Cerebral blood flow (CBF), defined as the volume of blood (mL)/100 g of brain tissue/min, is primarily determined by autoregulation, cerebral perfusion pressure (CPP), CO2 reactivity, O2 reactivity, cerebral metabolic rate of O2 (CMRO2) coupling, temperature, viscosity, and some autonomic influences. Normal CBF is 45–60 mL/100 g/min.
Through autoregulation, the CBF is kept constant despite changes in CPP or mean arterial pressure (MAP). This feature enables the normal brain to tolerate large swings in blood pressure. Autoregulation occurs between MAP of 50 and 150 mm Hg (Figure 123-1).
Autoregulation of cerebral blood flow. (Reproduced with permission from Butterworth JF, Mackey DC, Wasnick JD. Morgan and Mikhail’ s Clinical Anesthesiology, 5th ed. McGraw-Hill; 2013.)
Any decrease in CPP or MAP leads to cerebral vasodilation and increase in CPP or MAP leads to cerebral vasoconstriction. Outside of these limits, CBF is pressure dependent. High MAPs could greatly increase CBF and lead to cerebral edema or hemorrhage. Low MAPs may greatly decrease CBF and lead to injury from hypoxia/anoxia.
In patients who are chronically hypertensive, the cerebral autoregulation curve is shifted to the right for both the lower and upper limits. Some studies suggest it may be possible to restore normal cerebral autoregulatory limits with chronic antihypertensive therapy.
CEREBRAL PERFUSION PRESSURE
Cerebral perfusion pressure determines CBF at the extremes of MAP where there is no cerebral autoregulation or in situations where cerebral autoregulation has been compromised (traumatic brain injury [TBI], increased intracranial pressure [ICP], tumor, meningitis, etc). Cerebral perfusion pressure is MAP—ICP or central venous pressure (CVP) or cerebral venous pressure (cVP), whichever is greatest. Because the ICP, CVP, and cVP are usually less than 10 mm Hg, CPP is primarily determined by MAP.
Normal CPP is approximately 80–100 mm Hg. Cerebral perfusion pressure progressively decreases as ICP or CVP increases until the body’ s compensatory sympathetic nervous system begins to activate. Likewise, CPP decreases as MAP decreases. CPP less than 50 mm Hg shows slowing on EEG, CPP of 25–40 mm Hg shows flat EEG, and CPP sustained at less than 25 mm Hg results in irreversible brain damage.
CBF changes proportionately to changes in PaCO2 (1–2 mL/100 g/min per mm Hg change in PaCO2 (Figure 123-2). This effect is thought to be due to CO2 diffusing across the blood–brain barrier (BBB) and inducing changes in the pH of the CSF and the cerebral tissue. This feature is referred to as CO2 reactivity. Immediate changes with metabolic acidosis are not evident because bicarbonate and other ions do not cross the BBB easily.