Brain tissue oxygen tension response to induced hyperoxia reduced in hypoperfused brain

Object. Increasing PaO2 can increase brain tissue PO2 (PbtO(2)). Nevertheless, the small increase in arterial O-2 content induced by hyperoxia does not increase O-2 delivery much, especially when cerebral blood flow (CBF) is low, and the effectiveness of hyperoxia as a therapeutic intervention remains controversial. The purpose of this study was to examine the role of regional (r)CBF at the site of the PO2 probe in determining the response of PbtO(2) to induced hyperoxia. Methods. The authors measured PaO2 and PbtO(2) at baseline normoxic conditions and after increasing inspired O-2 concentration to 100% on I I I occasion. in 83 patients with severe traumatic brain injury in whom a stable xenon-enhanced computed tomography measurement of CBF was available. The 0, reactivity was calculated as the change in PbtO(2) X 100/change in PaO2. Results. The O-2 reactivity was significantly different (p < 0.001) at the 5 levels of rCBF (< 10, 11-15, 16-20, 21-40, and > 40 ml/100 g/min). When rCBF was < 20 ml/100 g/min, the increase in PNO2 induced by hyperoxia was very small compared with the increase that occurred when rCBF was > 20 ml/100 g/min. Conclusions. Although the level of CBF is probably only one of the factors that determines the PbtO(2) response to hyperoxia, it is apparent from these results that the areas of the brain that would most likely benefit from improved oxygenation are the areas that are the least likely to have increased PbtO(2).