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Ventricular
tachycardia is ≥ 3 consecutive
ventricular beats at a rate ≥ 120
beats/min. Symptoms depend on duration and vary from none to palpitations
to hemodynamic collapse and death. Diagnosis is by ECG. Treatment
of more than brief episodes is with cardioversion or antiarrhythmics depending
on symptoms. If necessary, long-term treatment is with an implantable
cardioverter defibrillator.
Some experts use a cutoff rate of ≥ 100 beats/min for ventricular tachycardia (VT). Repetitive ventricular rhythms at slower rates are called accelerated idioventricular rhythms or slow VT; they are usually benign and are not treated unless associated with hemodynamic symptoms.
Most patients with VT have a significant heart disorder, particularly prior MI or a cardiomyopathy. Electrolyte abnormalities (particularly hypokalemia or hypomagnesemia), acidemia, hypoxemia, and adverse drug effects contribute. The long QT syndrome (congenital or acquired) is associated with a particular form of VT, torsades de pointes.
VT may be monomorphic or polymorphic and nonsustained or sustained. Monomorphic VT results from a single abnormal focus or reentrant pathway and has regular, identical-appearing QRS complexes. Polymorphic VT results from several different foci or pathways and is thus irregular, with varying QRS complexes. Nonsustained VT lasts < 30 sec; sustained VT lasts ≥ 30 sec or is terminated sooner because of hemodynamic collapse. VT frequently deteriorates to ventricular fibrillation and thus cardiac arrest (see Respiratory and Cardiac Arrest: Cardiac Arrest).
Symptoms and Signs
VT of short duration or slow rate may be asymptomatic. Sustained VT is almost always symptomatic, causing palpitations, symptoms of hemodynamic compromise, or sudden cardiac death.
Diagnosis
Diagnosis is by ECG (see Fig. 17: Arrhythmias and Conduction Disorders: Broad QRS ventricular tachycardia. ). Any wide QRS complex tachycardia (QRS ≥ 0.12 sec) should be considered VT until proved otherwise. Diagnosis is supported by ECG findings of dissociated P-wave activity, fusion or capture beats, uniformity of QRS vectors in the V leads (concordance) with discordant T-wave vector (opposite QRS vectors), and a frontal-plane QRS axis in the northwest quadrant. Differential diagnosis includes supraventricular tachycardia conducted with bundle branch block or via an accessory pathway (see Table 1: Arrhythmias and Conduction Disorders: Modified Brugada Criteria for Ventricular Tachycardia ). However, because some patients tolerate VT surprisingly well, concluding that a well-tolerated wide QRS complex tachycardia must be of supraventricular origin is a mistake. Using drugs appropriate for supraventricular tachycardia (eg, verapamil , diltiazem ) in patients with VT may cause hemodynamic collapse and death.
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Fig. 17
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Broad QRS ventricular tachycardia.
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The QRS duration is 160 msec. An independent P wave can be seen in V1 (arrow). There is a leftward mean frontal axis shift.
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Treatment
Acute:
Treatment depends on symptoms and duration of VT. Hypotensive VT requires synchronized direct-current cardioversion with ≥ 100 joules. Stable sustained VT can be treated with IV drugs, usually lidocaine (see Table 2: Arrhythmias and Conduction Disorders: Antiarrhythmic Drugs (Vaughan Williams Classification) ), which acts quickly but is frequently ineffective. If lidocaine is ineffective, IV procainamide may be given, but it may take up to 1 h to work. Failure of IV procainamide is an indication for cardioversion.
Nonsustained VT does not require immediate treatment unless the runs are frequent or long enough to produce symptoms. In such cases, antiarrhythmics are used as for sustained VT.
Long-term:
The primary goal is preventing sudden death, rather than simply suppressing the arrhythmia. It is best accomplished by use of an implantable cardioverter-defibrillator (ICD—see Arrhythmias and Conduction Disorders: Implantable cardioverter-defibrillators (ICDs)). However, the decision about whom to treat is complex and depends on the estimated probability of life-threatening VTs and the severity of underlying heart disorders (see Table 5: Arrhythmias and Conduction Disorders: Indications for Implantable Cardioverter-Defibrillators in Ventricular Tachycardia and Ventricular Fibrillation).
Long-term treatment is not required when the index episode of VT resulted from a transient cause (eg, during the 48 h after onset of MI) or a reversible cause (acid-base disturbances, electrolyte abnormalities, proarrhythmic drug effect).
In the absence of a transient or reversible cause, patients who have had an episode of sustained VT typically require an ICD. Most patients with sustained VT and a significant structural heart disorder should also receive a β-blocker. If an ICD cannot be used, amiodarone may be the preferred antiarrhythmic for prevention of sudden death.
Because nonsustained VT is a marker for increased risk of sudden death in patients with a structural heart disorder, such patients (particularly those with an ejection fraction < 0.35) require further evaluation. Such patients should receive an ICD.
When prevention of VTs is important (usually in patients who have an ICD and are having frequent episodes of VT), antiarrhythmics or transcatheter radiofrequency or surgical ablation of the arrhythmogenic substrate is required. Any class Ia, Ib, Ic, II, or III drug can be used. Because β-blockers are safe, they are the first choice unless contraindicated. If an additional drug is required, sotalol is commonly used, then amiodarone .
Transcatheter radiofrequency ablation is used most commonly in patients who have VT with well-defined syndromes (eg, right ventricular outflow tract VT or left septal VT [Belhassen VT, verapamil -sensitive VT]) and otherwise healthy hearts.
Long
QT Syndrome and Torsades de pointes Ventricular Tachycardia
Torsades
de pointes is a specific form of polymorphic VT in patients with
a long QT interval. It is characterized by rapid, irregular QRS
complexes, which appear to be twisting around the ECG baseline.
This arrhythmia may cease spontaneously or degenerate into ventricular
fibrillation. It causes significant hemodynamic compromise and often death.
Diagnosis is by ECG. Treatment is with IV Mg, measures to shorten
QT interval, and DC defibrillation when ventricular fibrillation
is precipitated.
The long QT interval responsible for torsades de pointes can be congenital or drug-induced. QT-interval prolongation predisposes to arrhythmia by prolonging repolarization, which induces early after-depolarizations and spatial dispersion of refractoriness.
Congenital:
At least 10 distinct forms of congenital long QT syndrome have been described. Most cases fall into the first 3 subgroups:
These forms are inherited as autosomal dominant disorders with incomplete penetrance and, in the past, were referred to as Romano-Ward syndrome. In rare patients with 2 abnormal copies of the genetic abnormality (particularly LQT1), the disorder is associated with congenital deafness and, in the past, was referred to as the Jervell and Lange-Nielsen syndrome. Patients with long QT syndrome are prone to recurrent syncope secondary to torsade de pointes and to sudden death secondary to torsade de pointes degenerating into ventricular fibrillation.
Drug-induced:
More commonly, torsades de pointes results from a drug, usually a class Ia, Ic, or III antiarrhythmic. Other drugs that can induce torsades de pointes include tricyclic antidepressants, phenothiazines, and certain antivirals and antifungals (see www.torsades.org for an up-to-date list).
Symptoms and Signs
Patients often present with syncope because the underlying rate (200 to 250 beats/min) is nonperfusing. Palpitations are common among conscious patients. Sometimes the long QT interval is detected after resuscitation.
Diagnosis
Diagnosis is by ECG showing an undulating QRS axis, with the polarity of complexes shifting around the baseline (see Fig. 18: Arrhythmias and Conduction Disorders: Torsades de pointes ventricular tachycardia.). ECG between episodes shows a long QT interval after correction for heart rate (QTc). Normal values average about 0.44 sec, although they vary among individuals and by sex. A family history may suggest a congenital syndrome.
Treatment
An acute episode prolonged enough to cause hemodynamic compromise is treated with unsynchronized cardioversion, beginning with 100 joules. Nevertheless, early recurrence is the rule. Patients often respond to Mg: MgSO4 2 g IV over 1 to 2 min. If this treatment is unsuccessful, a 2nd bolus is given in 5 to 10 min, and an Mg infusion of 3 to 20 mg/min may be started in patients without renal insufficiency. Lidocaine (class Ib) shortens the QT interval and may be effective especially for drug-induced torsades de pointes. Class Ia, Ic, and III antiarrhythmics are avoided.
If a drug is the cause, it is stopped, but until drug clearance is complete, patients with frequent or long runs of torsades de pointes require treatment to shorten the QT interval. Because increasing the heart rate shortens the QT interval, temporary pacing, IV isoproterenol , or both are often effective. Long-term treatment is required for patients with a congenital long QT-interval syndrome. Treatment choices include β-blockers, permanent pacing, ICD, or a combination. Family members should be evaluated by ECG.
Patients with congenital long-QT syndrome should clearly avoid drugs that prolong the QT interval, and patients with exercise-related symptoms (usually LQT1 or LQT2) should avoid strenuous exercise. Treatment options include β-blockers, pacing to maintain faster heart rates (which shortens the QT interval), and the ICD, alone or in combinations. Current guidelines recommend the ICD for patients resuscitated from cardiac arrest and those with syncope despite β-blocker treatment.
Last full review/revision January 2008 by L. Brent Mitchell, MD
Content last modified January 2008
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