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What is cerebral autoregulation?
Cerebral autoregulation is the control process by which cerebral blood flow (CBF) is maintained constant over a wide range of cerebral perfusion pressures (CPP) (Figure 17.1). CPP represents the difference between mean arterial pres-sure (MAP) and ICP. Autoregulation adjusts cerebral vessel caliber as CPP changes. Normal CBF is 45–65 ml/100 g of brain tissue per minute. It is coupled to alterations in cere-bral metabolic rate, which is linked to oxygen consumption (CMRO2). CBF parallels the changes in CMRO2. Several parameters affect CBF.
Autoregulation maintains CBF between a CPP of 50 and 150 mmHg. Below 50 mmHg, cerebral blood vessels achieve maximal dilation; resistance to flow is low; and CBF falls in direct proportion to CPP. Chronically hypertensive patients undergo an upward shift of autoreg-ulation to higher perfusion pressures. Consequently, these patients require higher CPP to maintain normal CBF. At the upper level of autoregulation, cerebral blood vessels are maximally constricted, and CBF will rise linearly with increasing CPP. Integrity of the blood–brain barrier is lost at these high pressures; transudation of fluid occurs; and cerebral edema forms. Autoregulatory compensation generally occurs over 1–3 minutes.
The second parameter affecting CBF is arterial carbon dioxide tension (PaCO2). Increasing levels of PaCO2 produce elevated levels of extracellular hydrogen ion concen-trations, which induce cerebral vessel smooth muscle relaxation and vasodilation. Consequently, cerebral vascular resistance falls, increasing CBF by as much as twofold. This effect plateaus at a PaCO2 of approximately mmHg. Conversely, decreasing PaCO2 increases cere-bral vasoconstriction and CBF decreases. At a PaCO2 of mmHg, cerebral vasoconstriction is maximal and CBF decreases by 50%. Further decreases in PaCO2 have no greater vacoconstricting influence. These physiologic principles remain in effect for several hours, after which cerebral spinal fluid (CSF) bicarbonate levels drop to compensate for the induced CSF alkalosis. Once CSF pH returns toward normal, respiratory alkalosis no longer provokes cerebral vasoconstriction. The PaCO2 response at the limits of autoregulation can be blunted. If CPP is low and cerebral vessels are maximally dilated, lowering PaCO2 will have little beneficial effect on cerebral vascular resistance.
The third parameter affecting CBF is arterial oxygen tension (PaO2). At a PaO2 below 50 mmHg, CBF rises linearly with falling PaO2. Local accumulation of acidic metabolites such as lactate results in cerebral vasodilation. In contradistinction, hyperoxia has no effect on cerebral vascular tone.
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