Antiarrhythmics

Antiarrhythmics are drugs used to prevent or terminate arrhythmias — heart rhythms that are too fast, too slow, or irregular. They work by modifying the ion currents that create the cardiac action potential, changing how quickly heart cells depolarize, conduct impulses, or recover between beats.

The standard framework is the Vaughan-Williams classification. Class I drugs block sodium channels and slow depolarization; they are subdivided into IA (quinidine, procainamide), IB (lidocaine), and IC (flecainide, propafenone) based on how strongly they bind. Class II drugs are beta blockers (metoprolol, propranolol) that slow the sinoatrial and atrioventricular nodes. Class III drugs block potassium channels and prolong repolarization (amiodarone, sotalol). Class IV drugs are the non-dihydropyridine calcium channel blockers (verapamil, diltiazem), which slow nodal conduction. Several important agents fall outside the four classes, including adenosine and digoxin.

These drugs are clinically important and pharmacologically delicate: many can themselves provoke arrhythmias (proarrhythmia), and agents that prolong the QT interval carry a risk of torsades de pointes. Amiodarone is a frequent exam subject because of its long half-life and its pulmonary, thyroid, hepatic, and ocular side effects.

Antiarrhythmics appear across several exams. The USMLE Step 1 exam tests the Vaughan-Williams classes, their effects on the cardiac action potential, and signature toxicities; the PTCE tests drug names, classes, and common side effects among cardiovascular medications; and the CCMA exam covers them in the context of electrical heart disorders and patient care.