PCO2 modulation of ventilation and HCO3- buffer during chronic metabolic acidosis

Ventilation and acid-base balance were studied in 6 conscious dogs during chronic eucapnic and hypocapnic metabolic acidosis. The dogs had tracheostomas for respiratory studies, exteriorized carotid arteries for obtaining arterial blood and cannulae for sampling cisternal cerebrospinal fluid (CSF). Measurements were obtained on a control diet, and then, during metabolic acidosis induced by adding HCl (7 mmol/kg per day). Initially during metabolic acidosis, PaCO2 was maintained normal by having the dogs breathe 3% CO2 (eucapnia); then the dogs breathed air (hypocapnia). Chronically, arterial and CSF [HCO-3] were related to PCO2. No respiratory compensation occurred during chronic hypocapnic metabolic acidosis since [HCO-3] decreased more than PCO2; consequently, the acidosis worsened. At any [H+], ventilation was related to PCO2. Thus, during hypocapnic metabolic acidosis, ventilation was not increased relative to increase in arterial and CSF [H+]. Modulation of ventilation by PCO2 during severe acidosis may be crucial because stimulation of ventilation by [H+] of arterial blood or CSF would have progressively reduced PCO2 and [HCO-3], resulting in a worsening of the metabolic acidosis.