Oxygen Amiodarone

Amiodarone dilates arteriolar vascular smooth muscle, especiady coronary arteries, and thus exhibits antianginal effects. Its effects on the peripheral vasculature to decrease resistance leads to a decrease in left ventricular stroke work and a decrease in myocardial oxygen consumption. The dmg rarely produces hypotension that requires discontinuation of the dmg (1,2). 

Amiodarone relaxes vascular smooth muscle one of its most prominent effects is on the coronary circulation, reducing coronary vascular resistance and improving regional myocardial blood flow. In addition, its effects on the peripheral vascular bed lead to a decrease in left ventricular stroke work and myocardial oxygen consumption. Therefore, amiodarone improves the relationship between myocardial oxygen demand and oxygen supply. IV administration may be associated with profound hypotension requiring volume expansion therapy. 

Lung damage due to amiodarone usually develops slowly, but it can occasionally have a rapid onset, particularly in patients who are given high concentrations of inspired oxygen, and there is experimental evidence that amiodarone enhances the toxic effects of oxygen on the lungs (70). 

Donica SK, Paulsen AW, Simpson BR, Ramsay MA, Saunders CT, Swygert TH, Tappe J. Danger of amiodarone therapy and elevated inspired oxygen concentrations in mice. Am J Cardiol 1996 77(1) 109-10. 

The UK manufacturer of amiodarone suggests caution in patients receiving high-dose oxygen therapy. Others have suggested that the concentration of oxygen should be maintained at the lowest possible level consistent with adequate oxygenation. ... 

High-dose oxygen may increase the risks of amiodarone-induced postoperative adult respiratory distress syndrome. 

A retrospective review of 20 patients who underwent cardiac surgery found that pulmonary complications were more common in those receiving amiodarone (73% versus 25%). Moreover, the incidence of pulmonary complications in patients taking amiodarone was higher in those exposed to 100% oxygen (6 of 7) than those not (2 of 4). ... 

Increased pulmonary toxicity (pulmonary oedema) with the combination of amiodarone and 100% oxygen has been confirmed in mice. ... 

Pulmonary toxicity may occur in about 10% of patients given amiodarone. Pulmonary toxicity due to cyclophosphamide may occur between 1 to 6 months after exposure or occttr as a more insidiotts form after about 6 months. The early onset of symptorrrs in the patients described above suggests accelerated mechanisms of ptrlmonary toxicity. Both cyclophosphamide and amiodarone pulmonary toxicity appear to be erthanced by oxygen and the combination of cyclophosphamide with amiodarone may enhance oxidative stress and therefore ptrlmonary toxicity. 

Amiodarone lung toxicity, exceedingly rare in children, has been described in a child with supraventricular tachycardia after repair of a transposition of the great vessels, who developed acute amiodarone-induced pulmonary toxicity [30" ]. Recent cardiac surgery, a high concentration of inspired oxygen during mechanical ventilation, and chest trauma were considered associated susceptibility factors. 

L 8040 ( ), an analog of the coronary vasodilator amiodarone, was shown to be effective in decreasing myocardial oxygen consumption by an adrenergic blocking effect, but not by competitive 3-blockade.Cardiac output was not reduced. 

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