*3.2.1 Polymorphic VT/ventricular fibrillation*

Polymorphic VT is most commonly caused by abnormalities of ventricular muscle repolarization. The predisposition to this problem usually manifests on the ECG as a prolongation of the QT interval. Congenital problems include long QT syndrome and catecholaminergic polymorphic ventricular tachycardia. Acquired problems are usually related to drug toxicity or electrolyte abnormalities, myocardial ischemia. Class III anti-arrhythmic drugs such as sotalol and amiodarone prolong the QT interval and may in some circumstances be pro-arrhythmic. Other relatively common drugs include some antibiotics and antihistamines [37–44].

#### *Clinical Use of Electrocardiogram*

Ventricular fibrillation is a terminal arrhythmia in which ventricular contractions are uncoordinated and too weak to eject blood. The ECG shows irregular, chaotic deflections of varying amplitude and shape [37–44].


The ECG demonstrates a polymorphic VT characterized by the QRS complexes of changing amplitude that appear to twist around the isoelectric line and occur at the rates of 200 to 250 beats/min. Most data suggest that early afterdepolarizations are responsible for both the QT prolongation and the torsades de pointes. The most common causes are congenital severe bradycardia, potassium depletion and use of class IA and IC drugs. Clinical features depend on whether torsades de pointes is due to acquired or congenital long QT syndrome. Some episodes may persist and progress to ventricular fibrillation, leading to sudden death. In congenital long QT syndrome, long QT intervals predispose the patient to an R-on-T phenomenon, wherein the R-wave, representing ventricular depolarization, occurs during the relative refractory period at the end of repolarization [37–44].

• AF or atrial flutter or focal atrial tachcyardia with varying block conducted with aberration
