Electrophysiology and Arrhythmia Mechanisms
Core concepts
Normal myocardial cells have a resting membrane potential near −90 mV maintained largely by the Na+/K+ pump; the fast-response action potential has phases 0 (rapid Na+ influx), 1 (transient K+ efflux), 2 (plateau from Ca2+ influx balancing K+ efflux), 3 (K+ efflux repolarization), and 4 (resting). Pacemaker cells (SA node) lack a stable phase 4 and instead show spontaneous depolarization driven by the funny current (If) and Ca2+ currents - this automaticity is why they fire without external stimulus.
Arrhythmias arise from three broad mechanisms: abnormal automaticity (enhanced or ectopic pacemaker firing), triggered activity (early and delayed afterdepolarizations, often Ca2+-mediated - e.g., digoxin toxicity, long QT), and reentry. Reentry requires a unidirectional block plus slowed conduction around a circuit; it underlies most paroxysmal supraventricular tachycardias, atrial flutter, and scar-related ventricular tachycardia. The refractory period determines whether a circuit can be sustained; drugs that prolong refractoriness (class III) terminate or prevent reentry.
Question traps
- Attributing all tachycardias to reentry; automaticity and triggered activity are distinct and have different drug sensitivities.
- Mixing up which ion dominates which phase (Na+ = phase 0 in fast cells; Ca2+ = phase 0 in nodal cells).
- Forgetting that the autonomic nervous system modulates automaticity (vagal slowing, sympathetic speeding).
Rule of thumb
"Sudden onset/offset, regular, narrow-complex" suggests reentry; "gradual, warm-up, catecholamine-driven" suggests automaticity. Match the mechanism to the clinical pattern before choosing a drug.