Two mechanisms have been postulated to explain torsade de pointes. The first is that the drugs exert an inhomogeneous effect on cellular repolarization leading to an increased dispersion of refractoriness and an increase in the inhomogeneity of the recovery of excitability which serves as a substrate for reentry. The second postulated mechanism is that the drugs lead to the development of early after-depolarizations occuring during phase 3 of the action potential and that these initiate the arrhythmia.
I. INCREASED DISPERSION OF RECOVERY OF EXCITABILITY
II. EARLY AFTER-DEPOLARIZATIONS