a standard cali-
Rhythm Sinus rhythm bration setting of 10 mm/mV. In other words, a
voltage of 1 mV will cause a 10 mm deflection in
QRS axis Normal (+32°) the ECG tracing.
P waves Normal • The calibration setting is usually indicated on
the ECG by an annotation (in this case ‘Limb:
20 mm/mV Chest: 20 mm/mV’ along the bottom
QRS duration Normal (70 ms) of the ECG), and/or by a calibration marker (the
T waves Normal upright ‘box’ at the far right of this recording,
which shows what deflection is made by a voltage
of 1 mV). It is good practice to check the calibra-
tion settings on every ECG you examine.
Additional comments
• Many ECG machines will allow the calibration
of the limb leads and the chest leads to be set
The voltage calibration setting is 20 mm/mV, double independently.
the ‘standard’ setting. • For the vast majority of ECGs, a standard setting
of 10 mm/mV is appropriate. For patients with
very large QRS complexes (e.g. as seen in left ven-
ANSWERS tricular hypertrophy), sometimes at the standard
setting the QRS complexes on adjacent lines can
1. At first glance, this ECG might appear to meet overlap and make interpretation difficult. Under
a number of the diagnostic criteria for left ven- these circumstances, a calibration of 5 mm/mV
tricular hypertrophy (see Case 35). However, will halve the size of the complexes and may make
on closer inspection, it can be seen that the the ECG easier to interpret. The use of double the
voltage calibration has been set at 20 mm/mV, normal calibration (20 mm/mV) is very unusual.
which is double the standard setting (10 mm/
mV). Therefore, all the waves/complexes on Further Reading
the ECG will be twice their ‘usual’ size. When
Making Sense of the ECG 6th edition: Performing an ECG
this is taken into account, the ECG is in fact
recording, p 21; Incorrect calibration, p 158.
normal. Campbell B et al. Clinical guidelines by consensus: Recording a
2. Repeat the ECG at the standard calibration set- standard 12-lead electrocardiogram. An approved method
ting of 10 mm/mV (unless a different nonstan- by the Society for Cardiological Science and Technology
dard setting is required for a particular purpose). (SCST). 2017. Downloadable from www.scst.org.uk.
CASE 50
CLINICAL SCENARIO
Pulse: 48/min, some variation with respiration.
Chest pain. JVP: not elevated.
Usually fit and well. Patient was at a party with No peripheral oedema.
friends and had consumed quite a lot of alcohol
– more than he usually drank. Friends reported Investigations
that he then developed severe central chest pain FBC: Hb 139, WCC 8.1, platelets 233.
which got progressively worse. They were con- U&E: Na 137, K 4.2, urea 5.3, creatinine 88.
cerned so called for an ambulance. Admitted to Troponin I: negative.
coronary care unit with a suspected acute myo- Chest X-ray: normal heart size, clear lung fields.
cardial infarction. Echocardiogram: normal valves. Left ventricular
function normal (ejection fraction 67%).
Nil of note.
Heavy smoker.
QUESTIONS
DOI: 10.1201/9781003472186-50

Rate 48/min • Vasospastic or Prinzmetal’s angina occurs almost
Rhythm Sinus rhythm (with a degree of exclusively at rest, is not usually brought on by
sinus arrhythmia) exertion or emotion, and is associated with ST
segment elevation, which can occur in any lead –
the risk of sudden death is increased if seen in
P waves Normal both anterior and inferior leads. It may be asso-
ciated with myocardial infarction and cardiac
arrhythmias, including ventricular tachycardia,
QRS duration Normal (114 ms) ventricular fibrillation and sudden death.
T waves Tall in V2–V4 (‘hyperacute’) • Variant angina tends to affect younger patients
than does chronic stable angina or unstable
angina. Most will have few conventional risk
factors other than smoking. Illicit drug use with
Additional comments cannabis, a coronary vasoconstrictor and plate-
There is ST segment elevation in leads V2–V6. let activator, and cocaine, which causes alpha
adrenergically mediated coronary constriction
when ‘snorted’, should always be considered in a
ANSWERS young person with severe chest pain, ST segment
elevation and few risk factors.
1. ST segment elevation most marked in the ante-
rior chest leads. If these changes resolve as the
• In patients prone to coronary artery spasm,
coronary artery tone and responsiveness to
chest pain resolves, and there is no subsequent constrictor stimuli are increased. A number of
high-sensitivity troponin rise, this is consistent provocative tests have been developed, the most
with myocardial ischaemia due to coronary sensitive being ergonovine, an ergot alkaloid
artery vasospasm (‘Prinzmetal’s angina’). that stimulates alpha adrenergic and serotonin
2. Coronary artery vasospasm leads to a reduction receptors, which have a direct vasoconstric-
in blood supply to the myocardium supplied by tive effect on vascular smooth muscle. It may
the affected artery. ECG changes are not confined be administered when coronary angiography
to the ST segment – hyperacute T waves, T wave has demonstrated normal coronary arteries.
inversion or transient intraventricular conduc- Hyperventilation is only slightly less sensitive
tion defects, such as bundle branch or fascicular than ergonovine. Most patients have underlying
block may be evident. coronary disease and spasm tends to occur close
3. While it can occur in normal arteries (it may be to existing coronary lesions.
seen at coronary angiography on cannulating • Treatment is based on relieving the coronary
the right coronary artery, and cocaine is a potent spasm:
stimulus), in 90% of patients coronary artery vaso- • Calcium channel blockers
spasm occurs at the site of atheroma. ST segment • Nitrates
elevation may suggest an acute myocardial infarc-
tion, but with resolution of chest pain, the ST seg-
• Beta-blockers may worsen coronary spasm and
should be avoided.
ments return to normal. It usually occurs at rest.
Patients may also report symptoms of Raynaud’s
phenomenon. The patient in this case had been
using cannabis prior to admission. Further Reading
4. Treatment for vasospastic angina should include Making Sense of the ECG 6th edition: Vasospastic
a calcium channel blocker and/or a nitrate. (Prinzmetal) angina, p 120.
CASE 51
CLINICAL SCENARIO
Patient comfortable at rest. Alert and oriented.
Presenting complaint Pulse: 96/min, regular, slow rising.
Syncopal episode while walking uphill. Blood pressure: 108/86.
JVP: not elevated.
History of presenting complaint Precordium: left parasternal heave.
Three-month history of gradually worsening Heart sounds: loud (4/6) ejection systolic mur-
breathlessness and dizziness on exertion, culmi- mur heard in the aortic area, radiating to both
nating in a brief syncopal episode while walking carotid arteries.
uphill. An ambulance was called and the patient Chest auscultation: unremarkable.
was brought to the hospital where this ECG was No peripheral oedema.
recorded.
Investigations
Nil. U&E: Na 141, K 4.4, urea 6.8, creatinine 112.
QUESTIONS
2. What investigation would help to confirm this?
3. What can cause these appearances? What is the likely cause here?
DOI: 10.1201/9781003472186-51
ECG ANALYSIS valve must be assessed by echocardiography

(or cardiac magnetic resonance scanning) and,
Rate 96/min if severe symptomatic aortic stenosis is con-
Rhythm Sinus rhythm firmed, make plans for aortic valve replacement.
P waves Normal COMMENTARY

PR interval Normal (160 ms) • The diagnostic ECG criteria for left ventricular
QRS duration Normal (80 ms) hypertrophy were discussed earlier in Case 35.
The ECG in the present case meets several of
T waves Inverted in leads I, aVL,
these diagnostic criteria:
V4–V6, and also in lead II
• R wave of 25 mm or more in the left chest
QTc interval Prolonged (500 ms) leads
• S wave of 25 mm or more in the right chest
Additional comments leads
There are very deep S waves (up to 48 mm) in leads • Sum of S wave in lead V1 and R wave in lead
V2–V3 and very tall R waves (up to 44 mm) in leads V5 or V6 greater than 35 mm (Sokolow–Lyon
V5–V6. criteria)
• Sum of tallest R wave and deepest S wave in
the chest leads greater than 45 mm
ANSWERS • The Cornell criteria are met:
• The Cornell criteria involve measuring the
1. This ECG shows very deep S waves (up to 48 S wave in lead V3 and the R wave in lead aVL.
mm) in leads V2–V3 and very tall R waves (up to Left ventricular hypertrophy is indicated by
44 mm) in leads V5–V6, together with inverted T a sum of >28 mm in males and >20 mm in
waves in leads I, aVL, V4–V6 (and also in lead II). females
These appearances are indicative of left ventricu-
lar hypertrophy with ‘strain’.
• The ECG also meets the Romhilt–Estes cri-
teria for left ventricular hypertrophy, scoring
2. An echocardiogram (or cardiac magnetic reso- 6 points:
nance scan) would allow direct visualization • S wave in right chest leads of 25 mm or more,
of the left ventricle, assessment of the extent of and also R wave in left chest leads of 25 mm or
left ventricular hypertrophy, assessment of left more (3 points)
ventricular systolic (and diastolic) function, and
also assessment of the structure and function of
• ST segment and T wave changes (‘typi-
cal strain’) in a patient not taking digitalis
the aortic valve. (3 points)
3. Left ventricular hypertrophy can result from:
• Hypertension
• The presence of ST segment depression and/or
T wave inversion in the context of left ventricular
• Aortic stenosis hypertrophy are taken to indicate left ventricu-
• Coarctation of the aorta lar ‘strain’. However, it is important to assess the
• Hypertrophic cardiomyopathy clinical context – ST/T wave changes, particularly
The clinical findings indicate that aortic stenosis if dynamic, associated with symptoms of chest
is the most likely cause of left ventricular hyper- pain may instead indicate myocardial ischaemia.
trophy in this case. • The risk of myocardial infarction and stroke in
4. Where left ventricular hypertrophy is second- patients with left ventricular hypertrophy with
ary to pressure overload of the left ventricle, the a strain pattern is approximately double that of
appropriate treatment is that of the underlying patients who have left ventricular hypertrophy
cause. In the case of aortic stenosis, the aortic without strain.
Case 51 123
Further Reading
Making Sense of the ECG 6th edition: Left ventricular Peguero JG et al. Electrocardiographic criteria for the
hypertrophy, p 98; Ventricular hypertrophy with diagnosis of left ventricular hypertrophy. Journal of
‘strain’, p 130. the American College of Cardiology (2017). PMID
28359515.
CASE 52
CLINICAL SCENARIO
Severe chest pain (‘tight band’ around chest), JVP: elevated by 3 cm.
associated with breathlessness. Felt dizzy and Heart sounds: normal.
fainted. Chest auscultation: unremarkable.
Mild peripheral oedema.
Digging in garden all day. Ignored chest pain Investigations
earlier in day. FBC: Hb 144, WCC 11.2, platelets 332.
Past medical history Troponin I: elevated.
High blood pressure for several years. Chest X-ray: normal heart size, clear lung fields.
Was a heavy smoker until 4 weeks ago. Echocardiogram: normal valve function. Inferior
Strong family history of coronary artery disease. hypokinesia of left ventricle (ejection fraction
48%); right ventricle – impaired function.
QUESTIONS
1. What sort of ECG recording is this?
3. Why is this finding important?
DOI: 10.1201/9781003472186-52
ECG ANALYSIS (elevated jugular venous pressure and peripheral

oedema). The left ventricle may be functioning
Rate 90/min normally, so the lungs are clear. If these patients
develop hypotension, it is usually because their
Rhythm Sinus rhythm
left-sided filling pressure is too low (as the sup-
QRS axis Normal (+20°) ply of blood from the damaged right ventricle is
P waves Normal inadequate). Vasodilator drugs must be avoided.
Intravenous fluids may be needed to maintain
PR interval Normal (160 ms) right ventricular output, thus ensuring sufficient
QRS duration Normal (110 ms) blood is supplied to the left ventricle.
T waves Normal

COMMENTARY
• The prognosis in inferior myocardial infarc-
tion is generally very good. However, when the
Additional comments infarction involves the right ventricle (about
There is inferior ST segment elevation with recipro- 50% of cases), the risk of severe complications is
cal lateral ST segment depression. The right-sided increased almost sixfold:
chest leads show ST segment elevation in leads • Death, ventricular fibrillation, re-infarction
V3R–V6R.
• Risk of right-sided heart failure (elevated JVP,
peripheral oedema, low output state but with
no evidence of pulmonary oedema)
ANSWERS
• It may seem paradoxical to give intravenous flu-
1. This is an ECG showing the usual limb leads but ids to patients who already appear to be in right
right-sided chest leads (V1R–V6R). Perform an ECG heart failure, unless the reasons for doing so
with right-sided chest leads in all patients present- are understood. If haemodynamically compro-
ing with an acute inferior myocardial infarction, to mised, consideration can be given to the use of
look for evidence of right ventricular involvement a pulmonary artery catheter, which measures
(as shown by ST segment elevation in lead V4R). right-sided and, indirectly, left-sided filling
2. The ECG shows an acute inferior STEMI (ST pressure.
segment elevation in leads II, III, aVF) with
reciprocal ST segment depression laterally Further Reading
(leads I and aVL). There is ST segment elevation
Making Sense of the ECG 6th edition: ST segment elevation
in leads V3R–V6R. The presence of ST segment
myocardial infarction, p 114; Why is right ventricu-
elevation in lead V4R is indicative of right ven- lar infarction important? p 119.
tricular involvement. Chockalingam A et al. Right ventricular myocardial infarc-
3. Patients with right ventricular infarction may tion: Presentation and acute outcomes. Angiology
develop the signs of right-sided heart failure (2005). PMID 16079918.
CASE 53
CLINICAL SCENARIO
Fatigue. JVP: not elevated.
Longstanding history of fatigue. No peripheral oedema.
No other associated symptoms.
Investigations
Childhood asthma – no longer uses inhalers. U&E: Na 143, K 4.9, urea 3.6, creatinine 67.
QUESTIONS
3. What is the cause of this patient’s fatigue?
DOI: 10.1201/9781003472186-53

Rate 58/min • The standard ECG paper speed in the UK and
the US is 25 mm/s, which makes each small
Rhythm Sinus rhythm (slight bradycardia)
square equivalent to 0.04 s and each large square
QRS axis Unable to assess (single lead) equivalent to 0.2 s. By counting large and/or
P waves Present small squares, you can calculate such parameters
as heart rate and PR and QT intervals.
• If a ‘non-standard’ paper speed is used, the
QRS duration Normal (80 ms) ‘time value’ of small and large squares need to
be adjusted accordingly. At 50 mm/s, the small
T waves Normal
squares will equal 0.02 s and the large squares
QTc interval Normal (413 ms) 0.1 s. All measurements and calculations must
take the new speed setting into account.
Additional comments • A speed setting of 50 mm/s is sometimes used
to make measurements easier (by doubling the
The paper speed is set at 50 mm/s, double the nor- width of every wave, some features can be seen
mal recording speed. and/or measured more easily). A paper speed of
50 mm/s is used as the standard setting in some
ANSWERS parts of Europe rather than 25 mm/s.
• Annotate all ECGs with the paper speed that was used
1. This ECG shows normal sinus rhythm with a for the recording. If a non-standard paper speed was
heart rate of 58/min (slight bradycardia). At first used, highlight this clearly to avoid misinterpretation.
glance, the rate looks like it might be slower than • When an ECG has been recorded using a non-
that (29/min), but that is because the recording standard paper speed in error, repeat it using the
has been made at double the normal paper speed appropriate paper speed.
(50 mm/s rather than the standard 25 mm/s).
The paper speed is shown at the lower left corner Further Reading
of the rhythm strip.
2. Repeat the ECG at the standard paper setting of
recording, p 21; Incorrect paper speed, p 159.
25 mm/s.
Campbell B et al. Clinical guidelines by consensus:
3. This ECG rhythm strip does not reveal an expla- Recording a standard 12-lead electrocardio-
nation for this patient’s fatigue – his heart rate is gram. An approved method by the Society for
virtually normal at 58/min. Further clinical assess- Cardiological Science and Technology (SCST). 2017.
ment is required to identify the cause of his fatigue. Downloadable from www.scst.org.uk.
CASE 54
CLINICAL SCENARIO
Male, aged 22 years. JVP: not elevated.
Heart sounds: quiet; heard best on right side of
Presenting complaint chest.
Admitted with lower respiratory tract infection. Chest auscultation: bronchial breathing right
lower lobe.
Cough, productive of blood-stained sputum;
Investigations
fever; tachycardia
Chest X-ray: dextrocardia; consolidation right
Nil of note. lower lobe.
Echocardiogram: dextrocardia. Normal valves.
Examination Left ventricular function normal (ejection frac-
Pulse: 76/min, irregularly irregular. tion 67%).
QUESTIONS
1. What abnormalities does this ECG show?
DOI: 10.1201/9781003472186-54
ECG ANALYSIS that the finding of dextrocardia be recorded

prominently in a patient’s notes to prevent mis-
Rate 76/min haps. Manage the patient’s atrial fibrillation in
the same way as any other patient with atrial
Rhythm Atrial fibrillation
fibrillation (see Case 6).
QRS axis Extreme right axis deviation (+124°)
P waves Absent (atrial fibrillation) COMMENTARY

PR interval
QRS duration
N/A
Normal (112 ms)

• The term situs describes the position of the car-
diac atria and viscera, cardiac situs being deter-
T waves Normal mined by atrial location, so:
• Situs solitus – this is the normal orientation of
viscera and a left-sided heart
• Situs inversus – this is reversal of all the major
Additional comments structures in the thorax and abdomen
There is a decrease in QRS complex size from lead • Situs ambiguous – the orientation of heart
and viscera conform to neither situs soli-
V1 to lead V6.
tus nor inversus (any structure with a right-
left asymmetry can be normal, completely
ANSWERS reversed or neither)
1. The rhythm is atrial fibrillation. Leads I and aVL

• In situs inversus with levocardia, the apex of
the heart points to the left; with dextrocardia,
are negative and leads II, III and aVR are posi- it points to the right. Dextrocardia on its own is
tive – this is extreme right axis deviation. The R known as situs solitus with dextrocardia.
waves are generally small across the chest leads,
and decrease in size from V1 to V6 (normally, the
• Other congenital cardiovascular abnormalities
can be associated with dextrocardia, such as sin-
R waves are small in V1, equipolar at V3 or V4 and gle ventricle, atrial or ventricular septal defects,
largest at V6). anomalous pulmonary venous return, and trans-
2. This is dextrocardia. Dextrocardia is a naturally position of the great arteries. When dextrocardia
occurring anomaly, seen in 1:10,000 people. The occurs with just the heart incorrectly positioned,
ECG ‘abnormalities’ occur because the record- functionally significant complex cardiac abnor-
ing reflects the heart’s abnormal position in the malities are more likely.
thorax. The ECG will ‘normalize’ if the chest
leads are reversed so that lead V1 is recorded
• Situs inversus totalis may be associated with cili-
ary dysfunction (Kartagener’s syndrome) in which
from the left sternal edge and V6 from the right patients experience repeated sinus and respira-
axilla. The patient’s atrial fibrillation is likely tory infections resulting in bronchiectasis, chronic
to have been triggered by the lower respiratory sinusitis and nasal polyposis. Life expectancy is
tract infection, but always undertake a careful normal if bronchiectasis is adequately treated.
review for other possible causes.
3. The ECG ‘abnormalities’ seen in dextrocardia
must not be considered pathological – the heart Further Reading
is usually structurally normal. It is important Making Sense of the ECG 6th edition: Dextrocardia, p 101.
CASE 55
CLINICAL SCENARIO
Pulse: 102/min, irregular (ectopic beats).
Asymptomatic. Routine ECG performed as a No peripheral oedema.
preoperative assessment.
Investigations
Osteoarthritis (awaiting knee surgery). U&E: Na 139, K 4.4, urea 7.4, creatinine 102.
QUESTIONS
2. What can cause this abnormality?
DOI: 10.1201/9781003472186-55
ECG ANALYSIS QT intervals are associated with a risk of poly-

morphic ventricular tachycardia (torsades de
Rate 102/min pointes), which is discussed in Case 61.
Rhythm Sinus rhythm with an atrial and a • Many hereditary syndromes are now recognized
ventricular ectopic beat in which an abnormality of the sodium or potas-
sium ion channels causes a susceptibility to ven-
QRS axis Normal (+27°) tricular arrhythmias and sudden cardiac death.
P waves Normal These syndromes include long QT syndrome
(LQTS), in which genetic abnormalities of the
potassium or sodium channels lead to prolonged
QRS duration Normal (80 ms) ventricular repolarization and hence prolonga-
T waves Normal tion of the QT interval.

• Several genetic abnormalities have now been
identified, the three most common being termed
LQT1 and LQT2 (potassium channel abnormali-
ties) and LQT3 (sodium channel abnormality).
ANSWERS
• Many different drugs can cause prolongation of
1. This ECG shows a very prolonged QTc interval the QT interval. These include anti-arrhythmics
of 574 ms. (e.g. sotalol, flecainide, amiodarone), antibiotics
(e.g. erythromycin, clarithromycin), antidepres-
2. Causes of QTc prolongation include:
sants (e.g. amitriptyline, citalopram) and anti-
• Congenital long QT syndromes
histamines (e.g. terfenadine). Details of specific
• Electrolyte abnormalities (e.g. hypocalcae-
drugs categorized by their potential to cause
mia, hypokalaemia, hypomagnesaemia)
QT internal prolongation can be found on the
• Drug effects CredibleMeds® website. Drug-induced QT inter-
• Acute myocarditis val prolongation is associated with an increased
QTc prolongation can sometimes also be seen risk of torsades de pointes, which can lead to
in cases of acute myocardial infarction, cere- ventricular fibrillation and sudden cardiac
bral injury, hypertrophic cardiomyopathy and death. Awareness of the risk of drug-induced QT
hypothermia. prolongation is therefore important, particu-
larly when managing individuals with increased
susceptibility to such effects. This includes
COMMENTARY those with simultaneous treatment with more
than one QT-prolonging drug, overdose with
• The normal QT interval varies with heart rate, a QT-prolonging drug, pre-existing QT inter-
becoming shorter at faster rates. Measurements val prolongation, electrolyte abnormalities and
of the QT interval therefore need to be cor- underlying cardiovascular disease.
rected for heart rate. The most common method
for calculating the corrected QT interval (QTc)
is Bazett’s formula, dividing the measured QT Further Reading
interval by the square root of the RR interval (all Making Sense of the ECG 6th edition: Is the QTc interval
measurements in seconds). long? p 145.
• Bazett’s formula has limitations, however, and Giudicessi JR et al. The QT interval. Circulation (2019).
PMID 31180747.
tends to overcorrect or undercorrect the QT
interval at extremes of heart rate. Other formu- Rautaharju PM et al. AHA/ACCF/HRS recommendations
for the standardization and interpretation of the elec-
lae are also used, and so-called linear formulae
trocardiogram: Part IV: The ST segment, T and U
tend to be more uniform over a wide range of
waves, and the QT interval. Journal of the American
heart rates. College of Cardiology (2009). PMID 19281931.
• QT intervals tend to be a little longer in females Shah SR et al. Long QT syndrome: A comprehensive
than in males, and so a normal QTc is up to review of the literature and current evidence. Current
450 ms in males and 460 ms in females. Long Problems in Cardiology (2019). PMID 29784533.
CASE 56
CLINICAL SCENARIO
Severe central chest pain. JVP: not elevated.
Patient currently an inpatient on the coronary No peripheral oedema.
care unit. He had an acute myocardial infarction
36 h previously. Investigations
Hypertension. Troponin I: elevated.
Type 2 diabetes mellitus. Chest X-ray: mild cardiomegaly, early pulmonary
congestion.
Echocardiogram: left ventricular systolic function
impaired (ejection fraction 47%).
QUESTIONS
DOI: 10.1201/9781003472186-56
ECG ANALYSIS 4. The rhythm abnormality is benign and treat-

ment is necessary only if there is haemodynamic
Rate 36/min compromise.
Rhythm Regular
COMMENTARY
QRS axis Left axis deviation (–90°)
P waves Absent • Idioventricular rhythm is sometimes called ‘slow

VT’:
PR interval N/A
• It is a benign form of ventricular tachycardia.
QRS duration Prolonged (220 ms) • It is equally common in inferior and anterior
T waves Normal myocardial infarction
• It has a rate of less than 50/min with a QRS
complex duration >120 ms
• Rarely, the ventricular rate may increase, caus-
ing ventricular tachycardia or ventricular fibril-
ANSWERS lation. Treatment then involves increasing the
sinus rate with atropine or atrial pacing.
1. The QRS complexes are wide and appear in a
regular rhythm. This is a ‘slow’ form of mono- • Accelerated idioventricular rhythm is identified
when the heart rate is between 50 and 120 beats/
morphic ventricular ‘tachycardia’, called idio-
min. It occurs when an ectopic focus within the
ventricular rhythm.
ventricles starts firing with a rate just higher
2. Idioventricular rhythm is caused by suppres-
than that of the sinoatrial node – this ventricular
sion or block of the sinoatrial node, allowing the
focus then takes over the cardiac rhythm. This
emergence of a ventricular escape rhythm.
typically occurs when there is increased vagal
3. It is usually seen under specific metabolic con- tone with a decrease in sympathetic tone.
ditions such as acute myocardial ischaemia (the
most common). Other causes include electrolyte
abnormalities (which may require correction), Further Reading
drug toxicity (e.g. digoxin), myocarditis, cardio- Making Sense of the ECG 6th edition: Escape rhythms,
myopathy and following cardiac arrest. p 209; Accelerated idioventricular rhythm, p 190.
CASE 57
CLINICAL SCENARIO
Clammy, pale.
Haematemesis and melaena. Blood pressure: 86/46.
JVP: not seen.
Patient had been taking non-steroidal anti- Chest auscultation: unremarkable.
inflammatory drugs for the past 4 weeks to No peripheral oedema.
obtain pain relief from her osteoarthritis. She
presented with haematemesis, having vomited Investigations
approximately 500 mL of fresh blood, and sub- FBC: Hb 68, WCC 13.2, platelets 309.
sequently developed melaena. U&E: Na 137, K 4.1, urea 16.7, creatinine 93.
Past medical history Gastroscopy: large, actively bleeding duodenal
Osteoarthritis. ulcer.
Ischaemic heart disease.
QUESTIONS
2. What would you do about the heart rate?
DOI: 10.1201/9781003472186-57
ECG ANALYSIS • Supraventricular tachycardia (SVT) with

aberrant conduction
Rate 120/min • Ventricular pacing
Rhythm Sinus tachycardia
• If a patient has a pre-existing bundle branch
block in normal sinus rhythm, that bundle
QRS axis Normal (+48°) branch block will also remain present during epi-
P waves Present sodes of SVT. However, some patients may have
normal QRS complexes while in normal sinus
rhythm but develop a bundle branch block only
QRS duration Broad (130 ms) during episodes of tachycardia (‘functional’ bun-
dle branch block). In such cases, the development
T waves Normal
of functional right bundle branch block (RBBB)
QTc interval Normal (450 ms) is more common than functional LBBB. Sudden
changes in RR interval (as seen, for example, in
atrial fibrillation) are particularly likely to cause
Additional comments functional bundle branch block – this is referred
The QRS complexes have a left bundle branch block to as the Ashman phenomenon.
morphology. • SVT with aberrant conduction also includes SVT
occurring with ventricular preexcitation, such as
ANSWERS antidromic atrioventricular re-entry tachycardia
or atrial fibrillation with pre-excitation, both
1. This ECG shows a tachycardia (heart rate 120/ of which can occur in Wolff–Parkinson–White
min) with broad QRS complexes (QRS duration syndrome (see Case 59).
130 ms). The QRS complexes have a left bundle • Distinguishing between VT and SVT with aber-
branch block (LBBB) morphology. On careful rant conduction can be challenging. If the QRS
inspection, P waves can be seen before the QRS morphology has a typical RBBB or LBBB, then
complexes – the P waves are most easily seen in it is likely to be SVT with aberrant conduction.
lead V1. This broad-complex tachycardia is there- However, this is certainly not diagnostic as some
fore sinus tachycardia with aberrant conduction forms of VT can resemble LBBB or RBBB very
(LBBB). closely. If the QRS complexes are very broad
2. This patient’s sinus tachycardia is appropriate to (RBBB morphology with QRS duration >140
her haemodynamic state – she has lost blood and ms, LBBB morphology with QRS duration >160
is hypotensive and has therefore developed a sinus ms), then VT is more likely. An extreme QRS axis
tachycardia to help maintain cardiac output. (between –90° and –180°) also points towards
Trying to slow down the tachycardia in these cir- VT, as do concordant negative QRS complexes in
cumstances would be dangerous, causing haemo- the chest leads. One of the most valuable criteria
dynamic decompensation. The management of for diagnosing VT is the presence of independent
sinus tachycardia therefore depends critically on atrial activity (see ‘Commentary’, Case 58).
the identification and, where possible, treatment • Broad-complex tachycardia should always be
of the underlying cause. The appropriate action managed as VT until proven otherwise.
here would be to correct the hypovolaemia and to
prevent any further blood loss.
Further Reading
Making Sense of the ECG 6th edition: Sinus tachycardia,
COMMENTARY p 165; How do I distinguish between VT and SVT?
p 194; Bundle branch block, p 205.
• Broad-complex tachycardia (QRS complex dura- Alzand BSN et al. Diagnostic criteria of broad QRS com-
tion >120 ms) can result from: plex tachycardia: Decades of evolution. Europace
• Ventricular tachycardia (VT) (2011). PMID 21131372.
Case 57 137
Brugada P et al. A new approach to the differential diag- Jastrzebski M et al. Comparison of five electrocardiographic
nosis of a regular tachycardia with a wide QRS com- methods for differentiation of wide QRS-complex
plex. Circulation (1991). PMID 2022022. tachycardias. Europace (2012). PMID 22333239.
CASE 58
CLINICAL SCENARIO
Chest pain and breathlessness. JVP: not elevated.
Patient was woken from sleep by severe chest No peripheral oedema.
pain and breathlessness.
Investigations
Myocardial infarction 12 months previously. U&E: Na 135, K 3.2, urea 8.2, creatinine 138.
Occasional chest pain on exertion at intervals Thyroid function: normal.
since. Had reduced activities to avoid chest Troponin I: negative.
pain. Chest X-ray: marked cardiomegaly with signs of
pulmonary congestion.
Echocardiogram: moderate mitral regurgita-
tion into moderately dilated left atrium. Left
ventricular function severely impaired (ejection
fraction 25%).
QUESTIONS
DOI: 10.1201/9781003472186-58
ECG ANALYSIS • Ablation or surgery can be used to remove a

ventricular focus or re-entry circuit identified
Rate 152/min by electrophysiological testing.
Rhythm Ventricular tachycardia • Implantable cardioverter defibrillators (ICDs)
can be implanted to deliver anti-tachycardia
QRS axis +93° pacing and/or shocks for recurrent episodes
P waves Not seen of VT and VF.
PR interval N/A

COMMENTARY
T waves Not clearly seen • It can be difficult to differentiate VT and SVT
QTc interval T waves not clearly seen with aberrant conduction (if in doubt, always
manage as VT until proven otherwise).
• ECG findings favouring VT:
ANSWERS
• A broad-complex tachycardia in a patient
with a history of coronary disease (especially
myocardial infarction)
1. This ECG shows a broad-complex tachycardia.
There is positive concordance of the anterior • QRS duration in tachycardia – the wider the
QRS, the more likely the rhythm is to be VT
chest leads (the QRS complexes in the anterior
(VT is the most common cause of tachycardia
leads are all positive). This is monomorphic ven-
with a broad QRS)
tricular tachycardia (VT).
2. Acute management: • Normal QRS duration in sinus rhythm but
>140 ms during tachycardia
• Cardiopulmonary resuscitation – if the
• Marked change in axis (whether to the left or
patient is haemodynamically compromised,
follow the appropriate life support proto- right), compared with ECG in sinus rhythm
cols including electrical cardioversion as • Concordance – the QRS complexes in the
appropriate. chest leads are all positive or negative
• Manage the underlying cause (e.g. acute coro- • Evidence of atrioventricular dissociation is
nary syndrome) as appropriate. strongly supportive of a diagnosis of VT:
Long-term management: • Independent P wave activity – P waves occur
with no relation to the QRS complexes
• Following the initial management and cor-
• Capture beats – an atrial impulse manages to
rection of VT, longer-term management
should be discussed with a cardiologist. ‘capture’ the ventricles for one beat, causing
a normal QRS complex, which may be pre-
• Long-term prophylaxis is usually not neces-
ceded by a P wave
sary for VT occurring within the first 48 h
following an acute myocardial infarction. • Fusion beats – these appear when the ventri-
cles are activated by an atrial impulse and a
• Where prophylaxis is needed, pharmaco-
ventricular impulse simultaneously
logical options include such drugs as beta-
blockers, sotalol and amiodarone. However,
the selection of appropriate drug therapy for Further Reading
VT can be complex and requires a careful bal-
Making Sense of the ECG 6th edition: Monomorphic ven-
ance between efficacy and potential adverse
tricular tachycardia, p 191; How do I distinguish
effects, including possible pro-arrhythmic between VT and SVT? p 194.
actions. Alzand BSN et al. Diagnostic criteria of broad QRS com-
• VT related to bradycardia should be treated plex tachycardia: Decades of evolution. Europace
by pacing. (2011). PMID 21131372.
Case 58 141
Brugada P et al. A new approach to the differential diag- Whitaker J et al. Diagnosis and management of ventricu-
nosis of a regular tachycardia with a wide QRS com- lar tachycardia. Clinical Medicine (2023). PMID
plex. Circulation (1991). PMID 2022022. 37775174.
Jastrzebski M et al. Comparison of five electrocardio- Zeppenfeld K et al. 2022 ESC guidelines for the manage-
graphic methods for differentiation of wide QRS- ment of patients with ventricular arrhythmias and
complex tachycardias. Europace (2012). PMID the prevention of sudden cardiac death. European
22333239. Heart Journal (2022). PMID 36017572.
CASE 59
CLINICAL SCENARIO
Syncope. Heart sounds: normal.
Two abrupt syncopal events during the last
month. Investigations
Angina, hypertension, diabetes mellitus, chronic Thyroid function: normal.
kidney disease.
QUESTIONS
1. What key features are shown on this ECG?
2. What is this condition called?
3. Is this related to the patient’s syncope?
DOI: 10.1201/9781003472186-59
ECG ANALYSIS bundle branch block (RBBB), left bundle branch

block (LBBB), left anterior fascicular block (LAFB)
Rate 60/min and left posterior fascicular block (LPFB).
Rhythm Sinus rhythm
• When these blocks occur in combination, the
possible permutations include:
QRS axis Left axis deviation (–81°)
P waves Normal
• LAFB + LPFB = LBBB
• RBBB + LAFB = bifascicular block
• RBBB + LPFB = bifascicular block
QRS duration Broad complexes (180 ms) • RBBB + LAFB + first-degree AV block =
T waves Biphasic in lead I and inverted in lead aVL
trifascicular block
QTc interval Borderline prolonged (463 ms)

• RBBB + LPFB + first-degree AV block =
trifascicular block
• RBBB + LBBB = third-degree AV block (com-

Additional comments plete heart block)
The QRS complexes have a right bundle branch • RBBB + LAFB + LPFB = third-degree AV
block (complete heart block)
block morphology.
ANSWERS
• Permanent pacing is indicated when there is
bifascicular or trifascicular block with a clear
history of syncope, or documented intermittent
1. This ECG shows:
failure of the remaining fascicle.
• First-degree atrioventricular block (PR inter-
val 266 ms)
• Left axis deviation (QRS complex axis –81°) Further Reading
• Right bundle branch block Making Sense of the ECG 6th edition: Conduction prob-
2. This combination of conduction abnormalities is lems, p 201; Cardiac implantable electronic devices,
called trifascicular block. p 223.
3. Trifascicular block can progress to third-degree Glikson M et al. 2021 ESC guidelines on cardiac pacing
atrioventricular block (‘complete heart block’). and cardiac resynchronization therapy. European
This can occur intermittently and may therefore Heart Journal (2021). PMID 34455430.
Kusumoto FM et al. 2018 ACC/AHA/HRS guideline on
account for the syncopal events.
the evaluation and management of patients with
bradycardia and cardiac conduction delay. Journal
COMMENTARY of the American College of Cardiology (2018). PMID
30412710.
• Many different types of conduction block are
possible at different levels of the conduction sys-
tem, including atrioventricular (AV) block, right
CASE 60
CLINICAL SCENARIO
Breathlessness, intermittent chest pain and JVP: not elevated.
palpitations. Heart sounds: soft ejection systolic murmur in
aortic area and lower left sternal edge.
Been slowing down a lot recently; had to aban- No peripheral oedema.
don walking holiday in Scotland as very breath-
less on attempting to walk up hills. Investigations
FBC: Hb 129, WCC 7.8, platelets 259
Non-smoker. Troponin I: negative.
No family history of cardiovascular disease but Chest X-ray: mild cardiomegaly.
her sister is undergoing investigations for similar
problems.
QUESTIONS
DOI: 10.1201/9781003472186-60
ECG ANALYSIS defibrillator (ICD). Beta-blockers or verapamil

will reduce gradient across the outflow tract and
Rate 84/min control angina. In patients with more severe
symptoms – reduce outflow tract obstruction by
Rhythm Sinus rhythm
septal myomectomy either surgically or by alco-
QRS axis Normal (–15°) hol ablation. Dual-chamber pacing may improve
symptoms and increase exercise tolerance.
P waves Normal
Screening of first-degree relatives is important.

COMMENTARY
T waves Inverted I, aVL, V6
QTc interval Normal (450 ms) • Hypertrophic cardiomyopathy is a heterogeneous

disease of the sarcomere with at least 150 differ-
ent mutations in 10 different sarcomeric proteins.
Additional comments Certain mutations may delay penetrance so that
There are deep Q waves in the anterior leads. the disease presents late (>60 years).
• The 12-lead ECG is abnormal in at least 75% of
cases of hypertrophic cardiomyopathy. It may
ANSWERS
show a mild degree of hypertrophy, or show left
1. The deep anterior Q waves are suggestive of ventricular hypertrophy and ‘strain’, or sharply
septal hypertrophy. Echocardiography con- negative T waves in precordial leads V1–V3, deep
firmed that the patient had severe asymmetrical Q waves, atrial fibrillation, ventricular ectopics
hypertrophy of the interventricular septum with or ventricular tachycardia. ECG changes are
obstruction to the left ventricular outflow tract – often evident before phenotypical features, espe-
this is hypertrophic obstructive cardiomyopa- cially in the young.
thy (HOCM). • Characteristic features to look for on imaging –
2. ECG changes are due to thickened septal mus- asymmetrical left ventricular hypertrophy, small
cle – the most common variety of HOCM. If left ventricular cavity, systolic anterior motion of
this is in the outflow tract, the Venturi effect the mitral valve, mitral regurgitation, and mid-
of increased blood flow velocity during systole systolic closure of the aortic valve.
causes systolic anterior motion of mitral valve • On identifying the index case, arrange a 12-lead
(and mitral regurgitation). ECG and echocardiogram for first-degree
3. In 70%, there is a genetic mutation in the gene relatives.
coding for beta myosin, alpha-tropomyosin • Factors associated with a poor prognosis:
and troponin T. Inheritance is autosomal • Personal history of sudden cardiac death
dominant, though 50% of cases are sporadic. events, ventricular fibrillation or sustained
4. An accurate diagnosis is important to establish ventricular tachycardia
whether there is obstruction to outflow from the • Personal history of sudden cardiac death
left ventricle – the obstructive variety of cardio- events
myopathy carries a worse prognosis than non- • Unexplained syncope
obstructive. Investigate and monitor for rhythm • Documented non-sustained ventricular
abnormalities and treat with antiarrhyth- tachycardia
mic drugs as appropriate – high- risk patients • Maximal left ventricular wall thickness
may benefit from an implantable cardioverter ≥3 cm
Case 60 147
Further Reading
Making Sense of the ECG 6th edition: Left ventricular Arbelo E et al. 2023 ESC guidelines for the management of
hypertrophy, p 98. cardiomyopathies. European Heart Journal (2023).
PMID 37622657.
CASE 61
CLINICAL SCENARIO
Clinical features of alcoholic liver disease with
Presenting complaint ascites.
Syncope. Pulse: too fast to record manually.
History of presenting complaint JVP: elevated by 6 cm.
Patient admitted to hospital complaining of Heart sounds: gallop rhythm.
fatigue and muscle weakness after a week’s his- Chest auscultation: bilateral pleural effusions.
tory of diarrhoea and vomiting. She had a syn- Moderate peripheral oedema.
copal event shortly after admission and ECG
monitoring was commenced. Shortly afterwards Investigations
the patient had another syncopal episode and FBC: Hb 108, WCC 18.1, platelets 124.
this ECG was recorded. U&E: Na 127, K 2.3, urea 4.9, creatinine 85.
Magnesium: 0.61 mmol/L (normal range 0.7–1.0
Past medical history mmol/L).
Alcoholic cirrhosis of the liver. Chest X-ray: small bilateral pleural effusions.
QUESTIONS
1. What rhythm is shown on this rhythm strip?
2. What is the likely cause of this arrhythmia?
3. What treatment would be appropriate?
DOI: 10.1201/9781003472186-1
ECG ANALYSIS • When the underlying QT interval is normal,

polymorphic VT may be due to myocardial
Rate 230/min ischaemia/infarction, coronary reperfusion (fol-
Rhythm Polymorphic ventricular
lowing myocardial infarction), structural heart
tachycardia disease or the rare condition of catecholaminer-
gic polymorphic VT.
QRS axis Varying
• When polymorphic VT is seen in the context of
P waves Not visible a prolonged QT interval, it is commonly called
PR interval –
torsades de pointes (‘twisting of the points’).
There are several causes of QT interval prolonga-
QRS duration Broad tion, including hypocalcaemia, acute myocardi-
T waves Not visible tis, long QT syndrome and certain drugs.
QTc interval Not measurable on this
• Polymorphic VT carries a risk of precipitating
ventricular fibrillation and so urgent assess-
rhythm strip (but was
prolonged at 510 ms on
ment (with involvement of a cardiologist) is war-
admission 12-lead ECG) ranted. In an emergency, follow standard adult
life support protocols including urgent defibril-
lation if required. Treat underlying causes, such
ANSWERS as myocardial ischaemia/infarction or electro-
lyte abnormalities, and stop any causative drugs.
1. Polymorphic ventricular tachycardia (VT), • If the underlying QT interval is prolonged, use-
which in the setting of a prolonged QT interval ful measures can also include the administration
is commonly referred to as torsades de pointes. of intravenous magnesium and consideration of
2. The prolonged QT interval predisposes to poly- temporary transvenous pacing (which increases
morphic VT. In this patient’s case the likely the heart rate and thereby shortens the QT inter-
aetiology of the QT interval prolongation is the val). In the longer term, an implantable cardio-
electrolyte abnormalities (hypokalaemia and verter defibrillator may be required if the patient
hypomagnesaemia). is judged to be at high risk of recurrent arrhyth-
3. The electrolyte abnormalities need to be corrected. mias and sudden cardiac death.
Follow standard adult life support protocols.
Further Reading
COMMENTARY Making Sense of the ECG 6th edition: Polymorphic ven-
tricular tachycardia, p 196; Is the QTc interval long?
• Polymorphic VT is distinguished by a varying p 145.
Al-Khatib SM et al. 2017 AHA/ACC/HRS guideline for
QRS complex morphology.
• Polymorphic VT falls into two distinct catego- management of patients with ventricular arrhyth-
mias and the prevention of sudden cardiac death.
ries based upon the duration of the QT interval
Circulation (2018). PMID 29097296.
(measured during sinus rhythm): Zeppenfeld K et al. 2022 ESC guidelines for the manage-
• Polymorphic VT in the setting of a normal ment of patients with ventricular arrhythmias and
QT interval the prevention of sudden cardiac death. European
• Polymorphic VT in the setting of a prolonged Heart Journal (2022). PMID 36017572.
QT interval
CASE 62
CLINICAL SCENARIO
No specific complaints. JVP: not elevated.
Patient had been diagnosed with complete Peripheral oedema: nil.
heart block a few years ago when she presented
with dizziness and fatigue. Attended family doc- Investigations
tor surgery for routine ‘well woman’ check and FBC: Hb 105, WCC 3.9, platelets 145.
was concerned when ECG performed by the U&E: Na 133, K 4.8, urea 5.9, creatinine 129.
practice nurse was shown to a doctor. Chest X-ray: normal heart size, clear lung fields.
Echocardiogram: mild mitral regurgitation
Past medical history into mildly dilated left atrium. Left ventricu-
Angina, hypertension, diabetes mellitus. Had lar
function mildly impaired (ejection fraction
experienced feeling weak and dizzy last year – 51%).
fractured her hip following a fall but now fully
independent again.
QUESTIONS
DOI: 10.1201/9781003472186-62
ECG ANALYSIS and ventricles, ensuring that atrial and ven-

tricular stimuli are coordinated, avoiding ‘pace-
Rate 60/min maker syndrome’– atrial contraction against an
atrioventricular valve closed by asynchronous
Rhythm Atrial and ventricular
sequential pacing
ventricular contraction. Dual-chamber pacing
mimics the normal physiological action of the
QRS axis Left axis deviation (−61°) heart.
P waves Very small, visible just after 4. Pacemaker function needs checking a few weeks
the atrial pacing ‘spike’ after implantation and at regular intervals
thereafter. ‘End of battery life’ can be predicted
PR interval 160 ms
to within a few weeks and unit replacement
QRS duration Prolonged (186 ms) planned.
T waves Normal

COMMENTARY
ANSWERS • The symptoms of complete heart block (dizzi-

ness, lack of energy, breathlessness and syncope)
1. A small pacing ‘spike’ is seen immediately before are usually relieved by a permanent pacemaker.
each wide QRS complex – this is a ventricular • The choice of pacemaker is important.
pacing spike. In addition, there is an additional Atrioventricular sequential pacing is preferred
pacing spike visible about 160 ms before most of if there is any atrial activity, to avoid pacemaker
the QRS complexes – these are the pacemaker syndrome.
signals to the atria which trigger atrial systole.
This is atrioventricular sequential (or dual-
• Pacemakers may be single-chamber (pacing the
atrium in AAI mode or the ventricle in VVI
chamber) pacing. mode) or dual-chamber (pacing both atrium
2. The atrial lead only generates an electrical and/or ventricle).
impulse if the sinoatrial node fails to do so; here,
every atrial impulse is pacemaker-activated, Further Reading
according to a preset rate. The ventricular lead
only generates an electrical impulse if ventricu- Making Sense of the ECG 6th edition: Cardiac implantable
lar contraction does not occur within a fixed electronic devices, p 223.
Glikson M et al. 2021 ESC guidelines on cardiac pacing
time period after the atria have been paced.
Here, every ventricular contraction is also pace-
Heart Journal (2021). PMID 34455430.
maker activated. Kusumoto FM et al. 2018 ACC/AHA/HRS guideline
3. The patient had episodes of collapse due to on the evaluation and management of patients
complete heart block. As the individual was with bradycardia and cardiac conduction delay:
very active and the ECG showed P waves, a Executive summary. Journal of the American College
dual-chamber pacemaker was implanted. This of Cardiology (2019). PMID 30412710.
restores the electrical connection between atria
CASE 63
CLINICAL SCENARIO
Dizzy spells. JVP: not elevated.
Intermittent dizzy spells for one month. No peripheral oedema.

Angina. Diabetes mellitus. FBC: Hb 134, WCC 7.8, platelets 220.
Echocardiogram: normal cardiac structure and
function.
QUESTIONS
1. Describe the appearances seen in this ECG.
2. What arrhythmia is this?
3. How would you manage this arrhythmia?
DOI: 10.1201/9781003472186-63

Rate Atrial – 96/min • Second-degree atrioventricular block of the 2:1
subtype means that only every alternate P wave
Ventricular – 48/min
will be conducted via the atrioventricular node.
Rhythm Sinus rhythm with Thus, the ventricular (QRS complex) rate will be
second-degree exactly half of the atrial (P wave) rate.
atrioventricular block (2:1) • Second-degree atrioventricular block is often cate-
QRS axis Normal (+16°) gorized as Mobitz type I or Mobitz type II, depend-
ing upon whether or not the PR interval lengthens
P waves Normal
before a P wave fails to conduct. However, in 2:1
PR interval Normal for conducted atrioventricular block it is impossible to say whether
beats (150 ms) the PR interval would have lengthened or not, as
QRS duration Normal (94 ms) there is only one PR interval to measure before
the non-conducted P wave occurs. It is therefore
T waves Normal
impossible to place this into either the Mobitz type I
QTc interval Normal (384 ms) or the Mobitz type II category, and so this form of
second-degree atrioventricular block is placed in
its own category of 2:1 atrioventricular block.
ANSWERS
1. Every alternate P wave is followed by a QRS
Further Reading
complex. Making Sense of the ECG 6th edition: Second-degree atrio-
2. Second-degree atrioventricular block (2:1 ventricular block, p 203; 2:1 Atrioventricular block,
subtype). p 203.
Glikson M et al. 2021 ESC guidelines on cardiac pacing
3. Review the patient’s medication for any drugs
that may cause atrioventricular block (e.g. beta- Heart Journal (2021). PMID 34455430.
blockers, rate-limiting calcium channel block- Kusumoto FM et al. 2018 ACC/AHA/HRS guideline on
ers, digoxin). In the absence of a reversible cause, the evaluation and management of patients with
patients with second-degree atrioventricular bradycardia and cardiac conduction delay: execu-
block (2:1) will usually need permanent pacing tive summary. Journal of the American College of
and should therefore be referred to a cardiologist. Cardiology (2019). PMID 30412710.
CASE 64
CLINICAL SCENARIO
Pulse: <30/min, irregular.
Dizziness. JVP: normal.
Heart sounds: normal first and second sound;
History of presenting complaint quiet ejection systolic murmur.
Recently moved into sheltered accommoda- Chest auscultation: a few basal crackles.
tion to live near his daughter following his wife’s No peripheral oedema.
death. Was found collapsed by warden. Seen
in the emergency department and found to be Investigations
extremely bradycardic. No further information FBC: Hb 117, WCC 8.1, platelets 178.
available at time of admission. U&E: Na 131, K 3.9, urea 12.3, creatinine 221.
Prescription in pocket – history of hypertension Chest X-ray: mild cardiomegaly, early pulmo-
(on three anti-hypertensive agents). Permanent nary congestion.
pacemaker implanted 11 years earlier. Echocardiogram: thickened aortic valve with
pressure gradient of 22 mmHg. Concentric
left ventricular hypertrophy, systolic function
impaired (ejection fraction 44%).
QUESTIONS
DOI: 10.1201/9781003472186-64
ECG ANALYSIS with the pacemaker system itself, it may require

reprogramming, or repositioning/replacement
Rate <30/min of the pacing lead.
Rhythm Pacing spikes with intermittent failure
to capture
COMMENTARY
QRS axis N/A
P waves Present, with an atrial rate of 80/min • Pacemaker problems include failures in sensing
and failures in pacing.
PR interval N/A
• Failure to sense: the intrinsic intra-cardiac
QRS duration Prolonged (132 ms) activity is not recognized by the pacemaker
T waves N/A
because of:
• Inappropriate lead placement
QTc interval N/A
• Lead displacement – this can happen usually
within a few weeks of pacemaker implantation
ANSWERS • Lead fracture or insulation defect – this can
occur months or years after implantation. The
1. This rhythm strip shows leads I, II and III. P manufacturer will advise if problem occurs
waves can be seen (most clearly in lead II) with with a faulty batch; advise the manufacturer if
an atrial rate of around 80/min. There are also lead fracture identified. Occasionally, this may
occasional pacing spikes, with a pacing rate of be due to ‘twiddler’s syndrome’ (tendency for
66/min, but only two of these pacing spikes are the patient to rotate the pacemaker unit itself –
followed by QRS complexes. A ventricular pace- avoidable by ensuring the size of the pacemak-
maker is therefore trying to pace the ventricles er’s pocket is minimized during wound closure)
at 66/min, but only intermittently succeeding in • Connector problem – the lead connection to
doing so. This is therefore underlying complete pacemaker is poor
heart block and ventricular (VVI) pacing with • Inappropriate programming
intermittent failure to capture. • Component failure – e.g. magnetic reed switch
2. The pacing stimulus is delivered by the pace- jammed (rare)
maker but the ventricular myocardium fails to • Failure to pace: a pacing stimulus is not delivered
depolarize. This can be caused by: when expected, or a stimulus is delivered but the
• Displacement of the ventricular lead from its myocardium does not depolarize. A stimulus will
optimal position adjacent to the ventricular not be delivered with:
myocardium • Connector problem – a ratchet screwdriver
• Malfunction of the pacing lead (e.g. lead with preset torque ensures satisfactory
fracture) attachment of the lead to the pacemaker unit.
• A change in the pacing threshold (the voltage More of a problem if an ‘old style’ lead is con-
needed to depolarize the ventricle), as a result nected to a ‘modern’ pacemaker unit
of myocardial infarction or ischaemia, elec- • Lead fracture – this is rare but will trigger a
trolyte abnormalities or drug therapy manufacturer’s alert
• Inappropriate programming (inadequate • Pulse generator failure – pacemaker failure is
voltage) usually due to battery depletion
3. The underlying cause of the loss of capture • Oversensing: Pacemaker detects signals other
needs to be identified and addressed (see previ- than those intended (e.g. ‘cross talk’ between
ous). A chest X-ray will show the position of the atrial and ventricular components of dual-cham-
pacing lead and whether it has become damaged ber pacemaker); this can usually be electrically
or dislodged. If the problem is due to a problem ‘tuned out’ by the cardiac physiologist.
Case 64 157
Further Reading
• Lead displacement may occur: Making Sense of the ECG 6th edition: Cardiac implantable
• Early (within 6 weeks) – about 1% of ventricu- electronic devices, p 223.
lar leads and 4% of atrial leads get displaced
• Late – most commonly affecting the atrial lead
CASE 65
CLINICAL SCENARIO
Resting tremor affecting the hands.
Exertional breathlessness. Orthopnoea. Blood pressure: 118/74.
JVP: elevated by 3 cm.
History of presenting complaint Heart sounds: soft (2/6) pan-systolic murmur at
One-year history of gradually worsening breath- apex.
lessness with a reduction in exercise capac- Chest auscultation: bi-basal inspiratory crackles.
ity – the patient can now walk only 100 m No peripheral oedema.
on level ground. Recent orthopnoea – the
patient sleeps with four pillows. Investigations
Inferior myocardial infarction 7 years ago. Chest X-ray: moderate cardiomegaly, pulmo-
Anteroseptal myocardial infarction 4 years ago. nary oedema.
Essential tremor. Echocardiogram: dilated left ventricle with
severely impaired systolic function (ejection frac-
tion 34%). Mild functional mitral regurgitation.
QUESTIONS
1. What heart rhythm is evident on this ECG?
2. Are there any other ECG findings?
3. What are the likely causes of these findings?
DOI: 10.1201/9781003472186-65
ECG ANALYSIS infarction), poor anterior R wave progression

(old anteroseptal myocardial infarction), left
Rate 90/min axis deviation (which can be a consequence
of inferior myocardial infarction) and mild
Rhythm Sinus rhythm
impairment of atrioventricular conduction.
QRS axis Normal (–56°)
P waves Normal
COMMENTARY

• The ECG records the electrical activity of the
heart, but this is not the only source of electri-
T waves Normal cal activity in the body. Skeletal muscle activity
QTc interval Normal (442 ms) is also picked up on the ECG.
• Where possible, patients should lie still during
an ECG recording to minimize skeletal muscle
Additional comments artefact, but this is not always possible, particu-
There are inferior Q waves and there is poor R wave larly if the patient
progression in leads V1–V5. • is uncooperative or agitated,
• is in respiratory distress, or
ANSWERS • has a movement disorder.
• The presence of electrical artefact which is much
1. Sinus rhythm, which is best appreciated in the more marked in the limb leads than in the chest
chest leads (V1–V6). leads (as in this example) strongly suggests that
2. There are several findings: skeletal muscle interference from limb move-
• The baseline in the limb leads is erratic and ment is the cause.
masks the P waves, making it difficult to dis- • The use of signal-averaged ECGs (to ‘average out’
cern the underlying rhythm in these leads. random electrical artefacts by combining a num-
The rhythm is seen much more clearly in the ber of PQRST complexes) can help to reduce the
chest leads. impact of skeletal muscle artefact, particularly
• There are inferior Q waves. during exercise treadmill testing. However, sig-
• There is poor anterior R wave progression nal-averaged recordings can introduce artefac-
(affecting leads V1–V5). tual changes of their own and so always interpret
• There is left axis deviation. such recordings with discretion.
• There is mild first-degree atrioventricular
block (PR interval 205 ms). Further Reading
3. There are two causes:
• The erratic baseline is a consequence of the recording, p 21; Patient movement, p 159.
essential tremor, producing musculoskeletal Srikureja W et al. Tremor-induced ECG artifact mim-
artefact on the ECG recording. icking ventricular tachycardia. Circulation (2000).
• Ischaemic heart disease would account for PMID 10982552.
the inferior Q waves (old inferior myocardial
CASE 66
CLINICAL SCENARIO
Female, aged 58 years. Blood pressure: 110/50.
JVP: not visible.
Presenting complaint Heart sounds: hard to assess (tachycardia).
Palpitations of sudden onset. Chest auscultation: fine basal crackles.
Woken from sleep with racing heartbeat and Investigations
breathlessness. FBC: Hb 139, WCC 8.1, platelets 233.
Nil significant. Troponin I: negative.
Chest X-ray: mild cardiomegaly, early pulmo-
Examination nary congestion.
QUESTIONS
DOI: 10.1201/9781003472186-66
ECG ANALYSIS delta waves as a result of ventricular pre-excita-

tion (see Case 16). Some impulses will be con-
Rate 228/min ducted normally via the atrioventricular node
and so normal QRS complexes may be visible at
Rhythm Atrial fibrillation with
ventricular pre-excitation
intervals.
3. At very fast heart rates there is a risk of ven-
QRS axis Left axis deviation (−49°) tricular fibrillation, so consider an urgent
P waves Not visible cardioversion.
PR interval N/A

COMMENTARY
T waves Inverted in anterolateral • Atrial fibrillation in WPW syndrome can resem-
leads ble ventricular tachycardia, but AF is irregular
QTc interval Difficult to assess at such whereas ventricular tachycardia is regular.
high heart rates • In WPW syndrome with atrial fibrillation, the
ventricular rate can be very fast due to conduc-
tion via the accessory pathway. Blocking the
atrioventricular node can paradoxically increase
ANSWERS the heart rate even more, by directing all the
1. This ECG shows irregularly irregular QRS impulses down the accessory pathway, precipi-
complexes with no discernible P waves, the tating ventricular fibrillation. Drugs such as
hallmark of atrial fibrillation. The ventricular adenosine, beta-blockers, verapamil and digoxin
rate is very fast. The QRS complexes are some- must therefore be avoided in these patients.
what broad and have an odd morphology, not • Urgent electrical cardioversion is the preferred
typical of a left or right bundle branch block. treatment, especially if the patient is hypotensive
This is atrial fibrillation with ventricular pre- or in heart failure.
excitation in Wolff–Parkinson–White (WPW) • Atrial fibrillation, atrial flutter and atrial tachy-
syndrome. cardia carry considerable risk of sudden cardiac
2. Conduction from atria to ventricles is usually death in patients with an accessory pathway, and
through a single connection involving the atrio- patients who have experienced these arrhyth-
ventricular node and bundle of His. The ven- mias should be considered for urgent catheter
tricles are normally protected from rapid atrial ablation.
activity by the refractory period of the atrioven-
tricular node. In WPW syndrome, there is an Further Reading
additional accessory pathway which conducts
Making Sense of the ECG 6th edition: Wolff–Parkinson–
electrical activity to the ventricles at a faster rate White syndrome, p 80; Atrial fibrillation in Wolff–
than the atrioventricular node. If atrial fibrilla- Parkinson–White syndrome, p 180.
tion develops, most impulses will be conducted Brugada J et al. 2019 ESC guidelines for the manage-
via the accessory pathway, so high ventricular ment of patients with supraventricular tachycardia.
rates can be achieved. These beats will contain European Heart Journal (2020). PMID 31504425.
CASE 67
CLINICAL SCENARIO
Patient comfortable at rest but breathless on
Presenting complaint exertion.
Breathlessness and peripheral oedema. Pulse: 78/min, regular.
History of presenting complaint JVP: elevated.
Three-month history of progressive breathless- Heart sounds: normal.
ness and peripheral oedema, with a steady fall Chest auscultation: bilateral expiratory wheeze.
in exercise capacity. Moderate peripheral oedema.

Hypertension. FBC: Hb 108, WCC 8.3, platelets 174.
Chronic obstructive pulmonary disease. U&E: Na 139, K 4.5, urea 8.2, creatinine 141.
Chest X-ray: pulmonary oedema.
Echocardiogram: moderate hypertrophy of left
and right ventricles, and evidence of diastolic
dysfunction (‘stiff ventricles’). Dilatation of left
and right atria.
QUESTIONS
1. What abnormalities are seen on this ECG?
2. How do these abnormalities relate to the echocardiographic findings?
3. What is the likely clinical diagnosis?
DOI: 10.1201/9781003472186-67
ECG ANALYSIS 3. The presence of left ventricular hypertrophy

is likely a result of the patient’s hypertension.
Rate 78/min The presence of right ventricular hypertrophy
is likely secondary to pulmonary hypertension,
Rhythm Sinus rhythm
which is due to the chronic obstructive pulmo-
QRS axis Normal (+30°) nary disease.
P waves Normal
PR interval Borderline short (110 ms) COMMENTARY

QRS duration Normal (90 ms) • Right ventricular hypertrophy causes a ‘domi-
T waves Widespread inversion nant’ R wave (i.e. bigger than the S wave) in the
leads that ‘look at’ the right ventricle, particu-
larly V1. Right ventricular hypertrophy can also
cause:
Additional comments • Right axis deviation
There is a dominant R wave in lead V1, and tall R • Deep S waves in leads V5 and V6
waves in leads V3–V5. • Right bundle branch block (RBBB)
• ST depression and/or T wave inversion in the
right precordial leads (when severe)
ANSWERS
• Right ventricular hypertrophy is not the only
1. This ECG contains several abnormalities. The cause of a positive R wave in lead V1. Other
main ones are: causes include:
• Dominant R waves in the right precordial • Posterior myocardial infarction
leads • Wolff–Parkinson–White syndrome Type
• Tall R waves in leads V3–V5 A (left-sided accessory pathway)
• ST depression and T wave inversion in the • Causes of right ventricular hypertrophy include
anterolateral leads pressure overload on the right ventricle (e.g.
• T wave inversion in leads II and aVF pulmonary stenosis, pulmonary hypertension)
or hypertrophic cardiomyopathies affecting the
2. The dominant R waves in the right precordial
right ventricular myocardium. The treatment
leads are consistent with right ventricular hyper-
of right ventricular hypertrophy is that of the
trophy. The tall R waves in leads V3–V5 are consis-
underlying cause.
tent with left ventricular hypertrophy, and the ST
segment and T wave abnormalities are consistent
with ventricular ‘strain’ in association with the Further Reading
hypertrophy. The echocardiogram supports these Making Sense of the ECG 6th edition: Left ventricular
findings, revealing moderate hypertrophy of left hypertrophy, p 98; Right ventricular hypertrophy,
and right ventricles. p 100.
CASE 68
CLINICAL SCENARIO
Found collapsed at home. JVP: not elevated.
Collapsed without warning at home. On arrival No peripheral oedema.
of the paramedics, he was found to be in ven-
tricular fibrillation and sinus rhythm was restored Investigations
following defibrillation. FBC: Hb 154, WCC 6.2, platelets 212.
Nil of note – normally fit and well. Chest X-ray: normal heart size, clear lung fields.
Echocardiogram: normal aortic and mitral
valves. Left ventricular function good (ejection
fraction 68%).
QUESTIONS
2. What is the likely cause of the collapse?
3. What is the underlying mechanism?
DOI: 10.1201/9781003472186-68

Rate 61/min • Epidemiology:
Rhythm Sinus rhythm
• 60% of patients with aborted SCD with typi-
cal Brugada ECG have a family history of
QRS axis Normal (+34°) sudden death or a family with similar ECGs
P waves Bifid • Brugada syndrome probably accounts for
about half of all cases of idiopathic ventricu-
lar fibrillation
QRS duration Normal (100 ms) • Incidence probably underestimated: inci-
T waves Inverted in lead V2
dence varies with population (26–38/100,000
per year in South-East Asia)
• Recognized worldwide but greatest preva-
lence in the Far East: 1:2000 of adult Japanese;
1:30,000 in Belgium
Additional comments
There is ST segment elevation in leads V1–V3 and a
• Most common cause of sudden death in South
Asians under 50 with apparently structurally
right bundle branch block morphology. normal heart
• 40% with typical ECG will have a first episode
of ventricular tachycardia or sudden death in
ANSWERS
3 years, unless asymptomatic with abnormal
1. There is ST segment elevation in the right chest ECG after drugs
leads (V1–V3) and a right bundle branch block • Three different ECG patterns have been described
(RBBB) morphology – this combination of ECG in Brugada syndrome. All three have ST segment
signs is suggestive of Brugada syndrome. elevation (≥2 mm elevation of the J point), but
2. In patients with a structurally normal heart vary in other ways:
but with the ECG characteristics shown earlier, • Type 1 has ‘coved’ ST segment elevation with
Brugada syndrome is associated with syncopal inverted T waves. The terminal portion of the
or sudden death episodes. The collapse may be ST segment gradually descends until it meets
due to fast, polymorphic ventricular tachycar- the inverted T wave
dia or ventricular fibrillation, usually occurring • Type 2 has saddle-shaped ST segment eleva-
without warning. tion with positive or biphasic T waves. The
3. Inheritance is autosomal dominant in around terminal portion of the ST segment is ele-
50% of cases, and there is an 8:1 male-to-female vated by ≥1 mm
ratio. Abnormalities have been identified in the • Type 3 has saddle-shaped ST segment ele-
genes coding for ion channels, in particular the vation with positive T waves. The termi-
sodium channel gene SCN5A. nal portion of the ST segment is elevated
4. The diagnosis of Brugada syndrome can be diffi- by <1 mm
cult as the ECG changes mentioned may be inter- • Recording the 12-lead ECG with leads V1 and
mittent or their significance overlooked. ECG V2 in the second (rather than fourth) intercostal
abnormalities may be ‘unmasked’ pharmacologi- space has been reported to increase the diagnos-
cally with flecainide or ajmaline. This particular tic sensitivity of the ECG. Some patients require
ECG was recorded during an ajmaline challenge. an intravenous challenge with a sodium channel
It is important to exclude electrolyte disorders blocking drug (such as flecainide or ajmaline)
(hyperkalaemia and hypercalcaemia) and struc- to unmask the ECG appearances. This is not
tural heart disease. No drug has been proven helpful in those with a Type 1 ECG but can help
effective at preventing arrhythmias or reducing diagnostically in those with Type 2 or 3 ECG
mortality in sudden cardiac death (SCD) survi- appearances. Such a test should only be per-
vors, and so there is a low threshold for using an formed by individuals trained and experienced
implantable cardioverter defibrillator (ICD). in the technique.
Case 68 167
Further Reading
Making Sense of the ECG 6th edition: Brugada syndrome, Wilde AAM et al. Proposed diagnostic criteria for the
p 124. Brugada syndrome: Consensus report. Circulation
(2002). PMID 12417552.
CASE 69
CLINICAL SCENARIO
Four-month history of episodic palpitations – No peripheral oedema.
sudden onset rapid heartbeat, lasting up to 15
min, followed by sudden termination of palpita- Investigations
tions. The patient was asymptomatic during the FBC: Hb 147, WCC 5.8, platelets 339.
recording of this ECG rhythm strip. U&E: Na 142, K 5.1, urea 4.5, creatinine 76.
Nil.
QUESTIONS
1. This rhythm strip is taken from a 24 h ambulatory ECG recording – what does it show?
2. What can cause this?
DOI: 10.1201/9781003472186-69
ECG ANALYSIS in patients who have received a heterotopic ‘pig-

gyback’ heart transplant, in which a donor heart
Rate Difficult to assess in view is connected to the patient’s own heart. Both
of bizarre rhythm hearts operate independently, and so an ECG
Rhythm Bizarre – there appear to
will show two distinct heart rhythms, one from
be two distinct each heart.
overlapping rhythms 3. Discard this recording and arrange a new 24 h
ECG recording.
QRS axis Unable to assess (single
lead)
P waves Difficult to assess in view COMMENTARY

of bizarre rhythm
PR interval Difficult to assess in view

• Always consider the possibility of artefact in
‘bizarre’ ECGs, particularly when they do not
of bizarre rhythm
correlate with what you know about the patient’s
QRS duration Difficult to assess in view clinical details.
of bizarre rhythm
• Rare artefactual errors of this kind highlight the
T waves Difficult to assess in view importance of taking a careful and structured
of bizarre rhythm approach to ECG interpretation, and to ensure
QTc interval Difficult to assess in view
that any abnormalities you see can be accounted
of bizarre rhythm for.
• This kind of recording error should no longer be
possible now that cassette tapes have been super-
ANSWERS seded by digital recording onto memory cards in
ambulatory ECG monitoring.
1. This is a very odd ECG recording. On close
inspection there appear to be two distinct
• In patients with a heterotopic ‘piggy-back’ heart
transplant, a similar ‘double ECG’ can be seen.
heart rhythms occurring simultaneously, with
In this type of heart transplant, the recipient’s
no obvious correlation between them. In some
heart is left in situ to supplement the function of
cases two distinct QRS complexes occur on top
the donor heart. Heterotopic heart transplants
of, or close to, each other.
are rarely performed but may be appropriate if
2. In this case, the rhythm strip was made using an the donor heart is unable to function alone (for
old 24 h ECG recorder that used cassette tapes example, if the recipient’s body size is much
to record the ECG. The cassette tape had been greater than that of the donor’s, or if the recipi-
accidentally reused without the previous record- ent has pulmonary hypertension).
ing having been deleted, and so two recordings
from different patients ended up on the same
cassette tape. When the tape was analysed, the Further Reading
two recordings appeared simultaneously on one Making Sense of the ECG 6th edition: Artefacts on the
rhythm strip. A similar appearance can be seen ECG, p 157.
CASE 70
CLINICAL SCENARIO
Breathlessness on exertion. JVP: not elevated.
Patient was fit and well until 12 months earlier. No peripheral oedema.
Heart failure had developed after a flu-like ill-
ness – viral myocarditis diagnosed. Assessed for Investigations
cardiac transplant but turned down as had had FBC: Hb 159, WCC 6.6, platelets 222.
problems with depression, including one (much U&E: Na 143, K 4.1, urea 4.7, creatinine 106.
regretted) suicide attempt. An alternative oper- Thyroid function: normal.
ation had been offered and performed, and this Troponin I: negative.
ECG was recorded post-surgery. Chest X-ray: mild cardiomegaly, early pulmo-
nary congestion.
Past medical history Echocardiogram: moderate mitral regurgitation
Viral myocarditis. and dilated left atrium. Left ventricular function
Depression. severely impaired (ejection fraction 23%).
QUESTIONS
2. What operation has this patient undergone?
DOI: 10.1201/9781003472186-70
ECG ANALYSIS • A chronic girdling effect due to the wrap-

ping of latissimus dorsi around the heart,
Rate 96/min
resulting in stabilization of the ventricular
Rhythm Sinus rhythm remodelling process and a decrease in left
ventricular dilatation
• Active systolic assistance to decrease myo-
P waves Normal cardial stress
PR interval Normal (184 ms) The operation was performed for patients with
heart failure which was symptomatic despite
maximal medical treatment. The skeletal muscle
T waves Inverted in inferior and had to be ‘trained’ to work like cardiac muscle –
anterolateral leads a pacing electrode was placed within the muscle
QTc interval Normal (440 ms) and over a period of weeks stimulated by an
impulse generator synchronized with cardiac
contraction.
Additional comments
After some of the QRS complexes, there is a pacing
spike followed by a burst of electrical ‘noise’ from COMMENTARY
skeletal muscle.
• Dynamic cardiomyoplasty was once used as an
alternative to cardiac transplantation.
ANSWERS • Perioperative mortality was about 10%.
1. The ECG shows a normal P wave, PR interval
• ‘Muscle transformation’ – training the latissi-
mus dorsi muscle by pacing every fourth, third,
and QRS duration and multiple pacing spikes, alternate and finally every cardiac contraction –
which occur after many of the QRS complexes. would take at least 8 weeks.
This is the ECG from a patient who has under-
gone a dynamic cardiomyoplasty.
• Trials reported an increase in left ventricular
ejection fraction, left ventricular stroke index
2. This operation, which was sometimes under- and stroke work.
taken during the 1980s and 1990s, involved
mobilizing the patient’s left latissimus dorsi
• Outcomes were disappointing and the operation
was abandoned in the US and the UK.
muscle as a pedicle graft, wrapping the free end
around the heart and stimulating it to contract
in synchrony with cardiac systole. Based on Further Reading
animal and human studies, the benefits of this
Treasure T. Cardiac myoplasty with the latissimus dorsi
operation were believed to be due to: muscle. Lancet (1991). PMID 1674768.
Appendix 1: List of Cases
This appendix lists the principal diagnosis for each ECG case, to facilitate finding cases for revision. Please
note that this appendix contains ‘spoilers’, so if you wish to test yourself on the ECGs, then be sure to do so
before looking through this list!
Case 1 Normal ECG (mild sinus bradycardia)
Case 2 Sinus arrhythmia
Case 3 Atrial ectopic beat
Case 4 First-degree atrioventricular block
Case 5 Sinus bradycardia
Case 6 Atrial fibrillation with a fast ventricular response
Case 7 Acute inferior ST segment elevation myocardial infarction
Case 8 Left bundle branch block
Case 9 Ventricular ectopic beat
Case 10 Sinus tachycardia
Case 11 Atrial flutter with 4:1 atrioventricular block
Case 12 Myocardial ischaemia (unstable angina)
Case 13 Ventricular tachycardia triggered by a ventricular ectopic beat
Case 14 Mobitz type I second-degree atrioventricular block (Wenckebach phenomenon)
Case 15 Hyperkalaemia
Case 16 Wolff–Parkinson–White ECG pattern
Case 17 Inferolateral non-ST segment elevation myocardial infarction
Case 18 Right bundle branch block
Case 19 Atrioventricular re-entry tachycardia (AVRT)
Case 20 Sinoatrial block
Case 21 Broad and bifid P waves (‘P mitrale’)
Case 22 Atrial ectopic beats (atrial trigeminy)
Case 23 Left axis deviation
Case 24 Downsloping ‘reverse tick’ ST segment depression (digitalis effect)
Case 25 Acute pulmonary embolism
Case 26 Atrial fibrillation with a slow ventricular response
Case 27 Pulseless electrical activity (PEA)
(Continued )
174 Appendix 1 List of Cases
(Continued )
Case 28 Acute lateral ST segment elevation myocardial infarction
Case 29 Atrioventricular nodal re-entry tachycardia (AVNRT)
Case 30 Atrial tachycardia with variable atrioventricular block
Case 31 Lown–Ganong–Levine syndrome
Case 32 Old anterior myocardial infarction
Case 33 Third-degree atrioventricular block
Case 34 Hypokalaemia
Case 35 Left ventricular hypertrophy
Case 36 Ventricular pacing
Case 37 Atrioventricular nodal re-entry tachycardia
Case 38 Sinus arrest
Case 39 Misplacement of the right and left arm electrodes
Case 40 Acute posterior ST segment elevation myocardial infarction
Case 41 Hypothermia
Case 42 Left ventricular aneurysm
Case 43 Ventricular bigeminy
Case 44 Ventricular tachycardia
Case 45 Pericarditis
Case 46 Atrial flutter
Case 47 Atrial pacing
Case 48 Atrial parasystole
Case 49 Incorrect voltage calibration
Case 50 Coronary artery vasospasm (‘Prinzmetal’s angina’)
Case 51 Left ventricular hypertrophy with ‘strain’
Case 52 Acute inferior ST segment elevation myocardial infarction with right ventricular involvement
Case 53 Incorrect paper speed setting
Case 54 Dextrocardia
Case 55 Prolonged QT interval
Case 56 Idioventricular rhythm
Case 57 Sinus tachycardia with aberrant conduction
Case 58 Monomorphic ventricular tachycardia
Case 59 Trifascicular block
Case 60 Hypertrophic obstructive cardiomyopathy
Case 61 Polymorphic ventricular tachycardia (torsades de pointes)
(Continued )
Appendix 1 List of Cases 175
(Continued )
Case 62 Atrioventricular sequential (or dual-chamber) pacing
Case 63 Second-degree atrioventricular block (2:1 subtype)
Case 64 Ventricular pacing with intermittent failure to capture
Case 65 Electrical artefact (skeletal muscle interference)
Case 66 Atrial fibrillation with ventricular pre-excitation
Case 67 Left and right ventricular hypertrophy
Case 68 Brugada syndrome
Case 69 Artefact resulting in a ‘double’ ECG recording
Case 70 Dynamic cardiomyoplasty

Index
Note: Page numbers in bold indicate a table on the corresponding page.
A ECG analysis, 170

questions, 169
Acute coronary syndromes (ACS), 42 Atrial ectopic beat, 52
Acute inferior ST segment elevation myocardial answers, 8
infarction, 126 clinical scenario, 7
answers, 18 commentary, 8
clinical scenario, 17 ECG analysis, 8
commentary, 18 questions, 7
ECG analysis, 18 Atrial ectopic beats (atrial trigeminy)
questions, 17 answers, 52
Acute inferior ST segment elevation myocardial clinical scenario, 51
infarction with right ventricular involvement commentary, 52
answers, 126 ECG analysis, 52
clinical scenario, 125 questions, 51
commentary, 126 Atrial extrasystoles, 8, 52
ECG analysis, 126 Atrial fibrillation (AF) with fast ventricular response
Acute lateral ST segment elevation myocardial clinical scenario, 13
infarction (STEMI) commentary, 14
commentary, 64 Atrial fibrillation with slow ventricular response
ECG analysis, 64 answers, 60
questions, 63 clinical scenario, 59
Acute posterior ST segment elevation myocardial commentary, 60
infarction (STEMI) ECG analysis, 60
answers, 94 questions, 59
clinical scenario, 93 Atrial fibrillation with ventricular pre-excitation
commentary, 94 answers, 162
ECG analysis, 94 clinical scenario, 161
questions, 93 commentary, 162
Acute pulmonary embolism ECG analysis, 162
clinical scenario, 57 Atrial flutter, 24, 162
commentary, 58 answers, 110
Adenosine diphosphate (ADP), ECG analysis, 110
30, 64 questions, 109
Alcohol, 8, 14, 22, 52, 119, 149 Atrial flutter with 2:1 block, 26, 88
Artefact resulting in ‘double’ ECG recording Atrial flutter with 4:1 atrioventricular block
answers, 170 answers, 26
clinical scenario, 169 atrial fibrillation, 27
commentary, 170 atrial tachycardia, 27
178 Index

commentary, 26 – 27 questions, 45
ECG analysis, 26 Atrioventricular sequential (dual-chamber) pacing
Atrial pacing, 134 clinical scenario, 151
ECG analysis, 112
questions, 111 B
Atrial parasystole
answers, 116 Bartter’s syndrome, 78
clinical scenario, 115 Beta-blockers
commentary, 116 acute posterior ST segment elevation myocardial
ECG analysis, 116 infarction, 94
questions, 115 AF, 14
Atrial premature beats (APBs), 8, 52 atrial ectopic beat, 8
Atrial premature complexes (APCs), 8, 52 atrial ectopic beats (atrial trigeminy), 52
Atrial tachycardia with variable atrioventricular block atrial fibrillation with a slow ventricular
answers, 70 response, 60
clinical scenario, 69 atrial fibrillation with ventricular pre-excitation, 162
commentary, 70 AV, 76
ECG analysis, 70 AVNRT, 66
questions, 69 AVRT, 46
Atrial trigeminy, see Atrial ectopic beats (atrial coronary artery vasospasm, 120
trigeminy) first-degree atrioventricular block, 10
Atrioventricular (AV) HOCM, 146
atrial fibrillation with a fast ventricular response, 14 monomorphic ventricular tachycardia, 140
atrial flutter, 110 myocardial ischaemia (unstable angina), 30
AVRT, 46 normal ECG (mild sinus bradycardia), 2
Lown–Ganong–Levine syndrome, 72 second-degree atrioventricular block, 154
Mobitz type I second-degree atrioventricular block sinoatrial block, 48
(Wenckebach phenomenon), 36 sinus bradycardia, 12
third-degree atrioventricular block, 76 sinus tachycardia, 24
trifascicular block, 144 STEMI, 64
Wolff–Parkinson–White ECG pattern, 40 VEBs, 22
Atrioventricular dissociation, 102, 140 VT, 102
Atrioventricular nodal re-entry tachycardia Broad and bifid P waves (P mitrale)
clinical scenario, 87 clinical scenario, 49
commentary, 88 commentary, 50
ECG analysis, 88 ECG analysis, 50
questions, 87 questions, 49
Atrioventricular nodal re-entry tachycardia (AVNRT), Brugada syndrome
46, 88 answers, 166
answers, 66, 87 clinical scenario, 165
clinical scenario, 65, 87 commentary, 166
commentary, 66, 87 ECG analysis, 166
ECG analysis, 66, 87 questions, 165
questions, 65, 87
Atrioventricular re-entry tachycardia (AVRT), 40, 66,
C
72, 88
answers, 46 Caffeine, 8, 22, 24, 52
clinical scenario, 45 Carotid sinus massage, 26, 88
commentary, 46 Chagas disease, 98
Index
179
Ciliary dysfunction, see Kartagener’s syndrome H

Conn’s syndrome, 78
Cornell criteria, 80, 122 His-Purkinje system, 100
Coronary artery vasospasm (Prinzmetal’s angina) Hyperkalaemia, 62, 78
clinical scenario, 119 arrhythmias/malignant, 56
commentary, 120 clinical scenario, 37
ECG analysis, 120 commentary, 38
questions, 119 ECG analysis, 38
Cushing’s syndrome, 78 questions, 37
Hypertrophic cardiomyopathy, 132, 146
Hypertrophic obstructive cardiomyopathy (HOCM)
D answers, 146
Dextrocardia, 92 clinical scenario, 145
ECG analysis, 130 Hypokalaemia, 56, 70
Digitalis (digoxin) effect clinical scenario, 77
ECG analysis, 56 Hypothermia, 12, 62, 132
Dual-chamber pacing, see Atrioventricular sequential clinical scenario, 95
(dual-chamber) pacing commentary, 96
Dynamic cardiomyoplasty ECG analysis, 96
clinical scenario, 171 Hypothyroidism, 12
commentary, 172
ECG analysis, 172
I
questions, 171
Idioventricular rhythm
E answers, 134
clinical scenario, 133
Echocardiography, 14, 20, 22, 106, commentary, 134
122, 146 ECG analysis, 134
Electrical artefact (skeletal muscle questions, 133
interference) Implantable cardioverter defibrillators (ICDs), 140, 146
answers, 160 Incorrect paper speed setting
clinical scenario, 159 answers, 128
Electromechanical dissociation (EMD), 62 questions, 127
Incorrect voltage calibration
F answers, 118
First-degree atrioventricular block commentary, 118
commentary, 10 Inferolateral non-ST segment elevation myocardial
ECG analysis, 10 infarction (NSTEMI)
180 Index

ECG analysis, 42
questions, 41
M
K Massive pulmonary embolism, 58, 62

Mild hypokalaemia, 78
Kartagener’s syndrome, 130 Misplacement of right and left arm electrodes
answers, 92
L
commentary, 92
Left and right ventricular hypertrophy ECG analysis, 92
clinical scenario, 163 Mobitz type I second-degree atrioventricular block
commentary, 164 (Wenckebach phenomenon)
Left axis deviation, 144, 160 commentary, 36
commentary, 54 Monomorphic ventricular tachycardia (VT)
Left bundle branch block (LBBB), commentary, 140
102, 136 ECG analysis, 140
clinical scenario, 19 Myocardial ischaemia, 12, 20, 22, 56, 150
commentary, 20 coronary artery vasospasm, 120
ECG analysis, 20 Myocardial ischaemia (unstable angina)
Left ventricular aneurysm, 18, 64, 106 clinical scenario, 29
ECG analysis, 98
questions, 97 N
Left ventricular hypertrophy, 20, 56, 118, 122,
146, 164 Nicotine, 8, 52
answers, 80 Non-ST segment elevation acute coronary syndrome
clinical scenario, 79 (NSTEACS), 30, 42
commentary, 80 – 81 Normal ECG (mild sinus bradycardia)
Left ventricular hypertrophy with ‘strain’ commentary, 2
commentary, 122
ECG analysis, 122
O
questions, 121
Lown–Ganong–Levine (LGL) syndrome Old anterior myocardial infarction
clinical scenario, 71 clinical scenario, 73
commentary, 72 commentary, 74
Index
181

Osborn waves, 96 ECG analysis, 154
questions, 153
Sick sinus syndrome, 112
P
Sinoatrial block, 90
Percutaneous coronary intervention (PCI), 18, 30, 42, answers, 48
64, 94 clinical scenario, 47
Pericarditis, 18, 64 commentary, 48
commentary, 106 Sinus arrest, 48
P mitrale, see Broad and bifid P waves (P mitrale) commentary, 90
Polymorphic ventricular tachycardia (VT) (torsades de ECG analysis, 90
pointes) questions, 89
answers, 150 Sinus arrhythmia
Premature atrial contractions (PACs), 8, 52 questions, 5
Premature ventricular contractions (PVCs), 22 Sinus bradycardia, 2, 48, 90, 96
Prinzmetal’s angina, see Coronary artery vasospasm answers, 12
(Prinzmetal’s angina) clinical scenario, 11
Prolonged QT interval, 150 commentary, 12
commentary, 132 Sinus node dysfunction (SND), 90
ECG analysis, 132 Sinus tachycardia, 58, 62, 70, 96, 136
Pulseless electrical activity (PEA) clinical scenario, 23
ECG analysis, 62 Sinus tachycardia with aberrant conduction
commentary, 136
R
ECG analysis, 136
Right bundle branch block (RBBB), 14, 70, 102, 136, 166 questions, 135
answers, 44 Skeletal muscle interference, see Electrical artefact
clinical scenario, 43 (skeletal muscle interference)
commentary, 44 ST segment elevation myocardial infarction (STEMI),
ECG analysis, 44 18, 42, 64, 94, 106
questions, 43 Supraventricular tachycardia (SVT), 102,
Romhilt–Estes scoring system, 80 136, 140
S T
Second-degree atrioventricular block (2:1 subtype) Third-degree atrioventricular block, 10, 144
182 Index

ECG analysis, 76 Ventricular (VVI) pacing with intermittent failure
questions, 75 to capture
Torsades de pointes, see Polymorphic ventricular answers, 156
tachycardia (VT) (torsades de pointes) clinical scenario, 155
Trifascicular block commentary, 156 – 157
commentary, 144 Ventricular premature beats (VPBs), 22
ECG analysis, 144 Ventricular premature complexes
questions, 143 (VPCs), 22
Ventricular tachycardia (VT), 22, 32, 136
answers, 102
U
Unstable angina (UA), 30, 42, 120 commentary, 102
ECG analysis, 102
monomorphic, 140
V
polymorphic, 150
Valsalva manoeuvre, 46, 66, 88 questions, 101
Ventricular bigeminy Ventricular tachycardia triggered by ventricular
answers, 100 ectopic beat
Ventricular ectopic beat (VEB), 32, 100 questions, 31
answers, 22
clinical scenario, 21 W
commentary, 22
ECG analysis, 22 Wenckebach phenomenon, see Mobitz type I
questions, 21 second-degree atrioventricular block
Ventricular extrasystoles, 22, 60 Wolff–Parkinson–White (WPW) ECG pattern, 46, 66,
Ventricular fibrillation (VF), 32, 96 72, 136, 162
Ventricular pacing, 54, 112, answers, 40
136, 152 clinical scenario, 39

Making Sense of the ECG

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MAKING SENSE OF

Making Sense of the Chest X-Ray: A Hands-on Guide

Making Sense of Clinical Teaching: A Hands-on Guide to Success

Making Sense of Fluids and Electrolytes: A Hands-on Guide

Making Sense of Lung Function Tests: A Hands-on Guide, 2E

Making Sense of Exercise Testing

Making Sense of Sleep Medicine: A Hands-on Guide

Making Sense of the EEG: From Basic Principles to Clinical Applications

Making Sense of the Pediatric EEG

Making Sense of the ECG: A Hands-on Guide, 6E

Making Sense of the ECG: Cases for Self Assessment, 3E

For more information about this series please visit: www.routledge.com/Making-Sense-of/book-series/

Third edition published 2025

and by CRC Press

CRC Press is an imprint of Taylor & Francis Group, LLC

© 2025 Andrew R Houghton

ISBN: 978-1-032-75057-6 (hbk)

Typeset in Minion Pro

Preface to the Third Edition xi

Case 60 145

Mookhter Ajij Lawrence Green V B S Naidu

Full Blood Count (FBC)

Urea and Electrolytes (U&E)

Past medical history Investigations

ECG ANALYSIS You can therefore count the number of QRS

Additional comments COMMENTARY

ECG ANALYSIS the medulla oblongata. One centre, the nucleus

ANSWERS • Sinus arrhythmia is of no pathological

ECG ANALYSIS atrial premature beats (APBs) or premature

COMMENTARY Further Reading

ECG ANALYSIS 60 years and around 6% of those over 60 years.

ECG ANALYSIS COMMENTARY

ECG ANALYSIS screen for structural heart disease. Risk stratify

ECG ANALYSIS COMMENTARY

ECG ANALYSIS more commonly causes right bundle branch

ECG ANALYSIS ventricular contractions (PVCs), are a common

COMMENTARY Further Reading

ECG ANALYSIS to slow an ‘appropriate’ sinus tachycardia can

QTc interval Normal (440 ms)

ECG ANALYSIS • There is a thromboembolic risk, and so con-

Additional comments COMMENTARY

ECG ANALYSIS COMMENTARY

ECG ANALYSIS peripheral perfusion, cardiac rhythm, neurolog-

ECG ANALYSIS there is a stronger indication for pacing, even if

ECG ANALYSIS • At higher potassium levels, the QRS com-

• In general, hyperkalaemia causes a sequence of 134.

ECG ANALYSIS atrial activity, as the refractory period of the

Additional comments COMMENTARY

ECG ANALYSIS ST segment elevation myocardial infarction

ECG ANALYSIS cardiomyopathy, atrial septal defect, Ebstein’s

ECG ANALYSIS options for orthodromic AVRT include beta-

P waves Inverted P waves after each

ECG ANALYSIS sinus node dysfunction should be withdrawn).

P waves Normal (when present)

ECG ANALYSIS COMMENTARY

ECG ANALYSIS 2. A pacemaker is not indicated. This is atrial tri-

Past medical history Investigations

ECG ANALYSIS • If the QRS complex is positive in leads I and

QRS duration Normal (90 ms)

ECG ANALYSIS concomitant prescribing with verapamil or amio-

Preface to the Third Edition xi

Case 60 145