Acute Haemodynamic Effects of Sodium Bicarbonate Administration in Respiratory and Metabolic Acidosis in Anaesthetized Dogs

Abstract

Twenty-seven halothane-anaesthetized, mechanically ventilated adult mongrel dogs were randomly assigned to either respiratory acidosis group [pHa 7.22 (0.03, SD), PaCO2 9.6 (1.1) kPa, base excess –0.5 (1.4) mmol.l–1, n=9], metabolic acidosis group [pHa 7.20 (0.05), PaCO2 5.5 (0.4) kPa, base excess –11.1 (2.1) mmol.l–1, n=9], or non-acidosis group [pHa 7.37 (0.07), PaCO2 5.2 (0.4) kPa, base excess –1.1 (1.5) mmol.l–1, n=9]. Respiratory acidosis and metabolic acidosis were induced by decreasing respiratory rate and continuous infusion of 2 mmol.l–1 hydrochloric acid, respectively. Sodium bicarbonate solution 1 mmol.kg–1 was injected into the right atrium over five seconds when haemodynamic stability was obtained. In all three groups, acute administration of sodium bicarbonate produced transient decreases in mean arterial pressure and RV dP/dtmax, and transient increase in right atrial pressure 30 seconds after injections, but these variables returned to the pre-injection values by the end of the three minutes observation period. Although no significant differences were seen in haemodynamic variables among the three groups at 30 seconds, one and three minutes, maximum reductions in both RV dP/dtmax and PBF in the metabolic acidosis group (260 (143) mmHg.s–1 and 0.38 (0.26) l.min–1) were significantly greater than those in the non-acidosis group (127 (34) mmHg.s–1 and 0.08 (0.09) l.min–1; P<0.05).