• Can J Anaesth · Aug 1993

    Review

    Vasodilators during cerebral aneurysm surgery.

    • K Abe.
    • Department of Anaesthesia, Osaka Police Hospital, Japan.
    • Can J Anaesth. 1993 Aug 1; 40 (8): 775-90.

    AbstractThe objective of this review is to review the anaesthetic implications of vasoactive compounds particularly with regard to the cerebral circulation and their clinical importance for the practicing anaesthetist. Material was selected on the basis of validity and application to clinical practice and animal studies were selected only if human studies were lacking. Hypotensive drugs have been used to induce hypotension and in the treatment of intraoperative hypertension during cerebral aneurysm surgery. After subarachnoid haemorrhage, cerebral blood flow is reduced and cerebral vasoreactivity is disturbed which may lead to brain ischaemia. Also, cerebral arterial vasospasm decreases cerebral blood flow, and may lead to delayed ischaemic brain damage which is a major problem after subarachnoid haemorrhage. Recently, the use of induced hypotension has decreased although it is still useful in patients with intraoperative aneurysm rupture, giant cerebral aneurysm, fragile aneurysms and multiple cerebral aneurysms. In this review, a variety of vasodilating agents, prostaglandin E1, sodium nitroprusside, nitroglycerin, trimetaphan, adenosine, calcium antagonists, and inhalational anaesthetics, are discussed for their clinical usefulness. Sodium nitroprusside, nitroglycerin and isoflurane are the drugs of choice for induced hypotension. Prostaglandin E1, nicardipine and nitroglycerin have the advantage that they do not alter carbon dioxide reactivity. Local cerebral blood flow is increased with nitroglycerin, decreased with trimetaphan and unchanged with prostaglandin E1. Intraoperative hypertension is a dangerous complication occurring during cerebral aneurysm surgery, but its treatment in association with subarachnoid haemorrhage is complicated in cases of cerebral arterial vasospasm because fluctuations in cerebral blood flow may be exacerbated. Hypertension should be treated immediately to reduce the risk of rebleeding and intraoperative aneurysmal rupture and the choice of drugs is discussed. Although the use of induced hypotension has declined, the control of arterial blood pressure with vasoactive drugs to reduce the risk of intraoperative cerebral aneurysm rupture is a useful technique. Intraoperative hypertension should be treated immediately but the cerebral vascular effects of each vasodilator should be understood before their use as hypotensive agents.

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