Worldwide, sudden cardiac death (SCD) is a major problem. It is most frequently caused by ventricular tachyarrhythmias: Monomorphic and polymorphic ventricular tachycardia (VT), torsade de pointes (TdP), and ventricular fibrillation (VF). Beta blockade, ACE inhibition, coronary reperfusion and other treatments have reduced the incidence of VT but pulseless electrical activity (PEA) is increasingly seen, particularly in patients with advanced chronic heart disease. From existing data, bradyarrhythmia in the form of asystole (usually complete heart block without escape rhythm) causes only a minor proportion (10-15%) of SCD. In patients aged 50 years and more, coronary artery disease plays a dominant role causing more than 75% of SCD cases, either by acute ischemia and ventricular fibrillation or by chronic scar formation and reentrant VT. In younger patients, SCD may occur in patients with structurally normal hearts. A number of arrhythmogenic disorders with an increased risk of SCD have been detected and better understood recently, such as long and short QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, and the early repolarization syndrome. Most importantly, ECG signs and clinical features indicating high risk for SCD have been identified. Knowledge of the exact electrophysiologic mechanisms of ventricular tachyarrhythmias at the cellular level has been improved and mechanisms such as phase 2 reentry and reflection proposed to better understand why and how SCD occurs.