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Part II
June Edhouse
This article continues the discussion,
started last week, on ventricular tachycardias and also examines how to
determine whether a broad complex tachycardia is ventricular or
supraventricular in origin.
Fascicular tachycardia

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Fascicular ventricular tachycardia (note the right bundle branch
block pattern and left axis deviation)
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Ventricular tachycardias
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Ventricular tachycardias
Broad complex tachycardias of...
Differentiating between...
Fascicular tachycardia is uncommon and not usually associated
with underlying structural heart disease. It originates from the region
of the posterior fascicle (or occasionally the anterior fascicle) of
the left bundle branch and is partly propagated by the His-Purkinje
network. It therefore produces QRS complexes of relatively short
duration (0.11-0.14 s). Consequently, this arrhythmia is commonly
misdiagnosed as a supraventricular tachycardia.

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Right ventricular outflow track tachycardia
The QRS complexes have a right bundle branch block pattern, often with a small Q wave rather than primary R wave in lead V1 and a deep S wave in lead V6. When the tachycardia originates from the posterior fascicle the frontal plane axis of the QRS complex is deviated to the left; when it originates from the anterior fascicle, right axis deviation is seen.
Right ventricular outflow tract tachycardia
This tachycardia originates from the right ventricular outflow
tract, and the impulse spreads inferiorly. The electrocardiogram
typically shows right axis deviation, with a left bundle branch block
pattern. The tachycardia may be brief and self terminating or
sustained, and it may be provoked by catecholamine release, sudden
changes in heart rate, and exercise. The tachycardia usually responds
to drugs such as
blockers or calcium antagonists. Occasionally the
arrhythmia stops with adenosine treatment and so may be misdiagnosed as
a supraventricular tachycardia.
Torsades de pointes tachycardia
Torsades de pointes ("twisting of points") is a type of
polymorphic ventricular tachycardia in which the cardiac axis rotates
over a sequence of 5-20 beats, changing from one direction to another
and back again. The QRS amplitude varies similarly, such that the
complexes appear to twist around the baseline. In sinus rhythm the QT
interval is prolonged and prominent U waves may be seen.
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Torsades de pointes may be drug induced or secondary to electrolyte disturbances |
Torsades de pointes is not usually sustained, but it will recur unless the underlying cause is corrected. Occasionally it may be prolonged or degenerate into ventricular fibrillation. It is associated with conditions that prolong the QT interval.
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Transient prolongation of the QT interval is often seen in the
acute phase of myocardial infarction, and this may lead to torsades de pointes. Ability to recognise
torsades de pointes is important because its management is different
from the management of other ventricular tachycardias.
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Causes of torsades de pointes
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Polymorphic ventricular tachycardia
Polymorphic ventricular tachycardia has the electrocardiographic characteristics of torsades de pointes but in
sinus rhythm the QT interval is normal. It is much less common than
torsades de pointes. If sustained, polymorphic ventricular tachycardia
often leads to haemodynamic collapse. It can occur in acute myocardial
infarction and may deteriorate into ventricular fibrillation.
Polymorphic ventricular tachycardia must be differentiated from atrial
fibrillation with pre-excitation, as both have the appearance of an
irregular broad complex tachycardia with variable QRS morphology (see
last week's article).
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Differentiation between ventricular tachycardia and
supraventricular tachycardia with bundle branch block
If the tachycardia has a right bundle branch block morphology (a predominantly positive QRS complex in lead V1), a ventricular origin is suggested if there is:
If the tachycardia has a left bundle branch block morphology (a predominantly negative deflection in lead V1), a ventricular origin is suggested if there is:
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Broad complex tachycardias of supraventricular origin |
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In the presence of aberrant conduction or ventricular pre-excitation, any supraventricular tachycardia may present as a broad complex tachycardia and mimic ventricular tachycardia.
Atrial tachycardia with aberrant conduction
Aberrant conduction is defined as conduction through the
atrioventricular node with delay or block, resulting in a broader QRS
complex. Aberrant conduction usually manifests as left or right bundle
branch block, both of which have characteristic features. The bundle
branch block may predate the tachycardia, or it may be a rate related
functional block, occurring when atrial impulses arrive too rapidly for
a bundle branch to conduct normally. When atrial fibrillation occurs
with aberrant conduction and a rapid ventricular response, a totally
irregular broad complex tachycardia is
produced.
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The Wolff-Parkinson-White syndrome is discussed in more detail in an earlier article, on junctional tachycardias |
Wolff-Parkinson-White syndrome
Broad complex tachycardias may also occur in the
Wolff-Parkinson-White syndrome, either as an antidromic atrioventricular re-entrant tachycardia or in association with atrial
flutter or fibrillation.
Antidromic atrioventricular re-entrant
tachycardia
In this relatively uncommon tachycardia the impulse is
conducted from the atria to the ventricles via the accessory pathway.
The resulting tachycardia has broad, bizarre QRS complexes.
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Atrial fibrillation
In patients without an accessory pathway the atrioventricular
node protects the ventricles from the rapid atrial activity that occurs
during atrial fibrillation. In the Wolff-Parkinson-White syndrome the
atrial impulses are conducted down the accessory pathway, which may
allow rapid conduction and consequently very fast ventricular rates.
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Drugs
that block the atrioventricular node |
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Differentiating between ventricular and supraventricular origin |
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Clinical presentation
Age is a useful factor in determining
the origin of a broad complex tachycardia: a tachycardia in patients aged over 35 years is more likely to be ventricular in origin. A
history that includes ischaemic heart disease or congestive cardiac
failure is 90% predictive of ventricular tachycardia.
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Danger of misdiagnosis
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The symptoms associated with broad complex tachycardia depend
on the haemodynamic consequences of the arrhythmia
that is, they
relate to the heart rate and the underlying cardiac reserve rather than
to the origin of the arrhythmia. It is wrong to assume that a patient
with ventricular tachycardia will inevitably be in a state of collapse;
some patients look well but present with dizziness, palpitations,
syncope, chest pain, or heart failure. In contrast, a supraventricular
tachycardia may cause collapse in a patient with underlying poor
ventricular function.
Clinical evidence of atrioventricular dissociation
that is,
"cannon" waves in the jugular venous pulse or variable intensity of
the first heart sound
indicates a diagnosis of a ventricular tachycardia The absence of these findings, however, does not exclude the diagnosis.
Electrocardiographic differences
Direct evidence of independent P wave activity is highly
suggestive of ventricular tachycardia, as is the presence of fusion
beats or captured beats. The duration of QRS complexes is also a key
differentiating feature: those of >0.14 s generally indicate a
ventricular origin. Concordance throughout the chest leads also
indicates ventricular tachycardia.
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In ventricular tachycardia the rhythm is regular or almost regular; if the rhythm is obviously irregular the most likely diagnosis is atrial fibrillation with either aberrant conduction or pre-excitation |
A previous electrocardiogram may give valuable information. Evidence of a myocardial infarction increases the likelihood of ventricular tachycardia, and if the mean frontal plane axis changes during the tachycardia (especially if the change is >40° to the left or right) this points to a ventricular origin.
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Adenosine can also be used to block conduction temporarily through the atrioventricular node to ascertain the origin of a broad complex tachycardia, but failure to stop the tachycardia does not necessarily indicate a ventricular origin |
Ventricular tachycardia and supraventricular tachycardia with bundle branch block may produce similar electrocardiograms. If a previous electrocardiogram shows a bundle branch block pattern during sinus rhythm that is similar to or identical with that during the tachycardia, the origin of the tachycardia is likely to be supraventricular. But if the QRS morphology changes during the tachycardia, a ventricular origin is indicated.
The emergency management of a broad complex tachycardia
depends on the wellbeing of the patient and the origin of the
arrhythmia. Vagal stimulation
for example, carotid sinus massage or
the Valsalva manoeuvre
does not usually affect a ventricular
tachycardia but may affect arrhythmias of supraventricular origin. By
transiently slowing or blocking conduction through the atrioventricular
node, an atrioventricular nodal re-entrant tachycardia or
atrioventricular re-entrant tachycardia may be terminated. In atrial
flutter transient block may reveal the underlying flutter waves.
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Footnotes |
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The ABC of clinical electrocardiography is edited by Francis Morris, consultant in emergency medicine at the Northern General Hospital, Sheffield; June Edhouse, consultant in emergency medicine, Stepping Hill Hospital, Stockport; William J Brady, associate professor, programme director, and vice chair, department of emergency medicine, University of Virginia, Charlottesville, VA, USA; and John Camm, professor of clinical cardiology, St George's Hospital Medical School, London. The series will be published as a book in the summer.
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