Arrhythmogenesis occurs through three primary electrophysiological mechanisms. Abnormal automaticity involves enhanced spontaneous phase 4 depolarization in cells that normally lack pacemaker function (atrial, ventricular, or Purkinje cells) — ischemia, catecholamine excess, hypokalemia, and digoxin toxicity can shift the resting membrane potential toward threshold, enabling spontaneous firing. Enhanced normal automaticity occurs when the SA node or subsidiary pacemakers (AV junction at 40-60 bpm, His-Purkinje at 20-40 bpm) fire faster than their intrinsic rate due to sympathetic stimulation, fever, or thyrotoxicosis. Reentry is the most clinically important mechanism, responsible for AVNRT, AVRT (WPW), atrial flutter, and most monomorphic VTs. Reentry requires three conditions: (1) two functionally distinct pathways with different conduction velocities and refractory periods, (2) unidirectional block in one pathway, and (3) slow conduction through the alternate pathway, allowing the blocked pathway to recover excitability. Triggered activity arises from afterdepolarizations — early afterdepolarizations (EADs) occur during phase 2-3 repolarization when action potential duration is prolonged (QTc prolongation from drugs, hypokalemia, hypomagnesemia), producing torsades de pointes; delayed afterdepolarizations (DADs) occur after complete repolarization from intracellular calcium overload (digitalis toxicity, catecholamine excess, heart...