Occasionally an atrial impulse arrives when the AV node and the His-Purkinje system are not refractory and AV conduction can occur. This results in a capture beat in which ventricular conduction occurs over the normal pathways, resulting in a normal-appearing (narrow) QRS complex. A capture beat occurs at a shorter RR interval than the RR interval of the VT. AV conduction also may occur simultaneously with depolarization of the ventricular focus. In this instance, the ventricle will be depolarized in part over the normal pathway and in part from the ventricular focus. The resulting QRS complex will be intermediate in morphology between a normal QRS and a QRS of ventricular origin. In this instance, the RR interval will not change. This is called a fusion beat. Ventricular tachycardia may be monomorphic (all QRSs with the same shape) or polymorphic (varying QRS shapes during the tachycardia).

Ventricular tachycardia can be referred to as sustained or nonsustained. Sustained refers to an episode that lasts at least 30 seconds and generally requires termination by antiarrhythmia drugs, antitachycardia pacing techniques or electrical cardioversion. Nonsustained ventricular tachycardia suggests that the episodes are short (three beats or longer) and terminate spontaneously. In general, ventricular tachycardia affects the diseased heart, although it has been described in patients with apparently normal hearts. It is usually associated with coronary artery disease. Patients who have ventricular tachycardia in the absence of coronary artery disease have other cardiac abnormalities, including cardiomyopathy, mitral valve prolapse, valvular heart disease, QT interval prolongation and, in an otherwise normal heart, an abnormality described as primary electrical instability. Other causes of ventricular tachycardia include sarcoidosis, beginning treatment in patients with myxedema and drugs such as digitalis, sympathomimetic amines and antiarrhythmia agents. Occasional runs of tachycardia are initiated by a change in posture, exercise, emotional excitement or vagal stimulation.

Treatment
Ventricular tachycardia when sustained but hemodynamically stable is initially treated with lidocaine, procainamide or bretylium. Ventricular tachycardia that is hemodynamically unstable should be treated the same as VF.

Summary of ECG criteria

• There are no normal-looking QRS complexes.
• Rate: Greater than 100 beats/minute and usually not faster than 200 beats/minute.
• Rhythm: Usually regular but may be irregular.
• P waves: In rapid VT the P waves are usually not recognizable. At slower ventricular rates, P waves may be recognized and may represent normal atrial depolarization from the sinus node at a rate slower than VT, but the electrical activities do not affect one another.
• QRS, ST segment, T wave:
  • The PVC is premature; i.e., it must occur before the next expected sinus beat unless atrial fibrillation is present since preactivity cannot be assessed.
  • The width of the QRS is 0.12 second or greater.
  • The QRS morphology is often bizarre, with notching.
  • The ST segment and T wave are usually opposite in polarity to the QRS.
  • When multiformed (or multifocal), the coupling interval and morphology of the QRS vary.

Figure 8. ECG of Ventricular Rhythm Disturbances

• Atrioventricular dissociation
• QRS axis between -90 degrees and plus or minus 180 degrees
• Positive QRS concordance (positive QRS V1 -V6)
• QRS duration of 140 msec or more with right bundle branch block pattern and 160 msec or more with left bundle branch block pattern
• Combination of left bundle branch block pattern and right axis
• Monophasic or biphasic QRS complex with right bundle branch block pattern and slurred or prolonged S wave in V1 with left bundle branch block morphology

Occasionally a narrow QRS complex may occur with a slightly shorter RR interval (capture beat), or a QRS complex may be seen with morphological features intermediate between a beat of ventricular origin and one of supraventricular origin but with a constant RR interval (fusion beat).

A number of fairly specific types of ventricular tachycardia have been identified, related either to a constellation of distinctive electrocardiographic and electrophysiological features or to a specific set of clinical events.

Specific types of ventricular tachycardia

Arrhythmogenic right ventricular dysplaysia
These patients present with ventricular tachycardia that generally has a left bundle branch block contour, often with right-axis deviation, with T waves inverted over the right precordial leads. The ventricular tachycardia may be due to reentry. Supraventricular arrhythmias also can occur, and exercise can induce the ventricular tachycardia in some patients.

Arrhythmogenic right ventricular dysplasia is due to a type of cardiomyopathy, possibly familial in some patients, with hypokinetic areas involving the wall of the right ventricle. ECG during sinus rhythm exhibits complete or incomplete right bundle branch block. Signal-averaged ECG is abnormal. Although the conventional pharmacological approaches to therapy may be appropriate, surgical manipulations have been successful in some of these patients, as has been implantable defibrillator therapy. Radiofrequency catheter ablation can be tried.

Accelerated idioventricular rhythm
The term accelerated idioventricular rhythm describes ventricular rates slower than usual tachycardia rates but faster than the ventricular escape rhythm. Rates of 75–100 beats/minute are usual. Accelerated idioventricular rhythm probably represents enhanced automaticity in the ventricles and manifests itself when sinus rates slow. The arrhythmia usually starts late in the cycle and frequently begins with a fusion beat. It may spontaneously terminate, or sinus rhythm acceleration may eventually capture the ventricles. It can be regular or irregular and occasionally can show sudden coupling, suggesting the presence of exit block. Many characteristics incriminate enhanced automaticity as the responsible mechanism.

This arrhythmia occurs as a rule in patients who have heart disease, e.g., those with acute myocardial infarction or with digitalis toxicity. It is transient and intermittent, with episodes lasting a few seconds to a minute, and does not appear to seriously affect the patient's clinical course or the prognosis. It commonly occurs at the moment of reperfusion of a previously occluded coronary artery, and it can be found during resuscitation. Suppressive therapy rarely is necessary because the ventricular rate is generally less than 100 beats/min.

Torsades de pointes
Torsades de pointes is a form of VT in which the QRSs appear to be constantly changing. Its name derives from the fact that its electrical activity appears to be twisted into a helix. This form of VT is due to drug toxicity or idiosyncratic reaction to type IA antiarrhythmic agents such as quinidine, procainamide or disopyramide, or other agents that prolong the QT interval. Hypokalemia, hypomagnesemia and bradycardias can also initiate torsades de pointes. This arrhythmia is usually accompanied by prolongation of the QT interval. The QT interval is measured from the onset of the QRS complex to the end of the T wave of the beat or beats just preceding the onset of torsades de pointes. At most rates, the QT interval is 0.40 second or less, though it may be prolonged at slow rates. If the QT is abnormally prolonged in a patient receiving a type IA antiarrhythmic agent, consider the possibility of inducing torsades.

Treatment
Discontinuation of offending agents is crucial. Other treatments include magnesium sulfate and overdrive pacing.

This content is reviewed regularly. Last updated 12/5/08.