Atrial fibrillation is a common arrhythmia in the intensive care unit (ICU) setting. The mainstay of therapy is rate control, with beta-blockers being the first-line agent. However, frequently the decision is made to use rhythm-converting agents, such as amiodarone. Amiodarone is a complex antiarrhythmic agent (predominantly class III) that shares at least some of the properties of each of the other three Vaughn-Williams classes of antiarrhythmics. Amiodarone is commonly used for the treatment and prevention of persistent atrial and ventricular tachyarrhythmias, although it is only FDA approved for management of ventricular arrhythmias. It is one of the few agents that can be used safely in individuals with congestive heart failure. Contraindications to amiodarone include severe sinus node dysfunction with marked sinus bradycardia or syncope, second- or third-degree heart block, known hypersensitivity to its contents, cardiogenic shock, possibly severe chronic lung disease.

Amiodarone is highly lipid soluble, extensively distributed in the body, and highly concentrated in many tissues, especially in the liver and lungs. After variable (30% to 50%) and slow gastrointestinal absorption, amiodarone is very slowly eliminated, with a half-life of about 25 to 110 days. The onset of action after oral administration is delayed and a steady-state drug effect may not be established for several months unless large loading doses are used. It undergoes extensive hepatic metabolism to the pharmacologically active metabolite desethylamiodarone (DEA). Amiodarone is not excreted by the kidneys but rather by the lacrimal glands, the skin, and the biliary tract. Neither amiodarone nor DEA is dialyzable.

Amiodarone is both an antiarrhythmic and a potent vasodilator. Amiodarone lengthens the effective refractory period by prolonging the action potential duration in all cardiac muscles, including bypass tracts (class III activity). It also has a powerful class I antiarrhythmic effect that works by inhibiting inactivated sodium channels at high stimulation frequencies. Amiodarone slows phase 4 depolarization of the sinus node as well as conduction through the atrioventricular (AV) node. It also decreases Ca²⁺ current (class IV effect) and transient
outward delayed rectifier and inward rectifier K⁺ currents. Amiodarone noncompetitively blocks α- and β-adrenergic receptors (class II effect); this effect is additive to competitive receptor inhibition by beta-blockers.