Electroencephalographic consequences of alkalinization therapy during lactic acidosis: Different effects of sodium bicarbonate and carbicarb

To explore the differences between sodium bicarbonate and an experimental buffer, Carbicarb in the therapy of lactic acidosis, we performed the following studies. Rats were subjected to a combined respiratory and metabolic acidosis designed to simulate clinical lactic acidosis following cardiac arrest and resuscitation. The electroencephalogram (EEG) was monitored during induction and therapy of acidosis. The acidosis model was associated in a 22% fall in the amplitude of the EEG along with marked decreases in mean blood pressure, arterial PO₂, and pH, as well as increases in arterial PCO₂. Bicarbonate infusion was associated with a marked fall in mean blood pressure along with transient increases in arterial PCO₂, which were accompanied by significant and sustained decreases in the amplitude of the EEG. In contrast, Carbicarb did not lower blood pressure and had only transient effects on the amplitude of the EEG. These data suggested that bicarbonate therapy had deleterious effects on cerebral electric activity in this model of acidosis that were not shared by Carbicarb. if these data are confirmed in humans, Carbicarb may have advantages over bicarbonate in the clinical therapy of acute acidosis.