Drug-induced QTc prolongation occurs through blockade of the human ether-a-go-go-related gene (hERG) potassium channel (IKr current), which is responsible for the rapid component of delayed rectifier potassium current during cardiac repolarization (phase 3 of the action potential). When antipsychotics block hERG channels, potassium efflux is delayed, prolonging the action potential duration and the QT interval on surface ECG. Prolonged repolarization creates a vulnerable window during which early afterdepolarizations (EADs) can trigger re-entrant circuits, leading to torsades de pointes (TdP), a polymorphic ventricular tachycardia with the characteristic twisting morphology around the isoelectric baseline. TdP can degenerate into ventricular fibrillation and sudden cardiac death. QTc prolongation risk varies significantly across antipsychotics: thioridazine carries the highest risk (FDA black box warning, removed from first-line use) > ziprasidone > IV haloperidol > chlorpromazine, while aripiprazole and lurasidone have minimal QTc effects. The risk of TdP increases exponentially when QTc exceeds 500 ms or when QTc increases by >60 ms from baseline. Risk is compounded by electrolyte derangements (hypokalemia and hypomagnesemia reduce repolarization reserve), drug interactions with CYP3A4 or CYP2D6 inhibitors that increase antipsychotic serum...