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A Murine Model of Subarachnoid Hemorrhage
Published on: November 21, 2013
Vasopressor Infusion After Subarachnoid Hemorrhage Does Not Increase Regional Cerebral Tissue Oxygenation
Khalil M Yousef1, Elizabeth Crago, Yuefang Chang
1Elizabeth Crago, PhD RN, School of Nursing, University of Pittsburgh, Pittsburgh, PA. Yuefang Chang, PhD, Department of Neurological Surgery, University of Pittsburgh Medical Center, Pittsburgh, PA. Theodore F. Lagattuta, RN, School of Nursing, University of Pittsburgh, Pittsburgh, PA. Khadejah Mahmoud, BSN RN, School of Nursing, University of Pittsburgh, Pittsburgh, PA. Lori Shutter, MD, University of Pittsburgh School of Medicine, and Department of Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA. Jeffrey R. Balzer, PhD, School of Nursing, University of Pittsburgh, and Department of Neurological Surgery, University of Pittsburgh Medical Center, Pittsburgh, PA. Michael R. Pinsky, MD CM DrHC, University of Pittsburgh School of Medicine, and Department of Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA. Robert M. Friedlander, MD, Department of Neurological Surgery, University of Pittsburgh Medical Center, Pittsburgh, PA. Marilyn Hravnak, PhD RN ACNP-BC FCCM FAAN, School of Nursing, University of Pittsburgh, Pittsburgh, PA.
Introduction:
Vasopressors are commonly used after aneurysmal subarachnoid hemorrhage (aSAH) to sustain cerebral pressure gradients. Yet, the relationship between vasopressors and the degree of cerebral microcirculatory support achieved remains unclear. This study aimed to explore the changes in cerebral and peripheral regional tissue oxygen saturation (rSO2) as well as blood pressure (BP) before and after vasopressor infusion in patients with aSAH.
Methods:
Continuous noninvasive cerebral and peripheral rSO2 was obtained using near-infrared spectroscopy for up to 14 days after aSAH. Within-subject differences in rSO2 before and after the commencement of vasopressor infusion were analyzed controlling for Hunt and Hess grade and vasospasm.
Results:
Of 45 patients with continuous rSO2 monitoring, 19 (42%) received vasopressor infusion (all 19 on norepinephrine, plus epinephrine in 2 patients, phenylephrine in 4 patients, and vasopressin in 2 patients). In these 19 patients, their vasopressor infusion times were associated with higher BP (systolic [b = 15.1], diastolic [b = 7.3], and mean [b = 10.1]; P = .001) but lower cerebral rSO2 (left cerebral rSO2 decreased by 4.4% [b = -4.4, P < .0001]; right cerebral rSO2 decreased by 5.5% [b = -5.5, P = .0002]).
Conclusions:
Despite elevation in systemic BP during vasopressor infusion times, cerebral rSO2 was concurrently diminished. These findings warrant further investigation for the effect of induced hypertension on cerebral microcirculation.
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