Ventricular tachycardia
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Ventricular
tachycardia (V-tach
or VT) is a tachycardia, or fast heart rhythm, that originates in one of the ventricles of the heart. The ventricles are the main pumping
chambers of the heart. This is a potentially life-threatening arrhythmia because it may lead to ventricular fibrillation, asystole, and sudden death.
Classification[edit]
12 lead electrocardiogram showing a run of monomorphic
ventricular tachycardia (VT)
Ventricular
tachycardia can be classi fied
based on its morphology:
- Monomorphic
ventricular tachycardia means that the appearance of all the beats match each other in each lead of a surface electrocardiogram (ECG).
- Scar
related monomorphic ventricular tachycardia is the most common type and a
frequent cause of death in patients who have survived a heart attack or myocardial infarction especially if they have weak
heart muscle.[1]
- RVOT
tachycardia is a type of monomorphic ventricular tachycardia originating
in the right ventricular outflow tract. RVOT
morphology refers to the characteristic pattern of this type of
tachycardia on an ECG.
- Polymorphic
ventricular tachycardia, on the other hand, has beat-to-beat variations in
morphology. This may appear as a cyclical progressive change in cardi ac axis, previously
referred to by its French name
torsades de pointes ("twisting of the
points"). However, currently the term torsades is reserved for
polymorphic VT occurring in the context of a prolonged resting QT
interval.
Another way
to classify ventricular
tachycardias is the duration of the episodes: Three or more beats in a
row on an ECG that originate from the ventricle at a rate of more than 100
beats per minute constitute a ventricular tachycardia.
- If the
fast rhythm self-terminates within 30 seconds, it is considered a
non-sustained ventricular tachycardia.
- If the
rhythm lasts more than 30 seconds, it is known as a sustained ventricular
tachycardia (even if it terminates on its own after 30 seconds).
A third way to
classify ventricular tachycardia is on the basis of its symptoms:
Pulseless VT is associated with no effective cardiac output, hence, no
effective pulse, and is a cause of cardiac arrest. In this circumstance, it is
best treated the same way as ventricular fibrillation (VF), and is recognized
as one of the shockable rhythms on the cardiac arrest protocol. Some VT is
associated with reasonable cardiac output and may even be asymptomatic. The
heart usually tolerates this rhythm poorly in the medium to long term, and
patients may certainly deteriorate to pulseless VT or to VF.
Less common is
ventricular tachycardia which occurs in individuals with structurally normal
hearts. This is known as idiopathic ventricular tachycardia and in the
Monomorphic form appears with little or no incidence of increased risk of
sudden cardiac death. In general, idiopathic ventricular tachycardia occurs in
younger individuals diagnosed with VT. While the causes of idiopathic VT are MI
or cardiomyopathy, it is generally presumed to be congenital, and can be
brought on by any number of diverse factors.
Pathophysiology[edit]
The morphology
of the tachycardia depends on its cause.
In monomorphic
ventricular tachycardia, all the beats look the same because the impulse is
either being generated from increased automaticity of a single point in either the left or right ventricle, or due to a reentry circuit within
the ventricle. The most common cause of monomorphic ventricular tachycardia is myocardial scarring from a previous myocardial infarction (heart attack). This scar cannot conduct electrical
activity, so there is a potential circuit around the scar that results
in the tachycardia. This is similar to the re-entrant circuits that are the
cause of atrial flutter and the re-entrant forms of supraventricular tachycardia. Other rarer congenital causes of
monomorphic VT include right ventricular dysplasia, and right and left
ventricular outflow tract VT.
Polymorphic
ventricular tachycardia, on the other hand, is most commonly caused by
abnormalities of ventricular muscle repolarization. The predisposition to this
problem usually manifests on the ECG as a prolongation of the QT interval. QT
prolongation may be congenital or acquired. Congenital problems include Long QT syndrome and Catecholaminergic polymorphic
ventricular tachycardia. Acquired problems are usually related to drug toxicity
or electrolyte abnormalities, but can occur as a result of myocardial ischemia.
Class III anti-arrhythmic drugs such as sotalol and amiodarone prolong the QT interval and may in
some circumstances be pro-arrhythmic. Other relatively common drugs including
some antibiotics and antihistamines may also be a danger, particularly in
combination with one another. Problems with blood levels of potassium,
magnesium and calcium may also contribute. High dose magnesium is often used as
an antidote in cardiac arrest protocols.
Diagnosis[edit]
The diagnosis of ventricular tachycardia is made
based on the rhythm seen on either a 12 lead ECG or a telemetry rhythm strip.
It may be very difficult to differentiate between ventricular tachycardia and a
wide-complex supraventricular tachycardia in some cases. In particular,
supraventricular tachycardias with aberrant conduction from pre-existing bundle branch block are commonly misdiagnosed as ventricular tachycardia.
Other rarer phenomena include ashman beats and antedromic atrioventricular re-entry tachcyardias.[citation needed]
Various diagnostic
criteria have been developed to determine whether a wide complex tachycardia is
ventricular tachycardia or a more benign rhythm.[2][3] In addition to these diagnostic
criteria, if the individual has a past history of a myocardial infarction, congestive heart failure, or recent angina, the wide complex tachycardia is much
more likely to be ventricular tachycardia.[4]
The proper
diagnosis is important, as the misdiagnosis of supraventricular tachycardia
when ventricular tachycardia is present is associated with worse prognosis.
This is particularly true if calcium channel blockers, such as verapamil, are used to attempt to terminate a
presumed supraventricular tachycardia.[5] It is therefore wisest to assume that
all wide complex tachycardia is VT until proven otherwise...
Treatment[edit]
Therapy may be
directed at either terminating an episode of the arrhythmia or at suppressing a
future episode from occurring. The treatment for stable VT is tailored to the
specific patient, with regard to how well the individual tolerates episodes of
ventricular tachycardia, how frequently episodes occur, their comorbidities,
and their wishes. Patients suffering from pulseless VT or unstable VT are
hemodynamically compromised and require immediate cardioversion.
Synchronized electrical cardioversion[edit]
If the patient
still has a pulse, it is usually possible to terminate a VT episode with a
direct current shock across the heart, that is delivered from one side of the
chest to the other, or from the front to the back. This is ideally synchronized
to the patient's heartbeat, in order to avoid degeneration of the rhythm to ventricular fibrillation. As this is quite uncomfortable,
shocks should be delivered only to an unconscious or sedated patient. As a
reminder, this is different from defibrillating the patient; see next
paragraph.
Defibrillation[edit]
A patient with
pulseless VT or ventricular fibrillation will be unconscious and treated as an
emergency on an ACLS protocol, given high energy (360J with a monophasic
defibrillator, or 200J with a biphasic defibrillator) unsynchronised
cardioversion (defibrillation).
The shock may
be delivered to the outside of the chest using the two pads of an external
defibrillator, or internally to the heart by an implantable cardioverter-defibrillator (ICD) if one has previously been
inserted.
An ICD may also
be set to attempt to overdrive pace the ventricle. Pacing the ventricle at a
rate faster than the underlying tachycardia can sometimes be effective in
terminating the rhythm. If this fails after a short trial, the ICD will usually
stop pacing, charge up and deliver a defibrillation grade shock.
Cardiac ablation[edit]
Catheter
ablation is a key therapeutic modality for patients with recurrent VT.[6]
There was
consensus among the task force members that catheter ablation for VT should
generally be considered early in the treatment of patients with recurrent VT.
In the past, ablation was often not considered until pharmacological options
had been exhausted, often after the patient had suffered substantial morbidity
from recurrent episodes of VT and ICD shocks. Antiarrhythmic medications can
reduce the frequency of ICD therapies, but have disappointing efficacy and side
effects. Advances in technology and understanding of VT substrates now allow
ablation of multiple and unstable VTs with acceptable safety and efficacy, even
in patients with advanced heart disease.[7]
Remote magnetic navigation is recognized as an important method
for delivery of ablation therapy for these patients due to the ability of the
flexible magnetic catheter to carefully map the diseased tissue without
inadvertently inducing abnormal ventricular rhythms. In a series of 110
patients that included all morphologies of VT, 85% of patients treated with
magnetic ablation were free from VT at one year after the intervention and were
exposed to statistically reduced levels of radiation when compared to
non-magnetic VT ablations at the same center.[8] In patients with myocardial scarring
from a previous heart attack who were receiving excessive shocks from an ICD,
magnetic ablation was shown to be successful in reducing these shocks and
demonstrated a 67% reduction in imaging radiation needed to complete the
procedure compared to a historical non-magnetic group.[9] For monomorphic idiopathic VT which
may originate in thin-walled tissues, magnetic ablation offers catheter
flexibility, steering accuracy and reproducibility to navigate to a desired
location with a low probability of perforating the myocardium.[10]
Antiarrhythmic drug therapy[edit]
Drugs such as amiodarone or procainamide may be used in addition to defibrillation to terminate VT while the underlying
cause of the VT can be determined. As hypomagnesia is a common cause of VT,
stat dose magnesium sulphate can be given for torsades or if hypomagnesemia is
found/suspected.
Long term
anti-arrhythmic therapy may be indicated to prevent recurrence of VT.
Beta-blockers and a number of class III anti-arrhythmics are commonly used.
Lidocaine is now being replaced by amiodarone as the first line anti-arrhythmic
treatment of VT.
The
implantation of an ICD is more effective than drug therapy for prevention of
sudden cardiac death due to VT and VF, but may be constrained by cost
issues,(RDM) and well as patient co-morbidities and patient preference.
