Cerebrovascular reserve refers to the central response to physiological alterations following acute brain damage. In short, it is the ability of the brain to successfully compensate for physiological stresses (e.g., hypoglycemia, hypoxia, hypotension, and anemia). In all of these cases, vasodilation is required to compensate for the increased cerebral blood flow. If vasodilation is not maintained in response to these physiological stresses, there is a risk of brain damage. Animal studies have shown that an environment of disrupted cerebrovascular reserve can be created that increases the risk of cerebral infarction.29 For example, mild hypoxia produced by blockage of one side of the carotid artery or by itself would not produce symptoms because of compensatory cerebrovascular dilation. Some scholars believe that arterial hypoxemia occurring under normal cerebrovascular compensatory mechanisms does not lead to brain damage. Of course, this view could be explained by the fact that hypoxic heart failure leads to organ failure without isolated neurological damage. However, carotid artery block on top of hypoxia, or vice versa, results in stroke because the compensatory mechanisms are maximal and cannot adapt to a further decline in oxygen supply.29 There are abundant clinical cases of this condition.30 Examples of decreased cerebrovascular reserve include cerebral edema, hypoxia, anemia, carotid stenosis, and peri-infarct penumbra. In each case, although difficult to quantify, it is clear that further disruption of the cerebral oxygen supply increases the risk of neurological damage. The degree of cerebrovascular reserve can be evaluated by measuring cerebral blood flow before and after administration of acetazolamide. Figure 87-2 gives an example of this method. If cerebrovascular reserve is present, acetazolamide can produce local respiratory acidosis of brain tissue, which in turn leads to local vasodilation.32 If cerebrovascular reserve is disrupted, even if basal cerebral blood flow is normal, brain tissue can be damaged by the lack of vasodilatory response required for perioperative physiologic changes.33-35 The clinical relevance of this view is that some studies have found a correlation between stroke and hypoxia,29 hypotension,36-39 fever,40,41 and anemia29. This has led to a consensus that physicians should be proactive in considering the capacity of each patient’s cerebrovascular reserve. A so-called hemodynamic stroke, a stroke without thrombosis or embolism, may occur if the patient has arterial stenosis, cerebral edema, a brain tumor, or the presence of other factors that may disrupt the vasodilatory capacity (response to hypoxia, hypotension, erythrocytosis, fever, anemia, etc.).