Cerebral hypoxia–ischemia is an important cause of secondary brain injury and is associated with higher morbidity and mortality in patients with acute brain injury (ABI), including patients with traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), and intracerebral hemorrhage (ICH) [
1]. Improving cerebral oxygen delivery by increasing arterial oxygen content through the increase of the inspired oxygen fraction (FiO
2) could allow a shift toward an aerobic glycolytic pathway [
2] and overcome either brain tissue hypoxia due to reduced cerebral perfusion pressure (CPP)/increased intracranial pressure (ICP) or microvascular dysfunction [
3]. However, previous studies have reported conflicting results regarding the impact of hyperoxia on cerebral metabolism [
4,
5]. …