PHYSIOLOGY

Electrocardiogram and
arrhythmias

Learning objectives
After reading this article, you should be able to:
C
recognize two common variations of each of the normal P, QRS
and T waves
C
distinguish the three atrioventricular blocks
C
describe three common tachyarrhythmias.

Rajender Singh
Jeremy J Murphy

Abstract
Introduced by Einthoven, electrocardiography remains the most common
diagnostic procedure readily available to the physician in primary and
secondary care. It is a graphical display of the electrical potential difference as it spreads through the heart and is recorded at the body surface.
The electrocardiogram (ECG) is an indispensable tool to screen and
monitor cardiac patients. Exercise ECG is used to diagnose coronary artery
disease and ambulatory ECG to assess arrhythmias.

beneath the electrode because the heart is close to the chest wall.
(For detailed discussion about lead position and cardiac depolarization please refer to Anaesthesia and Intensive Care Medicine 2006; 7: 264e6.)

ECG waves

Keywords Atrial fibrillation; atrial flutter; atrioventricular block; brady-

P wave
P waves result from atrial activation by the sinoatrial (SA) node.
Because the SA node is situated in the right atrium, right atrial
activation begins first and is reflected by the proximal
(ascending) limb of the P wave. Left atrial activation begins 0.03
seconds later and is represented by the descending limb of the P
wave. Because of the orientation of the leads, this is best seen in
standard lead II and lead V1. The P wave in these leads is usually
positive, pyramidal and with a slightly rounded apex. It is normally inverted in aVR, and upright in aVF plus the left chest leads
(V4e6). Amplitude does not usually exceed 2e3 mm in any lead.

cardia; ECG waves and their variations; electrical impulse of the heart;
tachycardia; ventricular tachycardia
Royal College of Anaesthetists CPD matrix: 1A01

ECG lead system

Heart muscle generates an electrical current that can be recorded
from the surface of the body by the electrocardiogram (ECG). The
12 conventional ECG leads record the difference in potential
between the electrodes on the body surface.
ECG leads are divided into two groups: six limb leads and six
chest leads. Of the six limb leads, three are bipolar leads and
have been in use for more than a century (lead I, lead II and lead
III). These leads measure the difference in potential between
electrodes at two extremities: lead I, left armeright arm; lead II,
left legeright arm; and lead III, left legeleft arm.
All leads introduced later are unipolar leads and are termed
V leads. These measure the voltage (V) at one locus relative to a
common central terminal (indifferent electrode) that has
approximately zero potential. These comprise the three limb
leads aVR, aVL and aVF, where aVR is the right arm, aVL is the
left arm and aVF is the left leg (foot). These three limb leads
detect only a small deflection of current, which is augmented
50% by the machine. This augmentation of potential is designated by the prefix a. There are six unipolar chest (precordial)
leads that are designated V1eV6; these are placed directly over
the chest wall. Each chest lead records the impulse immediately

Variations of the P wave

Inversion: in leads where it is normally upright (or upright in
aVR), an inverted P wave would indicate that the impulse is
travelling in an unusual path (e.g. atrial ectopic, atrioventricular
(AV) junctional rhythm).
Increased amplitude: this is due to right atrial hypertrophy and
is seen in cor pulmonale and congenital heart disease.
Biphasic (descending limb more negative than the ascending
limb): P waves in leads III and V1 are a sign of left atrial
enlargement.
P mitrale: notched P waves (distance between two peaks more
than 0.04 seconds) owing to left atrial involvement in mitral
disease. It is usually notched and taller in lead I than in lead III.
QRS complex
The QRS complex reflects rapid ventricular depolarization. An
initial downward deflection is termed the Q wave and ensuing
deflections are labelled in alphabetical order. The first positive
deflection is designated R, whereas S is the first negative
deflection that follows the R wave. This represents the terminal
part of the ventricular activation.
The complex ventricular depolarization can be divided into
two sequential phases. The first phase is the activation of the
ventricular septum from left to right. The second phase is the
simultaneous activation of the right and left ventricles, usually
dominated by the bulky left ventricle.

Rajender Singh MBBS MD MRCP is a Medical Registrar at County Durham

& Darlington Foundation Trust, and is also an Honorary Research
Associate at the Centre of Integrated Health Care Research, Durham
University, UK. Conflicts of interest: none declared.
Jeremy J Murphy MSc(Med Ed) MBBS DM FRCP is a Consultant Cardiologist at
County Durham & Darlington Foundation Trust, and is also an Honorary
Senior Lecturer at Durham University, UK. Conflicts of interest: none
declared.

ANAESTHESIA AND INTENSIVE CARE MEDICINE 16:5

220

2015 Published by Elsevier Ltd.

PHYSIOLOGY

approximately 70 times per minute at rest. A rate less than 60

beats per minute is termed bradycardia, whereas the term tachycardia is reserved for rates in excess of 100 beats per minute.

In the chest leads, as a consequence of this normal depolarization process, the right-oriented leads (V1 and V2) show a small
upward deflection (septal R wave), followed by a deep S wave.
The same sequence in the left-sided chest leads (V6, aVL, lead I)
causes a small downward deflection (physiological Q wave)
followed by a tall R wave. In the intermediate chest leads, there is
a relative increase in the R wave and a reduction in the S wave
amplitude (normal R wave progression) from left to right. R and
S waves are approximately equal in the mid-chest leads (V3 and
V4); this is called the transition zone.
The QRS pattern in the limb leads varies and depends on the
mean QRS axis. Lead aVR, which records from the right shoulder, effectively looks from the cavity of the heart with all the
vectors directed away and thus has all negative deflections. The
normal duration of the QRS complex is 0.05e0.10 seconds.

Bradycardia
This is normally present during sleep and in fit athletes (athletes
heart syndrome). Pressure receptors (baroceptors) in the aorta
and carotid arteries respond to arterial pressure, altering vagal
tone through acetylcholine release. In carotid sinus syndrome,
there is increased sensitivity of the baroceptors located in the
carotid sinus region of the carotid artery. Therefore, pressure on
the neck can result in extreme bradycardia, dizziness and syncope. Sometimes, it can trigger asystole for up to 10 seconds.
Heart rate also varies with the phase of respiration; this is called
sinus arrhythmia (For further description, please refer to
Anaesthesia and Intensive Care Medicine 2006; 7: 264e6.)

Variations of the QRS complex

Prolonged QRS duration: a duration of 0.12 seconds or more
signifies conduction delay, such as in bundle branch block, but can
also be present with pre-excitation of the ventricles via an accessory pathway, such as in WolffeParkinsoneWhite syndrome.

Atrioventricular (AV) block

First-degree block: this is characterized by a prolonged PR interval (> 0.20 seconds), and is due to constant delay rather than
a block in conduction of the impulse from the atrium to the
ventricle. First-degree block is often present in athletes, but can
be associated with ischaemic heart disease, acute rheumatic
carditis and drugs such as digitalis and b-blockers. It causes no
symptoms and requires no treatment other than observation.

Right bundle branch block (RBBB): this occurs more

commonly than left bundle branch block, especially in people
with structurally normal hearts. RBBB can also occur in acquired
(valvular, ischaemic) and congenital heart disease, especially
atrial septal defects.

Second-degree block: type 1 second-degree AV block (Wenckebach, Mobitz type I); there is progressive prolongation of the PR
interval, before a QRS complex fails to appear after a P wave. The
block is usually in the AV node and the QRS is of normal duration. Causes are inferior wall myocardial infarction, drug intoxication with beta blockers, digoxin and calcium channel blockers.
Type 1 block can be present in normal individuals with increased
vagal tone, generally at night. If the ventricular rate is adequate
and the patient is asymptomatic, observation is sufficient.

Left bundle branch block (LBBB): this is usually due to ischaemic

heart disease, hypertension, severe aortic stenosis and cardiomyopathy. Bundle branch blocks (QRS duration of 0.12 seconds or
more) can be chronic or intermittent and they can be rate related as
well. Therefore, some patients with supraventricular tachycardia
(SVT) have broad complexes (aberrant conduction).
T wave
T wave: this is a marker of the ventricular recovery period
(repolarization) and is normally inscribed in the same direction
as the QRS complex. It is, therefore, normally upright in leads I
and II and in the left-sided chest leads and is inverted in the aVR
lead. It is variable in all other leads.

Type 2 second-degree AV block (Mobitz type II) (Figure 1

shows the 2:1 AV block): the PR interval remains constant
before a sudden and unexpected failure of the P wave to conduct.
It is usually due to disease of the HisePurkinje system and is
often associated with an abnormal QRS wave. When two or more
successive P waves are blocked, this is called high-grade AV
block. Type 2 block can occur in the setting of anteroseptal
myocardial infarction or sclerodegenerative disease of the fibrous
skeleton of the heart. This is very likely to progress to symptomatic third-degree block or ventricular standstill, so permanent
pacing is indicated. Physiological second-degree block is seen
with fast supraventricular rhythms such as atrial tachycardia and
atrial flutter.

Variations of the T wave

Tall positive T waves can be a normal variant, but are also seen
in hyperkalaemia, hyperacute myocardial ischaemia, cerebrovascular injury and left ventricular volume overload.
T wave inversion can be seen with cardiomyopathy, ischaemia,
ventricular hypertrophy, myocarditis and intracranial bleeds.
U wave
U waves usually follow the T wave as a small rounded deflection
( 1 mm). An abnormal increase in the amplitude is seen with
hypokalaemia, and with drugs such as quinidine and procainamide. This could be a sign of increased susceptibility to torsades
de pointes.

Third-degree block (complete heart block): this is characterized by complete cessation of the electrical impulses from the
atrium to the ventricle. P waves are dissociated from the ventricular complex and the two are asynchronously controlled by
independent pacemakers. This is the most advanced form of AV
block. It is mostly due to chronic degenerative changes in the
bundle branches due to Levs and Lenegres disease. It can also
occur with cardiomyopathy and inferior myocardial infarction.
Complete heart block can be congenital owing to maternal

Arrhythmias
It is beyond the scope of this article to discuss arrhythmias in
detail, but a brief overview is provided. The heart normally beats

ANAESTHESIA AND INTENSIVE CARE MEDICINE 16:5

221

2015 Published by Elsevier Ltd.

PHYSIOLOGY

Figure 1 Bradycardia: type II second-degree (Mobitz type II) atrioventricular block. There are two P waves for one QRS complex (2:1 block).

transmission of antinuclear (Ro/SSA and/or La/SSB) antibodies.

Treatment is permanent pacing because third-degree block
carries significant mortality.

SVT in origin, whereas regular broad complex tachycardia usually originates from the ventricle.
Atrial fibrillation
Atrial fibrillation (AF) can be paroxysmal or persistent and is
characterized by disorganized atrial activity with no discrete P
waves on the ECG. The mechanism of AF is unclear, but it is
believed that there are numerous micro-re-entry circuits or
stimuli that excite the atria, usually from where the pulmonary
veins enter the left atrium. The atrial rate is between 350 and 600
beats per minute (bpm), and this activity causes an undulating
baseline. Impulses reach the AV node through multiple paths at
frequent and irregular intervals. Rapidly entering atrial impulses
render the AV node partially refractory to subsequent impulses,
so the ventricular rate is somewhat slower and irregularly
irregular. Acute AF can be precipitated by infection, alcohol,

Tachycardia
Normally, myocardial cells do not discharge spontaneously.
Tachyarrhythmias can arise from any part of the heart. These can
be disorders of impulse formation (enhanced automaticity)
owing to exogenous catecholamines, hyperkalaemia, hypoxia
and digitalis; they can also arise from disorders of impulse spread
(re-entry), such as in sustained supraventricular tachycardias.
Tachyarrythmias can be further classified as (1) regular or
irregular and (2) narrow or broad complex, depending on the
QRS morphology. An irregular arrhythmia is usually atrial
fibrillation (or flutter with variable block), whether narrow or
broad complex. Regular narrow complex tachycardia is generally

Figure 2 Atrial flutter: regular narrow complex tachycardia showing 2:1 physiological block. P waves (arrows) are best seen in leads V1 and V2.

ANAESTHESIA AND INTENSIVE CARE MEDICINE 16:5

222

2015 Published by Elsevier Ltd.

PHYSIOLOGY

Figure 3 Regular broad complex ventricular tachycardia.

5 morphological patterns of QRS complex:

RBBB mono- or biphasic complex V1
RS (only with left axis deviation) or QS in V6
LBBB broad R wave in V1 or V2  0.04 seconds
onset of QRS to nadir of S wave in V1 or V2 of  0.07
seconds
notched downslope of S wave in V1 or V2; Q wave in V6.
VT is commonly seen with structural heart disease, especially
ischaemic heart disease. It can also occur with prolonged QT
syndrome, cardiomyopathies and metabolic and drug disorders.
VT without structural heart disease is usually benign; asymptomatic non-sustained VT is not treated, except the long-QT syndrome. VT with haemodynamic compromise should be terminated
immediately with direct current (DC) cardioversion.
A

dehydration, congestive cardiac failure and pulmonary embolism. In acute AF, treating the primary cause usually resolves the
arrhythmia. If the patient is compromised, electrical or chemical
cardioversion can be performed.
Atrial flutter
Atrial flutter (Figure 2) is characterized by rapid and regular atrial
activity, causing a saw-tooth or picket-fence appearance, typically
in the inferior leads. The mechanism is generally a macro-re-entry
circuit in the right atrium. The atrial rate is 250e350 bpm; the
ventricular rate is typically half the atrial rate, usually around 150
bpm. Atrial flutter, when it lasts for more than a week, frequently
converts to AF. Although the risk of systematic emobolization is
less than for AF, management is the same for both.
Ventricular tachycardia
Ventricular tachycardia (VT) (Figure 3) is defined as three or
more consecutive ectopic ventricular QRS complexes occurring at
a rate of >100 bpm. It is called sustained VT if it lasts for more
than 30 seconds or needs intervention. It is broad complex and
quite regular, arising as a result of abnormal automaticity or
(more commonly) re-entry distal to the His bundle. Broad complex tachycardia is most commonly VT, particularly if structural
heart disease is present. Certain ECG criteria support VT as
opposed to SVT with aberrant conduction.
ECG features that favour VT are:1
1 atrioventricular dissociation
2 QRS width:
>0.14 seconds with RBBB configuration
>0.16 seconds with LBBB configuration
3 QRS axis:
left axis with RBBB morphology
extreme left axis with LBBB morphology
4 concordance of QRS in precordial leads

ANAESTHESIA AND INTENSIVE CARE MEDICINE 16:5

REFERENCE
1 Josephson ME, Zimetbaum P. The tachyarrhythmias. In: Braunwald E,
Fauci AS, Kasper DL, et al., eds. Harrisons principle of internal medicine. 15th edn, vol. 1. New York: McGraw-Hill, 2001; 1303.
FURTHER READING
Marriott HJL. Practical electrocardiography. 8th edn. Baltimore, USA:
Williams & Wilkins, 1988.
Schamroth L. An introduction to electrocardiography. 7th edn. Oxford:
Blackwell Science, 1990.

Acknowledgement
This is an update of the original article by Emrys Kirkman (Kirkman E.
The electrocardiogram. Anaesthesia and Intensive Care Medicine
2006; 7: 264e6), which discusses some basic principles of the ECG.

223

2015 Published by Elsevier Ltd.