Ventricular tachycardia (VT) 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 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 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 is by ECG (see Fig. 18: 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 3: 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.
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 class I or class III drugs (see Table 1: Antiarrhythmic Drugs (Vaughan Williams Classification) ). Lidocaine 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 cause symptoms. In such cases, antiarrhythmics are used as for sustained VT.
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 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 4: 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.
Last full review/revision July 2012 by L. Brent Mitchell, MD
Content last modified September 2013