The cerebral metabolic rate

The brain consumes O₂ at a high rate. Although accounting for only about 2% of total body weight, the brain receives 12% to 15% of cardiac output. Normal CBF is approximately 50 mL·100 g⁻¹·min⁻¹. Normal CMR for O₂ (CMRO₂) is 3.0 to 3.5 mL·100 g⁻¹·min⁻¹. Increases in regional brain activity lead to local increases in CMR that, in turn, lead to proportional changes in CBF. This relationship is carefully maintained and is called flow-metabolism coupling.

Mechanisms involved are, as yet, undefined but appear to include local byproducts of metabolism (potassium, H⁺, lactate, adenosine triphosphate), glutamate, and nitric oxide. Peptides (vasoactive peptide, substance P, and others) exert effects on the nerves that innervate cerebral vessels. Neurogenic control of CBF occurs by sympathetic innervation and is independent of the influence of PaCO₂.

The CMR decreases during sleep, increases with increasing mental activity, and may reach an extremely high level with epileptic activity. The CMR is globally reduced in coma and may be only locally impaired after brain injury.

Autoregulation

Autoregulation is defined as the maintenance of CBF over a range of mean arterial pressure (MAP) (see Figure 42-1). Cerebral vascular resistance (CVR) is adjusted to maintain constant CBF. Cerebral perfusion pressure equals MAP minus intracranial pressure (ICP). Because ICP (and therefore cerebral perfusion pressure) is not commonly available, MAP is used as a surrogate of cerebral perfusion pressure.

Autoregulation occurs when MAP is between 70 and 150 mm Hg in the normal brain (see Figure 42-1). This is a conservative estimate, given that considerable interindividual variation occurs. The lower limit of autoregulation (LLA) is the point at which the autoregulation curve deflects downward and CBF begins to decrease in proportion to MAP.

CVR varies directly with blood pressure to maintain flow, taking 1 to 2 min for flow to adjust after an abrupt change in blood pressure. In hypertensive patients, the autoregulatory curve is shifted to the right (Figure 42-2). A hypertensive patient may be at risk for developing brain ischemia at a MAP of 70 mm Hg, for example, because the LLA will be higher than in a nonhypertensive patient. Several weeks of blood pressure control may return the curve to normal. Following significant hypotension (lower than the LLA), autoregulation is impaired, and hyperemia may occur when MAP returns to the normal range. CO₂ reactivity remains intact, and inducing hypocapnia may attenuate hyperemia.

Autoregulatory vasodilation may be limited by background sympathetic vascular tone. Systemic vasodilators (nitroprusside, nitroglycerin, hydralazine, adenosine, and calcium channel blockers) may extend the lower limit of tolerable hypotension (shift the LLA to a lower pressure). Other than their effect on global cerebral perfusion pressure, β-adrenergic receptor blocking agents likely have no adverse effects on patients with intracranial pathology.

Autoregulation is impaired in areas of relative ischemia, surrounding mass lesions, after grand mal seizures, after head injury, and during episodes of hypercarbia or hypoxemia. Figure 42-3 shows how lost autoregulation may lead to dangerously low CBF. Regional or global ischemia may ensue.