Medical Student Survival Skills ECG 2020 @Pdf4Med
Medical Student Survival Skills ECG 2020 @Pdf4Med
Medical Student Survival Skills ECG 2020 @Pdf4Med
+ Medical Student
Survival Skills
ECG
AL GRAWANY
+ Medical Student
Survival Skills
ECG
Philip Jevon RN BSc(Hons) PGCE
Academy Manager/Tutor
Walsall Teaching Academy, Manor Hospital, Walsall, UK
Consulting Editors
AL GRAWANY
+ Contents
Preface vii
About the companion website ix
v
25 Recording a 12 lead ECG 65
26 What the standard 12 lead ECG records 71
27 Interpretation of a 12 lead ECG 75
28 ECG changes associated with myocardial infarction 81
29 ECG changes associated with myocardial ischaemia 87
30 ECG changes associated with bundle branch block 91
31 Wolff–Parkinson–White syndrome 97
vi
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+ Preface
A
n electrocardiogram (ECG) is a recording of electrical waveforms pro-
duced by the electrical activity of the heart. ECG monitoring is probably
one of the most valuable diagnostic tools in modern medicine. It is
essential if cardiac arrhythmias are to be identified. It can help with diagnosis
and can alert clinical staff to changes in the patient’s condition. ECG
monitoring must be meticulously undertaken. Potential consequences of poor
technique include misinterpretation of cardiac arrhythmias, mistaken diagno-
sis, wasted investigations, and mismanagement of the patient.
Philip Jevon
Jayant Gupta
vii
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About the
companion website
ix
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Introduction to ECG
1 monitoring
Sinoatrial node
Electrically inert
atrioventricular
Left
Right region
atrium
atrium
Left bundle
branch
Atrioventricular
node
Left Left anterior
m hemifascicle
ventricle
Left posterior
hemifascicle
Right bundle branch
Figure 1.1 Conduction system of the heart.
P T
QRS
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
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1
Chapter 1 Introduction to ECG monitoring
2
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Principles of ECG
2 monitoring
Indications
Indications for ECG monitoring include:
• Critical illness
• Acute coronary syndromes
• Cardiac arrhythmias
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
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3
Chapter 2 Principles of ECG monitoring
NB Flat line ECG trace: always check the patient first – cardiac
arrest?
4
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Chapter 2 Principles of ECG monitoring
Electrical interference
This is usually caused by electrical interference from devices by the bedside,
e.g. infusion pumps (Figure 2.5). Remove the source of the interference
if possible.
5
Chapter 2 Principles of ECG monitoring
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Chapter 2 Principles of ECG monitoring
ECG monitoring
✔✔ Explain procedure to patient
✔✔ Prepare skin prior to application of electrodes
✔✔ Select lead II on ECG monitor
✔✔ Interpret ECG following six stage approach
7
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Six stage approach
3 to ECG interpretation
QRS rate?
• Count the number of large squares between adjacent QRS complexes
and dividing it into 300, e.g. the QRS rate in Figure 1.3 is about 75 (300/4)
• If the QRS rhythm is obviously irregular count the number of QRS
complexes in a defined number of seconds and then calculate the rate per
minute. For example, if there are 10 QRS complexes in a 10 second strip,
then the ventricular rate is 60 bpm (10 × 6)
Classify QRS rate:
• Normal: 60–100
• Bradycardia: < 60
• Tachycardia: > 100
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
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9
Chapter 3 Six stage approach to ECG interpretation
P present?
Check if P waves are present: calculate the rate, regularity, and morphology
10
Chapter 3 Six stage approach to ECG interpretation
11
4 Sinus tachycardia
Causes
Causes include:
• Shock
• Heart failure
• Anxiety
• Medications
Effects on patient
• Usually no symptoms, although the patient may be ‘aware’ of a fast bound-
ing pulse
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
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13
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Chapter 4 Sinus tachycardia
Treatment
• Identify and where appropriate treat the underlying cause
• Rarely: a beta‐blocker such as atenolol to slow the heart (caution), e.g.
persistent tachycardia associated with myocardial infarction
14
5 Sinus bradycardia
Causes
Causes include:
• Acute myocardial infarction, particularly inferior myocardial infarction
• Raised intracranial pressure
• Medications, e.g. beta‐blockers
• Vagal stimulation
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
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15
Chapter 5 Sinus bradycardia
Effects on patient
• May lead to a fall in cardiac output: adverse signs could include hypoten-
sion, chest pain, lightheadiness, dizziness, nausea, syncope, and palor
• Note that there are normal physiological findings in some patients, e.g.
athletes
Treatment
• Treatment is indicated only if adverse signs are present and/or there is a
risk of asystole (see Resuscitation Council [UK] bradycardia algorithm in
Appendix A)
16
6 Sinus arrhythmia
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
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17
Chapter 6 Sinus arrhythmia
Effects on patient
• Patient asymptomatic
Treatment
• No treatment required
18
7 Atrial ectopic beats
Causes
Cause include:
• Cardiac stimulants, e.g. tobacco, caffeine, and alcohol
• Ischaemic heart disease
• Chronic obstructive pulmonary disease (CPOD)
• Electrolyte imbalance
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
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19
Chapter 7 Atrial ectopic beats
Effects on patient
• Usually asymptomatic
Treatment
• Atrial ectopics are benign and no treatment is necessary
• Attention to causes may be appropriate
20
8 Atrial tachycardia
• Ectopic focus in the atria rapidly depolarizing and overriding the normal
pacemaker function of the SA node
• Often preceded by atrial ectopics (see Chapter 7)
• Characterised by a sudden onset and an abrupt end
• Atrial rate is normally between 150 and 200 bpm
Causes
Causes include:
• Ischaemic heart disease
• Rheumatic heart disease
• Cardiomyopathy
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
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21
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Chapter 8 Atrial tachycardia
• P waves: rate between 150 and 200 bpm, may not be visible, may be
merged into preceding T waves; if visible, different morphology to sinus
P waves
• Relationship between P waves and QRS complexes: difficult to ascertain
relationship; PR interval often cannot be determined because P waves are
not clearly distinguishable; if there is AV block, P waves may not be
conducted to the ventricles (usually 2 : 1 AV block, i.e. every other P wave
is blocked)
Effects on patient
• May be associated with palpitations and/or haemodynamic compromise
due to the loss of effective atrial contractions and a rapid ventricular rate
Treatment
• ABCDE approach
• Follow narrow complex tachycardia algorithm (see Resuscitation Council
[UK] tachycardia algorithm in Appendix B)
22
9 Atrial flutter
(a)
(b)
Figure 9.1 (a) Atrial flutter with varying AV block. (b) Atrial flutter with 4 : 1 AV block.
Causes
• Nearly always associated with significant cardiac disease, e.g. mitral valve
disease
• Complicates 2–5% of acute myocardial infarctions
• Usually arises in the right atrium and often associated with diseases of the
right side of the heart, e.g. chronic obstructive pulmonary disease (COPD),
massive pulmonary embolism, and chronic congestive heart failure
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
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23
Chapter 9 Atrial flutter
Effects on patient
• Patient may complain of rapid palpitations
• Sometimes atrial flutter is associated with haemodynamic compromise
owing to the loss of effective atrial contractions and a rapid ventricular
rate
Treatment
• ABCDE
• Consider pharmacology intervention as class 1 (e.g. sotolol, flecainide, or
disopyramide) and class 3 (e.g. amiodarone) anti-arrhythmic drug therapy
can terminate the tachycardia
• Seriously consider the early use of synchronised DC cardioversion where
relatively low intensity shocks (e.g. 50 joules) often will effectively cardiovert
and restore a sinus rhythm (must anticoagulate patients prior to DC cardio-
version if flutter present more than 24–48 hrs. Offer longer term anticoagu-
lation if flutter persists if CHADS2VASc score is 1 or more)
• Seek expert advice at an early stage
24
Chapter 9 Atrial flutter
25
10 Atrial fibrillation
(a)
(b)
Figure 10.1 (a) Atrial fibrillation with a fast ventricular response. (b) Atrial fibrillation with a slow
ventricular response.
Causes
Causes of atrial fibrillation include:
• Valvular heart disease
• Ischaemic heart disease
• Thyrotoxicosis
• Pulmonary disease
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
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27
Chapter 10 Atrial fibrillation
Effects on patient
• Can be asymptomatic
• Loss of ‘atrial kick’ (atrial contraction) can result in a decrease in cardiac
output by 20–30%; this, together with a rapid ventricular response, can
lead to a fall in cardiac output of up to 50%
• Heart failure may develop, particularly if the patient has coexistent valvular
heart disease or impaired left ventricular function
• Symptoms may include palpitations, weakness, shortness of breath, chest
pain, feeling faint, and syncope
• If atrial fibrillation persists > 48 hours, stasis of blood in the fibrillating atria can
lead to clot formation, i.e. increased risk of systemic thromboembolism
28
Chapter 10 Atrial fibrillation
Treatment
• ABCDE
• Follow tachycardia algorithm (see Resuscitation Council [UK] tachycardia
algorithm in Appendix B)
• Take into account clinical setting in which atrial fibrillation occurs; any reme-
diable factors should be addressed if possible
• Treatment aimed at:
–– Slowing down the ventricular response
–– Converting it to sinus rhythm (if possible)
–– Reducing the frequency and haemodynamic effects of subsequent atrial
–– Fibrillation or preventing further episodes
–– Correcting any electrolyte imbalances
29
AV junctional
11 ectopics
Causes
Causes include:
• Cardiac stimulants, e.g. tobacco, caffeine, and alcohol
• Ischaemic heart disease
• Electrolyte imbalance
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
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31
Chapter 11 AV junctional ectopics
Effects on patient
• Patient is usually asymptomatic
Treatment
• Treatment is not usually required
• Any electrolyte imbalances should be corrected
32
AV junctional
12 escape rhythm
• Junctional escape rhythm is said to be present when there are six or more
consecutive junctional escape beats
• This is not a primary diagnosis, rather a symptom of an underlying primary
disturbance (SA node malfunction) to which it is secondary
• Inherent rate of AV junction is 40–60 bpm
Causes
• SA node failure (or malfunction) to initiate impulse
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
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33
Chapter 12 AV junctional escape rhythm
Effects on patient
• If the rhythm is sustained, patient may become haemodynamically com-
promised, as loss of ‘atrial kick’ will contribute to the fall in cardiac output
Treatment
• Junctional escape rhythm itself does not require treatment and should not
be suppressed by drugs
• Treatment is aimed at stimulating a higher pacemaker, e.g. atropine; pacing
may be required
• Cause of SA node failure should be sought, e.g. medications, myocardial
ischaemia/infarction. Any electrolyte imbalances should be corrected
34
Junctional
13 tachycardia
Causes
Causes include:
• Ischaemic heart disease
• AV junctional disease
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
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35
Chapter 13 Junctional tachycardia
Effects on patient
• Most will complain of palpitations
• Patient may become haemodynamically compromised. This is influenced
by the rate, duration of the episode, and underlying cardiac disease
Treatment
• ABCDE
• Follow the tachycardia algorithm (see Resuscitation Council [UK] tachycar-
dia algorithm in Appendix B)
• Vagal manoeuvres may slow or terminate junctional tachycardia
• Adenosine is usually first drug of choice
• If the patient is severely compromised and adverse signs are present or if
other treatments fail, synchronised electrical cardioversion is usually
undertaken
• Long‐term treatment may include radiofrequency ablation
• Any electrolyte imbalances should be corrected
36
14 Ventricular ectopics
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
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37
Chapter 14 Ventricular ectopics
38
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Chapter 14 Ventricular ectopics
Causes
Causes include:
• Ischaemic heart disease
• Acute myocardial infarction
• Electrolyte imbalances
• Heart failure
Effects on patient
• The patient is usually aware of the premature beat itself, of the subsequent
pause often described as a missed beat, or of a stronger post‐ectopic beat
• More noticeable at night when the patient is in a left lateral position
• Patient may be asymptomatic
• Can be associated with a significant fall in stroke volume and are often not
pulse‐producing; frequent ventricular ectopics can therefore have signifi-
cant haemodynamic effects on the patient
Treatment
• Anti‐arrhythmic therapy to suppress ventricular ectopics is no longer
recommended
• When associated with acute myocardial infarction: adequate pain relief and
effective treatment of heart failure
• Correction of any electrolyte imbalance
39
Idioventricular
15 rhythm
Causes
Causes include:
• Acute myocardial infarction
• Reperfusion following reperfusion therapy
• Drugs
• Electrolyte imbalance
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
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41
Chapter 15 Idioventricular rhythm
Effects on patient
• The patient may be haemodynamically compromised, particularly if the
rhythm is sustained or slow. The loss of ‘atrial kick’ will contribute to the fall
in cardiac output; however, it is rarely sustained
Treatment
• Not usually required
• If treatment is required (rhythm sustained and patient haemodynamically
compromised) it will be aimed at stimulating a higher pacemaker, e.g. atro-
pine to speed up the underlying rhythm
• It may be necessary to identify and treat the cause of SA node and AV junc-
tion failure
42
Ventricular
16 tachycardia
Monomorphic Polymorphic
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
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43
Chapter 16 Ventricular tachycardia
Causes
Causes include
• Ischaemic heart disease
• Myocardial infarction
• Cardiomyopathy
• Electrolyte imbalance
44
Chapter 16 Ventricular tachycardia
Effects on patient
• Ventricular tachycardia is a serious cardiac arrhythmia. The patient will
often be haemodynamically compromised. In some patients cardiac output
will be lost
• It can degenerate into ventricular fibrillation (see Chapter 22)
Treatment
• Patient pulseless: immediate defibrillation – follow Resuscitation Council
(UK) advanced life support (ALS) algorithm (see Appendix C)
• Patient has a pulse: ABCDE and follow the Resuscitation Council (UK)
tachycardia algorithm (see Appendix B)
• Chemical cardioversion is usually required for sustain VT
• Electrical cardioversion may be indicated (see Appendix E)
• Any electrolyte imbalances should be corrected if possible
Uncommon presentations
Board complex tachycardia can occasionally be a supraventricular
tachycardia conducted with aberration, i.e. not VT.
45
17 Torsades de pointes
Causes
Torsades de points is usually associated with a prolonged QT interval, causes
of which include:
• Anti‐arrhythmic drugs
• Bradycardia due to sick sinus syndrome or AV block
• Congenital prolongation of the QT interval, e.g. Romano–Ward syndrome
• Electrolyte imbalance, e.g. hypokalaemia and hypomagnesaemia
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
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47
Chapter 17 Torsades de pointes
Effects on patient
• May become haemodynamically compromised
• Sometimes may degenerate into ventricular fibrillation and cardiac arrest
Treatment
• Effective treatment, i.e. prevention of recurrent episodes, involves attention
to the presumed predisposing cause(s), e.g. stopping offending drug and
correction of any electrolyte imbalances
• Overdrive pacing may be effective
• Measures to speed up the sinus rate may be effective in some situations
48
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First degree AV
18 block
(a)
(b)
V2
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
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49
Chapter 18 First degree AV block
Causes
Causes include:
• Inferior myocardial infarction
• Ischaemic heart disease
• Electrolyte imbalance
• Medications, e.g. beta‐blockers
Effects on patient
• The patient will be asymptomatic
Treatment
• Requires no specific treatment, although drugs that can prolong AV con-
duction, e.g. beta‐blockers, will probably need to be avoided
50
Second degree AV
19 block Mobitz type I
(Wenckebach
phenomenon)
Causes
Causes include:
• Inferior myocardial infarction
• Electrolyte imbalance
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
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51
Chapter 19 Second degree AV block Mobitz type I
Effects on patient
• Usually asymptomatic
• If the ventricular rate is slow, then the patient could become haemodynami-
cally compromised (rare)
Treatment
• Treatment not usually required
• Avoid drugs that may potentiate the AV block, e.g. beta‐blockers
• Follow the Resuscitation Council (UK) bradycardia algorithm (see
Appendix A) if necessary
52
Second degree AV
20 block Mobitz type II
• There are two classifications of second degree AV block (see Chapter 19)
• There is intermittent failure of transmission of the atrial impulse to the
ventricles
• The number of dropped beats is variable
• It is less common than second degree AV block type I, but its implications
are significantly more serious
• Block is usually at the level of the bundle branches, commonly resulting
in a wide QRS complex
• It can suddenly progress to third degree (complete) AV block (see
Chapter 21) or even ventricular standstill (see Chapter 23)
• It is never a normal clinical finding
Causes
Causes include:
• Acute myocardial infarction, particularly anterior
• Drugs that suppress AV conduction, e.g. beta‐blockers, digoxin, and cal-
cium channel blockers
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
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53
Chapter 20 Second degree AV block Mobitz type II
Effects on patient
• The patient is often haemodynamically compromised
• Progression to ventricular standstill and cardiac arrest is not uncommon
Treatment
• Prophylactic temporary pacing is usually required
Uncommon presentations
Second degree AV block Mobitz type II is rare but always serious: expert
help should always be sought.
54
Third degree
21 (complete) AV block
(a)
(b)
Figure 21.1 Third degree (complete) AV block with a ventricular rate of (a) 50 bpm and (b) 35 bpm.
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
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55
Chapter 21 Third degree (complete) AV block
develop second degree AV block Mobitz type II or left bundle branch block.
The QRS complex is wide, signifying a ventricular escape rhythm, unrelia-
ble and slow
• It is a common clinical finding in elderly patients admitted with a history of
weakness, fatigue, ‘off legs’, syncope, etc. (typically in the preceding few
weeks) – routine 12 lead ECG confirms diagnosis (a permanent pacemaker
is the usual treatment)
• Rate and morphology of the escape rhythm is determined by the origin
of the ventricular escape rhythm: if the pacemaker site is situated in the
AV junction or proximal aspect of the bundle of His (more reliable), then
the ventricular rate will be between 40 and 50 bpm (sometimes more)
and the QRS width will be narrow; if the pacemaker site is in the distal
His–Purkinje fibres or ventricular myocardium (less reliable), then the
ventricular rate will be between 30 and 40 bpm (sometimes less) and the
QRS width will be wide – sudden ventricular standstill and cardiac arrest
is possible
Causes
Causes include:
• Acute myocardial infarction
• Fibrosis of bundle of His
• Endocarditis
• Drugs
56
Chapter 21 Third degree (complete) AV block
Effects on patient
• Some patients will have an adequate escape rhythm that will maintain their
blood pressure, while others will be compromised requiring urgent
intervention
• Generally the effects on the patient will depend on the cause: when associ-
ated with an anterior myocardial infarction, the patient is haemodynamically
compromised. The risk of ventricular standstill and sudden cardiac arrest is
high. If associated with an inferior myocardial infarction the patient may be
haemodynamically stable. If chronic, the patient may present with a history
of blackouts or falls
Treatment
• ABCDE approach
• Follow the Resuscitation Council (UK) bradycardia algorithm (see
Appendix A)
57
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22 Ventricular fibrillation
‘The cardiac pump is thrown out of gear, and the last of its vital energy
is dissipated in a violent and prolonged turmoil of fruitless activity in the
ventricular walls…’
(Source: McWilliam 1889)
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
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59
Chapter 22 Ventricular fibrillation
Causes
Causes include:
• Ischaemic heart disease
• Heart failure
• Electrolyte imbalance
• Cardiomyopathy
Effects on patient
• Cardiac arrest
Treatment
• Rapid defibrillation is the definite treatment; give prompt cardiopulmonary
resuscitation (CPR) while awaiting the defibrillator – follow the Resuscitation
Council (UK) advanced life support (ALS) algorithm (see Appendix C)
60
23 Ventricular standstill
Causes
Causes of ventricular standstill include:
• Existing second degree AV block Mobitz type II or third degree (complete)
AV block in the presence of acute anterior myocardial infarction
• Severe myocardial disease
• Drugs
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
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61
Chapter 23 Ventricular standstill
Effects on patient
• Cardiac arrest
Treatment
• Start cardiopulmonary resuscitation and follow the Resuscitation Council
(UK) advanced life support (ALS) algorithm (see Appendix C)
• Emergency external pacing may be indicated. If capture is achieved and a
pulse producing rhythm ensures, consider transvenous pacing
62
24 Asystole
Causes
Causes of asystole include:
• Myocardial disease
• Hypoxia
• Drugs
• Death
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
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63
Chapter 24 Asystole
Effects on patient
• Cardiac arrest
Treatment
• Start cardiopulmonary resuscitation (CPR) immediately – follow the
Resuscitation Council (UK) advanced life support (ALS) algorithm (see
Appendix C)
64
Recording a
25 12 lead ECG
Common indications
Common indications for recording a 12 lead ECG include:
• Chest pain
• Myocardial infarction
• Sometimes prior to a general anaesthetic
• Cardiac arrhythmias
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
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65
Chapter 25 Recording a 12 lead ECG
Procedure
A suggested procedure for recording a standard 12 lead ECG is:
• Identify the patient
• Explain the procedure to the patient
• Assemble the equipment, ensuring that the ECG cables are not twisted as
this can cause interference
• Ensure the environment is warm and the patient is as relaxed as possible.
This will help produce a clear, stable trace without interference
• Ensure the patient is lying down in a comfortable position, ideally resting
against a pillow at an angle of 45° with the head well supported (an identi-
cal patient position should be adopted as with previous 12 lead ECGs as
this will help ensure standardisation). The inner aspects of the wrists should
be close to, but not touching, the patient’s waist
• Prepare the skin if necessary. If wet gel electrodes are used, shaving and
abrading the skin is not required. If solid gel electrodes are used, clean/
degrease and debrade the skin and shave if necessary
• Apply the electrodes and the limb leads:
–– Red to the inner right wrist
–– Yellow to the inner left wrist
–– Black to the inner right leg, just above the ankle
–– Green to the inner left leg, just above the ankle
• Apply the electrodes to the chest (Figure 25.1) and attach the chest leads:
–– V1 (white/red lead): 4th intercostal space, just to the right of sternum
–– V2 (white/yellow lead): 4th intercostal space, just to the left of sternum
–– V3 (white/green lead): midway between V2 and V4
–– V4 (white/brown lead): 5th intercostal space, mid‐clavicular line
–– V5 (white/black lead): on anterior axillary line, on the same horizontal
line as V4
–– V6 (white/violet lead): mid‐axillary line, on the same horizontal line as
V4 and V5
• Check the calibration signal on the ECG machine to ensure
standardisation
• Ask the patient to lie still and breathe normally
• Print out the ECG following the manufacturer’s recommendations
• Once an adequate 12 lead ECG has been recorded, disconnect the patient
from the ECG machine and clear equipment away and clean as necessary
following the manufacturer’s recommendations. Sometimes electrodes are
left on the patient if serial recordings are going to be required
66
Chapter 25 Recording a 12 lead ECG
V1 V2
V3
V6
V4 V5
• Ensure the ECG is correctly labelled. Report and store the ECG in the
correct patient’s notes following local procedures
67
Chapter 25 Recording a 12 lead ECG
Standardisation
• To help in the comparison of serial 12 lead ECGs, they should be recorded
with the patient in the same position. If this is not possible, e.g. if the patient
has orthopnoea, a note to this effect should be made because the electrical
axis of the heart (main direct of current flow) can be altered which makes
reviewing and comparing serial ECGs difficult
• Standard calibration is 1 mV vertical deflection on the ECG (Figure 25.2)
• Standard paper speed is 25 mm s−1
68
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Chapter 25 Recording a 12 lead ECG
69
What the standard
26 12 lead ECG records
Limb leads
• If leads are attached to the patient’s right arm, left arm, and left foot, the
three major planes for detecting electrical activity can be recorded (a fourth
lead, attached to the right leg serves as a neutral electrode and is not used
for recording)
• A hypothetical triangle (Einthoven’s triangle) is formed by these three axes,
with the heart in the middle (Figure 26.1)
• These three different views of the heart are designated standard leads I, II,
and III and each records the difference in electrical forces between the two
lead sites, hence the term bipolar leads. This electrode placement also
permits recording from three unipolar leads: aVR, aVL, and aVF
Chest leads
• The six chest leads view the heart in a horizontal plane from the front (ante-
rior) and from the side (lateral)
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Chapter 26 What the standard 12 lead ECG records
Frontal plane
Bipolar leads
Right Left
I
Einthoven’s
triangle II III
Electrode
+ aVL
aVR
+
I
+ +
+
III
II
aVF
Figure 26.1 Einthoven’s triangle.
72
Chapter 26 What the standard 12 lead ECG records
aVR aVL
V6
V5
V1 V2 V3 V4
III aVF II
Figure 26.2 Limb and chest leads and their relation to the surface of the heart.
73
Interpretation
27 of a 12 lead ECG
P waves
• Polarity: usually upright leads II, III, aVF
• Amplitude: not > 0.3 mV (3 small squares)
• Width: not > 0.11 seconds (2.75 small squares)
• Shape: round, not notched or pointed
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Chapter 27 Interpretation of a 12 lead ECG
PR interval
• Normal: 0.12–0.20 seconds (3–5 small squares)
• PR interval > 0.20seconds (> 5 small squares): first degree AV block
• PR interval < 0.12 seconds (< 3 small squares): AV junctional pacemaker or
accessory pathway, e.g. bundle of Kent in Wolff–Parkinson–White syndrome
QRS rate
• Normal: 60–100 bpm
• QRS rate < 60 bpm: bradycardia
• QRS rate > 100 bpm: tachycardia
QRS rhythm
• Irregular QRS rhythm: many causes including sinus arrhythmia, atrial fibril-
lation, extrasystoles, and AV block
QRS complexes
• Q wave: if first deflection QRS is negative
• R wave: first positive deflection
• S wave: negative deflection following R wave
• R1: if second positive deflection
• S1: if second negative deflection
• Normal width: < 0.12 seconds or 3 small squares; QRS width 0.12 seconds
or 3 small squares or greater indicates abnormal intraventricular c
onduction
(bundle branch block or ventricular arrhythmia)
Broad complex tachycardia is likely to be ventricular in origin if:
• R or qR (rabbit ear) in V1
• rS or QS in V6
• QRS complexes in V1–V6 are all either positive or negative
• Extreme axis deviation (–90° to ±180°) – positive aVR
• QRS complex > 0.14 seconds or 3.5 small squares
• Presence of fusion beats and/or capture beats
• AV dissociation
Broad complex tachycardia is likely to be supraventricular in origin if:
• rsR morphology in V1
• qRs morphology in V6
76
Chapter 27 Interpretation of a 12 lead ECG
Q waves
Small narrow Q waves (< 0.04 seconds or 1 small square wide and < 0.2 mV or
2 small squares deep) are normal in leads facing the left ventricle, i.e. I, aVL,
aVF, V5, and V6.
Wide (> 0.04 seconds or 1 small square) and deep (> 0.2 mV or 2 small
squares) Q waves indicate previous myocardial infarction.
T waves
• Polarity: upright in leads I, II, and V3–V6, inverted in aVR; variable in the
other leads. Inverted T waves can be associated with myocardial ischae-
mia, digoxin toxicity, or ventricular hypertrophy
• Morphology: normally slightly rounded and asymmetrical. Sharply pointed
T waves suggest myocardial infarction or hyperkalaemia. Notched T waves
may be associated with pericarditis. In myocardial ischaemia T waves can
be tall, flattened, inverted, or biphasic. In left ventricular hypertrophy,
T waves are inverted in the left ventricular leads, i.e. leads II, aVL, V5, and
V6 in right ventricular hypertrophy, T waves are inverted in the right
ventricular leads, i.e. V2 and V3
• Height: not > 0.5 mV (5 small squares) in the limb leads or not > 1.0 mV
(10 small squares) in the chest leads
77
Chapter 27 Interpretation of a 12 lead ECG
ST segment
• Isoelectric: normal
• Elevation > 0.1 mV (1 small square) in limb leads and/or > 0.2 mV (2 small
squares) in the chest leads: usually indicates myocardial infarction
• Widespread concave ST segment elevation: characteristic of pericarditis
• ST segment elevation can be normal in healthy young black men
• Depression > 0.5 mV (0.5 small squares): abnormal; horizontal depression
of the ST segment and upright T wave usually indicates myocardial
ischaemia
• ST segment down‐sloping or sagging (particularly noticeable in leads II and
III): suggests digoxin toxicity
QT interval
• Normal QT interval is usually less than half of the preceding RR interval;
upper limit of normal is 0.40 seconds or 2 large squares
• Prolonged QT interval can lead to the development of tachyarrhythmias
• Causes of a prolonged QT interval: hereditary, drugs, hypothermia, and
electrolyte abnormality
U waves
• Low voltage waves sometimes seen following the T waves
• Best seen in V3, share the same polarity as the T waves, and are usually
more evident in hypokalaemia
78
AL GRAWANY
Chapter 27 Interpretation of a 12 lead ECG
–120° –60°
–150° –30°
aVR aVL
180° 0°
I
150° 30°
120° 60°
III II
90°
aVF
(b)
I aVR
II aVL
III aVF
Figure 27.1 (a) Determining cardiac access using the hexaxial diagram. (b) Normal ECG axis.
79
Chapter 27 Interpretation of a 12 lead ECG
• Normal axis is between 0° and +90°, left axis deviation is between 0° and
–90°, and right axis deviation is between +90° and +180°
• Predominantly positive QRS in leads I and II: normal axis
• Predominantly positive QRS in lead I and predominantly negative QRS
in lead II (the QRS complexes have ‘left’ each other): left axis deviation
• Predominantly negative QRS in lead I and predominantly positive QRS
in lead II (QRS complexes are ‘right’ for each other): right axis deviation
• Causes of left axis deviation include left bundle branch block, left anterior
fasicular block, and ventricular arrhythmias
• Causes of right axis deviation include right bundle branch block, left
posterior fasicular block, and ventricular arrhythmias
Previous ECGs
• Compare with patient’s previous ECGs; sequential ECGs in acute coronary
syndrome can sometimes be particularly helpful in making a diagnosis
80
ECG changes
28 associated with
myocardial infarction
Degrees of ST
segment elevation
Figure 28.3 Degree of ST segment elevation.
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Chapter 28 ECG changes associated with myocardial infarction
Reciprocal changes
• ST depression in leads remote from the site of the infarct are referred to as
reciprocal changes. They are a highly sensitive indicator of acute myocardial
infarction. They may be seen in leads that do not directly view the affected
82
Chapter 28 ECG changes associated with myocardial infarction
83
Chapter 28 ECG changes associated with myocardial infarction
• The ECG in Figure 28.7 displays the characteristic ECG changes associ-
ated with inferior myocardial infarction. There is ST elevation in the inferior
leads (II, III, aVF). However, the T waves in these leads are beginning to
become negative. This, with the development of Q waves in the inferior
leads, is suggestive that the infarct is not acute. This patient was admitted
with a 24 hour history of central chest pain
• The ECG in Figure 28.8 displays the characteristic ECG changes associ-
ated with posterior myocardial infarction. Tall R waves and reciprocal
changes in anterior leads V1 and V2 and reciprocal changes in anterior
leads I and aVL suggest this diagnosis. Posterior wall chest leads would be
required to help confirm diagnosis of posterior myocardial infarction
84
Chapter 28 ECG changes associated with myocardial infarction
• The ECG in Figure 28.9 displays the characteristic ECG changes associ-
ated with anteroseptal or septal myocardial infarction. There is ST elevation
in leads aVL and V1–V4. In addition there is right bundle branch block and
left anterior fascicular block (bifascicular block), a complication of septal
infarction. Regarding the right bundle branch block, the familiar rSR mor-
phology has been replaced with QR morphology due to the infarction
• The ECG in Figure 28.10 displays the characteristic ECG changes associ-
ated with anterior myocardial infarction. The ST changes in the anterior
leads (I, aVL, V2–V6) are hyperacute. This patient was admitted with a
1 hour history of chest pain
85
ECG changes
29 associated with
myocardial ischaemia
ST segment depression
• Myocardial ischaemia typically causes ST segment depression (Figure 29.1).
In any given lead, the degree of ST segment depression is proportional to
the size of the R wave, i.e. it is more prominent in leads V4–V6
• ECG changes associated with myocardial ischaemia (Figure 29.2): ST
depression in the inferior (II, III, and aVL), and lateral (V4–V6) leads. This
patient was complaining of severe chest pain when the 12 lead ECG
was recorded
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Figure 29.1 Anterolateral ischaemia.
AL GRAWANY
Figure 29.2 Inferolateral ischaemia.
Chapter 29 ECG changes associated with myocardial ischaemia
T wave changes
T wave changes associated with myocardial ischaemia can present in a variety
of different ways:
• Tall T waves: in leads V1–V3 may be due to posterior wall myocardial
ischaemia (mirror image of T wave inversion)
• Biphasic T waves: particular seen in the anterior chest leads
• Inverted T waves (NB T waves are normally inverted in leads III, aVR,
and V1)
• Flattened T waves
90
ECG changes
30 associated with
bundle branch block
Figure 30.1 Left bundle branch block. The QRS width is 0.16 seconds or 4 small squares. The
W‐shaped morphology of the QRS complex in V1 and the M‐shaped morphology of the QRS
complex in V6 can be seen clearly.
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Chapter 30 ECG changes associated with bundle branch block
92
Chapter 30 ECG changes associated with bundle branch block
Figure 30.2 Right bundle branch block. The QRS width is 0.12 seconds or 3 small squares. The rSR
W‐shaped morphology of the QRS complex in V1 and the M‐shaped morphology of the QRS
complex in V6 can be seen clearly.
93
Chapter 30 ECG changes associated with bundle branch block
94
Chapter 30 ECG changes associated with bundle branch block
95
Wolff–Parkinson–
31 White syndrome
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Chapter 31 Wolff–Parkinson–White syndrome
Classification
The WPW syndrome is traditionally classified into two types (A and B)
according to the ECG morphology of in leads V1 and V2.
• Type A: left‐sided pathway resulting in a predominant R wave
• Type B: right‐sided pathway resulting in a predominant S or QS wave
Complications
• The frequency of paroxysmal tachycardia associated with WPW syndrome
increases with age
• If atrial fibrillation is present the ventricular response depends on the ante-
grade refractory period of the accessory pathway and may exceed
300 min−1, resulting in ventricular fibrillation and cardiac arrest
Treatment
• Patients who are symptomatic (palpitations or syncope) should be referred
for electrophysiology studies
• Catheter ablation has a high success rate
• Drugs that block the AV junction, e.g. digoxin, verapamil, and adenosine,
are particularly dangerous in WPW syndrome in the presence of atrial
fibrillation and should be avoided (they decrease the refractoriness of the
accessory pathways and increase the frequency of conduction, resulting in
a rapid ventricular response that may lead to ventricular fibrillation)
98
AL GRAWANY
Appendix A: Resuscitation
council (UK) bradycardia
algorithm
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99
Appendix A Resuscitation council (UK) bradycardia algorithm
2010 Resuscitation
Guidelines
Adverse features?
YES • Shock NO
• Syncope
• Myocardial ischaemia
• Heart failure
Atropine
500 mcg IV
Satisfactory YES
response?
NO
* Alternatives include:
• Aminophylline
• Dopamine
• Glucagon (if beta-blocker or calcium channel blocker overdose)
• Glycopyrrolate can be used instead of atropine
100
Appendix B: Resuscitation
council (UK) tachycardia
algorithm
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2010 Resuscitation
Guidelines
Adverse features?
Synchronised DC Shock Yes / Unstable • Shock
Up to 3 attempts • Syncope
• Myocardial ischaemia
• Heart failure
• Amiodarone 300 mg IV over 10-20 min
and repeat shock; followed by: No / Stable
• Amiodarone 900 mg over 24 h
Broad Is QRS narrow (< 0.12 s)? Narrow
!
Seek expert help Probable atrial fibrillation
if unsuccessful give further 12 mg.
• Monitor ECG continuously Control rate with:
• β-Blocker or diltiazem
• Consider digoxin or amiodarone
Sinus rhythm restored? if evidence of heart failure
102
Appendix C: Resuscitation
council (UK) advanced life
support (ALS) algorithm
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103
Appendix C Resuscitation council (UK) ALS algorithm
2010 Resuscitation
Guidelines
Unresponsive?
Not breathing or
only occasional gasps
Call
resuscitation team
CPR 30:2
Attach defibrillator / monitor
Minimise interruptions
Assess
rhythm
Shockable Non-Shockable
(VF / Pulseless VT) (PEA / Asystole)
Return of
1 Shock spontaneous
circulation
104
Appendix D: Vagal
manoeuvres
• Valsalva manoeuvre: forced expiration against a closed glottis, e.g. ask the
patient to blow into a 20 ml syringe with enough force to push the plunger
back
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Appendix E: Synchronised
electrical cardioversion
Shock energies
• Follow local protocols
• Broad complex tachycardia and atrial fibrillation: 120–150 J biphasic (200 J
monophasic) is recommended initially
• Regular narrow complex tachycardia or atrial flutter: 70–120 J biphasic
(100 J monophasic) is recommended initially
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Appendix E Synchronised electrical cardioversion
Procedure
• Record a 12 lead ECG, unless the patient is severely compromised and
doing so will delay the procedure
• Explain the procedure to the patient. Consent should be obtained if possi-
ble. If the patient is not unconscious, they must be anaesthetised or
sedated for the procedure
• Ensure the resuscitation equipment is immediately available
• Establish ECG monitoring using the defibrillator that will be used for
cardioversion
• Select an ECG monitoring lead that will provide a clear ECG trace, e.g. lead II
• Press the ‘synch’ button on the defibrillator
• Check the ECG trace to ensure that only the R waves are being synchro-
nised, i.e. a ‘synchronised’ dot or arrow should appear on each R wave
and nowhere else on the PQRST cycle, e.g. on tall T waves
• Prepare the chest: dry it and shave if necessary
• Apply large adhesive electrodes to the patient’s chest, one just to the right
of the sternum, below the right clavicle, and the other in the mid‐axillary
line, approximately level with the V6 ECG electrode or female breast
• Select the appropriate energy level on the defibrillator (see earlier for
recommended levels)
• Charge the defibrillator and shout ‘stand clear’
• Check all personnel are safely clear prior to defibrillation. No person should
be touching the patient or anything in contact with the patient, e.g. bed,
drip stand
• Ensure oxygen is remove at least 1 m away from the patient
• Check the ECG monitor to ensure that the patient is still in the tachyarrhyth-
mia that requires cardioversion, that the synchronised button remains
activated and that it is still synchronising with the R waves
• Press shock button to discharge the shock. There is usually a slight delay
between pressing the shock button and shock discharge
• Re‐assess the ECG trace. The ‘synch’ button will usually need to be reac-
tivated if further cardioversion is required (on some defibrillators it is neces-
sary to actually switch off the ‘synch’ button if further cardioversion is not
indicated). Stepwise increases in energy will be required if cardioversion
needs to be repeated
• After successful cardioversion, record a 12 lead ECG
• Monitor the patient’s vital signs until they have fully recovered from the
anaesthetic or sedative
108
Appendix E Synchronised electrical cardioversion
109
Appendix F: External
(transcutaneous) pacing
Indications
• Profound bradycardia, e.g. sometimes found in complete heart block, that
has not responded to pharmacological treatment, e.g. atropine
Advantages
• Can be quickly established
• Easy to undertake, minimal training
• Risks associated with central venous cannulation are avoided
• Can be undertaken by nurses
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111
Appendix G: Procedure
for transcutaneous pacing
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113
Appendix G Procedure for transcutaneous pacing
• Check the patient’s pulse. If they have a palpable pulse (mechanical cap-
ture), request expert help and prepare for transvenous pacing. If there is no
pulse, start CPR. If there is good electrical capture, but no mechanical
capture, this is indicative of a non‐viable myocardium. Note that there is no
electrical hazard if in contact with the patient during pacing
114
Appendix H: Definitions
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115
References
Fuster, V., Rydén, L.E., Cannom, D.S. et al. (2006). ACC/AHA/ESC 2006 guidelines for
the management of patients with atrial fibrillation: A report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines and the
European Society of Cardiology Committee for Practice Guidelines (Writing
Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial
Fibrillation): Developed in collaboration with the European Heart Rhythm Association
and the Heart Rhythm Society. Circulation 114: e257–e354.
Resuscitation Council (UK) (2018). Adult Advanced Life Support. London: Resuscitation
Council (UK) www.resus.org.uk (accessed November 2018.
McWilliam, J. (1889). Electrical stimulation of the heart in man. BMJ; 1: 348.
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/jevon/medicalstudent
117
Index
Medical Student Survival Skills: ECG, First Edition. Philip Jevon and Jayant Gupta.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
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119
Index
120
Index
121
Index
122
Index
123
Index
124
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