e 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 from one foci spreads varyingly.
Locating the ectopic foci causing ventricular tachycardia
The ECG provides valuable information regarding the location of the ectopic foci causing the tachycardia. This is done by classifying ventricular tachycardias broadly as either “left bundle branch appearance” or “right bundle branch appearance”. Ventricular tachycardias with ECG waveforms reminding of a left bundle branch block (dominant S-wave in V1) originate in the right ventricle. The opposite is also true, namely that ventricular tachycardias reminding of right bundle branch block (dominant R-wave in V1) originates in the left ventricle. This might be useful in trying to decipher what the cause of the ventricular tachycardia may be. Figure 4 and Figure 5 below shows examples.
Distinguishing ventricular tachycardia from supraventricular tachycardias with wide QRS complexes
Occasionally supraventricular tachycardias (which mostly have normal QRS complexes, i.e QRS duration <0.12 seconds) may display wide QRS complexes. This might be due to concomitant bundle branch block, aberration, hyperkalemia, pre-excitation or side effect of drugs (tricyclic antidepressants, antiarrhythmic drugs class I). It is fundamental to be able to differentiate supraventricular tachycardias with wide QRS from VT and the reason for this is simple: VT is potentially life-threatening, whereas supraventricular arrhythmias rarely are. Hence, wide QRS complexes do not guarantee that the rhythm is ventricular in origin.
Fortunately, there are several characteristics that separate ventricular tachycardia from supraventricular tachycardias (SVT). These characteristics can be used separately or in algorithms (Which are easy to use) to determine whether a tachycardia with wide QRS complexes (often called wide complex tachycardia) is a ventricular tachycardia or an SVT. Before dwelling into these characteristics and algorithm it should be noted that 90% of all wide complex tachycardias are ventricular tachycardias! If the patient suffers from any of the c