The spontaneous arterial blood pressure rise after aneurysmal subarachnoid hemorrhage

• Verfasst von: Fontana, Johann [VerfasserIn]
• Verfasst von: Scharf, Johann [VerfasserIn]
• Verfasst von: Weiß, Christel [VerfasserIn]
• Verfasst von: Schmieder, Kirsten [VerfasserIn]
• Verfasst von: Barth, Martin [VerfasserIn]
• Titel: The spontaneous arterial blood pressure rise after aneurysmal subarachnoid hemorrhage
• Titelzusatz: a biphasic phenomenon
• Verf.angabe: Johann Fontana, Johann Scharf, Christel Weiß, Kirsten Schmieder, Martin Barth
• E-Jahr: 2015
• Jahr: October 2015
• Umfang: 6 S.
• Fussnoten: Available online 19 June 2015 ; Gesehen am 20.12.2018
• Titel Quelle: Enthalten in: Clinical neurology and neurosurgery
• Ort Quelle: Amsterdam [u.a.] : Elsevier Science, 1974
• Jahr Quelle: 2015
• Band/Heft Quelle: 137(2015), Seite 22-27
• ISSN Quelle: 1872-6968
• DOI: doi:10.1016/j.clineuro.2015.06.014
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: Arterial blood pressure
• Sach-SW: Cerebral vasospasm
• Sach-SW: Subarachnoid hemorrhage
• K10plus-PPN: 1585784907

Abstract

Objectives: A spontaneous blood pressure (BP) rise is frequently observed after aneurysmal subarachnoid hemorrhage (aSAH). The current study was designed to characterize the time course of this BP rise and its relation to clinical and radiological parameters.Methods: The diastolic (DBP), mean (MAP), and systolic (SBP) BP values were determined in 61 aSAH patients from day 0 to 9. The patient's initial status was evaluated by the world federation of neurological surgeons scale and the Hijdra scale. The clinical outcome was quantified by the modified Rankin Scale, the Glasgow Outcome Scale Extended, and the National Institute of Health Stroke Scale. The degree of proximal and global vasospasm was calculated by comparison of the baseline angiography on day 0 and the control angiography on day 8. Furthermore, the influence of propofol and norepinephrine application was analyzed. Results: DBP, MAP, and SBP demonstrated an early rise in all patients from day 2 till 5 (p<0.001) and remained hypertensive until day 9. No significant correlation could be detected between this early BP rise and most clinical and radiological variables. From day 8 onwards, a divergence of the SBP courses was detected between patients with severe vs. non-severe global vasospasm. There was a secondary, norepinephrine independent SBP rise in patients with severe global vasospasm that significantly correlated with the initial Hijdra-scale and an unfavorable clinical outcome. Conclusions: The results demonstrate a biphasic BP course with a uniform early BP rise in all patients and an additional delayed SBP rise in patients with severe global vasospasm.