Elevated blood pressure is commonly associated with stroke syndromes and is often the result of a physiologic response to the stroke itself (to maintain adequate cerebral perfusion to the viable but edematous tissue surrounding the ischemic area) and not its immediate cause. In the area of the stroke, cerebral autoregulation is lost, causing tissue blood flow to become directly pressure dependent. Most patients suffering from embolic or thrombotic strokes without associated hemorrhage do not have substantial elevations in blood pressure and do not need aggressive antihypertensive treatment. Furthermore, if the patient has a long-standing history of hypertension, any rapid reduction in blood pressure may further reduce cerebral blood flow to watershed areas and cause increased ischemia. —I2. In the rare case of a stroke patient with extreme blood pressure elevation or sustained diastolic pressure greater than 140 mmHg, the blood pressure may be reduced in a controlled manner by no more than 20 percent with intravenous labetalol in small doses beginning with 5-mg increments.
In contrast to the relatively minor blood pressure elevations with most strokes, intracranial hemorrhage commonly results in profound reactive rise in blood pressure. Causes of intracranial hemorrhage include hypertensive vascular disease, arteriovenous anomalies, arterial aneurysms, bleeding associated with tumors, and trauma. Hypertension associated with hemorrhagic stroke is usually transitory and the result of increased intracranial pressure and irritation of the autonomic nervous system. The acute management of blood pressure associated with intracranial hemorrhage is controversial. In the case of subarachnoid hemorrhage, oral nimodipine (60 mg every 4 h) has been used to reverse the vasospasm associated with subarachnoid blood. Intravenous nicardipine (2-mg boluses followed by a 4- to 15-mg/h infusion) is also beginning to have a role in the management of hypertension during this type of hemorrhage.
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