Postoperative delirium is associated with increased morbidity and mortality. We hypothesised that restoration of regional cerebral oxygen desaturation would reduce the incidence of postoperative delirium in elderly patients after cardiac surgery. After institutional ethics review board approval and informed consent, a double-blinded, prospective, randomised, controlled trial was conducted in patients ≥ 60 years of age undergoing cardiac surgery with cardiopulmonary bypass. In the intervention group, an algorithm was commenced if regional cerebral oxygen saturation decreased below 75% of baseline value for 1 min or longer. In the control group, the cerebral oximetry monitor screen was electronically blinded. Assessment of delirium was performed with confusion assessment method for intensive care unit or confusion assessment method after discharge from intensive care unit at 12-h intervals for seven postoperative days. Postoperative delirium was present in 30 out of 123 (24.4%) and 31 out of 126 (24.6%) patients in the intervention and control groups, respectively, odds ratio 0.98 (95%CI 0.55-1.76), p = 0.97. Postoperative delirium was present in 20 (71%) out of 28 and in 41 (18%) out of 221 patients with baseline regional cerebral oxygen saturation ≤ 50, or > 50%, respectively, p = 0.0001. Higher baseline regional cerebral oxygen saturation and body mass index were protective against postoperative delirium. Restoration of regional cerebral oxygen desaturation did not result in lower postoperative delirium after cardiac surgery. Pre-operative regional cerebral oxygen saturation ≤ 50% was associated with increased postoperative delirium rates in elderly patients following cardiac surgery.

In studies on IOH, both the threshold to define hypotension and the method chosen to model IOH affects the association of IOH with outcome. This makes different studies on IOH less comparable and hampers clinical application of reported results.

Both hypoxia and carbon dioxide increase cerebral blood flow (CBF), and their effective interaction is currently thought to be additive. Our objective was to test this hypothesis. Eight healthy subjects breathed a series of progressively hypoxic gases at three levels of carbon dioxide. Middle cerebral artery velocity, as an index of CBF; partial pressures of carbon dioxide and oxygen and concentration of oxygen in arterial blood; and mean arterial blood pressure were monitored. The product of middle cerebral artery velocity and arterial concentration of oxygen was used as an index of cerebral oxygen delivery. Two-way repeated measures analyses of variance (rmANOVA) found a significant interaction of carbon dioxide and hypoxia factors for both CBF and cerebral oxygen delivery. Regression models using sigmoidal dependence on carbon dioxide and a rectangular hyperbolic dependence on hypoxia were fitted to the data to illustrate this interaction. We concluded that carbon dioxide and hypoxia act synergistically in their control of CBF so that the delivery of oxygen to the brain is enhanced during hypoxic hypercapnia and, although reduced during normoxic hypocapnia, can be restored to normal levels with progressive hypoxia.