Hemodynamic profile of amiodarone during acute and long-term administration in patients with ventricular dysfunction.

One of the potential adverse effects of anti-arrhythmic agents is an impairment of cardiac function as a result of their intrinsic negative inotropic properties. Amiodarone, in animals, also induces dose-related negative inotropic effects, in addition to coronary and systemic vasodilatation and slowing of the heart. Likewise, in most human studies, intravenous amiodarone gives rise to early systemic and coronary vasodilatation, followed by a reduction in contractility. Depending on the relative impact of these opposing effects on the left ventricle, the changes in heart rate, cardiac output and left ventricular filling pressure are variable. Particularly in patients with pre-existing ventricular dysfunction, cardiac pump function is impaired further when relatively high dosages of amiodarone are used without its solvent Tween 80. In contrast, fast bolus administrations, eg. 5 mg/kg amiodarone in 5 minutes, result in an improvement of cardiac output, albeit at the expense of an increase in left ventricular filling pressure. The latter observation suggests that intravenous amiodarone should be given with caution in patients with heart failure and elevated left ventricular filling pressures. When given by mouth, amiodarone does not have significant hemodynamic effects, other than a moderate reduction in heart rate and, occasionally, in diastolic blood pressure. Cardiac pump function is not affected, even in patients with ventricular dysfunction or heart failure, in whom chronic oral administration of the drug is well tolerated.