Dr FJM Walters,
Consultant Anaesthetist, Frenchay Hospital, Bristol, UK

Introduction		Cerebral blood flow
Intracranial pressure		Applied physiology - Head injury
Cerebral perfusion pressure		References

The physiological changes that maintain cerebral blood flow (CBF) and accommodate alterations in brain volume are relatively simple to understand. Following trauma or in the presence of major intracranial disease additional changes occur. Major advances in the care of patients with major neurosurgical problems have been developed over the last 10 years. These advances have evolved from a sound understanding of basic physiological rules and the pathological process of different disease situations as well as the pharmacology of anaesthetic drugs. Successful management of these patients relies on a clear understanding of these physiological mechanisms and of the added effect of anaesthesia and the manipulation of arterial pressure, CO₂ and O₂ tensions. Poor anaesthetic technique which allows coughing, straining, hypotension, exaggerated hypertension, hypoxia and hypercarbia will seriously damage the brain. Better results can be obtained by careful monitoring of the patient and attention to simple details than by complex pharmacological interventions. It is the purpose of this article to explain these factors and how an understanding of them can be applied to patients following head trauma or intracranial disease.

The brain is only able to withstand very short periods of ischaemia, unlike the kidney, liver or muscle. Thus cerebral blood flow must be maintained to ensure a constant delivery of oxygen and glucose as well as the removal of "waste" products. Maintenance of cerebral blood flow depends on a balance between the pressure within the skull, intracranial pressure (ICP) and the arterial pressure of the blood, mean arterial pressure (MAP). It is important to maintain a constant blood flow. Thus when blood pressure falls, physiological mechanisms attempt to maintain flow to prevent ischaemia. This process is autoregulation and is explained in detail later. Similarly, when blood pressure rises, the same mechanism stops the blood flow from increasing to excessive levels. If this did occur, cerebral oedema could develop and the brain would enlarge because of the increase in cerebral arterial blood volume.

A number of terms will be used in this article and are defined:

• ICP intracranial pressure is the pressure within the rigid skull.

• CBF cerebral blood flow is the flow of blood through the brain, important for delivery of oxygen and removal of "waste" products

• CPP cerebral perfusion pressure is the effective pressure driving blood through the brain. It is discussed in detail later

Teaching Point:High intracranial pressure (ICP) will cause internal or external herniation of the brain, distortion and pressure on cranial nerves and vital neurological centres. Cerebral perfusion will be impeded and operating conditions difficult or impossible. Loss of CSF and reduction of venous blood volume act to compensate for increases in brain volume. Once these mechanisms are exhausted, any further increase, however small, will cause a large increase in ICP.

The principle constituents within the skull are brain (80%), blood (12%) and CSF (8%). The total volume is 1600ml. The skull is thus a rigid fluid filled box. If the volume of the contents of a rigid fluid-filled container increase, the pressure inside will rise considerably unless some fluid is able to escape. So it is with the skull and brain within it.

If the brain enlarges, some blood or CSF must escape to avoid a rise in pressure. If this should fail, or be unable to occur there will be a rapid increase in ICP from the normal range (5-13 mmHg). If there is an increase in the volume of either the brain or blood the normal initial response is a reduction in CSF volume within the skull. CSF is forced out into the spinal sac. Thus the pressure within the skull, ICP, is initially maintained. If the pathological process progresses with further increase in volume, venous blood and more CSF is forced out of the skull.

Ultimately this process becomes exhausted, when the venous sinuses are flattened and there is little or no CSF remaining in the head. Any further increase in brain volume then causes a rapid increase in ICP. This chain of events is represented by the sequence in Fig 1a and 1b.

(Continued ...)

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