HYPOCAPNIA-INDUCED VENTILATION-PERFUSION MISMATCH - A DIRECT CO2 OR PH-MEDIATED EFFECT

The purpose of this study was to determine whether the increased venti lation/perfusion (VA/Q) mismatch caused by hypocapnic hyperventilation in dogs (J. Appl. Physiol. 1993; 74:1306-1314) is a direct CO2 or a P H-mediated effect. From an initial state of hyperventilated respirator y alkalosis (Fl(O2) = 0.21, VT = 18 ml/kg, RR = 35), we studied the ch anges in VA/Q distributions, respiratory gas exchange, and hemodynamic s when the acid-base status of the dogs was manipulated by combination s of acid or alkali infusion with or without CO2 inhalation. In this m anner, we studied respiratory alkalosis (high pH, low PCO2), normalize d acid-base status (normal pH, normal PCO2), metabolic acidosis (low p H, normal PCO2), metabolic alkalosis (high pH, normal PCO2), and a mix ed respiratory alkalosis and metabolic acidosis (normal pH, low PCO2). Cas exchange was evaluated using the multiple inert gas elimination t echnique. Pco(2) was reduced and Va/Q heterogeneity was increased in a ll conditions defined by a high pH, independent of the Pco(2) (respira tory alkalosis and metabolic alkalosis). In contrast, Pa-O2 and VA/Q h eterogeneity was unchanged in conditions defined by either a normal or low pH (normalized acid-base status, mixed respiratory alkalosis and metabolic acidosis, and metabolic acidosis). Therefore, we conclude th at hypocapnia-induced VA/Q mismatch in hyperventilated dogs is pH-medi ated and is not a function of PCO2 per se.