Effect of metabolic acidosis on pulmonary gas exchange of artificially ventilated dogs

Abstract

It is well established that metabolic acidosis induces a reduction in alveolar-arterial O2 difference [(A-a)Do2] in artificially ventilated dogs by shifting the oxyhemoglobin dissociation curve (ODC) and/or by improving the distribution of the ventilation-to-perfusion ratio (VA/Q) throughout the lung. To assess the influence of these two factors we examined eight artificially ventilated dogs before and after induction of metabolic acidosis by a perfusion of 0.3 mol HCl. We measured classic indexes of cardiopulmonary function. VA/Q distribution was estimated using the multiple inert gas elimination technique (MIGET). ODC and Bohr effect of each dog were obtained by a dynamic method. Acidosis increased CO2 excretion, respiratory quotient, blood PO2 at 50% saturation, and arterial PCO2 and PO2 with a simultaneous decrease in (A-a)DO2. In seven dogs, the distribution of VA and Q, as assessed by MIGET, was not substantially modified by HCl perfusion. In the eighth dog the distribution of Q and VA became more homogeneous after acidosis. This led us to conclude that the Bohr effect is the most important and most consistently observed factor responsible for the decrease in (A-a)DO2 found in metabolic acidosis. In rare cases the increase in pulmonary arterial pressure may complement this action by improving the distribution of the VA/Q ratio.