The Determinants of Cerebrospinal Fluid PO2

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Abstract
Arterial blood and lumbar cerebrospinal fluid (CSF) PQ2, PCO2, and pH were measured in six hospitalized patients without lung disease and in eleven patients with chronic lung disease (CLD). The same measurements were made on serial samples of arterial and jugular venous blood and lumbar CSF from the patients with CLD while they breathed 95% oxygen with 5% nitrogen and 95% oxygen with 5% carbon dioxide. The lumbar CSF P02 of the hypoxemic hypercapnic . patients with CLD was the same as that of patients without CLD. Breathing 95% oxygen with 5% carbon dioxide increased lumbar CSF PO2 more than breathing 95% oxygen with 5% nitrogen. The change in CSF PO2 was closely related to the change in arterial PCO2 and this relationship is similar to the relationship between arterial PCO2 and cerebral blood flow in patients with and without hypercapnia. The increases in CSF and jugular venous PO2 were essentially the same magnitude in response to breathing the oxygen and nitrogen mixture. These results suggest that increased central nervous system blood flow in response to hypercapnia may be one of the mechanisms which sustain CSF PO2 in hypoxemic hypercapnic patients. The similarity of jugular venous and CSF PO2 values of subjects breathing air and of the increase on breathing 95% oxygen with nitrogen suggest that both CSF and jugular venous PO2 may be in equilibrium with the same tissues or with each other and may reflect the magnitude of PO2 changes in some of the central nervous system tissue.