Abstract
Acute hypertensive response is the elevation of blood pressure (BP) above normal and premorbid values that initially occurs within the first 24 hours of symptom onset in patients with intracerebral hemorrhage (ICH).1 The acute hypertensive response is characterized by its high prevalence, self-limiting nature, and prognostic significance. To remain consistent with the 2003 World Health Organization/International Society of Hypertension statement,2 acute hypertensive response is defined as systolic BP (SBP)≥140 mm Hg demonstrated on 2 recordings taken 5 minutes apart within 24 hours of symptom onset. A total of 33 992 patients (75.0%) had an initial SBP≥140 mm Hg among 45 330 patients presenting with an ICH analyzed in the National Hospital Ambulatory Medical Care Survey.3 Acute hypertensive response is usually set on the platform of inadequately treated or undetected chronic hypertension. However, elevation and spontaneous reduction in the initial BP during the next few days support the role of other transient and stroke-specific mechanisms. Presumably, the primary cause of the acute hypertensive response is damage or compression of specific regions in the brain that mediate autonomic control with functional adaptation during the next few days.4,5 Hypertensive responses to other factors are exaggerated and additive because of impaired parasympathetic activity and baroreceptor sensitivity.6 This article addresses the state of knowledge about acute therapy for hypertensive response with ICH. The treatment of acute hypertensive response in ICH has been controversial for the past 3 decades. The Figure demonstrates the 4 periods of evolution in our understanding of pathophysiology and treatment. The current notion of treatment is based on the observation that one third of the subjects presenting with ICH demonstrate hematoma expansion (with subsequent deterioration and death) in the first few hours after onset.7 An initial SBP of ≥200 mm Hg is associated with …
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