Vasodilator therapy of idiopathic lactic acidosis

Abstract

Afterload reduction with sodium nitroprusside was performed in a patient with idiopathic lactic acidosis in whom sodium bicarbonate therapy had precipitated pulmonary edema. The drug reduced mean pulmonary-artery wedge pressure from 28 to 12 mm Hg, accompanied by a modest rise in left ventricular stroke work index from 33 to 43 g-m per square meter. Concomitantly, there was dramatic resolution of the metabolic acidemia, the arterial pH rising from 7.19 to 7.61, arterial carbon dioxide tension from 13 to 26 mm Hg, and bicarbonate content from 6 to 28 mEq per liter, and the anion gap falling from 32 to 11 mEq per liter. Metabolic improvement occurred despite a fall in cardiac output from 5.5 to 4.8 liters per minute. These findings support the concept that regional vasoconstriction plays a part in idiopathic lactic acidosis, and suggests that vasodilators may be an effective form of therapy for this almost uniformly fatal disorder.