Clinical meaning
Normal cardiac rhythm originates in the sinoatrial (SA) node via spontaneous phase 4 depolarization driven by the funny current (If), generating impulses at 60-100 bpm. The impulse propagates through atrial myocytes to the AV node (PR interval 0.12-0.20 sec), then through the bundle of His, bundle branches, and Purkinje fibers to produce coordinated ventricular depolarization (QRS < 0.12 sec). Arrhythmias arise from three fundamental mechanisms: (1) abnormal automaticity — enhanced or abnormal spontaneous depolarization in non-pacemaker cells due to ischemia, electrolyte imbalances, or catecholamine excess; (2) reentry — a self-sustaining circuit requiring unidirectional block, slow conduction, and a recovered excitable pathway, responsible for most clinically significant tachyarrhythmias including AVNRT, AVRT, atrial flutter, and monomorphic VT; (3) triggered activity — afterdepolarizations (early afterdepolarizations from prolonged QTc causing torsades, or delayed afterdepolarizations from calcium overload in digitalis toxicity). The NP must systematically classify arrhythmias by origin (supraventricular vs ventricular), rate (tachy vs brady), regularity, and QRS width (narrow < 0.12 sec vs wide ≥ 0.12 sec) to guide diagnosis and treatment.