Three or more ventricular complexes (wide QRS) occurring at a rate more than 100 per minute is taken as ventricular tachycardia (VT). Any wide QRS tachycardia is better considered as VT until proved otherwise. Presence of dissociated P waves, fusion beats and capture beats are the diagnostic features to differentiate VT from an SVT with aberrancy or pre-existing bundle branch block. Dissociated P waves are not so easy to identify in a fast rhythm and have to be sought out diligently as subtle variation in the shape of T waves or QRS.
VT lasting more than 30 seconds or requiring cardioversion due to hemodynamic compromise prior to that is called sustained VT. Non-sustained VT is one which lasts less than 30 seconds without hemodynamic compromise.
VT can be further classified into monomorphic or polymorphic depending on whether the complexes have same morphology or varying morphology. Polymorphic VT often occurs in the setting of QT prolongation and then it is called ‘torsades des pointes’. Initial treatment of monomorphic ventricular tachycardia is often amiodarone bolus followed by infusion. If there is hemodynamic compromise, electrical cardioversion may be resorted to. Monomorphic VT in the setting of acute ischemia may also respond to intravenous lignocaine. Polymorphic VT needs measures to bring down the QT interval if it is prolonged, like overdrive pacing. Occasionally isoprenaline infusion may also be resorted for this purpose. Intravenous magnesium is often useful in controlling polymorphic VT. It is also given as a bolus followed by infusion. Hypokalemia if present, has to be corrected. If it is secondary to a QT interval prolonging drug, it has to be withdrawn.