W Denney Zimmerman1, Wan-Tsu W Chang2. 1. Department of Neurology, University of Maryland Medical Center, Baltimore, MD, 21201, USA. 2. Departments of Emergency Medicine and Neurology, Program in Trauma, University of Maryland School of Medicine, 22 S. Greene St, Baltimore, MD, 21201, USA. wchang1@som.umaryland.edu.
Abstract
PURPOSE OF REVIEW: To review most recent literature on management of blood pressure in acute aneurysmal subarachnoid hemorrhage (SAH) and provide practice recommendations for the emergency clinician. RECENT FINDINGS: There is increased risk of aneurysmal rebleeding with systolic blood pressure (SBP) greater than 160 mmHg in the acute setting. Avoiding large degrees of blood pressure variability improves clinical outcomes in aneurysmal SAH. Acute lowering of SBP to a range of 140-160 mmHg decreases risk of rebleeding while also maintaining cerebral perfusion pressure (CPP) after aneurysmal rupture. Treatment with a short acting antihypertensive agent allows for rapid titration of blood pressure (BP) and reduces BP variability. Elevations in intracranial pressure occur commonly after SAH due to increased intracranial blood volume, cerebral edema, or development of hydrocephalus. Clinicians should be familiar with changes in cerebral autoregulation and effects on CPP when treating elevated BP, in order to mitigate the risk of secondary neurological injury.
PURPOSE OF REVIEW: To review most recent literature on management of blood pressure in acute aneurysmal subarachnoid hemorrhage (SAH) and provide practice recommendations for the emergency clinician. RECENT FINDINGS: There is increased risk of aneurysmal rebleeding with systolic blood pressure (SBP) greater than 160 mmHg in the acute setting. Avoiding large degrees of blood pressure variability improves clinical outcomes in aneurysmal SAH. Acute lowering of SBP to a range of 140-160 mmHg decreases risk of rebleeding while also maintaining cerebral perfusion pressure (CPP) after aneurysmal rupture. Treatment with a short acting antihypertensive agent allows for rapid titration of blood pressure (BP) and reduces BP variability. Elevations in intracranial pressure occur commonly after SAH due to increased intracranial blood volume, cerebral edema, or development of hydrocephalus. Clinicians should be familiar with changes in cerebral autoregulation and effects on CPP when treating elevated BP, in order to mitigate the risk of secondary neurological injury.
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