Anesthesia for Neurosurgery - Physiology
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Cerebral blood flow
Cerebral blood flow (CBF) is equal to cerebral perfusion pressure (CPP) divided by the cerebral vascular resistance. CPP is defined as the difference between the mean arterial pressure (MAP) and intracranial pressure (ICP) or central venous pressure, whichever is higher. CBF averages 50 mL/100 g of brain tissue per minute in the normal brain and is affected by blood pressure, metabolic demands, PaCO2, PaO2, blood viscosity, vasoactive agents, and neurogenic regulation. The brain receives approximately 15% of the cardiac output.
- CBF is maintained at a constant level by constriction and dilation of arterioles (autoregulation) (Fig. 25.1) when the MAP is between 50 and 150 mm Hg. When MAP is outside these limits, CBF varies directly with the MAP. Chronic hypertension shifts the autoregulatory curve to the right, rendering hypertensive patients susceptible to cerebral ischemia at blood pressures considered normal in healthy individuals. Chronic antihypertensive therapy may normalize the autoregulatory range. Cerebral ischemia, trauma, hypoxia, hypercarbia, edema, mass effect, and volatile anesthetics attenuate or abolish autoregulation and may make blood flow to the affected area dependent on MAP.
- PaCO2 has profound effects on CBF by its effect on the pH of the brain extracellular fluid (ECF). CBF increases linearly with increasing PaCO2 in the range from 20 to 80 mm Hg, with an absolute change of 1 to 2 mL/100 g/min for each mm Hg change in PaCO2. The effect of PaCO2 on CBF decreases over 6 to 24 hours because of slow adaptive changes in the brain ECF bicarbonate concentration. Sustained hyperventilation causes cerebrospinal fluid (CSF) bicarbonate production to decrease, allowing CSF pH to gradually normalize. Rapid normalization of PaCO2 after a period of hyperventilation results in a significant CSF acidosis with vasodilation and increased ICP.
- PaO2. Hypoxia is a potent cerebral vasodilator. CBF increases markedly below a PaO2 of 60 mm Hg. PaO2 above 60 mm Hg has little influence on CBF.
- Neurogenic regulation. The cerebral vasculature receives extensive cholinergic, adrenergic, serotonergic, and VIPergic innervation, although the exact role these systems play in regulation of CBF is not clear. Evidence suggests, however, that increased sympathetic tone in hemorrhagic shock shifts the lower end of the autoregulatory curve to the right and results in lower CBF at a given MAP.
- Viscosity. Normal hematocrit (33% to 45%) in a normal brain has little influence on CBF. During focal cerebral ischemia, however, reduction in viscosity by hemodilution (hematocrit 30% to 34%) may increase CBF to ischemic territories.