INVESTIGATIONS
The electrocardiogram
Patrick Davey
David Sharman
Abstract
This article describes the features that should be looked at on a 12-
lead electrocardiogram to determine whether or not it is normal. It de-
scribes the abnormalities found in certain conditions, including atrial
enlargement, ventricular hypertrophy, acute chest pain, ST elevation
myocardial infarction and syncope, with many illustrations.
Keywords Atrial enlargement; Brugada syndrome; cardiovascular
disorders; diagnosis; ECG; MRCP; ST elevation myocardial infarction;
syncope; ventricular hypertrophy
The normal electrocardiogram (ECG)
It is important to determine confidently whether an ECG is
normal, according to the following parameters (Figure 1):

The P wave is 110 ms or less, and 0.25 mV or less; the first
two-thirds of the P wave come from right atrial depolari-
zation and the last two-thirds from left atrial depolariza-
tion. In health, the P wave is upright in lead II and biphasic
in lead V1; the first, positive, deflection is larger than the
second, negative, one.

The PR interval is 140e210 ms. A short PR interval may
indicate an accessory pathway, which allows early ven-
tricular depolarization (pre-excitation). A long PR interval
reflects slow conduction through the atrioventricular (AV)
node and bundle of His, and can indicate disease of the
conduction tissue predisposing to bradyarrhythmia
through high-grade AV block.

The QRS axis is normal from 30 to þ90 (Figure 2). The
QRS complexes in leads I and II are ‘positive’ (R wave > S
wave), and the QRS in lead III is ‘negative’ (S wave > R
wave). Axis deviation implies either ventricular hypertro-
phy or disease of one of the left bundle hemifascicles (left
axis deviation indicates left anterior hemifascicular block,
right axis deviation indicates posterior hemifascicular
block).

The QRS amplitude, when large, implies thin stature or
ventricular hypertrophy. When small, it implies obesity,
hypothyroidism, pericardial effusion or diffuse loss of
myocytes as a result of ischaemic heart disease or
cardiomyopathy.
Patrick Davey DM FRCP is a Consultant Cardiologist at Northampton
General Hospital, Northampton, UK and the John Radcliffe Hospital,
Oxford, UK. His interests include heart failure and interventional and
nuclear cardiology. Competing interests: none declared.
David Sharman MB ChB BSc MRCP is a Consultant Cardiologist and
Lead for Cardiac Rhythm Management at Northampton General
Hospital, Northampton, UK. Competing interests: none declared.
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Key points
C The ability to interpret an electrocardiogram (ECG) accurately
and objectively is an important skill in cardiology
C The recognition of well-defined patterns is the key to safe ECG
interpretation

The QRS duration is 120 ms or less. A broad QRS usually
reflects disease of the right, the left or both bundle
branches.
The R wave and S wave
The R wave exhibits normal progression in the chest leads. Its
height increases from lead V1 to about V5, and then declines.
The S wave increases (becomes deeper) from lead V1 to V2
(sometimes V3), and then declines. The ‘transition point’ (where
the R wave equals the S wave) is usually seen in lead V3, and
reflects the position of the interventricular septum. The transition
point can be moved towards lead V2 in health (clockwise rota-
tion) or towards lead V4 in obesity (anticlockwise rotation).
‘Poor R wave progression’ (little/no increase in R wave height
until lead V4) may indicate an old anterior wall myocardial
infarction.
Non-pathological Q waves
Small Q waves (two small squares or less in amplitude) are seen
in lead III (varying with respiration) and laterally in the chest
leads, reflecting left-to-right septal depolarization. A large Q
wave is seen in lead aVR (as aVR examines the endocardial
surface of the heart, it registers the endocardial-to-epicardial
spread of depolarization as a Q wave).
The ST segment
The ST segment is isoelectric. ‘Physiological’ ST elevation is
usually restricted to leads V1eV3/V4.
T wave polarity reflects whether the R or S wave is dominant;
if R is greater than S, the T wave is upright, and vice versa. Thus,
the T wave is normally inverted in leads III, aVF, aVR and V1,
and upright elsewhere.
The QT interval
To determine whether the QT interval is abnormal, it is impor-
tant to correct for heart rate, as the normal physiological
response to increasing heart rate is for the QT interval to shorten.
To remove the confounding factor of heart rate, some form of
heart rate correction formula is needed so that the dependence of
the normal QT interval on heart rate is removed. Fridericia’s
correction (QTc ¼ 3O(QT/RR interval)), where RR interval is the
interval between QRS complexes measured in seconds (RR in-
terval relates to heart rate by the formula heart rate ¼ 60/RR
interval) is the ‘best’ heart rate correction formula. All such
formulae are, however, scientifically unsound, because they fail
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 INVESTIGATIONS
Figure 1 Normal ECG. This is the typical printout with the 12 leads running sequentially in the top three lines. The bottom line is the rhythm strip in
this case lead II, But it can be changed to other leads as required.
Determining the QRS axis
Step 1
Lead I
Step 4
Step 2 Step 3
Lead aVF
To determine the overall QRS vector, obtain the net
difference between the size of the lead R and S wave
in I and aVF (i.e. R–S in mV); then plot this to obtain the
overall vector (step 3 – positive numbers plotted
rightwards and upwards, and vice versa) that can be
measured (step 4) to give the QRS axis. Other leads can
be used if these complexes are too small – it is best to
choose leads at right angles to each other (e.g. lead aVL
and lead II).
Source: P Davey. ECG at a glance. Oxford Wiley-Blackwell,
2008.
Figure 2
to allow for individual QTeheart rate variation with day/night,
health/disease and many drugs.
Right and left atrial enlargement
The ECG is unreliable in the diagnosis of atrial enlargement. The
classic signs are as follows (Figure 3). In right atrial enlargement,
the P wave height in lead II increases to two and a half small
squares or more. In left atrial enlargement, the P wave is domi-
nated by the late, long, left atrial depolarization. This leads to a
late second peak in lead II, and a late negative deflection in lead
V1 greater than the early positive deflection. V1 is more sensitive
than lead II to left atrial enlargement.
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Right and left ventricular hypertrophy
Right ventricular hypertrophy (RVH)
The ECG is poor at diagnosing RVH/pulmonary hypertension
(Figure 4).

The earliest sign is a rightwards shift in the QRS axis,
followed by an increase in the size of the V1 R wave.

Subsequently, the V1 R wave becomes larger than the S
wave (i.e. dominant) (Table 1).

The T waves in leads V1eV3 invert (‘RV strain’).

Finally, right bundle branch block can occur, particularly
in acute right heart strain associated with pulmonary
embolism.
Left ventricular hypertrophy (LVH)

Initially, the R wave height increases in the left-sided
standard and chest leads (I, II, aVL and V4eV6), often
with commensurate deepening of the S wave in leads V2
and V3.

The small ‘septal’ Q waves in lead V5/V6 increase in size
with increasing hypertrophy.

As LVH increases, the QRS axis shifts to the left, and the
lateral-lead T waves flatten and then invert (‘strain’,
associated with a worse prognosis in hypertension).

Finally, the QRS broadens, with the development of com-
plete left bundle branch block.
It is not possible to define a QRS complex size that differentiates
normal from LVH. High limits are reliable, but miss most cases;
low limits catch many cases, but include many normal subjects.
Various scoring systems have been proposed (Table 2).
Acute chest pain
Acute coronary syndromes (ACSs) result from partial or complete
thrombotic occlusion of a coronary artery. The distribution of
ECG changes reflects which coronary artery is occluded (Table 3).
These changes include:

T wave flattening

T wave inversion (Figure 5)

ST depression (Figure 6; associated with as poor an
outlook as ST elevation)

occasionally, episodes of dynamic ST elevation.
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 INVESTIGATIONS
P wave changes in atrial enlargement
Lead II Lead VI
Normal
RAE
LAE
RAE + LAE
In right atrial enlargement (RAE), the P wave is dominated
by the wave of depolarization passing through the enlarged
right atrium; this passes towards both lead I and V1 and,
two-thirds of the P wave, changes in RAE are
the P wave. In left atrial enlargement (LAE), the P wave
is dominated by the wave of depolarization passing
through the enlarged left atrium; this is towards lead I
but away from lead V1. As the normal left atrium
depolarization occupies the latter two-thirds of the
P wave, abnormalities are found in this phase of the
P wave.
Figure 3 Source: Marriot’s practical electrocardiography, 10th edn.
Philadelphia: Lippincott Williams & Wilkins, 2001.
Deep T wave inversion throughout the anterior chest leads
usually relates to a high-grade lesion in the proximal left anterior
descending (LAD) artery; this is termed a ‘proximal LAD pattern’
or LAD syndrome ECG. Generally, the greater and more dynamic
the ECG changes, the worse the prognosis; however, the ECG is
only one of several variables that determine the outcome. The so-
called proximal LAD pattern ECG, like almost all ECGs, has a
differential diagnosis, and this includes Takotsubo cardiomyop-
athy, and sometimes also pulmonary embolism.
A normal ECG after many hours of continuous chest pain
suggests that the pain is non-cardiac, or that the territory is
Figure 4 ECG of pulmonary hypertension. The P-wave is tall in lead II, The QRS axis is shifted to the right, The R-wave in Leeds V1 is dominant,
and there is T-wave inversion in Leeds V1 to V3.
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electrically silent, i.e. it involves the circumflex artery and the
posterior wall (often, the only sign of ischaemia here is an up-
right, instead of inverted, T wave in lead V1).
ST elevation myocardial infarction (STEMI) is caused by
thrombotic coronary artery occlusion. There is a characteristic
sequence of ECG changes (Figure 7) in the distribution of the
affected artery. Posterior wall STEMI presents with ST depression
in leads V1eV3 (these leads examine the posterior wall from its
endocardial surface). This can be difficult to distinguish acutely
from LAD-territory ischaemia (as, chronically, posterior wall
infarction produces a dominant R wave in lead V1); the presence
of inferior lead ST elevation suggests that the diagnosis is infero-
posterior infarction (Figure 8). If this is not present, prolonged
pain with autonomic upset suggests posterior infarction rather
than LAD-territory ischaemia. Echocardiography can reliably
differentiate these two conditions.
Pericarditis often produces no ECG changes. In a few cases, ST
elevation occurs as a consequence of subepicardial myocardial
inflammation (Figure 9). Pericarditis can be distinguished from
STEMI by:

the shape of the ST elevation (concave upwards in peri-
carditis, convex upwards in STEMI)

the distribution of the ECG changes (in STEMI, changes are
restricted to the territory of a coronary artery; they can be
more extensive in pericarditis, but the patient remains
well)

echocardiography.
Pulmonary embolism usually causes no ECG changes beyond
sinus tachycardia. However, the ECG signs of acute right heart
strain may appear in patients with a large pulmonary embolism
(right axis deviation (S1Q3T3) and right bundle branch block).
Syncope
In the inter-attack evaluation of syncope (brief-duration loss of
consciousness with loss of postural tone), it is important to distin-
guish benign conditions from more dangerous forms that could lead
to premature death. The history (adverse family history, injury, no
warning) and examination (aortic stenosis, hypertrophic cardio-
myopathy, heart failure) can help, as can the ECG. Vasomotor
syncope is usually associated with a normal inter-attack 12-lead
ECG. Tilt-table testing may induce bradycardia/hypotension.
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Causes of a dominant R wave in lead V1 ECG criteria for diagnosing left ventricular hypertrophy
Cause Incidence QRS Associated ECG features RomhilteEstes criteria
width C Voltage criterion: R or S in any limb lead 3 points
>0.20 mV or S in lead V1
Right bundle Very Broad Long PR interval; right or C Left ventricular strain: ST segment and T

branch block common left axis deviation wave in opposite direction to QRS complex
indicates e Without digitalis 3 points
disease also of the left e With digitalis 1 point
bundle C Left atrial enlargement: terminal negativity 3 points
Posterior wall Common Narrow Sometimes inferior lead of the P wave in lead V1 >0.10 mV in depth
myocardial Q waves and 40 ms in duration
infarction C Axis shift: left axis deviation greater than 2 points
RVH Rare Narrow Right axis deviation, 30
right C QRS duration: >90 ms 1 point
atrial enlargement C Intrinsicoid deflection in lead V5 or V6 1 point
WolffeParkinsone Rare Broad Short PR interval >50 ms
White syndrome Maximum possible score 13 points
Skeletal myopathy Very rare Narrow Diffusely abnormal ECG 4 points ¼ probable LVH
(e.g. Friedreich’s 5 points ¼ definite LVH
ataxia) SokoloweLyon criteria
C S wave in lead V1 þ R wave in lead V5 or V6 >3.50 mV, or R wave
Table 1
in lead V5 or V6 >2.60 mV
Cornell sex-specific voltage criteria
Syncope resulting from ventricular outflow C Women: R wave in lead aVL þ S wave in lead V3 >2.00 mV

obstruction C Men: R wave in lead aVL þ S wave in lead V3 >2.80 mV

The ECG shows LVH (aortic stenosis, hypertrophic cardiomy- Cornell voltageeQRS duration product criteria
opathy) or RVH (pulmonary hypertension). C See Buchner et al., http://www.jcmr-online.com/content/11/1/18/

table/T1
Syncopal ventricular tachycardia (VT) GubnereUngerleider criteria
The diagnosis is straightforward if the patient arrives at hospital C R wave in lead I plus S wave in lead III >2.5 mV

in VT (see below). Problems arise if the VT stops before admis- Minnesota code 3e1
sion, or if the patient is seen some time after the event. C R wave in lead V5eV6 >2.6 mV or

The most common cause is ischaemic heart disease; VT usu- C R wave in leads II, III, aVF >2.0 mV or

ally occurs in patients who have an arrhythmic scar from an old C R wave in lead aVL >1.2 mV

myocardial infarction, so the ECG may show Q waves/loss of R Adapted from Romhilt et al., Sokolow and Lyon, and Casale et al.
wave height. In addition, any of the changes of an ACS (see
above) can be present. Table 2
Rarer causes are hypertrophic cardiomyopathy (prominent LV
voltages, often with bizarre T wave changes) and dilated car-
diomyopathy (reduced QRS height, T wave flattening and often Distribution of ECG changes in ACSs
left bundle branch block).
Distribution Name Artery affected
Even rarer are the long QT syndromes, which predispose to
polymorphic VT. Diagnosis is easy, provided the QT interval is
V1eV3, possibly I, II Antero-septal LAD or a major branch
measured (and corrected for heart rate). Prolongation is usually
I, II, aVL, V1eV4/V5 Antero-lateral LAD, probably proximal
significant if the QT interval is >450 ms in a man and 470 ms in a
I, II, aVL, V5/V6 Lateral Diagonal branch of LAD
woman. The most common long QT syndromes are acquired
or circumflex
(e.g. LV dysfunction with QT-prolonging drugs, such as macro- II, III, aVF Inferior Right coronary artery
lide antibiotics and non-sedating antihistamines). In the
(circumflex if ST elevation
extremely rare hereditary long QT syndrome, additional bizarre
in lead III is greater than
repolarization patterns are often seen.
that in lead II)
The autosomal dominant Brugada syndrome underlies some
V1eV3 Posterior Circumflex
cases of polymorphic VT and sudden cardiac death. Classically,
(ST depression)
the inter-attack ECG shows ST elevation in leads V1eV3, with a
Combinations of the above are common. ACS, acute coronary
hump on the downslope, sometimes misinterpreted as right
syndrome; LAD, left anterior descending.
bundle branch block. The ECG changes can be subtle, and can be
accentuated by class I drugs, most commonly intravenous Table 3
ajmaline.

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Figure 5 Proximal LAD syndrome with deep anterior T-wave inversion. The differential diagnosis includes high grade stenosis at the start of the left
anterior descending coronary artery and takotsubo cardiomyopathy.

Figure 6 Severe ischaemia. Widespread deep down sloping ST segment depression in 8 ECG leads. Also atrial fibrillation and high heart rate
response.

Syncopal atrial fibrillation (AF)
This is rare, unless there is severe underlying structural heart
disease or sinus node disease producing long pauses when the
AF stops, or the ventricular response to AF is very fast (>250/
minute e usually caused by pre-excitation in WolffeParkinson
eWhite syndrome).
Syncope from bradyarrhythmia
Causes include:

sinus node disease (often diagnosed from low heart rate
variability on a 24-hour ECG)

high-grade AV block.
In patients who are not in heart block on arrival in hospital,
the clue that intermittent heart block underlies syncope is usually
the finding of extensive conducting tissue disease on an inter-
attack 12-lead ECG (Figure 10).

Look for evidence of damage to the AV conduction system,
which is apparent on the ECG as a long PR interval.

Look for damage to the specialized conducting system of
the ventricle, which is seen as right or left bundle branch
block.

Look for partial damage to the left bundle. The left bundle
has two fascicles, one anterior and one posterior. Damage
to these respectively results in QRS axis deviation left-
wards or rightwards. The posterior hemifascicle is larger,
and damage to it is of greater importance than damage to
the left hemifascicle.

It is of particular importance to decide whether the damage
to the conducting tissue affects more than one site, e.g. AV
and ventricular conduction, which could be seen as a long PR
interval and either left bundle branch block or right bundle
branch block, with or without QRS axis deviation (implying
damage to one of the left bundle’s hemifascicles). Damage to
both the right bundle and one hemifascicle of the left bundle
is known as bifascicular block; the added presence of
impaired AV conduction is known as trifascicular block.
Diagnosis of VT
There are two main forms of VT:

monomorphic VT, the more common form (below),
defined as non-sustained (lasting <30 seconds) or sus-
tained (lasting >30 seconds), and terminating either
spontaneously or after treatment

polymorphic VT, the rarer kind, of which the most notable
form is torsade de pointes, and which has a very distinctive
pattern. The QRS complexes run one into the other, and
their amplitude is continually increasing then decreasing.
VT is strongly associated with underlying structural heart dis-
ease or genetic channelopathies, and has a high risk of degenerating

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Sequential changes of acute myocardial infarction
in leads facing the infarct (‘primary’ changes)
a b c very fast; it can be as fast as 220 beats per minute but is
d e
a The control, normal appearances are shown in the
lead, which, as can be seen by its QRS morphology,
lies facing the left ventricle.
b The typical, convex upwards S-T elevation is shown
occurring within hours of the onset of symptoms of
infarction. At this stage, there is no change in the
QRS complex.
c The appearances within days of the onset are shown.
There is loss of R wave height, abnormal Q waves (in
this case in both depth and duration) have developed,
and there is T wave inversion. The loss of R wave
height and the abnormal Q waves prove infarction.
The S-T segment and T wave changes indicate that
the event is recent.
d Resolution of the S-T segment change is shown. In
other respects, the appearances are similar to c. The
loss of R wave height and the abnormal Q waves
prove infarction. The normal S-T segment indicates
that the event is not very recent (i.e. not within days)
but T wave changes indicate that the event is
relatively recent (within weeks).
e Restoration of an upright T wave is shown, but this is
otherwise similar to d. The loss of R wave height and
the abnormal Q waves prove infarction. The normal
S-T segment indicates that the event is not very
recent (i.e. not within days) and the normal T wave
that the event is relatively old (not within weeks).
Figure 7
Figure 8 Substantial ST segment infarction with gross ST elevation in the inferior leads (II, III, aVF), lateral leads (aVL, V4 to V6), and posterior leads
where it is seen as ST depression (V1 to 3). Occlusion of a very large coronary artery probably a very dominant right or circumflex.
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into ventricular fibrillation. Reliable recognition is therefore
crucial. Clues that a tachyarrhythmia is VT are as follows:

A tachycardia is present (the heart rate is >120 beats per
minute). VT, contrary to expectation, does not have to be
often around 160e180 beats per minute. However, in in-
dividuals with significant heart disease, VT with a heart
rate (QRS complex rate) of 120e140 beats per minute is
not unusual. Do not use the heart rate as the sole means of
diagnosing VT.

The patient is often known to have background structural
heart disease, such as a previous myocardial infarction or
heart failure from any cause.

The ECG signs include a broad QRS complex (>120 ms),
implying a broad-complex tachycardia. The differential
diagnosis of such tachycardias lies between VT and a
supraventricular tachycardia (SVT) with an associated
bundle branch block (termed ‘aberrancy’ in this situation).
Distinguishing features are:

The broader the QRS, the more likely the rhythm is to be
VT, especially if >160 ms.

An extreme QRS axis makes VT likely.

If all the QRS complexes in the chest leads are positive,
or negative (precordial concordance), this makes VT
highly likely.

In VT, the QRS complexes usually look quite unlike
those of right or left bundle branch block.

In VT with a QRS complex that looks like right bundle
branch block, the first deflection is larger than the sec-
ond (RSr), unlike the situation in true right bundle
branch block, where the R wave is smaller than the R0
deflection (rSR).

The RR interval in most monomorphic VT is fairly
(although not completely) regular; if there is very
marked irregularity, AF with aberrancy, or with Wolff
eParkinsoneWhite syndrome (pre-excited AF) is the
likely diagnosis.
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 INVESTIGATIONS

Figure 9 ST elevation leads V1 through to V4. Pericarditis with the typical concave upwards ST elevation. Also old Q-wave inferior wall myocardial
infarct.

Anterior/posterior hemifascicular block

Mechanism of the
a b c
ECG appearance of
(a) normal function, and
of partial block of the
(b) left anterior fascicles I I I
and (c) left posterior
fascicles. When partial
block of the left bundle
occurs there is no III II III II III II
broadening of the QRS
complex, as the left
anterior and posterior
fascicles connect via
small branches over
their entire length, so
depolarization is not –90% –90%
prolonged. Instead, a –45%
–30%
shift in the QRS axis 180%
0% 0% 0%
occurs as shown,
caused by the
predominant early +110%
+90%
depolarization, which is
determined by which
fascicle remains viable.

Figure 10

AV dissociation (P waves marching through the tracing
independent of QRS activity) clinches the diagnosis of VT.

If one has a tracing of the patient’s usual rhythm (sinus
rhythm or AF), the diagnosis is usually very easy. If the
tachycardia looks similar to this ECG, the rhythm is
usually an SVT with aberrancy. Conversely, a marked
difference (particularly a large axis shift) makes VT
much more likely.
It is sometimes not possible to be certain whether one is
dealing with VT, or SVT with aberrancy. The safest approach in
this situation is to always treat the patient as if the rhythm is VT.
If the arrhythmia is sustained, DC cardioversion is unlikely to be
the wrong approach.
Pitfalls of the automated ECG report
Modern ECG machines, as well as acquiring a standard 12-lead
ECG, often provide a computerized interpretation of the
tracing. This has many advantages:

It alerts non-cardiologists and those untrained in ECG
analysis to potentially life-threatening diagnoses, such as
acute myocardial infarction or LVH; this is undeniably
important and saves lives.

It can alert clinicians to the presence of important ar-
rhythmias, such as AF; this is particularly important in
primary care, where these important arrhythmias can be
missed. Early anticoagulation in AF prevents strokes and is
clearly valuable.

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It can point the most experienced clinicians to a diagnosis
that they might miss on quick assessment of the ECG.

Finally, although not really part of the automated report,
the automatic data analysis provides useful information on
QRS duration and QTc interval.
For these reasons, computerized systems are useful, and all
clinicians should take heed of the automated report.
However, there are several associated problems including the
following. First, computers tend to overcall abnormalities and
fail to recognize variants of normal. In other words, computer-
ized systems have difficulty in reliably identifying a normal ECG.
On one level, this is appropriate, as it is best to overcall rather
than undercall abnormalities. However, it can lead to unnec-
essary anxiety, unnecessary further investigations (some of
which can be expensive) and potentially high-risk treatments.
A second, frequent, problem is the overcalling of a normal ECG
as one showing a previous myocardial infarction. For example,
poor anterior R wave progression caused by obesity is frequently
overcalled as a previous antero-septal infarct. Similarly, a physi-
ological deep S wave, or even an isolated Q wave, in lead III is
often overcalled as a previous inferior wall myocardial infarction.
All ST elevation tends to be diagnosed as acute STEMI,
even when caused by pericarditis, or, even more disturbingly,
when physiological (high ST segment take-off). This can lead
to serious problems if the computer report is used to deter-
mine the role of out-of-hospital reperfusion therapy, with the
potential for inappropriate administration of thrombolytic
therapy.
Finally, a noisy baseline, often resulting from muscle artefact,
can be interpreted as AF. Again, this can lead to the incorrect
administration of a therapy such as warfarin. Thus, while the
computer report should always be read, one should approach it
with a degree of objectivity, and be prepared to overrule it if
appropriate. A
FURTHER READING
Davey P. ECG at a glance. 1st edn. Wiley-Blackwell, 5 Sep 2008.
ISBN-10: 0632054050, ISBN-13: 978e0632054053.
Electrocardiography. http://en.wikipedia.org/wiki/Electrocardiography.
Guidelines for recording a clinical ECG. Guidelines by consensus. British
Cardiovascular Society. http://www.scst.org.uk/resources/consensus_
guideline_for_recording_a_12_lead_ecg_Rev_072010b.pdf.
Houghton A, Gray A. Making sense of the ECG. 4th edn. CRC Press,
2014. ISBN-10: 1444181823 ISBN-13: 978e1444181821.
Marriot’s practical electrocardiography. 10th edn. Philadelphia: Lip-
pincott Williams and Wilkins, 2001.

TEST YOURSELF
To test your knowledge based on the article you have just read, please complete the questions below. The answers can be found at the
end of the issue or online here.

Question 1
A 27-year-old man presented with a 2-day history of central chest
pains radiating to the neck and left shoulder. They were worse on
lying flat. He had recently been bed-bound with a flu-like illness.
He was usually well, and there was no past history of note.
On clinical examination, his temperature was 38.4 C, heart rate
120 beats/minute and regular, blood pressure 128/79 mmHg,
and respiratory rate 18/minute. Oxygen saturation was 98%.
Auscultation of the heart and lungs was normal.
Investigations

Chest X-ray showed a normal-sized heart and clear lung
fields

ECG showed sinus rhythm of 120 beats/minute, wide-
spread saddled ST segment elevation that was concave
upwards, and PR segment depression in lead ll

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 INVESTIGATIONS

What is the most likely diagnosis? On clinical examination, his temperature was 36.8 C, heart rate
A. Acute myocardial infarction 130 beats/minute, blood pressure 88/54 mmHg, and respiratory
B. Pericarditis rate 34/minute. Oxygen saturation was 82% on 15 litres of ox-
C. Pulmonary embolus ygen. On auscultation, lung fields were clear, and there was a
D. Myocarditis loud second sound but no murmurs.
E. Hyperkalaemia
Investigation
Question 2
ECG showed sinus rhythm of 130 beats/minute, with deep
A 67-year-old man presented as an emergency with collapse and S waves in lead 1, T wave inversion and Q waves in lead
severe breathlessness. He was not in pain. He had been dis- III. A chest X-ray demonstrated clear lungs.
charged 2 days previously after uncomplicated repair of a right
inguinal hernia.

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Please cite this article in press as: Davey P, Sharman D, The electrocardiogram, Medicine (2018), https://doi.org/10.1016/j.mpmed.2018.05.004
 INVESTIGATIONS

What is the most likely diagnosis? tation, heart sounds were normal, and there were bi-basal
A. Anterior myocardial infarction crackles in the lungs.
B. Acute pericarditis
C. Posterior myocardial infarction Investigations
D. Massive pulmonary embolus
ECG showed a broad-based tachycardia at 180 beats/
E. Postoperative hospital-acquired pneumonia minute.

Question 3
An 81-year-old woman presented with sudden collapse and What is the most likely primary diagnosis?
breathlessness. She had a history of a myocardial infarction 11 A. Monomorphic ventricular tachycardia
years previously. An echocardiogram last year had demonstrated B. Acute myocardial infarction
severe left ventricular dysfunction. C. Pulmonary oedema
On clinical examination, her temperature was 37.0 C, heart rate D. Massive pulmonary embolus
180 beats/minute, blood pressure 94/56 mmHg, and respiratory E. Polymorphic ventricular tachycardia
rate 24/minute. Oxygen saturation was 92% on air. On auscul-

MEDICINE --:- 10 Ó 2018 Elsevier Ltd. All rights reserved.

Please cite this article in press as: Davey P, Sharman D, The electrocardiogram, Medicine (2018), https://doi.org/10.1016/j.mpmed.2018.05.004