Are optimal cerebral perfusion pressure and cerebrovascular autoregulation related to long-term outcome in patients with aneurysmal subarachnoid hemorrhage?

BACKGROUND AND OBJECTIVES: Continuous assessment of the cerebrovascular autoregulation (CVA) through use of the pressure reactivity index (PRx), a moving linear correlation coefficient between mean arterial blood pressure and intracranial pressure, has been effective in optimizing cerebral perfusion pressure (CPPopt) in traumatic brain injured (TBI) patients. This study investigates the feasibility of measuring CPPopt in patients with aneurysmal subarachnoid hemorrhage (aSAH) by continuously assessing the CVA. METHODS: Twenty-nine aSAH patients were enrolled, and data from CVA status, CPPopt, and periods when CPP was below, within, or above CPPopt were computed daily. Outcome was assessed at 6 months with the Glasgow Outcome Scale. Mann-Whitney U test was used to analyze differences in the duration of impaired CVA and duration of CPP below CPPopt in patients with good and poor outcomes. Multivariable logistic regression analysis was used to identify independent predictors of outcome. RESULTS: CVA monitoring data were available for all 29 patients with a total monitoring time of 2757 h. The duration of impaired CVA was 36.5% (interquartile range: 24.6 to 49.8) of the total monitoring time in 15 patients with good outcome and 71.6% of the total monitoring time (51.2 to 80.0) in 14 patients with poor outcome (Mann-Whitney U test 3.295, P=0.0010). PRx-based CPPopt could be identified in 26 patients (89.6%) with a total monitoring time of 2691 h. The duration of CPP below the CPPopt range was 28.0% (interquartile range: 18.0 to 47.0) of the total monitoring time in patients with good outcome and 76.0% (48.5 to 82.5) in patients with poor outcome (Mann-Whitney U test 2.779, P=0.0054). Glasgow Coma Scale score and duration of impaired CVA were independently associated with 6-month outcome (Glasgow Coma Scale score odds ratio: 1.95, 95% confidence interval: 1.01-3.75; duration of impaired CVA odds ratio: 0.88, 95% confidence interval: 0.78-0.99). CONCLUSIONS: The assessment of CVA and CPPopt is feasible in aSAH patients and may provide important information regarding long-term outcome. A PRx above the 0.2 threshold and a CPP below the CPPopt range are associated with worse outcome.

Cerebrovascular reactivity and autonomic drive following traumatic brain injury.

INTRODUCTION: The autonomic nervous system exerts tonic control on cerebral vessels, which in turn determine the autoregulation of cerebral blood flow. We hypothesize that the impairment of cerebral autoregulation following traumatic brain injury might be related to the acute failure of the autonomic system. METHODS: This prospective, observational study included patients with severe traumatic brain injury requiring mechanical ventilation and invasive monitoring of intracranial pressure (ICP) and arterial blood pressure (ABP). Pressure reactivity index (PRx), a validated index of cerebrovascular reactivity, was continuously monitored using bedside computers. Autonomic drive was assessed by means of heart rate variability (HRV) using frequency domain analysis. FINDINGS: Eighteen TBI patients were included in the study. Cerebrovascular reactivity impairment (PRx above 0.2) and autonomic failure (low spectral power of HRV) are significantly and independently associated with fatal outcome (P = 0.032 and P < 0.001, respectively). We observed a significant correlation between PRx and HRV spectral power (P < 0.001). The high frequency component of HRV (HF, 0.15-0.4Hz) can be used to predict impaired autoregulation (PRx > 0.2), although sensitivity and specificity are low (ROC AUC = 0.67; P = 0.001). CONCLUSION: Following traumatic brain injury, autonomic failure and cerebrovascular autoregulation impairment are both associated with fatal outcome. Impairment of cerebrovascular autoregulation and autonomic drive are interdependent phenomena. With some refinements, HRV might become a tool for screening patients at risk for cerebral autoregulation derangement following TBI.