Ventricular tachycardia is a difficult clinical problem for physicians. Its evaluation and treatment are complicated because it often occurs in life-threatening situations that dictate rapid diagnosis and treatment.
Ventricular tachycardia is defined as three or more beats of ventricular origin in succession at a rate greater than 100 beats/minute. There are no normal-looking QRS complexes. The rhythm is usually regular, but on occasion it may be modestly irregular. The arrhythmia may be either well-tolerated or associated with grave, life-threatening hemodynamic compromise. The hemodynamic consequences of VT depend largely on the presence or absence or myocardial dysfunction (such as might result from ischemia or infarction) and on the rate of VT. Atrioventricular dissociation usually is present. This means that the sinus node is depolarizing the atria in a normal manner at a rate either equal to, or slower than, the ventricular rate. Thus, sinus P waves sometimes can be recognized between QRS complexes. They bear no fixed relation to the QRS complexes unless the atrial and ventricular rates happen to be equal. Conduction from atria to ventricles is usually prevented because the AV node or ventricular conduction system is refractory due to ventricular depolarization. Sometimes retrograde conduction from ventricles to atria occurs. In this instance, there will be a relation between the QRS complex and the retrograde P wave. Thus, it may be difficult to distinguish VT from a supraventricular tachycardia with aberrant ventricular conduction.
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.
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 ventricular fibrillation (VF)..