In this issue of Journal of Neuroscience Nursing, Yousef and colleagues1 report the findings of an intervention study conducted to assess the changes in cerebral and peripheral tissue oxygenation saturation among people with aneurysmal subarachnoid hemorrhage (aSAH) who received vasopressor infusion. This is an excellent example of an intervention study that demonstrates the effect of vasopressors in cerebral microcirculation.
Study Purpose
The purpose of this study was to explore the changes in regional cerebral and peripheral tissue oxygen saturation (rSO2) and blood pressure (BP) before and after the vasopressor infusion in patients with aSAH.
Significance
After aSAH, complications can lead to secondary insults by lowering levels of cerebral blood flow and oxygenation, which can cause poor functional and cognitive outcomes. It is known that vasopressors are used to improve mean arterial pressure and thereby the cerebral macrovascular perfusion pressure. However, the effectiveness of vasopressor infusion in improving cerebral microcirculation, as assessed by cerebral tissue oxygenation, is not known.
Methods
The study was conducted at a comprehensive stroke and level I regional resource trauma center in Western Pennsylvania. Participants were adults who had sustained aSAH within 5 days before admission and had a Fisher grade of greater than 1. They were monitored in the neurovascular intensive care unit for up to 14 days per institutional aSAH protocol. Patients with Hunt and Hess grades 3 to 5 and/or with hydrocephalus had external ventricular drain for cerebral fluid diversion and had to intermittently monitor intracranial pressure.
During the acute phase and vasopressor infusion, BP was continuously monitored primarily via arterial catheter and, later when the patient was stabilized, using a noninvasive BP cuff. To achieve the institutional aSAH care protocol goals, BP was first treated with fluid optimization and then supported with vasopressor infusion. The vasopressor of choice was norepinephrine, with the addition of epinephrine, phenylephrine, or vasopressin. Blood pressure monitoring started upon admission to the neurovascular intensive care unit; and rSO2 monitoring, after aneurysm securement.
Continuous cerebral and peripheral rSO2 was monitored using near-infrared spectroscopy, a noninvasive spectroscopy used to assess the concentration differences between oxygenated and deoxygenated hemoglobin. A decrease in near-infrared spectroscopy value indicated an increase in oxygen extraction or insufficient delivery, leading to cerebral ischemia. Continuous cerebral and peripheral rSO2 values were recorded every 5 milliseconds and then averaged on 5-minute intervals for statistical analyses.
Data Analyses
Only patients who received vasopressors were included in the sample, to serve as their own control (data during times vasopressor was not infusing) and cases (data during times when vasopressor was infusing). Mixed model linear regression was used to test whether cerebral rSO2, peripheral rSO2, and BP were statistically different between vasopressor infusion time and times off pressor. Multivariate analyses were conducted while controlling for Hunt and Hess grade and severe angiographic vasospasm.
Results
Nineteen of 45 patients (42%) with continuous rSO2 data received vasopressors. Their mean age was 56.7 +/- 10.5 years, 84% were female, and 79% were white. The mean time from injury to monitoring initiation was 10.2 +/- 11.6 hours for BP and 64.7 +/- 33.1 hours for continuous rSO2 monitoring. The mean monitoring duration was 322.6 +/- 30.5 hours (13.4 +/- 1.3 days) for BP and 242.8 +/- 68.4 hours (10.1 +/- 2.8 days) for rSO2. All 19 patients (100%) received norepinephrine infusion, of which 2 patients (11%) also received epinephrine, 4 (21%) received phenylephrine, and 6 (32%) received vasopressin. Six patients (32%) had severe angiographic vasospasm, and 5 (29%) had moderate vasospasm.
After controlling for Hunt and Hess grade and severe angiographic vasospasm, during vasopressor infusion times, the left cerebral rSO2 significantly decreased by 4.4% (P < .0001) and the right cerebral rSO2 significantly decreased by 5.5% (P = .0002), with a nonsignificant increase in peripheral rSO2 by 1.5% (P = .457), suggesting that the depression in cerebral rSO2 is not exclusively due to vasospasm but perhaps due to global microcirculatory vasoconstriction induced by vasopressors.
Implications
Nurses are responsible for hemodynamic and neurologic monitoring of patients with aSAH. This study demonstrates how targeted vasopressor infusion therapy at the bedside has the potential to improve outcomes and reduce aSAH burden on patients.
Reference