Ventricular Tachycardia (VT)
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.
(See also Overview of Arrhythmias.)
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 myocardial infarction 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.
Ventricular tachycardia may be monomorphic or polymorphic and nonsustained or sustained.
Monomorphic VT: Single abnormal focus or reentrant pathway and regular, identical-appearing QRS complexes
Polymorphic VT: Several different foci or pathways and irregular, varying QRS complexes
Nonsustained VT: Lasts < 30 sec
Sustained VT: Lasts ≥ 30 sec or is terminated sooner because of hemodynamic collapse
Diagnosis of ventricular tachycardia is by ECG (see Figure: 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: 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 of acute ventricular tachycardia depends on symptoms and duration of VT.
Pulseless VT requires defibrillation with ≥100 joules.
Stable sustained VT can be treated with synchronized direct-current cardioversion with ≥100 joules.
Stable sustained VT can also be treated with IV class I or class III antiarrhythmic drugs (see Table: 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. IV amiodarone is frequently used but does not usually work quickly. Failure of IV procainamide or IV amiodarone 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). 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: Indications for Implantable Cardioverter-Defibrillators in Ventricular Tachycardia and Ventricular Fibrillation).
Long-term treatment is not required when the index episode of ventricular tachycardia resulted from a transient cause (eg, during the 48 h after onset of myocardial infarction) 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 beta-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 or surgical ablation of the arrhythmogenic substrate is required. Any class Ia, Ib, Ic, II, or III antiarrhythmic drug can be used. Because beta-blockers are safe, they are the first choice unless contraindicated. If an additional drug is required, sotalol is commonly used, then amiodarone.
Transcatheter 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.
Any wide-complex (QRS ≥ 0.12 sec) tachycardia should be considered VT until proved otherwise.
Patients who do not have a pulse should be defibrillated.
Synchronized cardioversion or antiarrhythmic drugs may be tried if the patient is stable.
Patients who had an episode of sustained VT without a transient or reversible cause typically require an ICD.