- Cerebral perfusion pressure is the difference
between mean arterial pressure and intracranial pressure (ICP) (or
central venous pressure, whichever is greater).
- The cerebral autoregulation curve is shifted
to the right in patients with chronic arterial hypertension.
- 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.
- CBF changes 5–7% per 1°C change
in temperature. Hypothermia decreases both cerebral metabolic rate
and CBF, whereas pyrexia has the reverse effect.
- 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.
- The blood–brain barrier may be disrupted
by severe hypertension, tumors, trauma, strokes, infection, marked
hypercapnia, hypoxia, and sustained seizure activity.
- 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.
- With the exception of ketamine, all intravenous
agents either have little effect on or reduce cerebral metabolic
rate and CBF.
- 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
- The brain is very vulnerable to ischemic injury
because of its relatively high oxygen consumption and near-total
dependence on aerobic glucose metabolism.
- Hypothermia is the most effective method for
protecting the brain during focal and global ischemia.
- Both animal and human data suggest that barbiturates
are effective for brain protection in the setting of focal ischemia.
The anesthetic care of patients who undergo neurosurgery requires
a basic understanding of the physiology of the central nervous system
(CNS). The effects of anesthetic agents on cerebral metabolism,
blood flow, cerebrospinal fluid (CSF) dynamics, and intracranial
volume and pressure are often profound. In some instances, these
alterations are deleterious, whereas in others they may actually
be beneficial. This chapter reviews important physiological concepts
in anesthetic practice and then discusses the effects of commonly
used anesthetics on cerebral physiology. Although most of the discussion
focuses on the brain, the same concepts also apply, at least qualitatively,
to the spinal cord.
The brain is normally responsible for consumption of 20% of
total body oxygen. Most of cerebral oxygen consumption (60%)
is used in generating adenosine triphosphate (ATP) to support neuronal
electrical activity (Figure 25–1).
The cerebral metabolic rate (CMR) is usually expressed in terms
of oxygen consumption (CMRo2),
which 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