A Brief Review of Brain's Blood Flow–Metabolism Coupling and Pressure Autoregulation

Background The human brain, depending on aerobic glycolysis to cover its metabolic needs and having no energy reserves whatsoever, relies on a constant and closely regulated blood supply to maintain its structural and functional integrity. Cerebral autoregulation, that is, the brain's intrinsic ability to regulate its own blood flow independently from the systemic blood pressure and cardiac output, is an important physiological mechanism that offers protection from hypoperfusion injury. Discussion Two major independent mechanisms are known to be involved in cerebral autoregulation: (1) flow–metabolism coupling and (2) myogenic responses of cerebral blood vessels to changes in transmural/arterial pressure. A third, less prominent component of cerebral autoregulation comes in the form of neurogenic influences on cerebral vasculature. Conclusion Although fragmentation of cerebral autoregulation in separate and distinct from each other mechanisms is somewhat arbitrary, such a scheme is useful for reasons of simplification and to better understand their overall effect. Comprehension of cerebral autoregulation is imperative for clinicians in order for them to mitigate consequences of its impairment in the context of traumatic brain injury, subarachnoid hemorrhage, stroke, or other pathological conditions.

Arterial Oxygenation in Traumatic Brain Injury—Relation to Cerebral Energy Metabolism, Autoregulation, and Clinical Outcome

Background: Ischemic and hypoxic secondary brain insults are common and detrimental in traumatic brain injury (TBI). Treatment aims to maintain an adequate cerebral blood flow with sufficient arterial oxygen content. It has been suggested that arterial hyperoxia may be beneficial to the injured brain to compensate for cerebral ischemia, overcome diffusion barriers, and improve mitochondrial function. In this study, we investigated the relation between arterial oxygen levels and cerebral energy metabolism, pressure autoregulation, and clinical outcome. Methods: This retrospective study was based on 115 patients with severe TBI treated in the neurointensive care unit, Uppsala university hospital, Sweden, 2008 to 2018. Data from cerebral microdialysis (MD), arterial blood gases, hemodynamics, and intracranial pressure were analyzed the first 10 days post-injury. The first day post-injury was studied in particular. Results: Arterial oxygen levels were higher and with greater variability on the first day post-injury, whereas it was more stable the following 9 days. Normal-to-high mean pO2 was significantly associated with better pressure autoregulation/lower pressure reactivity index ( P = .02) and lower cerebral MD-lactate ( P = .04) on day 1. Patients with limited cerebral energy metabolic substrate supply (MD-pyruvate below 120 µM) and metabolic disturbances with MD-lactate-/pyruvate ratio (LPR) above 25 had significantly lower arterial oxygen levels than those with limited MD-pyruvate supply and normal MD-LPR ( P = .001) this day. Arterial oxygenation was not associated with clinical outcome. Conclusions: Maintaining a pO2 above 12 kPa and higher may improve oxidative cerebral energy metabolism and pressure autoregulation, particularly in cases of limited energy substrate supply in the early phase of TBI. Evaluating the cerebral energy metabolic profile could yield a better patient selection for hyperoxic treatment in future trials.