Neurosurgical Anaesthesia
APPLIED ANATOMY AND PHYSIOLOGY
Cerebral Blood Flow
Under normal conditions, the brain receives about 15% of the cardiac output, which corresponds to a cerebral blood flow (CBF) of approximately 50 mL 100 g– 1 tissue min– 1 or 600–700 mL min– 1. The cerebral circulation is able to maintain an almost constant blood flow between a mean arterial pressure of 60 and 140 mmHg by the process of autoregulation. This is mediated by a primary myogenic response involving local alteration in the diameter of small arterioles in response to changes in transmural pressure. Above and below these limits, or in the traumatized brain, autoregulation is impaired or absent, so that cerebral blood flow is closely related to cerebral perfusion pressure (CPP) (Fig. 32.3). This effect is also seen in association with cerebral hypoxia and hypercapnia, in addition to acute intracranial disease and trauma. Cerebral perfusion pressure may be reduced as a result of systemic hypotension or an increase in ICP; CBF is maintained until the ICP exceeds 30–40 mmHg. The Cushing reflex increases CPP in response to an increase in ICP by producing, first, reflex systemic hypertension and tachycardia and then bradycardia, despite these compensatory mechanisms also contributing to an increase in ICP. In the treatment of closed head injuries, if both ICP and mean arterial pressure are being monitored, it is essential to maintain the resultant CPP with vasopressor therapy if cerebral perfusion is borderline because even transient absence of flow to the brain may produce focal or global ischaemia with infarction. Figure 32.3 also demonstrates that haemorrhagic hypotension associated with excess sympathetic nervous activity results in a loss of autoregulation at a higher CPP than normal, while the use of vasodilators to induce hypotension shifts the curve to the left, maintaining flow at lower levels of perfusion pressure. Vasodilators also differ in their effects; autoregulation is preserved at a lower CPP with sodium nitroprusside than with autonomic ganglionic blockade (however, vasodilators are rarely used during neuroanaesthesia). Cerebral blood flow is closely coupled to cerebral metabolic rate. Local increases in cerebral metabolic rate are associated with very prompt increases in CBF. The increased electrical activity associated with convulsions produces an increase in lactic acid and other vasodilator metabolites. This, together with an increase in CO2 production, produces an increase in CBF. Conversely, cerebral metabolic depression, in association with either deliberate or accidental hypothermia or induced by drugs, reduces CBF.