ECG guide for uk

Airway Management |  Patient Monitoring & Diagnostics | Emergency Care
A Pocket Guide to
Common Arrhythmias
Interpretation and Management

Preface
In a patient with suspected or known heart disease, the electrocardiogram
should be regarded as an extension of the patient’s history and physical
examination. Indeed, electrocardiography is a fundamental part of any
cardiovascular assessment.As such, it is an essential tool for accurately
diagnosing cardiac-rhythm disorders, ischemic chest pain, and estimating
the extent of coronary artery disease. Moreover, the electrocardiogram
gives invaluable information about the workload of the individual chambers
of the heart, besides being helpful in diagnosing systemic diseases that
affect the heart and disturbances in electrolyte metabolism. Because the
electrocardiogram is such a powerful tool, it should be well understood for
use by medical practitioners, medical students, nurses in intensive and
coronary care units, and by paramedics in emergency services.
It should be kept in mind, however, that a patient with an organic heart
disorder could have a normal electrocardiogram, whereas a perfectly
healthy individual may display non-specific electrocardiographic abnormalities.
Thus the electrocardiogram should always be interpreted in conjunction
with the clinical findings and never in isolation.
This ECG booklet is part of the educational concept ”Professional Advisory”
that the Cardiology group from Ambu A/S is offering to provide users and
purchasers with greater knowledge by imparting new learning, supplying
better clinical documentation and sharing other helpful experiences.
Ambu has made this booklet in cooperation with Dr. Christian Lange,
Cardiologist, and it can be useful for doctors, nurses, technicians and
anybody working within cardiology to analyze ECG patterns.
It provides both examples of ECG patterns and diagnosis to match,
symptoms and signs to be aware of and what treatment to offer. It also
explains the function of the heart and the basic ECG pattern.
Thank you to Lars Ramløse for helping with illustrations in the book.
Another helpful tool Ambu has produced is an ECG ruler for fast and
accurate diagnosis based on an ECG pattern. Please contact your local
Ambu sales representative for more information.

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Contents
Anatomy and electricity of the heart.............................................4
Conduction system.......................................................................5
Heart rate, time and voltage.........................................................6
The 12-lead ECG..........................................................................8
P wave.......................................................................................10
PR interval.................................................................................11
QRS complex..............................................................................12
ST segment................................................................................14
T wave.......................................................................................15
QT interval.................................................................................16
U wave......................................................................................17
Sinus rhythm..............................................................................18
Sinus bradycardia.......................................................................19
Sinus tachycardia.......................................................................20
Sinus arrhythmia........................................................................22
Sinoatrial (SA) block...................................................................23
Second-degree SA block.............................................................24
Third-degree SA block and sinus arrest.......................................26
Atrial fibrillation (AF)..................................................................28
Atrial flutter...............................................................................32
Atrial tachycardia.......................................................................34
Multifocal supraventricular tachycardia.......................................36
AV nodal re-entry tachycardia.....................................................38
Ventricular tachycardia (VT)........................................................40
Ventricular fibrillation (VF)..........................................................44
Atrioventricular (AV) block..........................................................46
First-degree AV block..................................................................47
Second-degree AV block.............................................................48
Second-degree AV block – Mobitz type I (Wenckebach)...............49
Second-degree AV block – Mobitz type II....................................50
Advanced second-degree AV block.............................................52
Third-degree (complete) AV block...............................................54
Extrasystoles (ectopic beats).......................................................56
Ventricular extrasystoles (ventricular ectopic beats).....................58
Supraventricular extrasystoles (atrial ectopic beats).....................62
Escape rhythms..........................................................................64
Common Tracing Problems.........................................................66

Anatomy and electricity of the heart
Contraction and relaxation of cardiac muscle occurs as a result of electrical
changes within the myocardial cells, referred to as depolarisation and
re-polarisation. Electrodes attached to the skin on the limbs and chest wall
can sense this electrical activity and transmit it to an electrocardiograph.
The electrocardiograph then converts this information into waveforms, which
are recorded on graph paper to produce an electrocardiogram, commonly
known as an ECG.
Although the heart has four chambers, from the electrical point of view it can
be thought of as having only two, since the two atria contract simultaneously
and the two ventricles contract simultaneously.
The muscle mass of the atria is relatively small and the electrical changes
accompanying the contraction are therefore equally small. Contraction
(i.e. depolarisation) of the atria causes the ECG wave called P. Since the
ventricular mass is large, there is a large deflection of the ECG when the
ventricles contract (i.e. depolarise) and this is called the QRS complex.
The T wave of the ECG is caused by the return of this ventricular mass to
the resting electrical state called re-polarisation. Electrical events and corresponding ECG components.
The SA node depolarises - no
deflection
The atria depolarise
- P wave
The AV node and the
bundle of His depolarise - no
deflection
The free walls of the ventri-
cles depolarise
- QRS complex
The ventricles are totally
depolarised - no deflection
(ST segment)
The ventricles
repolarise - T wave

5
Conduction system
The myocardium contains a system of highly specialised tissue that can
conduct impulses faster than the surrounding muscle tissue. Parts of this
specialised conducting tissue can discharge spontaneously and set up a
wave of depolarisation through the rest of the conducting system of the
entire heart.
The sinoatrial (SA) or sinus node high in the right atrium, has the highest
spontaneous discharge rate of 60–100 beats/min at rest, and therefore
acts as a natural pacemaker and initiates atrial depolarisation.The impulse
spreads from the sinoatrial node through the muscle mass of the atria to
reach the atrioventricular (AV) node.
Here the impulse is delayed before rapidly continuing through the bundle
of His, which is normally the only pathway between the atria and the
ventricles. In the septum between the ventricles, this single pathway divides
into the right and left bundle branch.The left bundle branch then divides in
two, an anterior and a posterior fascicle.At the lower part of the ventricular
septum the conducting branches spread out in a complex network called
Purkinje fibres.Therefore, after a delay in the atrioventricular node, atrial
contraction is followed by rapid coordinated contraction of the ventricles.
The conduction system.
Sinoatrial node
Atrioventricular
node
Right bundle branch
Left posterior
hemifascicle
Left anterior hemi-
fascicle
Left bundle branch
Electrically inert
atrioventricular
region
Right
atrium
Left
atrium
Right
ventricle
Left
ventricle

The heart rate can be calculated rapidly by remembering the following
sequence:
Number of large squares
between 2 QRS complexes
Heart rate
(beats/min)
1 300
2 150
3 100
4 75
5 60
6 50
Rate rulers are sometimes used to calculate heart rate; these are used to
measure two or three consecutive R-R intervals, of which the average is
expressed as the rate equivalent.When using a rate ruler, one must take
care to count the correct numbers of beats (two or three) and restrict the
technique to regular rhythms.
Heart rate, time and voltage
The electrocardiogram is recorded on standard paper travelling at a rate of
25 mm/s.The paper is divided into large squares, each is 5 mm wide - the
equivalent of 0.2 seconds. Each large square is five small squares wide, and
each small square is 1 mm wide - the equivalent of 0.04 seconds.
The heart rate is the number of heartbeats occurring in 1 minute. On an
ECG, the heart rate is measured from R wave to R wave to determine the
ventricular rate, and P wave to P wave to determine the atrial rate.The QRS
complexes represent ventricular depolarisation and the P waves represent
atrial depolarisation.
The term tachycardia is used to describe a heart rate greater than 100
beats/min and bradycardia is defined as a rate less than 60 beats/min
(or < 50 beats/min during sleep).
One large square of recording paper is equivalent to 0.2 seconds, so 5 large
squares pass per second and 300 per minute.Thus, when the rhythm is regular
and the paper is moving at the standard speed of 25 mm/s, the heart rate can
be calculated by counting the number of large squares between two
consecutive R waves, and dividing this number into 300.

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When an irregular rhythm is present, the heart rate may be calculated from
the rhythm strip. It takes one second to record 2.5 cm of trace; therefore
the heart rate per minute can be calculated by counting the number of
intervals between QRS complexes every 6 seconds (namely, 15 cm of
recording paper) and multiplying by 10.
On the vertical axis, the electrical activity detected by the electrocardiogram
machine is measured in millivolts. Machines are calibrated so that a signal
with an amplitude or height of 1 mV moves the recording stylus vertically
1 cm (2 large squares). Most commonly and throughout this text, the
amplitude of waveforms is expressed as 0.1 mV = 1 mm = 1 small square.
Thus each small square is 1 mm high and each large square 5 mm high.
Time and voltage.
Vertical axis:
• 1 small square = 1 mm (0.1 mV)
• 1 large square = 5 mm (0.5 mV)
• 2 large squares = 10 mm (1.0 mV)
Horizontal axis:
• 1 small square = 0.04 s
• 1 large square = 0.2 s
• 5 large squares = 1.0 s
P-R
Interval
Q-T
Interval
QRS
Duration
1 sec
0.04 sec
0.2 sec
P
R
Q
S
T
U
1mm
5mm
1mV
PAPER SPEED - 25mm/sec

The 12-lead ECG
To make sense of an ECG, it is important to appreciate that the various
leads “view” the heart from different directions.The term “lead” does not
refer to the wires that connect the patient to the ECG machine, but rather
to different views of the heart’s electrical activity.An ECG machine uses the
information it collects via its four limb and 6 chest electrodes to compile a
comprehensive picture of the electrical activity in the heart as observed
from 12 different angles.
The six chest leads (V1
to V6
) “view” the heart from a horizontal plane.The
information from the limb electrodes is combined to produce the six limb
leads (I, II, III, aVR, aVL and aVF).The limb electrodes can be thought of as
looking at the heart in a vertical plane (that is, from the sides or the feet).
The information from these 12 leads is combined to form a standard
electrocardiogram.
Position of the six chest electrodes for
standard 12-lead electrocardiography.
V1
: right sternal border,
4th
intercostal space;
V2
: left sternal border,
4th
intercostal space;
V3
: between V2
and V4
;
V4
: mid-clavicular line,
5th
intercostals space;
V5
: anterior axillary line,
horizontally in line with V4
;
V6
: mid-axillary line,
horizontally in line with V4

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The positions of the leads produces the following anatomical relationships:
leads II, III and aVF view the inferior surface of the heart; leads V1
to V4
view the anterior surface; leads I, aVL,V5
and V6
view the lateral surface;
and leads V1
and aVR look through the right atrium directly into the cavity
of the left ventricle.
Anatomical relations of leads in a standard 12-lead ECG
II, III and aVF Inferior surface of the heart
V1
to V4
Anterior surface
I, aVL,V5
and V6
Lateral surface
V1
and aVR Right atrium and cavity of left ventricle

P wave
The sinoatrial (SA) node is high in
the wall of the right atrium and
initiates atrial depolarisation which
produces the P wave on the
electrocardiogram.The P wave thus
represents atrial depolarisation and
not SA node depolarisation, as is
sometimes mistakenly believed.
Although anatomically the atria are two distinct chambers, electrically they
act almost as one.They have relatively little muscle and generate a single,
small P wave.The duration of the P wave should not exceed 0.12 seconds.
P wave amplitude (height) rarely exceeds 0.25 mV. Sinus P waves are
usually most prominently seen in leads II and V1
.
Characteristics of the P wave
• Represents atrial depolarisation
• Positive (upright) in leads I and II
• Best seen in leads II and V1
• Duration < 0.12 s (three small squares)
• Amplitude < 0.25 mV (two and a half small squares)
P wave
Sinoatrial node
Atrioventricular
node
Right atrium
Wave of
depolarisation
Left atrium
Atrial depolarisation gives rise to the P wave.

11
PR interval
The PR interval is the time between the onset of atrial depolarisation and
the onset of ventricular depolarisation. It is measured from the beginning
of the P wave to the first deflection of the QRS complex; regardless of
whether this is a Q wave or an R wave.The normal duration of a PR interval
is 0.12 – 0.22 seconds.
The “PR segment” represents a brief return of the P wave to the isoelectric
line. During this time the electrical impulse is conducted through the
atrioventricular node, bundle of His, the bundle branches and the Purkinje
fibres.
Abnormalities of the conduction system may lead to transmission delays
that will prolong the PR interval.
Characteristics of the PR interval
• Measured from the beginning of the P wave to the beginning of the
QRS complex
• Duration 0.12 – 0.22 s (three to five and a half small squares)
P
PR segment
PR interval Q
R
S
T
U

QRS complex
The QRS complex represents the
electrical forces generated by
ventricular depolarisation.Thus, it
represents the spread of electrical
depolarisation through the
ventricular muscle mass.The Q wave
is the first negative (downward)
deflection; the R wave is the first positive (upward) deflection in the
complex; the S wave is a negative deflection in the complex that follows
an R wave.
With normal intraventricular conduction, depolarisation occurs in an
efficient, rapid fashion.The duration (width) of the QRS complex should
not exceed 0.12 seconds or three small squares.
Q
R
S
R
S
R
Q S
The QRS complex:
• The first downward deflection is a Q wave
• The first upward deflection is an R wave
• A downward deflection after an R wave is an S wave
R wave
S waveQ wave

13
Characteristics of the QRS complex
• Represents depolarisation of the ventricles
• Duration < 0.12 s (three small squares) Sinoatrial node
Atrioventricular
node
Right
atrium
Left
atrium
Right
ventricle Left
ventricle
A wave of depolarisation spreading throughout ventricles gives rise to
a QRS complex.

ST segment
The ST segment lies between the
terminal portion of the QRS complex
and the beginning of the T wave. It
represents the period between the
end of ventricular depolarisation and
the beginning of re-polarisation.
The junction between the terminal
portion of the QRS complex and the start of the ST segment is referred to
as the J point.
The interpretation of subtle abnormalities in the ST segment is one of the
more difficult areas of clinical electrocardiography. Nevertheless, any
elevation or depression of the ST segment must be explained rather than
dismissed.
Characteristics of the ST segment
• Measured from the end of the S wave to the beginning of the T wave
• Horizontal line
ST segment
J point

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T wave
Ventricular re-polarisation produces a
T wave.A normalT wave is asymmetrical.
The first half has a more gradual slope
than the second half.
T wave orientation usually corresponds
with that of the QRS complex.
Though no widely accepted criteria exist regarding T wave amplitude,
as a rule, it correlates with the amplitude of the preceding R wave.
Tall T waves may be seen in both acute myocardial ischemia and
hyperkalemia. Conversely hypokalemia results in a flatter T wave.
Characteristics of the T wave
• Represents re-polarisation of the ventricles
• T wave orientation usually follows the direction of the QRS complex
T wave

QT interval
The QT interval is measured from the
beginning of the QRS complex to the
end of the T wave and represents the
total time taken for depolarisation
and re-polarisation of the ventricles.
The QT interval lengthens as the
heart rate slows, and thus when
measuring the QT interval, the heart rate must be taken into account.As a
general guide, the QT interval should be 0.35 – 0.45 seconds and should
be no more than half of the interval between adjacent R waves (R – R
interval).The QT interval increases slightly with age and tends to be longer
in women than in men.
Prominent U waves can easily be mistaken for T waves, leading to
overestimation of the QT interval.
Characteristics of the QT interval
• Measured from the beginning of the QRS complex to the end of the T
wave
• Lengthens as the heart rate slows
• Duration 0.35 – 0.45 s
QT interval

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U wave
The U wave is a small deflection
that follows the T wave. It is
generally deflected in the same
direction as the preceding
T wave.Therefore, inverted
U waves usually follow inverted
T waves, as a result of the same
clinical abnormality.
It has been suggested that U waves result from re-polarisation of the
mid-myocardial cells – that is, those cells between the endocardium
and the epicardium – and the His-Purkinje system. However, this is by
no means certain.
Many electrocardiograms have no discernible U waves. Prominent U
waves may be found in athletes and are also associated with
hypokalemia, hypercalcemia and hyperthyroidism.
Characteristics of the U wave
• Small generally upright wave
• Follows the T wave
• Most prominent in leads V2
to V4
U wave

Diagnosis
• P waves have normal morphology
• Atrial and ventricular rate 60 – 100 beats/min
• Regular ventricular rhythm
• Every P wave is followed by a QRS complex
• PR interval 0.12 – 0.22 s (three to five and a half small squares)
• QRS complexes < 0.12 s (three small squares)
Signs and symptoms
Exercise and emotion are potent accelerators of sinus rhythm through
sympathetic, neural and catecholamine stimulation. Resting sinus rates of
60 to 100 beats/min classically represents the limits of a normal rate, but
much slower sinus rates occur in young persons, particularly trained
athletes.Thus, resting rates of < 60 beats/min (sinus bradycardia) are often
not pathologic. Sinus tachycardia describes rates of > 100 beats/min.
Normally, a marked diurnal variation in heart rate is common, with the
lowest rates just before early morning awakening.Absolute regularity of
sinus rhythm is pathologic and occurs with autonomic denervation, as seen
in advanced diabetes.
Sinus rhythm
A normal heart rhythm is initiated in the sinus node and proceeds to
depolarise the atria. P wave are recorded on the ECG, representing atrial
depolarisation.The cardiac impulse then travels to the AV node and the
bundle of His, traverses the bundle branches and the Purkinje fibres, and
a PR interval is recorded.The impulse then reaches the ventricular muscle,
and a QRS complex is displayed, representing ventricular depolarisation.
This complex is followed by an isoelectric ST segment and a T wave
representing ventricular re-polarisation.Altogether, this cycle is called
sinus rhythm.
Normal sinus rhythm.

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Signs and symptoms
Sinus bradycardia is common in individuals during sleep and in those with
high vagal tone such as athletes and healthy young adults.
Sinus bradycardia frequently occurs during digitalisation, treatment with
opiates and beta-blocking agents and is a predominant feature in
vasovagal attacks (episodes of bradycardia and hypotension related to
pain, arterial puncture, the Valsalva manoeuvre and carotid sinus massage).
Sinus bradycardia may also be seen in myxoedema, obstructive jaundice,
uraemia, increased intracranial pressure and glaucoma.
Treatment
If the bradycardia is symptomatic, atropine 0.5 to 1.0 mg can be given
intravenously in repeat doses every 3 to 5 minutes.
Transcutaneous pacing is always appropriate if the bradycardia is severe
and the clinical situation is unstable.
Sinus bradycardia
Sinus bradycardia is sinus rhythm with a heart rate of below 60 beats/
min.Atrial depolarisation resembles sinus rhythm with normal P waves,
and P-P intervals are usually regular. Every P wave is followed by a QRS
complex of normal duration and appearance.
Diagnosis
• Atrial and ventricular rate of < 60 beats/min
• One P wave precedes every QRS complex
• Normal QRS complexes < 0.12 s (three small squares)
Sinus bradycardia. Heart rate of 51 beats/min.

Sinus tachycardia
Sinus tachycardia is a sinus rhythm with a heart rate of greater than 100
beats/min.Atrial depolarisation occurs as in sinus rhythm with normal P
waves, and the P-P interval is usually regular.
The rate increases gradually and may show beat-to-beat variation but
rarely exceeds 140 beats/min in adults except during heavy exercise.
A QRS complex follows each P wave, and P wave morphology is normal.
The height of the P wave may increase and the PR interval will shorten
with the increase in heart rate.With rapid tachycardia, the P wave may
become embedded in the preceding T wave, so the rhythm can be
mistaken for atrioventricular nodal tachycardia.
Diagnosis
• Atrial and ventricular rate of 100 – 140 beats/min
• One P wave precedes every QRS complex
• QRS complexes < 0.12 s (three small squares)
Signs and symptoms
Sinus tachycardia is usually a normal physiological response to a need for
increased cardiac output, but may be precipitated by symphathomimetic
drugs or endocrine disturbances.
Common causes of sinus tachycardia include:
• Physiological Exertion, anxiety, pain
• Pathological Fever, anaemia, hypovolaemia,
hypoxaemia, heart failure
• Endocrine Thyrotoxicosis, phaeochoromocytoma
• Pharmacological Adrenalin, atropine, salbutamol, alcohol,
caffeine
Sinus tachycardia. Heart rate of 112 beats/min.

21
Recognition of the underlying cause usually facilitates diagnosis of sinus
tachycardia.A persistent tachycardia in the absence of an obvious
underlying cause should prompt consideration of atrial flutter or atrial
tachycardia.
Treatment
Therapy should be directed towards treating the primary disorder.This may
involve institution of digitalis and/or diuretics for heart failure, oxygen for
hypoxemia, treatment of thyrotoxicosis, volume repletion in dehydration,
aspirin for fever, or tranquillisers for emotional upset.
When a patient has an appropriate tachycardia (e.g. hypoxia or
compensating for low blood pressure such as with fluid loss), slowing it
with beta-blockers can lead to disastrous decompensation.The underlying
problem needs management. If, however, the sinus tachycardia is
inappropriate, as in conditions of anxiety or hyperthyroidism, treatment
with a beta blocking agent or verapamil may be helpful.

Sinus arrhythmia
Sinus arrhythmia, or irregular sinus rhythm, is characterised by a continuous
variation in heart rate.
The variation in cycle length is usually related to respiration and exhibits an
increase during expiration.
The PP and RR cycles usually vary for more than 0.16 of a second.
Diagnosis
• Heart rate varies with respiration
• Atrial and ventricular rate of 60 – 100 beats/min
• Every P wave is followed by a QRS complex
• QRS complex < 0.12 s (three small squares)
Signs and symptoms
Commonly in children and young adults, this is considered normal in the
context of a high vagal tone. The heart rate normally increases during
inspiration as a reflex response to an increased volume of blood returning
to the heart. Sinus arrhythmia is uncommon after the age of 40.
Treatment
The condition is completely harmless and no tests or treatment are
necessary.
Sinus arrhythmia. Sinus rhythm with continuous variation in the length of the PP (and RR) interval.

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Sinoatrial (SA) block
Sinoatrial (SA) block is defined as a reduced or blocked conduction of the
normal impulse spreading from the SA node to the surrounding atrial
muscle. Similar to AV block, it can be divided into three categories. Of
these, only second-degree SA block can be diagnosed using an ordinary
ECG. First-degree SA block is not recorded on an ECG because the
depolarisation of the SA node is not visible.With third-degree block, no P
waves or QRS complexes appear because conduction is totally blocked.
Therefore the ECG cannot be differentiated from the ECG of sinus arrest.

Second-degree SA block
Second-degree sinoatrial block denotes the intermittent failure of
conduction of sinus impulses to the surrounding atrial tissue.This is seen
as a sudden loss of P waves and corresponding QRS complexes. SA block
usually occurs irregularly and unpredictably.
Diagnosis
• P waves and QRS complexes do not appear in the expected position
• An escape beat may appear later in the cycle
• The duration of the block period is usually a multiple of the P-P interval
of the normal rhythm
Signs and symptoms
SA block is seldom clinically significant unless it is a manifestation of drug
toxicity with digitalis, quinidine or other antiarrhythmic drugs. It is
especially prevalent in athletes and youngsters with an increased vagal
tone and is also often associated with uraemia and occasionally
hyperaemia.
Treatment
If the SA block is symptomatic, intravenous atropine may be given.
Second-degree SA block with drop-out of P waves and QRS complex.

Third-degree SA block and sinus arrest
Third-degree SA block and sinus arrest are both characterised by asystole
(isoelectric line) on the ECG because activation of the atria does not occur.
Usually 2-3 seconds pass before an escape rhythm - usually an AV
junctional escape rhythm - supervenes.With SA block, conduction of
impulses from the SA node to the atrium is blocked, while in sinus arrest
the SA node fails to depolarise. It is difficult to differentiate between the
two conditions, but with SA block, the distance between the P waves
before and after the dropped beats is a multiple of the P–P interval.
Diagnosis
• Absence of three or more P waves
• An escape beat may appear later in the cycle
Signs and symptoms
Asymptomatic SA block, with an occasionally dropped P-QRS cycle, is a
relatively common phenomenon especially in children, young adults and
well-trained athletes.
Long periods of sinus arrest may cause fainting attacks but prolonged
unconsciousness is rarely seen.The cause may by increased vagal tone due
to pain, fear, or procedures such as arterial puncture, gastroscopy,
broncoscopy, pleurocentesis etc. SA block is also prevalent during the first
hours after acute myocardial infarction. In the elderly, carotid sinus
stimulation or the valsalva manoeuvre can trigger SA block. Over doses of
digitalis, beta blocking agents or verapamil can be complicated by SA
block. In the so-called sick sinus syndrome, a chronic disease usually
starting after the age of 60, recurrent attacks of fainting or near-fainting
due to third-degree SA block or sinus arrest can be seen.
Third-degree SA block or sinus arrest with missing P waves and QRS complexes.

27
Treatment
In acute episodes, intravenous atropine is given. Recurrent syncope or
presyncope is an indication for permanent pacemaker insertion. Digitalis,
beta-blocker agents, or verapamil toxicity should be considered.

Diagnosis
• P waves absent; oscillating baseline with f (fibrillatory) waves
• Atrial rate of 350 – 600 beats/min
• Irregular ventricular rhythm
• Ventricular rate of 100 – 180 beats/min
Atrial fibrillation (AF)
Atrial fibrillation (AF) is caused by multiple re-entrant circuits of activation
sweeping around the atrial myocardium. It is characterised by irregular
depolarisation in the atria at a rate of 350-600 beats/min appearing as an
irregular wavy base line made up of f (fibrillatory) waves with absent
P waves.
Conduction of atrial impulses to the ventricles is variable and unpredictable
as only a few of the impulses transmit through the atrioventricular node to
produce an irregular ventricular response.This combination of absent
P waves, fine baseline f-wave oscillation and irregular ventricular
complexes is characteristic of atrial fibrillation.The ventricular rate depends
on the degree of atrioventricular conduction, and with normal conduction it
varies between 100 and 180 beats/min.Atrial fibrillation is the most
common sustained arrhythmia in adult populations.
Atrial fibrillation with a fibrillatory line and irregular ventricular complexes.

29
Signs and symptoms
Because of the completely irregular atrial rate, the function of the atria is
disorganised and chaotic with no effective systolic contraction.This
predisposes to thrombus formation in the atria and consequent systemic
emboli. If the ventricular rate is rapid, diastolic filling is reduced and the
patient may experience dyspnoea and peripheral or pulmonary oedema.
The aetiology of atrial fibrillation is closely associated with myocardial
damage and increased atrial pressure.The causes include hypoxaemia,
anaemia, hypertension, congestive heart failure, mitral regurgitation,
thyrotoxicosis, alcohol misuse, cardiomyopathy and post-cardiac surgery.
Treatment
Major goals in the management of atrial fibrillation are ventricular rate
control, assessment of anticoagulation needs and restoration of sinus
rhythm. Reversible and underlying causes of atrial fibrillation should be
investigated and, if possible, corrected.
Haemodynamically unstable atrial fibrillation with a rapid ventricular rate
of (> 120 beats/min) should be electrically cardioverted immediately,
regardless of the duration of the arrhythmia.
Sinoatrial node
Atrioventricular
node
Right atrium
Left atrium
Atrial fibrillation is the result of multiple wavelets of depolarisation
moving around the atria in a chaotic fashion.

Pharmacological rate control is the recommended initial treatment for
stable, rapid atrial fibrillation (ventricular rate of > 120 beats/min)
regardless of its duration. Specific drug treatment depends on the presence
or absence of impaired left ventricular function:
• In patients with preserved left ventricular function, beta-blockers,
calcium blockers (verapamil or diltiazem) and digitalis are reasonable
agents for rate control.
• In patients with congestive heart failure, (ejection fraction of < 40%),
digitalis, diltiazem, and amiodarone are recommended.
Efforts should be made to minimise the risk of thromboembolic
complications that are strongly related to the duration of the arrhythmia
before cardioversion. If atrial fibrillation has been present for > 48 hours,
a risk of systemic embolisation exists with cardioversion to sinus rhythm
unless patients are adequately anticoagulated for at least 3 weeks.
Electrical cardioversion and the use of antiarrhythmic agents should be
avoided unless the patient is unstable or haemodynamically compromised.
If pharmacologic measures fail to prevent recurrence of atrial fibrillation
or control the ventricular rate, non-pharmacologic strategies should be
considered.These include pacemakers, atrial defibrillators, catheter ablation
for either rate control or prevention of atrial fibrillation, and surgery.

Atrial flutter
Atrial flutter is characterised by an atrial rate of between 250 and 350 beats/
min. P waves may be obscured by flutter waves.The AV node has a refractory
period that prevents it from conducting impulses at more than about 230/
min.This results in a degree of atrioventricular block, commonly 2:1 or 3:1
and in a ventricular rate of a half or one third of the atrial rate, typically 150
beats/min.
Diagnosis
• Abnormal P wave morphology, flutter waves
• Atrial rate 250 – 350 beats/min
• Ventricular rhythm usually regular
• Variable ventricular rate
• QRS complex < 0.12 s (three small squares)
Signs and symptoms
This arrhythmia occurs most often in patients with organic heart disease.
Flutter may be paroxysmal, in which case there is usually a precipitating
factor such as pericarditis or acute respiratory failure, or it may be persistent.
Atrial flutter is usually more temporary than atrial fibrillation and commonly,
if it lasts for more than a week, converts into atrial fibrillation. Systemic
embolisation is less common in atrial flutter than in atrial fibrillation.
In contrast to atrial fibrillation, atrial depolarisation in flutter is regular.
Atrial flutter is associated with varying degrees of heart failure depending
on the ventricular response.The most common symptoms are palpitations
and dyspnoea induced by even slight physical exercise.
Atrial flutter showing obvious flutter waves.

33
Treatment
The same applies as for atrial fibrillation.
Sinoatrial node
Atrioventricular
node
Right atrium
Left atrium
Atrial flutter is usually the result of a re-entrant circuit in the right atria.

Atrial tachycardia
Atrial tachycardia differs from sinus tachycardia in that the impulses are
generated by an ectopic focus somewhere within the atrial myocardium
rather than the sinus node.
The P waves are different in configuration to the sinus P wave but usually
of the same polarity, as the pacemaker is most often located in the upper
part of the right atrium.
The atrial (P wave) rate is 140 – 220 beats/min and may be as high as
250 beats/min.At atrial rates of above 200 beats/min, the AV node
struggles to keep up with impulse conduction and AV block may occur.
Sometimes however, the P waves are hidden within the preceding T wave
and are not visible.
Diagnosis
• Abnormal P wave morphology
• Atrial rate of usually 140 – 220 beats/min
• Ventricular rhythm usually regular
• Normal QRS complexes < 0.12 sec. (three small complexes)
Atrial tachycardia interrupted by sinus complexes.

35
Signs and symptoms
Periodic paroxysmal atrial tachycardia can occur in apparently healthy
individuals as well as in individuals with cardiac disease. Most forms of
heart disease are complicated by atrial tachycardia, including ischemic
heart disease, rheumatic heart disease and cardiomyopathy. In addition, it
also manifests in severe chronic lung disease, pulmonary embolism or
digoxin toxicity.
Patients with significant heart disease, such as severe ischemic heart
disease or tight mitral stenosis, may develop congestive heart failure or
pulmonary oedema even though the tachycardia is not very rapid. However,
unless the ventricular rate is very high, individuals without concomitant
heart disease can tolerate atrial tachycardia for longer periods with minimal
or no symptoms.
Treatment
Digitalis intoxication should always be suspected in paroxysmal atrial
tachycardia with block. If however, digitalis is not the cause then it can be
used to control the ventricular response, as can verapamil or a beta-blocker.
Sinoatrial node
Atrioventricular
node
Right atrium
Left atrium
Atrial tachycardia is characterised by an ectopic atrial focus.

Multifocal supraventricular tachycardia
Multifocal supraventricular tachycardia is a type of atrial tachycardia that
occurs when multiple sites in the atria are discharging due to increased
automaticity. It is characterised by P waves of varying morphologies and PR
intervals of different lengths. In contrast to atrial fibrillation, distinct P
waves are seen, separated by isoelectric periods. Every P wave reflects
synchronised atrial depolarisation and a coordinated contraction.The QRS
complexes are usually normal, but widened complexes may be seen if the
atrial rate is high.
Diagnosis
• P waves of varying shape and direction from beat to beat
• P wave frequency of 120 – 150 beats/min
• Varying PR interval
• Irregular rhythm
• Normal QRS complexes of < 0.12 s (three small squares)
Signs and symptoms
Multifocal supraventricular tachycardia can be confused with atrial
fibrillation and is often preceded or followed by atrial fibrillation or
atrial flutter.
Multifocal supraventricular rhythm with P waves of changing shape and varying PR intervals.

37
This relatively uncommon arrhythmia is most frequently seen in patients
with chronic pulmonary disease with cor pulmonale, but may also be seen
in patients with pulmonary emboli, left heart failure, acute myocardial
infarction and hypoxaemia. It may also occur as a terminal feature in
elderly sick patients.
Multifocal supraventricular tachycardia is a bad prognostic sign because it
usually indicates serious underlying heart disease.At rates < 100 beats/min
it is called a multifocal supraventricular rhythm.The ECG picture appears
similar to multifocal supraventricular tachycardia but it is harmless and
does not usually require treatment.
Treatment
Treat the underlying heart disease. In some cases, careful digitalisation may
be warranted, taking note that very ill patients are often sensitive to over
digitalisation.

Diagnosis
• Rapid regular rhythm
• Heart rate of 140 – 220 beats/min
• Normal QRS complexes < 0.12 s (three small squares)
• P waves are often hidden within the QRS complex and are not visible
Signs and symptoms
Episodes of atrioventricular nodal re-entrant tachycardia may begin at any
age.They tend to start and stop abruptly, can occur spontaneously, or are
precipitated by simple movements and may last a few seconds, several
hours, or days.The frequency of episodes varies between several a day to
AV nodal re-entry tachycardia
AV junctional tachycardia is defined as three or more consecutive beats
originating from the AV node or the surrounding area.This paroxysmal
regular, narrow QRS tachycardia involves so-called re-entry either within or
beside the atrioventricular node.
Retrograde atrial depolarisation occurs (backwards) up through the AV
node, which causes the P wave to invert (retrograde). However, since atrial
and ventricular depolarisation often occur simultaneously, the P waves are
frequently buried in the QRS complex and may be totally obscured.
During sinus rhythm the electrocardiogram is normal.
AV junctional (supraventricular) tachycardia with a regular rate of 240 beats/min. P waves visible.

39
one episode in a lifetime. Most patients have only mild symptoms such
as palpitations or the sensation of a rapidly beating heart. More severe
symptoms include dizziness, dyspnoea, weakness, neck pulsation and
central chest pain. Some patients report polyuria.
Treatment
Vagotonic manoeuvres (Valsalva manoeuvre, carotid sinus massage,
swallowing ice cold water), particularly if used before the arrhythmia has
stabilised, may terminate the paroxysm. If these methods are ineffective,
attacks will often stop during sleep.
Acute symptomatic attacks usually respond dramatically to intravenous
adenosine or amiodarone, and beta or calcium channel blockers.
Prophylaxis is difficult, but beta or calcium channel blockers, alone or in
combination, may prove effective. Most patients troubled with this
arrhythmia are suitable candidates for electrophysiological testing and
possibly radio frequency (RF) pathway ablation.

Ventricular tachycardia
Ventricular tachycardia (VT) is defined as a broad-complex tachycardia
consisting of three or more consecutive ventricular beats at a rate of higher
than 120 beats/min. Episodes can be self-terminating, sustained or may
degenerate into ventricular fibrillation.
Impulses originate in pacemakers located distal to the bundle of His, in the
bundle branches, Purkinje fibres or, rarely, in the working myocardium of
the ventricles.The ventricular complexes are widened and bizarre in
appearance because of the abnormal impulse spreading through the
ventricular myocardium. P waves are usually difficult to identify.
Ventricular tachycardia with varying QRS morphology is called polymorphic
VT, which is usually irregular in rate, haemodynamically unstable and likely
to quickly degenerate into ventricular fibrillation (VF). It is often associated
with ischemic heart events, electrolyte imbalance or toxic conditions.A
unique form of polymorphic VT is called torsades de pointes, which usually
Fast ventricular tachycardia (rate of 210 beats/min) precipitated by a ventricular extrasystole.

41
occurs in a setting of bradycardia and prolongation of the QT interval.
Both polymorphic VT and torsades de pointes frequently terminate
spontaneously, but the arrhythmia may recur and seldom remains stable.
Diagnosis
• Independent activation of the atria and ventricles (AV dissociation)
• Wide QRS complexes > 0.12 s of abnormal shape
• Ventricular rate > 120 beats/min
• T waves usually in opposite direction to the QRS complexes
Signs and symptoms
Sustained VT normally occurs at a rate of 150 – 250 beats/min, but the
diagnosis can be difficult.VT can be remarkably well tolerated and may
not cause haemodynamic disturbance. Do not assume therefore, that if
the patient appears well that it is not VT.Any broad QRS tachycardia
(QRS > 0.12 s) should be considered to be VT until proven otherwise.
Sinoatrial node
Atrioventricular
node
Right atrium
Left atrium
Ventricular tachycardia showing abnormal direction of wave of
depolarisation giving rise to abnormal, bizarre QRS complexes.
Right ventricle

The symptoms of ventricular tachycardia can vary from mild palpitations
to dizziness, syncope and cardiac arrest.Always look for an underlying
treatable cause.The causes of ventricular tachycardia include:
• Acute myocardial infarction
• Chronic coronary artery disease
• Cardiomyopathy
• Valvular heart disease (particularly aortic valve disease)
• Mitral valve prolapse
• Myocarditis
• Congenital heart disease
• Electrolyte disturbance (particularly low and high serum potassium)
• Antiarrhythmic drugs
Torsades de pointes ventricular tachycardia with
the cardiac axis rotating, changing from one direction to another and back again.

43
Treatment
When haemodynamic impairment is present, ventricular tachycardia
becomes a medical emergency and warrants immediate synchronised
cardioversion.
However, stable patients can be cardioverted medically.The recommended
treatments for haemodynamically stable VT are intravenous procainamide,
sotalol, amiodarone, or beta-blockers. Each of these is considered
preferable to intravenous lidocaine.
Brief salvos of unsustained VT are common in acute myocardial infarction
but have no immediate or late prognostic significance and should not be
treated.
If any doubt exists as to whether the broad complex tachycardia is a
genuine VT or in fact a SVT with aberrancy, the therapeutic options should
be limited to DC cardioversion, intravenous procainamide or intravenous
amiodarone.
The selection of optimal long-term prophylactic treatment requires an
understanding of the mechanism of the arrhythmia and the disease process
that provides the substrate for the arrhythmia.All patients with sustained
VT should be investigated using invasive electrophysiology and therapy
selected accordingly. Effective drugs include beta-blockers verapamil,
procainamide, propafenone and amiodarone, but bear in mind that
antiarrhythmic agents can produce or exacerbate the very arrhythmias
that they are meant to prevent.
Radio frequency (RF) catheter ablation or surgery can be used to remove
a ventricular focus identified by electrophysiological testing. Finally,
automatic implantable cardiovertor defibrillator (ICD) devices can be used
to deliver low energy DC shocks for recurrent episodes of VT (and VF).

Ventricular fibrillation
Ventricular fibrillation (VF) is the most common initial arrhythmia causing
cardiac arrest and appears as a chaotic rhythm on the ECG.
Ventricular fibrillation can be described as different parts of the ventricular
myocardium depolarising in a chaotic manner independently of each other,
and at a fast and irregular rate. Coordinated ventricular activity and
muscular contraction cease, producing essentially zero cardiac output.
Completely irregular, chaotic and abnormal deflections of varying height
and width are seen on the ECG, which has an irregular base line with no
real QRS complexes.Ventricular fibrillation, in association with acute
myocardial infarction is often provoked by a ventricular extrasystole that
occurs during the first 2/3 of the preceding T wave, the so-called R-on-T
phenomenon. In chronic ischemic heart disease, ventricular fibrillation is
usually preceded by an episode of ventricular tachycardia that may
suddenly degenerate into ventricular fibrillation without warning.
Diagnosis
• Rapid irregular rough base line
• Bizarre ventricular patterns of varying size and configuration
• Frequency of 250-600 beats/min
Onset of ventricular fibrillation precipitated by a ventricular extrasystole falling on the T wave (R on T phenomenon).

45
Signs and symptoms
During ventricular fibrillation, the heart ceases to pump after approximately
10 seconds and clinical cardiac arrest accompanied by loss of consciousness.
If left untreated, death follows after a few minutes.The cause of ventricular
fibrillation is mainly coronary artery disease, which occurs most frequent
during the first few hours after myocardial infarction (primary VF).Ventricular
fibrillation can be caused by electrical accidents, serious electrolyte
disturbances, drowning, choking, hypothermia and drug toxicity (digoxin,
tricyclic antidepressants, quinidine and others).
VF that occurs in the absence of myocardial infarction is usually related to
severe underlying coronary artery disease and is likely to recur in patients
who survive. Such patients warrant detailed investigation, including exercise
testing, coronary angiography and invasive electrophysiology.
Treatment
VF is fatal unless reversed by immediate DC cardioversion. Success rates of
95% are common for DC cardioversion of primary VF, and short-term and
long-term prognoses are excellent.The success of defibrillation is time
dependent with a 2 to 10 % decline in success rate per minute of cardiac
arrest. Prompt DC cardioversion is far more efficient in resuscitation than
pharmacological therapy.
If an immediate DC shock of 200 joules is unsuccessful, a second shock of
200 to 300 joules is given and a third of 360 joules is used if VF persists.
These three shocks should be delivered consecutively without interruption
for CPR or drug therapy.After three unsuccessful defibrillation attempts,
rescuers must move quickly to accomplish tracheal intubation and gain
access to the circulation with an intravenous line. Once the intravenous line
is established, epinephrine 1 mg is administered, followed by another
attempt to defibrillate at 360 joules.The dose of epinephrine may be
repeated after intervals of 3 to 5 min. Following each dose of epinephrine,
attempts to defibrillate at 360 joules are repeated within 30 to 60 seconds.
After the initial unsuccessful defibrillation attempts, or with persistent
electrical instability, a rapid infusion of 300 mg amiodarone is given. For
persistent or recurrent ventricular fibrillation, a second dose of 150 mg is
given intravenously.As an alternative, a bolus of 1.5 mg/kg lidocaine is
given intravenously and the dose is repeated after 2 min in those patients
who have persistent ventricular arrhythmias or remain in ventricular
fibrillation.

Atrioventricular (AV) block
Atrioventricular (AV) block is characterised by a delay or failure in impulse
conduction from the atria to the ventricles. It occurs in three degrees of
severity: first-degree AV block simply lengthens the PR interval by delaying
conduction through the AV node, in second-degree AV block, some atrial
impulses fail to be conducted to the ventricles, and in third-degree AV
block, there is no conduction between atria and ventricles.

47
First-degree AV block
Prolongation of the PR interval is a common finding and indicates that
conduction through the AV node has been delayed.When this delay is
constant for each cardiac cycle, and a QRS complex follows each P wave,
it is referred to as first-degree AV block.
Diagnosis
• PR interval > 0.22 s (five and a half small squares)
• Normal P wave and QRS complex
• All P waves are followed by a QRS complex
Signs and symptoms
First-degree AV block in itself is asymptomatic and does not generally
progress to other more serious sorts of heart block. It is normal when
it accompanies a vagally induced bradycardia, as an increase in vagal tone
decreases AV nodal conduction.A prolonged conduction time is frequently
found in well-trained athletes and the elderly. First-degree AV block may
occur after beta-blocker or digitalis treatment and in electrolyte
disturbances such as hyperkalemia. It is also associated with ischemic heart
disease, myocarditis, acute rheumatic fever and sarcoid heart disease.
Intermittent first-degree AV block often accompanies acute infections.
Treatment
No specific treatment is necessary for first-degree AV block in its own right,
but may suggest further investigation is required.
Sinus rhythm with first-degree AV block (PR interval 0.26 s).

Second-degree AV block
Second-degree AV block occurs when there is intermittent failure or
absence of atrioventricular conduction, which is characterised by some P
waves failing to produce a QRS complex. It is subdivided into Mobitz type I
block (Wenckebach), Mobitz type II block and advanced AV block.

49
Signs and symptoms
Mobitz type I AV block is thought to result from abnormal conduction
through the AV node itself and can simply occur during periods of high
vagal activity as it does during sleep. It may also occur in generalised
disease of the conducting tissue, is usually periodic and of shorter
duration than Mobitz type II AV block and can commonly be seen in
digitalis overdose and inferior wall infarction. Haemodynamic
compromise is not usually a feature of this condition.
Treatment
Mobitz type I AV block is regarded as a relatively benign form of AV
block, but in rare cases where it is complicated by severe symptomatic
bradycardia, intravenous atropine given in
repeat doses of 0.5 to 1.0 mg every 3 to 5
minutes usually proves effective in
immediately accelerating heart rate and
alleviating all bradycardia-related symptoms.
Second-degree AV block - Mobitz type I is characterised by a progressive
increase in the conduction time over several beats, until an impulse is
totally blocked and the corresponding QRS complex does not appear.This
phenomenon repeats itself with a gradual prolongation of the PR interval
over 3 to 6 beats until a P wave occurs without a following QRS complex.
Diagnosis
• Normal P wave and QRS complex
• Gradual increase in the PR interval until a P wave is not followed by
a QRS complex
• PR interval resets to normal and the cycle repeats itself
Sinus rhythm with progressive lengthening of the PR interval until a QRS
complex is dropped completely: second-degree AV block Mobitz type I.
Second-degree AV block - Mobitz type I (Wenckebach)

Signs and symptoms
The block in conduction is thought to result from abnormal conduction
below the AV node (in the bundle of His or bilaterally in the bundle branches).
Haemodynamic upset is common with signs of circulatory disturbance
accompanied by a feeling of remoteness. Clinical symptoms include chest
pain, shortness of breath and decreased level of consciousness. Common
signs are low blood pressure, shock, pulmonary congestion or congestive
heart failure.
If the block has an acute onset, it is often associated with an acute
myocardial infarction (anteroseptal or inferior), while chronic AV block is
Second-degree AV block - Mobitz type II
Second-degree AV block - Mobitz type II - is characterised by an occasional
dropped QRS complex without preceding changes in the PR interval.The PR
interval may be either normal or slightly prolonged, but remains constant
from one P-QRS complex to the next.
Diagnosis
• Normal P waves and QRS complexes
• PR interval normal and constant
• Some P waves are not followed by a QRS complex
Sinus rhythm with occasional drop-out of a QRS complex; second-degree AV block Mobitz type II.

51
catecholamines such as epinephrine or isoproterenol at rates of 2 to
10 µg/min can be used for short-term therapy.
The use of atropine, transcutaneous pacing or intravenous infusion of
catecholamines are usually the first line of treatment before the insertion
of a temporary pacing electrode for ventricular pacing.Temporary pacing
is usually achieved by the transvenous insertion of an electrode catheter,
with the catheter positioned in the right ventricular apex and attached to
an external pulse-generator.
Catecholamines should be used with extreme caution or not at all in
patients who have acute myocardial infarction.
Drugs do not have any significant role to play in the long-term
management of patients with symptomatic AV block.The only final
treatment of patients who have an AV block and are symptomatic,
is the subcutaneous or retropectoral implantation of a permanent
cardiac pacemaker.
often due to degenerative changes in the conduction system. Mobitz type II
AV block is often caused by irreversible damage and is considered more
serious than Mobitz type I, as it can progress without warning to total AV
block.
Treatment
If the patient has serious signs and symptoms, make sure they are related
to the slow rate and not for example, to hypotension due to myocardial
dysfunction or hypovolemia. If the bradycardia is severe and the clinical
condition is unstable, atropine 0.5 to 1.0 mg can be given intravenously in
repeat doses every 3 to 5 minutes.Transcutaneous pacing is always
appropriate and should be initiated quickly in patients who do not respond
to atropine or who are severely symptomatic, especially when the block is
at or below the His-Purkinje level. Dopamine (at rates of 2 to 5 µg/kg per
minute) can be added and increased quickly to 5 to 20 µg/kg per minute if
low blood pressure is associated with the bradycardia.Alternatively, other

With advanced AV block, a mathematical relationship exists between
P waves and QRS complexes, e.g., 2:1, 3:1 or 4:1. It thus encompasses:
• 2:1 AV block with AV conduction of every second P wave and a
corresponding drop-out of every second QRS complex
• 3:1 AV block with AV conduction of every third P wave and a
corresponding drop-out of two in every three QRS complexes
• 4:1 AV block with AV conduction of every fourth P waves and a
corresponding drop-out of three in every four QRS complexes
Advanced second-degree AV block
Advanced AV or high-grade AV block is characterised by an alternate
drop-out of the QRS complex, or the drop-out of two or more QRS
consecutive complexes.Advanced AV block cannot be categorised as
Mobitz type I or type II because it is impossible to say whether the PR
interval for the non-conducted P waves would have been the same as,
or longer than, the conducted P waves.
Advanced second-degree AV block with AV conduction of every other P wave (2:1 AV block).

53
Diagnosis
• Normal P waves
• Alternate P waves are not followed by a QRS complex
Signs and symptoms
Same as for Mobitz type II AV block.
Treatment
Same as for Mobitz type II AV block.

Diagnosis
• Normal P waves with regular rhythm
• QRS complexes with an almost regular rhythm but unrelated to P waves
• Slow QRS frequency (< 60 beats/min)
• QRS complexes normal or widened depending on site of ventricular
pacemaker
Third-degree (complete) AV block
Third-degree AV block is the most advanced state of AV block in which
there is complete absence of conduction of impulses from the atria to the
ventricles. Independent pacemakers asynchronously control the arteria and
ventricles.
In most cases, the ventricular pacemaker function is taken over by a focus
below the block, and the heartbeat can then be sustained by impulses from
the area around the AV node or the ventricles.A nodal escape rhythm often
gives a ventricular rate of 40–60/min and a ventricular escape rhythm a
rate of 30–40 beats/min. If an escape rhythm does not develop, it is called
ventricular standstill, which is fatal if untreated.
Third-degree AV block with AV junctional escape rhythm. Sinus P waves in a regular rhythm at a rate
of 76 beats/min and narrow QRS complexes at a regular but slower rate of 38 beats/min.

55
Signs and symptoms
Clinical symptoms include chest pain, shortness of breath and decreased
level of consciousness while common signs are low blood pressure, shock,
pulmonary congestion or congestive heart failure.
If the cause is acute inferior myocardial infarction, drug toxicity or acute
peri/-myocarditis, total AV block is normally a temporary phenomenon. On
the other hand, anteroseptal infarctions will lead to irreversible damage.
Congenital AV block and blocks seen in elderly patients are also
irreversible. Complete AV block may be entirely asymptomatic but is often
associated with syncopal attacks. Heart failure develops less commonly,
and prolonged ventricular arrest causes sudden death.
Treatment
For short-term therapy, when the block is likely to be fleeting but still
requires treatment or until adequate pacing therapy can be established,
isoproterenol infusion can be used transiently. It should be remembered
however, that catecholamines cannot be relied on to increase the heart rate
for more than several hours to several days in patients with symptomatic
heart block without producing significant side effects.
Permanent pacemaker implantation is clearly indicated in all symptomatic
patients with third-degree AV block, and should be seriously considered in
asymptomatic cases.

Extrasystoles (ectopic beats)
Extrasystoles or ectopic beats are triggered by premature depolarisation of
an ectopic focus outside the sinus node. Usually, a fixed distance exists
between the normal beat and the extrasystole, which is called the constant
coupling interval. In some cases, the extrasystoles occur irregularly among
the normal beats while in others, extrasystoles can be frequent and occur
at regular intervals, e.g. every second, third or fourth beat can be an
extrasystole termed bigeminy, trigeminy or quadrigeminy, respectively.
Depending on its origin, it is possible to differentiate between ventricular
and supraventricular extrasystoles.

configuration, but if those derived from more than one focus have different
shapes they are called multifocal ventricular extrasystoles.
Diagnosis
• Premature QRS complex
• A wide, tall and abnormal QRS complex (>0.12 s)
• T wave, often inverted
• Fully compensatory postextrasystolic pause
Ventricular extrasystoles or ventricular ectopic beats are caused by an
electric impulse from an area in either the right or the left ventricle
occurring before the impulse from the SA node has passed the AV node.
The impulse conduction through the ventricles becomes abnormal, and the
resultant QRS complexes are widened and abnormal.The extrasystoles are
followed by a pause (the postextrasystolic pause) but the interval between
the preceding and following beat is still twice as long as the normal
interval in the basic sinus rhythm.The postextrasystolic pause is said to be
fully compensatory. Extrasystoles from the same focus have the same ECG
Sinus rhythm with one ventricular extrasystole.
Ventricular extrasystoles (ventricular ectopic beats)

59
Signs and symptoms
Ventricular extrasystoles are very common, especially after acute myocardial
infarction or heart surgery and are also associated with hyperkalemia,
hypoxemia and digoxin toxicity.Ventricular extrasystoles produce a reduced
or impalpable peripheral pulse because of poor diastolic filling, but do not
usually cause any haemodynamic upset unless they occur very frequently.
In bigeminy the pulse rate and effective cardiac output may be halved,
possibly provoking or worsening heart failure in the sick patient. During
ventricular re-polarisation, the heart is electrically unstable for a period
corresponding to the first 2/3 of the T wave, also called the vulnerable
period.A ventricular extrasystole occurring during this period (“the R-on-T
phenomenon”) might lead to ventricular fibrillation in patients with acute
myocardial infarction.
Sinus rhythm with ventricular bigeminy.

the ventricular ectopics with antiarrhythmic agents. Beta-blockers may be
successful in managing ventricular extrasystoles that occur primarily in the
daytime or under stressful situations and in specific cases, such as mitral
valve disease or thyrotoxicosis.
In the setting of chronic cardiac disease, the presence of multifocal
ventricular ectopics, bigeminy, short coupling intervals (R-on-T-
phenomenon), and salvos of three or more ectopic beats are suggestive of
Treatment
In the absence of cardiac disease, isolated asymptomatic ventricular ectopics
regardless of their configuration and frequency, need not be treated. Routine
treatment with antiarrhythmic drugs has not been shown to decrease risk of
sudden death. However, some patients may be significantly troubled by
symptoms caused by the ectopic beat, the compensatory pause or the
following sinus beat.These symptoms should first be addressed by allaying
the patient’s anxiety, or if this is not successful, reducing the frequency of
Sinus rhythm with multifocal ventricular extrasystoles.

61
increased risk of sudden cardiac death. In these instances invasive
electrophysiologic testing and catheter ablation or implantable
cardioverter/defibrillator (ICD) placement should be considered.

originates from a nodal focus, the P wave will usually be inverted and may
be seen before or after the QRS complex, or may even be completely
hidden. Impulse conduction from the AV node through to the ventricles
occurs along the normal pathway, thus producing a normal QRS complex.
In this case, the postextrasystolic pause is said to be not fully compensatory.
Diagnosis
• The P wave and the corresponding QRS complex appear prematurely
• The P wave differs in shape from the P wave in sinus rhythm
• Normal QRS complex < 0.12 s (three small squares)
• No compensatory pause
Signs and symptoms
Supraventricular extrasystoles are very common, but are rarely of any
clinical significance. Common causes are beta 2 agonist therapy, chronic
obstructive pulmonary disease or alcohol intake.Three or more consecutive
supraventricular extrasystoles are called supraventricular tachycardia and
an increase in their frequency may signify impending atrial fibrillation.
Supraventricular extrasystoles
(atrial ectopic beats)
A supraventricular extrasystole or atrial ectopic beat originates in the atria
or around the AV node and is called an atrial or nodal extrasystole,
respectively.The P wave appears prematurely and differs in form from the
normal sinus P wave.The PR interval is usually shorter. If the extrasystole
Sinus tachycardia with one supraventricular extrasystole.

63
Treatment
Supraventricular extrasystoles are usually harmless and do not require
treatment unless the patient complains of palpitations. In this case,
a beta blocking agent or verapamil may be helpful.

The AV junctional pacemaker will continue until it again starts to be
inhibited by impulses from the SA node. If the AV junction pacemaker fails
or its impulses are blocked, a ventricular pacemaker will take over. Its
rhythm is even slower, at 30 – 40 beats/min, and the QRS complexes will
be wide and abnormal.
Escape rhythms
Escape rhythms are a form of a “safety net” for the heart and develop in
response to a block or bradycardia. It serves to maintain the vital activation
of the ventricles and in turn the pumping activity of the heart.The heart
has a number of subsidiary ectopic pacemakers that can assume control if
normal impulse generation or conduction fails.
The subsidiary pacemakers are located in the AV junction and the ventricular
myocardium. If the AV junction fails to receive impulses as a result of SA
arrest or block, or even during severe sinus bradycardia, it will take over as
the cardiac pacemaker.The QRS complexes generated will have the same
morphology as normal but at a slower rate of around 40 – 60 beats/min.
Sinus rhythm with second-degree SA block and two AV junctional escape beats.

65
Diagnosis
AV junctional escape rhythm:
• Normal QRS complexes < 0.12 s (three small complexes)
• Ventricular rate 40 – 60 beats/min
• P waves retrograde (inverted) and most often hidden within the QRS
complex
Ventricular escape rhythm:
• Wide QRS complexes > 0.12 s (three small complexes) of abnormal
shape
• Ventricular rate 30 – 40 beats/min
Signs and symptoms
Episodes of AV junctional escape rhythm may be induced by high vagal
tone and are not uncommon findings in apparently healthy athletes and
children.They develop secondarily to sinus bradycardia and AV block but
may also occur as an early sign of digitalis over-dosage.
The most common cause of ventricular escape rhythm is third-degree AV
block.
Treatment
Because escape rhythms exist as a safety net, they must not be suppressed.
Attempts should rather be made to determine the cause of the escape
rhythm and correct the underlying problem.
Two sinus complexes followed by third-degree SA block (or sinus arrest) and ventricular escape rhythm.

Alternating current interference. This appears as fluctuations with a
constant amplitude and frequency (50Hz) superimposed on the waveform.
It can be remedied by:
• Ensuring the best possible electrode contact.
• Switching off radios and lamps.
• Moving the patient away from plugs and cables in the wall.
• Placing the ECG electrodes parallel to the patient’s vertical axis.
Common Tracing Problems
Large amplitude deflections. The amplitude of the signal in patients
with ventricular hypertrophy may be halved by adjusting the test signal to
give deflections of 5 mm (1 mV).
Poor electrode technique. This appears as irregular fluctuations in the
recording. Obtain better contact with the skin, change the electrodes or, if
using dry (non-gelled) electrodes, apply more electrode paste.
Defective cables. Sharp fluctuations or an isoelectric waveform may be
seen. If disturbances can be produced by gently pulling the cable, change
the cable.
Muscular activity. This appears as fast irregular fluctuations with an
amplitude exceeding that of the ECG.This can be remedied by making the
patient more comfortable, and by asking him to relax.
The electrodes may be moved so that they are overlying bone. If possible,
connect a filter to limit electrical interference.

67
All rights reserved. No part of this publication may be reproduced, stored in a retrieval system or transmitted in
any form by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior written
permission of Ambu A/S.
Ambu is one of the world’s leading suppliers of innovative diagnostic and
life-support devices, carefully designed to provide genuine value and ultimately
improve the quality of patient care. Key business areas include respiratory care,
cardiology, neurology, training, and immobilization.
Headquartered in Copenhagen, Denmark,Ambu’s products are sold worldwide
through an international network of subsidiaries and distributors.The company
has over 900 employees at its manufacturing and sales facilities in Europe,
Asia, and North America, and is publicly traded on the Copenhagen Stock
Exchange.

Ambu Ltd.
Burrel Road
St. Ives
Cambridgeshire PE27 3LE
T +44 1 480 498 403
F +44 1 480 498 405
www.ambu.co.uk
Ambu A/S
Baltorpbakken 13
DK-2750 Ballerup
Denmark
T +45 72 25 20 00
F +45 72 25 20 50
www.ambu.com
ambu@ambu.com
496103221-05/2008ISBN978-87-984226-2-4

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