Antiarrhythmic drugs
Antiarrhythmic drugs suppress or terminate abnormal cardiac rhythms by blocking sodium, potassium, or calcium currents or by beta-adrenergic blockade, chosen by arrhythmia mechanism and the presence of structural heart disease, with rhythm control (flecainide, sotalol, dofetilide, amiodarone) reserved once rate control and anticoagulation are addressed.
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What this article covers
- Overview
What the class is: antiarrhythmic drugs suppress abnormal automaticity, reentry, or triggered activity by altering the sodium, potassium, or calcium currents of the cardiac action potential, or by blunting autonomic input.
- Epidemiology
Who receives these drugs: most prescriptions are for AF, the most common sustained arrhythmia, whose prevalence rises after age 65 and with hypertension, heart failure, and valvular disease.
- Risk factors
Structural or ischemic heart disease: prior myocardial infarction or reduced ejection fraction raises proarrhythmia risk with class IC and, less so, class IA agents.
- Pathophysiology
Class I, sodium channel blockade: slows phase 0 depolarization, strongest at fast rates from preferential binding to open or inactivated channels, most pronounced in IC, intermediate in IA, weakest in IB.
- Clinical features
Class IA: procainamide causes a reversible lupus-like syndrome; quinidine causes cinchonism; disopyramide has marked negative inotropy and anticholinergic effects.
- Differential diagnosis
Class IC versus class III for AF without structural disease: flecainide or propafenone suits a structurally normal heart, but once coronary disease or reduced ejection fraction is present, class IC is avoided for a class III agent.
- Diagnosis
What establishes the correct agent: the appropriate antiarrhythmic is established by the arrhythmia mechanism on a 12-lead electrocardiogram (ECG) correlated with symptoms, plus the presence or…
- Management
First, address hemodynamic stability: for an unstable tachyarrhythmia, give synchronized cardioversion first; reserve the drugs below for the stable patient or maintenance afterward.
- Complications
Torsades de pointes: the principal risk of class IA and III agents, most frequent with quinidine, sotalol, dofetilide, and ibutilide, within hours to days of initiation or uptitration.
- Prognosis
Rhythm control efficacy: amiodarone is the most effective agent for AF sinus rhythm maintenance but is reserved for refractory or structural-disease cases; sotalol and dofetilide have intermediate efficacy with a narrower safety margin.
- Prevention
Amiodarone monitoring: baseline and every-6-month TSH and liver function tests, periodic chest imaging or pulmonary function testing, and an annual ophthalmologic exam if visual symptoms develop.
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