Brain tissue oxygen reactivity: clinical implications and pathophysiology

INTRODUCTION It is generally accepted that PbO2 reflects the balance between O2 delivery and consumption (Diringer et al., 2007; Diringer, 2008). However, implementation in the perioperative period of various ventilatory modes using high FiO2 leads to a dramatic and non-physiologic increase in PbO2 with approximating levels of 147 ± 36 mmHg (McLeod et al., 2003). This phenomenon doesn’t correlate with the extent of slight increase in arterial O2 content. At the same time, the jugular venous PO2 increases only slightly (37–40 mmHg) (Forkner et al., 2007). Moreover, hyperoxia does not affect significantly the regional CBF, and there is no improvement in cerebral metabolism with oxygen therapy (Magnoni et al., 2003; Diringer et al., 2007; Diringer, 2008; Xu et al., 2012). The PbO2 increase is more pronounced in edematous (but not necrotized) brain tissues compared to normal areas (Meixensberger et al., 1993). Although, this can be considered a positive phenomenon, it masks the real state of rCBF and local oxidative metabolism. Recording of high PbO2 absolute values may create a false impression of safety and negatively impact the clinical decision making. Apparently, better indicators of the status of energy exchange in the brain tissue are needed for practical use in the perioperative and critical care settings.