Amiodarone is the most effective, and certainly the strangest, antiarrhythmic drug ever developed. Anyone being treated with amiodarone should understand the idiosyncrasies - and the risks - associated with this highly effective drug.
Amiodarone is used to correct abnormal rhythms of the heart (an antiarrhythmic medication). Amiodarone was discovered in 1961. Amiodarone was approved by the FDA for clinical use as an antiarrhythmic agent in December of 1985. Although amiodarone has many side effects, some of which are severe and potentially fatal, it has been successful in treating many arrhythmias where other antiarrhythmics fail. Amiodarone is considered a "broad spectrum" antiarrhythmic medication, that is, it has multiple and complex effects on the electrical activity of the heart which is responsible for the heart's rhythm. In addition to being an antiarrhythmic medication, amiodarone also causes blood vessels to dilate (enlarge). This effect can result in a drop in blood pressure. Because of this effect it also may be of benefit in patients with congestive heart failure.
Amiodarone hydrochloride is a Class III antiarrhythmic agent. The active ingredient of Amiodarone Hydrochloride Injection Concentrate is amiodarone hydrochloride (2-n-butyl-3(4-(2-diethylaminoethoxy)-3,5-diiodobenzoyl) benzofuran hydrochloride). Amiodarone hydrochloride is a fine white crystalline powder. It is slightly soluble in water and is soluble in alcohol and chloroform. It is an amphiphilic compound and contains iodine in its formulation.
Amiodarone is a "broad spectrum" antiarrhythmic structurally similar to thyroxine with multiple and complex electrophysiologic effects. Although its exact mechanism of action is not completely known, using the traditional Vaughn-Williams classification scheme for antiarrhythmic compounds, amiodarone is considered a class III compound. Like the other class III antiarrhythmic agents, bretylium and sotalol, amiodarone acts directly on the myocardium to delay repolarization and increase the duration of the action potential. This results in prolongation of the effective refractory period in the atria, ventricles, AV node, and His-Purkinje system. Amiodarone exerts these electrophysiologic effects without significantly altering the myocardial membrane potential.
By definition, class III agents act only on the repolarization phase of the action potential and therefore should leave conduction unchanged. However, sinus node automaticity (and function) is depressed, AV conduction in prolonged, and conduction is slowed in the His-Purkinje system, primarily as a result of the class II and IV effects of amiodarone. The drug also exhibits significant class I properties including inhibition of "fast" sodium channels, with subsequent impaired recovery of the myocardium due to its membrane stabilizing properties. Conduction in the accessory pathway of patients with Wolff-Parkinson-White syndrome is prolonged by amiodarone. Amiodarone also noncompetitively inhibits ›- and œ-receptors, and possesses both vagolytic and calcium-channel blocking properties. The drug relaxes both smooth and cardiac muscle, causing decreases in coronary and peripheral vascular resistance, left ventricular end-diastolic pressure (LVEDP) and systolic blood pressure, thereby decreasing afterload. Transient, dose-related increases in coronary blood flow may occur following intravenous amiodarone administration, and is thought to be due to direct relaxation of coronary arteries, reductions in myocardial contractility and LVEDP. This activity may result in a decrease in myocardial oxygen demand (MVOA), and decrease the potential for myocardial ischemia.