Amiodarone is an extremely attractive antiarrhythmic drug in the setting of the critically ill patient. It is effective against a wide spectrum of both supraventricular and ventricular arrhythmias. Its effects on the inotropic state of the myocardium are significantly less than those of the vast majority of antiarrhythmic drugs. There is less concern in the acutely ill patient about the extensive long-term toxicity that is seen with chronic oral usage.

Amiodarone has a complex mode of action with activity across the Vaughan Williams classification. It has a delayed onset of action which necessitates aggressive intravenous loading (usually 300 mg over 30 min followed by a maintenance infusion of 900 to 1200 mg/24 h) preferably via central venous access to avoid phlebitis. Acute infusion at high rates may lead to significant hypotension due to an a-receptor-blocking effect. Even with such loading, effective antiarrhythmic action may not be seen for 1 to 24 h. Metabolism is principally hepatic to desethylamiodarone, which has antiarrhythmic action in its own right. Amiodarone potentiates oral anticoagulation and increases blood levels of digoxin, quinidine, and flecainide. Although the drug prolongs the QT interval, drug-induced torsade de pointes is less common than with other class III antiarrhythmic drugs. Despite its delayed onset of action, it has recently proven efficacious and better tolerated in trials comparing it with bretylium in patients with malignant ventricular arrhythmias ( Kowey.®L§/ 1995). It is also useful in pediatric patients, particularly in the context of postsurgical junctional ectopic tachycardia, an arrhythmia with a very high mortality. It is currently being assessed in the setting of the post-myocardial infarction patient perceived to be at high risk of death in large placebo-controlled randomized trials as small pilot studies have shown potential benefit.

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