s non-sustained ventricular tachycardia. Sustained ventricular tachycardia has duration >30 seconds.
Monomorphic ventricular tachycardia
In monomorphic ventricular tachycardia all QRS complexes display the same morphology (minor differences are allowed). This indicates that the impulses originate in the same ectopic focus. In structural heart disease (coronary heart disease, heart failure, cardiomyopathy, valvular disease etc) monomorphic ventricular tachycardia is typically caused by re-entry. Refer to Figure 1.
The Purkinje fibers in the interventricular septum appear to have an important role in ventricular tachycardia among patients with coronary heart disease. These Purkinje fibers appear to be highly arrhythmogenic in the setting of myocardial ischemia, particularly re-ischemia. Because any impulse arising in the interventricular septum will enter the Purkinje network (to some degree) the QRS complexes tend to be shorter than arrhythmias originating in the free ventricular walls. QRS duration is generally 120 to 145 ms in ventricular tachycardias arising in the septum.
Fascicular ventricular tachycardia is an idiopathic form of VT. It is caused by re-entry in the fascicles of the left bundle branch (i.e in the Purkinje fibers). Fascicular ventricular tachycardia occurs in people aged less than 50 years of age, and predominantly in males. The QRS complexes display morphology similar to right bundle branch block and there is left axis deviation.
Right ventricular outflow tract (RVOT) ventricular tachycardia is a monomorphic VT originating in the outflow tract of the right ventricle. The arrhythmia is mostly idiopathic but some patients may have ARVC (arrhythmogenic right ventricular cardiomyopathy). Because the impulses originate in the right ventricle, the QRS complexes have left bundle branch appearance and the electrical axis is around 90°. Refer to Figure 2.
Polymorphic ventricular tachycardia
A ventricular tachycardia with varying QRS morphology or varying electrical axis is classified as polymorphic. The rhythm may be irregular. Polymorphic ventricular tachycardia is typically very fast (100–320 beats per minute) and unstable. There are several types of polymorphic ventricular tachycardia. The most common cause is myocardial ischemia. The second most common cause is prolonged QTc interval (Long QT syndrome).
Familial catecholaminergic polymorphic ventricular tachycardia (CPVT) is an hereditary ventricular tachycardia in which emotional or physical stress induce the arrhythmia, which may lead to circulatory colapse and cardiac arrest. This type of ventricular tachycardia may be bidirectional (see below). The diagnosis is established by means of exercise stress testing since the sympathetic activity induces the tachycardia.
Brugada syndrome causes polymorphic VT (mostly during sleep or fever).
Early repolarization and hypertrophic obstructive cardiomyopathy also causes polymorphic VT.
Bidirectional ventricular tachycardia means that the QRS morphology alternates from one ebat to another. In most cases it alternates between two variants of the QRS complex. Bidirectional ventricular tachycardia is seen in familial CPVT, digoxin overdoes and long QT syndrome. Refer to Figure 3.
Ventricular tachycardia in ischemic heart disease
Coronary artery disease (ischemic heart disease) is by far the most common cause of ventricular tachycardia and the mechanism is mostly re-entry. As mentioned earlier in this chapter, re-entry occurs when there is a central block ahead of the depolarizing impulse and the cells surrounding the block has varying conductivity. In ischemic heart disease, the central block is typically ischemic/necrotic myocardium (which do not conduct any impulses) while the surrounding cells have dysfunctional conduction due to ischemia. Ventricular tachycardia due to ischemia poses a high risk of degenerating into ventricular fibrillation and cardiac arrest.
Hence, ventricular tachycardia in coronary artery disease is mostly monomorphic. It may be polymorphic, if there are several ectopic foci or if the impulse 