Pathophysiology of Cardiac Arrhtymias

Pathophysiology of Cardiac Arrhtymias

Cardiac arrhythmia is the irregularity in heart beats. The types of cardiac arrhythmias includes supraventricular, atrial fibrillation, ventricular tachycardia.
Regardless of the specific arrhythmia, the pathogenesis of the arrhythmias falls into one of three basic mechanisms—enhanced or suppressed automaticity, triggered activity, or re-entry. Automaticity is a natural property of all myocytes. Ischemia, scarring, electrolyte disturbances, medications, advancing age, and other factors may suppress or enhance automaticity in various areas. Suppression of automaticity of the sinoatrial (SA) node can result in sinus node dysfunction, and sick sinus syndrome (SSS), which is still the most common indication for permanent pacemaker implantation . In contrast to suppressed automaticity, enhanced automaticity can result in multiple arrhythmias, both atrial and ventricular. Triggered activity occurs when early afterdepolarizations and delayed afterdepolarizations initiate spontaneous multiple depolarizations, precipitating ventricular arrhythmias. Examples include torsades de pointes and ventricular arrhythmias caused by digitalis toxicity. Probably the most common mechanism of arrhythmogenesis results from re-entry. Requisites for re-entry include bidirectional conduction and unidirectional block. “Micro” level re-entry occurs with ventricular tachycardia from conduction around the scar of myocardial infarction, and “macro” level
re-entry occurs via conduction through (Wolff-Parkinson-White [WPW] syndrome) concealed accessory pathways.