Amiodarone is used to manage virtually all forms of supraventricular and ventricular tachycardia and has therefore become one of the most frequently used antiarrhythmic drugs in clinical practice. Amiodarone has a variable oral bioavailability. After absorption, the drug undergoes extensive enterohepatic circulation. A large first pass effect results in desethylamiodarone, which is active and has similar electrophysiologic effects as the parent compound. Peak amiodarone serum levels, after oral dosing, are achieved within 3-7 hours. Acute amiodarone therapy results in a use-dependent inhibition of inward sodium and inward calcium currents, as well as a non-competitive alpha- and beta-blockade effect. Acute amiodarone therapy has no consistent effects on the repolarization phase of action potentials. The major effect of chronic amiodarone therapy is an inhibition of outward potassium currents resulting in a prolongation of action potential duration, not only in atrial and ventricular muscles but also in the sinoatrial node and atrioventricular nodes. A basic understanding of the pharmacokinetics is important for the clinician to understand the antiarrhythmic properties of both the oral and intravenous preparation.