Cerebral Venous and Tissue Gases and Arteriovenous Shunting in the Dog

Abstract

Cerebral venous blood gas values have been used to indicate brain tissue oxygenation. However, it is not clear how cerebral tissue and venous measures may vary under physiologic conditions caused by arteriovenous shunt. The purpose of this study was to measure brain tissue and local cerebral venous oxygen (PO2) and carbon dioxide (PCO2) partial pressure during changes in ventilation and to calculate shunt fraction. Eight dogs were anesthetized with isoflurane. After a craniotomy, a Neurotrend probe (Diametrics Inc., St. Paul, MN) that measures PO2, PCO2, pH, and temperature was inserted into brain tissue, and a small vein that drained the same tissue was catheterized. Arterial, cerebral venous, and brain tissue PO2 and PCO2 were measured during random changes in ventilation to produce five different levels of inspired oxygen (room air, 40%, 60%, 80%, 95%) at each of three different end-tidal PCO2 (20 mm Hg, 40 mm Hg, 60 mm Hg). Arteriovenous shunt was calculated from oxygen and CO2 content in artery, vein, and tissue, representing capillary. Tissue PCO2 was 8 mm Hg greater than vein PCO2 during hypocapnia and this difference increased to 20 mm Hg during hypercapnia. Vein PO2 was 8 mm Hg higher than tissue PO2 during hypocapnia, and this difference increased to 40 mm Hg during hypercapnia. Shunt fraction increased from 10%–20% during hypocapnia to 50%–60% during hypercapnia. These results show that brain vein and tissue PO2 and PCO2 differ because of arteriovenous shunting and this difference is increased as end-tidal PCO2 increases. Implications We found, in dogs, that the gradient between brain venous and tissue PO2 and PCO2 is increased with increased arterial PCO2. The divergence between tissue and venous gases can be described by arterial to venous shunting.