Optimizing blood pressure in neurological emergencies

Abstract

Excessive hypertension can challenge the brain's capacity to autoregulate cerebral blood flow, and can aggravate increased intracranial pressure (ICP) and cerebral edema. Hypotension may worsen ischemic damage in marginally perfused tissue, and in some cases can trigger cerebral vasodilation and ICP plateau waves. There is a lack of high-quality data regarding optimal BP management in these conditions. Existing guidelines for target BP levels are based largely on class III evidence. Class I data only exist for enteral candesartan and nimodipine use in acute ischemic stroke and aneurismal subarachnoid hemorrhage (SAH), respectively, and for parenteral magnesium use in eclampsia. Class II data exist for reducing BP to <180/105 mmHg in patients with ischemic stroke who are treated with intravenous tissue plasminogen activator, for elevating systolic BP to 180-220 mmHg in SAH patients with symptomatic vasospasm, and for maintaining cerebral perfusion pressure (CPP)>60 mmHg in traumatic brain injury. Short-acting continuous-infusion agents with a reliable dose-response relationship and favorable safety profile are desirable. To reduce BP, labetalol, esmolol, and nicardipine best meet these criteria. Sodium nitroprusside should be avoided in most neurological emergencies because of its tendency to raise ICP and cause toxicity with prolonged infusion. To elevate BP, the preferred agents are phenylephrine, dopamine, and norepinephrine.