Arrhythmia Mechanisms Fundamental Assessment

Cardiac arrhythmias arise from three fundamental electrophysiologic mechanisms including reentry enhanced automaticity and triggered activity. Reentry is the most common mechanism requiring two pathways with different conduction velocities and refractory periods that allow circular impulse propagation. Anatomic and functional reentry circuits underlie atrial flutter ventricular tachycardia after myocardial infarction and atrioventricular reentrant tachycardia.

Enhanced automaticity occurs when cells outside the sinus node spontaneously generate impulses faster than the sinus rate. This mechanism underlies inappropriate sinus tachycardia some atrial tachycardias and accelerated junctional rhythms. Triggered activity arises from afterdepolarizations either early in the action potential associated with prolonged QT and torsades de pointes or delayed associated with digitalis toxicity and catecholaminergic polymorphic ventricular tachycardia.

Mechanism understanding informs treatment selection. Reentry circuits are amenable to catheter ablation that interrupts the critical isthmus or pathway. Enhanced automaticity is typically controlled with medications including beta blockers calcium channel blockers and antiarrhythmic drugs. Triggered activity related to early afterdepolarizations responds to magnesium and pacing while delayed afterdepolarizations require correction of underlying triggers. Diagnostic electrophysiology study clarifies mechanism in complex cases and guides definitive ablation therapy.