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  • Image not available. Cerebral perfusion pressure is the difference between mean arterial pressure and intracranial pressure (or central venous pressure, whichever is greater).
  • Image not available. The cerebral autoregulation curve is shifted to the right in patients with chronic arterial hypertension.
  • Image not available. The most important extrinsic influences on cerebral blood flow (CBF) are respiratory gas tensions—particularly Paco2. CBF is directly proportionate to Paco2 between tensions of 20 and 80 mg Hg. Blood flow changes approximately 1-2 mL/100 g/min per mm Hg change in Paco2.
  • Image not available. CBF changes 5% to 7% per 1°C change in temperature. Hypothermia decreases both cerebral metabolic rate and CBF, whereas pyrexia has the reverse effect.
  • Image not available. The movement of a given substance across the blood-brain barrier is governed simultaneously by its size, charge, lipid solubility, and degree of protein binding in blood.
  • Image not available. The blood-brain barrier may be disrupted by severe hypertension, tumors, trauma, strokes, infection, marked hypercapnia, hypoxia, and sustained seizure activity.
  • Image not available. The cranial vault is a rigid structure with a fixed total volume, consisting of brain (80%), blood (12%), and cerebrospinal fluid (8%). Any increase in one component must be offset by an equivalent decrease in another to prevent a rise in intracranial pressure.
  • Image not available. With the exception of ketamine, all intravenous agents either have little effect on or reduce cerebral metabolic rate and CBF.
  • Image not available. With normal autoregulation and an intact blood-brain barrier, vasopressors increase CBF only when mean arterial blood pressure is below 50-60 mm Hg or above 150-160 mm Hg.
  • Image not available. The brain is very vulnerable to ischemic injury because of its relatively high oxygen consumption and near total dependence on aerobic glucose metabolism.
  • Image not available. Hypothermia is the most effective method for protecting the brain during focal and global ischemia.

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Anesthetic agents may have profound effects on cerebral metabolism, blood flow, cerebrospinal fluid (CSF) dynamics, and intracranial volume and pressure. In some instances, these alterations are deleterious, whereas in others they may be beneficial. This chapter reviews important physiological concepts in anesthetic practice and discusses the effects of commonly used anesthetics on cerebral physiology.

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Cerebral Metabolism

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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 (Figure 26-1). 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 electrical 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.

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Figure 26-1
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