KEY POINTS

1. The brain has a rapid metabolic rate, and it receives approximately 15% of the cardiac output. Under normal circumstances, CBF is approximately 50 mL/100 g/min. The gray matter receives 80% and the white matter receives 20% of this blood flow.
2. Approximately 60% of the brain's energy consumption is used to support electrophysiologic function. The remainder of the energy consumed by the brain is involved in cellular homeostatic activities.
3. CBF is tightly coupled to local cerebral metabolism. When cerebral activity in a particular region of the brain increases, a corresponding increase in blood flow to that region occurs. Conversely, suppression of cerebral metabolism leads to a reduction in blood flow.
4. CBF is autoregulated and maintained constant over a MAP range of 65 to 150 mm Hg. CBF is pressure passive when MAP is either below the lower limit or above the upper limit of autoregulation.
5. CBF is also under chemical regulation. It varies directly with arterial carbon dioxide tension (PaCO₂ ) in the range of 25 to 70 mm Hg. With a reduction in PaO₂ to less than 60 mm Hg, CBF increases dramatically. Changes in temperature affect CBF primarily by suppression of cerebral metabolism.
6. Systemic vasodilators (nitroglycerin, nitroprusside, hydralazine, calcium channel blockers) vasodilate the cerebral circulation and can, depending on MAP, increase CBF. Vasopressors such as phenylephrine, norepinephrine, ephedrine, and dopamine do not have significant direct effects on cerebral circulation. Their effect on CBF is dependent on their effect on systemic blood pressure. When MAP is less than the lower limit of autoregulation, vasopressors increase systemic pressure and thereby increase CBF. If systemic pressure is within the limits of autoregulation, vasopressor-induced increases in systemic pressure have little effect on CBF.
7. All modern volatile anesthetics suppress CMR and, with the exception of halothane, can produce burst suppression of the EEG. At that level, CMR is reduced by about 60%. Volatile agents have dose-dependent effects on CBF. In sub-MAC doses, CBF is not significantly altered. Beyond 1 MAC doses, direct cerebral vasodilation results in an increase in CBF.
8. Barbiturates, etomidate, and propofol decrease CMR and can produce burst suppression of the EEG. At that level, CMR is reduced by about 60%. Flow and metabolism coupling is preserved, and therefore CBF is decreased. Opiates and benzodiazepines effect minor decreases in CBF and CMR, whereas ketamine

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   can increase CMR (with a corresponding increase in blood flow) significantly.
9. Brain stores of oxygen and substrates are limited, and the brain is exquisitely sensitive to reductions in CBF. Severe reductions in CBF (<10 mL/100 g/min) lead to rapid neuronal death. Ischemic injury is characterized by early excitotoxicity and delayed apoptosis.
10. Barbiturates, propofol, ketamine, and the volatile anesthetics have neuroprotective efficacy and can reduce ischemic cerebral injury. In the case of volatile anesthetics, the reduction in cerebral injury is transient, and long-term protection of neurons is not achieved. Etomidate administration is associated with regional reductions in CBF, which can exacerbate ischemic brain injury.