• Robert L Talbert.
• College of Pharmacy, University of Texas at Austin, Austin, Texas, USA. talbert@uthscsa.edu
• Pharmacotherapy. 2006 Aug 1; 26 (8 Pt 2): 123S-130S.

AbstractHypertensive crises are commonly seen in the emergency department, and acute stroke is often the inciting etiology of a hypertensive crisis. Cerebral autoregulation is disrupted in acute stroke, and efforts to lower blood pressure may reduce cerebral perfusion and worsen outcomes. Although most patients with stroke have elevated blood pressure, evidence from clinical trials to guide therapy are scarce. Current national guidelines recommend lowering blood pressure after stroke only if end-organ damage is present or if systolic/diastolic blood pressures exceed 220/120 or 185/110 mm Hg in patients ineligible and in those eligible to receive thrombolytic drug therapy, respectively. Recommended pharmacologic interventions for elevated blood pressure after acute ischemic stroke include labetalol, nicardipine, or nitroprusside, depending on the severity of the elevation. Similar recommendations have been made for intracerebral hemorrhage. Subarachnoid hemorrhage is managed with nimodipine and other calcium channel blockers to prevent vasospasm and improve clinical outcomes. Data from ongoing clinical trials may improve guidance about the management of elevated blood pressure after acute stroke.

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