Management of blood pressure during neuroanaesthesia

Abstract C3

It has been accepted knowledge that in normal individuals the cerebral blood flow is kept constant between cerebral perfusion pressures of approximately 50-150 mmHg through compensatory changes in cerebral vascular resistance ^[1]. Therefore variations in blood pressure should not pose serious harm in normal patients. However, there is a growing body of evidence suggesting that the lower limit of autoregulation in humans may be much higher, around 70-80 mmHg ^[2,3].

A number of entities exist where the cerebral vasculature either globally or regionally loses its ability to respond to the changes in pressure. As a result cerebral blood flow will passively follow any change in cerebral perfusion pressure and cause significant alterations in cerebral blood volume and perfusion. This scenario becomes reality with intracranial pathology such as head trauma, tumour, haemorrhage, stroke or due to the administration of vasoactive drugs, for example anaesthetic agents or vasodilators.

In general, blood pressure should be controlled meticulously and kept within 20 mmHg of normal. Specifically sudden hypoor hypertension must be avoided. Hypotension on induction may be attenuated by preinduction volume loading (10 ml kg⁻¹) whereas hypertension due to laryngoscopy and intubation can be avoided by lignocaine(1.5-2.0 mg kg⁻¹), urapidil (10-20 mg) or esmolol (0.5 mg kg⁻¹).

Despite this general rule there exist quite a number of situations where alterations in blood pressure during neuroanaesthesia might be of some benefit.

The elevation of arterial blood pressure is clearly indicated in patients with chronic hypertension. It is well documented that in these patients the upper and lower limits of autoregulation have been shifted to the right ^[4].

Less definite is the indication for an elevated blood pressure in patients with subarachnoidal haemorrhage to treat or avoid vasospasm ^[5]. Although hypervolaemia, haemodilution and hypertension is associated with less vasospasm it is not clear whether it is the hypervolaemia or the hypertension that is the most important factor in ameliorating vasospasm ^[6-8]. Recommended is a blood pressure increase to 100-150 mmHg with unclipped aneurysm and to 160-200 mmHg if the aneurysm has been clipped.

A deliberate increase in intra-operative blood pressure during carotid endarterectomy has been advocated as autoregulation should keep blood flow normal in areas of healthy brain but might increase flow in hypoperfused regions. However, apart from an increased risk of haemorrhage and oedema formation associated with hypertension the drugs and effects commonly employed for hypertension may impair myocardial oxygen balance ^[9]. The available evidence does not support the introduction of hypertension, but several studies show that hypotension must be avoided during carotid endarterectomy ^[10].

Another area where the evidence supports the introduction of deliberate hypertension is during the management of head injured patients. It is known that hypotension leading to reduced cerebral perfusion pressure is a major determinant of secondary brain injury^[11,12]. Recent studies suggest that outcome after severe head injury is improved if cerebral prefusion pressure is maintained above 70-80 mmHg ^[13]. Taking this into consideration the American Association of Neurological Surgeons and the Brain Trauma Foundation^[14] as well as the European Brain Injury Consortium have mentioned the maintenance of a cerebral perfusion pressure at a minimum of 70 mmHg as a therapeutic option ^[15].

On the other hand there exist few disease entities where a reduction in blood pressure has been recommended ^[16]. Induced hypotension may lower the risk of rupture during microscopic dissection of a cerebral aneurysm and in addition will allow for a clearer view of the anatomy as it will decrease bleeding. However, avoidance of cerebral ischaemia and maintenance of organ perfusion are of the utmost importance. As arterial blood pressure has been shown to be a determinant of collateral blood flow during focal cerebral ischaemia, the deliberate reduction in blood pressure is controversial ^[10,17]. As a result many prefer to use clips for temporary artery occlusion and thus reduce the risk of aneurysm rupture without using induced hypotension ^[17-20]. Even after rupture of the aneurysm, induction of hypotension must be considered carefully. Under these circumstances tamponade and temporary artery clipping led to a better outcome than hypotension ^[21]. Therefore it is now accepted that cerebral perfusion pressure should be maintained at pre-operative levels during cerebral aneurysm surgery ⁽²²⁾. However, if intraoperative rupture occurs and temporary clipping is not feasible transient decreases in mean arterial blood pressure to 50 mmHg or even lower can be indicated to facilitate surgical control ^[23].

Intra-operative attention to blood pressure control must be continued into the post-operative period as post-operative hypertension and tachycardia are present in up to 80% of neurosurgical patients and increase the risk of post-operative intracerebral haemorrhage and myocardial ischaemia^[24].