Abstract

Cerebral autoregulation (CA) describes the capability of the brain to maintain its flow as relatively stable over a wide rage of mean arterial pressures (MAPs), for example, from 60 to 150 mm Hg. Because the brain is encompassed in the skull, CA is vital for preventing cerebral edema and hemorrhage, as illustrated in some patients experiencing acute liver failure.1 Also, CA counteracts the effect on cerebral blood flow (CBF) of a reduction in MAP in response to, for example, hemorrhage or a change in body position. Yet, when rising from a supine or seated position, one sometimes experiences symptoms indicative of a reduced CBF, like blurred vision.2 Thus, CA is of general clinical interest. For example, diabetic patients have increased risk of developing ischemic or hemorrhagic stroke, and in some diabetic patients CA is affected. Evidence for CA was provided in the 1930s when Fog,3 through a cranial window, observed the pial artery reaction to manipulation of MAP. For humans, CBF was measured with introduction of the method of Kety-Schmidt in 1948,4 and it was used in 1954 by Finnerty et al5 to determine cerebral hemodynamics of the ischemic brain after an acute reduction in MAP in attempt to define what now would be considered the lower limit of CA. However, it was the review by Lassen6 that introduced the concept of CA by plotting CBF against MAP to illustrate the relative stability of CBF over a wide range of blood pressure. Also, the lower and upper limits of CA were identified by a decrease in CBF at a low MAP and an increase …

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