Topic overview

Start with the big picture

Arrhythmias arise from abnormal impulse formation, such as enhanced automaticity or triggered activity, or from abnormal conduction, including re-entry and block. Their consequences—from palpitations and syncope to sudden cardiac death—help guide treatment choices alongside the underlying cardiac substrate. Antiarrhythmic drugs may suppress ectopic activity, prolong refractoriness, or slow conduction. The Vaughan Williams system groups agents by primary target: sodium channels, beta receptors, potassium channels, or calcium channels. The lesson introduces distinctions within Class I, the action and proarrhythmic concerns of Class III, and rate- versus rhythm-control approaches in atrial fibrillation. It also previews acute management concepts and safety considerations, including the need to weigh drug risks against options such as ablation or an implantable cardioverter-defibrillator.