Hyperventilation-induced cerebral hypoxia

Acute respiratory alkalosis decreases cerebral blood flow, increases the affinity of hemoglobin for oxygen, and can result in cerebral hypoxia. This experiment was designed to study this phenomenon in dogs, and to demonstrate the effect of an increased concentration of inspired oxygen. Seven mongrel dogs were anesthetized with pentobarbital and ventilated with a constant volume respirator. A Telfon-coated stainless steel catheter was placed through a craniotomy into the parietal lobe and advanced through the corona radiata to monitor cerebral PO2 and PCO2 with a mass spectrometer. Steady state cerebral and arterial gas tensions were recorded during eucapnic ventilation with air, eucapnic ventilation with 100% oxygen, hypocapnic ventilation with air, and hypocapnic ventilation with 100% oxygen. Decreased cerebral tissue oxygen tension was demonstrated in hypocapnic dogs ventilated with air. When the concentration of inspired oxygen was increased, the relatively small increase in artrial oxygen content was associated with a marked increase in PO2 at the cerebral tissue level. This may be of clinical importance in therapeutic or centrally mediated hyperventilation.