Revue médicale de Bruxelles
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Bicarbonate administration during lactic acidosis seems logical in view of the myocardial depression associated with the decrease in intracellular pH. This treatment has been recently challenged on the basis of observations showing an increase in the veno-arterial gradient for CO2 during acute circulatory failure. The partial transformation of bicarbonate in CO2 carries the risk of aggravating the phenomenon and thereby decreasing intracellular pH. Alternatives to sodium bicarbonate--carbicarb, THAM and dichloroacetate--are discussed.