Am. J. Respir. Crit. Care Med., Vol 152, No. 5, 11 1995, 1534-1539.
Hypocapnia-induced ventilation/perfusion mismatch: a direct CO2 or pH- mediated effect?
KB Domino, ER Swenson and MP Hlastala
Department of Anesthesiology, University of Washington School of Medicine, Seattle, USA.
The purpose of this study was to determine whether the increased
ventilation/perfusion (VA/Q) mismatch caused by hypocapnic hyperventilation
in dogs (J. Appl. Physiol. 1993; 74:1306-1314) is a direct CO2 or a
pH-mediated effect. From an initial state of hyperventilated respiratory
alkalosis (FIO2 = 0.21, VT = 18 ml/kg, RR = 35), we studied the changes in
VA/Q distributions, respiratory gas exchange, and hemodynamics when the
acid-base status of the dogs was manipulated by combinations of acid or
alkali infusion with or without CO2 inhalation. In this manner, we studied
respiratory alkalosis (high pH, low PCO2), normalized acid-base status
(normal pH, normal PCO2), metabolic acidosis (low pH, normal PCO2),
metabolic alkalosis (high pH, normal PCO2), and a mixed respiratory
alkalosis and metabolic acidosis (normal pH, low PCO2). Gas exchange was
evaluated using the multiple inert gas elimination technique. PaO2 was
reduced and VA/Q heterogeneity was increased in all conditions defined by a
high pH, independent of the PCO2 (respiratory alkalosis and metabolic
alkalosis). In contrast, PaO2 and VA/Q heterogeneity 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 that hypocapnia-induced VA/Q mismatch in
hyperventilated dogs is pH-mediated and is not a function of PCO2 per se.
