The brain normally consumes 20% of total body oxygen. Most cerebral oxygen consumption (60%) is used to generate adenosine triphosphate (ATP) to support neuronal electrical activity ( Figure26–1). The cerebral metabolic rate (CMR) is usually expressed in terms of oxygen consumption (CMRo2) and averages 3–3.8 mL/100 g/min (50 mL/min) in adults. CMRo2 is greatest in the gray matter of the cerebral cortex and generally parallels cortical elec-trical activity. Because of the relatively high oxygen consumption and the absence of significant oxygen reserves, interruption of cerebral perfusion usually results in unconsciousness within 10 sec, as oxygen tension rapidly drops below 30 mm Hg. If blood flow is not reestablished within 3–8 min under most conditions, ATP stores are depleted, and irreversible cellular injury begins to occur. The hippocampus and cerebellum seem to be most sensitive to hypoxic injury.
Neuronal cells normally utilize glucose as their primary energy source. Brain glucose con-sumption is approximately 5 mg/100 g/min, of which more than 90% is metabolized aerobically. CMRo2 therefore normally parallels glucose con-sumption. This relationship is not maintained dur-ing starvation, when ketone bodies (acetoacetate and β-hydroxybutyrate) also become major energy substrates. Although the brain can also take up and metabolize lactate, cerebral function is nor-mally dependent on a continuous supply of glu-cose. Acute sustained hypoglycemia is injurious to
the brain. Paradoxically, hyperglycemia can exac-erbate global and focal hypoxic brain injury by accelerating cerebral acidosis and cellular injury. Tight control of perioperative blood glucose con-centration has been advocated in part because of adverse effects of hyperglycemia during ischemic episodes; however, overzealous blood glucose con-trol can likewise produce injury through iatrogenic hypoglycemia.