Canadian Journal of Anesthesia, Vol 21, 205-214, Copyright © 1974 by Canadian Anesthesiologists' Society

Cerebral Response to Hypocapnia in Normal and Brain-Injured Dogs

¹ Department of Anaesthesia, University of Toronto, St. Michael's Hospital, Toronto
² Department of Neurosurgery, Toronto Western Hospital, Toronto

The cerebral blood flow response to hypocapnia was quantitated utilizing two methods of ventilation. Increased volume hyperventilation produced hypocapnia and decreased CBF but was associated with cardiopulmonary changes which raised mean intrathoracic pressure, decreased venous return and decreased cardiac output. This resulted in increased CSFP, decreased cerebral perfusion pressure and decreased CMRO₂ at PaCO₂ values below 20 mm Hg which was indicative of hypoxia. Constant volume hyperventilation with incremental removal of mechanical dead space was considered as hypocapnia where PaCO₂ was the singular variable because associated cardiopulmonary changes were minimized. This resulted in no CSFP changes and no changes in CMRO₂ even at low PaCO₂ values below 20 mm Hg.

It is concluded that hypocapnia per se does not produce brain tissue hypoxia in normal or brain injured dogs. Hypoxia secondary to hypocapnia is the result of the associated cardiopulmonary and cerebrovascular changes associated with mechanical hyperventilation.