The normal cerebral blood flow is 45-50ml 100g^-1 min^-1, ranging from 20ml 100g^-1 min^-1 in white matter to 70ml 100g^-1 min^-1 in grey matter. There are two essential facts to understand about cerebral blood flow. Firstly, in normal circumstances when the flow falls to less than 18-20ml 100g^-1 min^-1, physiological electrical function of the cell begins to fail. Secondly, an increase or decrease in CBF will cause an increase or decrease in cerebral arterial blood volume because of arterial dilatation or constriction. Thus in a brain which is decompensated as a result of major intracranial pathology, increases or decreases in CBF will in turn lead to a significant rise or fall in ICP. The physiological factors which can alter CBF and hence ICP are listed in  Table 2. There are also a number of drugs which can induce arterial dilatation, the most well known being high concentrations of volatile agents. These will be discussed in detail in a subsequent article.

Autoregulation. CBF is maintained at a constant level in normal brain in the face of the usual fluctuations in blood pressure by the process of autoregulation. It is a poorly understood local vascular mechanism. Normally autoregulation maintains a constant blood flow between MAP 50 mmHg and 150 mmHg. However in traumatised or ischaemic brain, or following vasodilator agents (volatile agents and sodium nitroprusside) CBF may become blood pressure dependent. Thus as arterial pressure rises so CBF will rise causing an increase in cerebral volume. Similarly as pressure falls so CBF will also fall, reducing ICP, but also inducing an uncontrolled reduction in CBF.

More recent work has shown that following trauma autoregulation may still be functioning. Bouma reported that it was present in up to 69% patients with head injuries [5].

In this situation if CPP falls below the critical value of 70 mmHg, the patient will have inadequate cerebral perfusion. Autoregulation will cause cerebral vasodilatation leading to a rise in brain volume. This in turn will lead to a further rise in ICP and induce the vicious circle described by the vasodilatation cascade (fig 3a) which results in cerebral ischaemia.

This process can only be broken by increasing the blood pressure to raise CPP, inducing the vasoconstriction cascade (fig 3b). This explains why the maintenance of arterial blood pressure at adequate level by careful monitoring and rapid correction if it falls is so important.

Carbon dioxide causes cerebral vasodilation. As the arterial tension of CO₂ (fig 4) rises, CBF increases and when it is reduced vasoconstriction is induced.

Thus hyperventilation can lead to a mean reduction in intracranial pressure of about 50% within 2-30 minutes [6]. When PaCO2 is less than 25 mmHg (3.3kPa) there is no further reduction in CBF. Therefore there is no advantage in inducing further hypocapnia as this will only shift the oxygen dissociation curve further to the left, making oxygen less available to the tissues.

Acute hypocapnic vasoconstriction will only last for a relatively short time (5 hours). While hypocapnia is maintained, there is a gradual increase in CBF towards control values leading which will lead to cerebral hyperaemia (over-perfusion) if the PaCO₂ is returned rapidly to normal levels (7). When long term ventilation is required, only mild hypocapnia (34-38 mmHg: 4.5-5.1 kPa) should be induced. Worse outcome was reported in patients after head injuries at 3 and 6 months in those who had been hyperventilated to low PaCO₂ levels for long periods [8].

Teaching Point. When there is an acute rise in ICP, for example after an acute head injury ICP can be reduced by hyperventilation to lower arterial CO₂ tension. This technique is used during neurosurgery to reduce brain size to improve access for the surgeon. In CONTRAST only mild hyperventilation should be used for long term ventilation of patients as described above.

Oxygen. Low arterial oxygen tension also has profound effects on cerebral blood flow (Fig 5). When it falls below 50 mmHg (6.7 kPa), there is a rapid increase in CBF and arterial blood volume.

(Continued ...)

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