Effect of non-carbonic acidosis on total splanchnic perfusion and cardiac output during anaesthesia with O2-N2O-halothane.

Six dogs, premedicated with pethidine 10 mg kg-1 b.w, were anaesthetized with mebumal natrium (NFN) 25 mg kg-1 b.w. and 80 mg gallamoni jodidum (NFN). Anaesthesia was continued with O2-N2O-halothane and artificial ventilation. Non-carbonic acidosis was induced by i.v. infusion of hydrochloric acid, during which the related values of pulse, blood pressure, cardiac output, total splanchnic prefusion and portal pressure were measured. The pulse remained unchanged down to pH 7.0. At this pH, arrhythmia suddenly occured and developed into ventricular fibrillation. Before this occured falling cardiac output was observed (cardiac output 1 min-1 = -21.49+3.21 x pH, N = 23, r = 0.75, P less than 0.001) and rising oxygen consumption (O2 ml min-1 kg-1 = 25.79--2.96 x pH, N =28, r = 0.52, P less than 0.01), rising oxygen extraction and rising peripheral resistance, while the mean pressure in the aorta was almost unaltered. During this course towards circulatory failure, an unchanged to slightly rising total splanchnic perfusion (Qsp1) was demonstrated, which with the lowest pH, represented up to 40% of the cardiac output (Qtot): Qsp1/Qtot = 3.11--0.39 x pH (N = 28, r = 0.52, P less than 0.01). Portal pressure rises slightly during acidosis, and oxygen saturation in the portal vein is high. It is probable that the retained splanchnic blood flow is caused by retention of the portal flow. This is quite different from observations during anaesthesia with barbiturates. It is concluded that halothane modifies considerably the circulatory response in the systemic circulation and the splanchnic region during non-carbonic acidosis.