Nicardipine may give smoother blood pressure control than labetalol135 and sodium nitroprusside,136 although data showing different clinical outcomes are lacking. Although lowering cerebral perfusion pressure may lead to cerebral ischemia, a cohort study of neurologically critically ill patients did not find an association between use of nicardipine and reduced brain oxygen tension.137 Clevidipine, a very short-acting calcium channel blocker, is another option for acute control of hypertension, but data for aSAH are lacking at this time. Antifibrinolytic therapy has been shown to reduce the incidence of aneurysm rebleeding when there is a delay in aneurysm obliteration. One referral center instituted a policy of short-term use of aminocaproic acid to prevent rebleeding during patient transfer. Such use led to a decreased incidence in rebleeding without increasing the risk of DCI, but 3-month clinical outcomes were not affected.138 There was an in- creased risk of deep venous thrombosis but not pulmonary embolism. Neither aminocaproic acid nor tranexamic acid is approved by the US Food and Drug Administration for prevention of aneurysm rebleeding. Medical Measures to Prevent Rebleeding After aSAH: Recommendations 1. Between the time of aSAH symptom onset and aneurysm obliteration, blood pressure should be controlled with a titratable agent to balance the risk of stroke, hypertension-related rebleeding, and maintenance of cerebral perfusion pressure (Class I; Level of Evidence B). (New recommendation) 2. The magnitude of blood pressure control to reduce the risk of rebleeding has not been established, but a decrease in systolic blood pressure to <160 mm Hg is reasonable (Class IIa; Level of Evidence C). (New recommendation) 3. 