Chapter 14: Drugs for Cardiac Dysrhythmia

Drugs for Cardiac Dysrhythmia begins by outlining the normal cardiac action potential, detailing the specific ion currents—including sodium, calcium, and potassium influx and efflux—that drive depolarization and repolarization in the sinoatrial node, atrioventricular node, and His-Purkinje system. The text explains how pathophysiology arises from disturbances such as impulse formation defects like increased automaticity and afterdepolarizations, as well as impulse conduction abnormalities like reentry, which is a primary cause of paroxysmal supraventricular tachycardia. A significant portion of the chapter is dedicated to the Vaughan-Williams classification system, which categorizes antidysrhythmic drugs based on their channel-blocking properties. Class I agents are described as sodium channel blockers that slow Phase 0 depolarization; they are further subdivided into Class IA drugs like quinidine and procainamide which prolong repolarization, Class IB drugs like lidocaine which primarily affect ischemic tissue with minimal ECG changes, and Class IC agents like flecainide which markedly slow conduction. The discussion moves to Class II beta-adrenoceptor antagonists like metoprolol and esmolol, highlighting their role in reducing sympathetic stimulation and slowing AV node conduction to treat supraventricular issues and reduce post-infarction mortality. Class III drugs, including amiodarone, sotalol, and dofetilide, are characterized by their ability to block potassium channels, thereby prolonging the action potential duration and refractory period, though this mechanism carries the risk of inducing torsades de pointes due to QT interval prolongation. Amiodarone is singled out for its multi-channel effects and complex pharmacokinetic profile, including a long half-life and potential for thyroid and pulmonary toxicity. Class IV calcium channel blockers, specifically non-dihydropyridines like verapamil and diltiazem, are explained in the context of slowing AV nodal conduction to control ventricular rates in atrial fibrillation. The chapter also covers miscellaneous agents such as adenosine, which is used for rapid termination of acute supraventricular tachycardia through transient AV node block, and magnesium sulfate for treating drug-induced polymorphic ventricular tachycardia. Finally, the text integrates these pharmacologic principles into clinical management strategies for conditions like atrial fibrillation, distinguishing between rate control and rhythm control approaches, and addressing the treatment of life-threatening ventricular fibrillation.