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. 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 electrical activity. Because of the rapid oxygen consumption and the absence of significant oxygen reserves, interruption of cerebral perfusion usually results in unconsciousness within 10 s. If blood flow is not reestablished within 3–8 min under most conditions, ATP stores are depleted, and irreversible cellular injury occurs. The more rostral, “higher” brain regions (cortex, hippocampus) are more sensitive to hypoxic injury than the brainstem.
Neuronal cells normally utilize glucose as their primary energy source. Brain glucose consumption is approximately 5 mg/100 g/min, of which more than 90% is metabolized aerobically. CMRO2 therefore normally parallels glucose consumption. This relationship is not maintained during 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 normally dependent on a continuous supply of glucose. Acute sustained hypoglycemia is injurious to the brain. Paradoxically, hyperglycemia can exacerbate global and focal hypoxic brain injury by accelerating cerebral acidosis and cellular injury. Adequate control of perioperative blood glucose concentration is advocated in part to prevent adverse effects of hyperglycemia during ischemia; however, overzealous blood glucose control can likewise produce injury through iatrogenic hypoglycemia.
Cerebral blood flow (CBF) varies with metabolic activity. Regional CBF parallels metabolic activity and can vary from 10 to 300 mL/100 g/min. For example, motor activity of a limb is associated with a rapid increase in regional CBF of the corresponding motor cortex. Similarly, visual activity is associated with an increase in regional CBF of the corresponding occipital visual cortex.
Indirect measures are often used to estimate the adequacy of CBF and brain tissue oxygen delivery in clinical settings. These methods include:
The velocity of CBF can be measured using transcranial Doppler (TCD). An ultrasound probe (2 MHz, pulse wave Doppler) is placed in the temporal area above the zygomatic arch, which allows insonation of the middle cerebral artery. Normal velocity in the middle cerebral artery is approximately 55 cm/s. Velocities greater than 120 cm/s can indicate cerebral artery vasospasm following subarachnoid hemorrhage (SAH) or hyperemic blood flow. Comparison between the velocities in the extracranial internal carotid artery and the middle cerebral artery (the Lindegaard ratio) can distinguish between these conditions. Middle cerebral artery velocity three times that of the velocity measured in the extracranial internal carotid artery more likely reflects cerebral artery vasospasm.
Near-infrared spectroscopy is discussed in Chapter 4. Decreased saturation ...