Blood Pressure Variability and Optimal Cerebral Perfusion Pressure—New Therapeutic Targets in Traumatic Brain Injury

BACKGROUND Optimal cerebral perfusion pressure (CPPopt) is an autoregulatory-oriented target in the neurointensive care (NIC) of patients with traumatic brain injury (TBI), and deviation from CPPopt is associated with poor outcome. We recently found that blood pressure variability (BPV) is associated with deviation from CPPopt. OBJECTIVE To evaluate BPV and other variables related to deviation from CPPopt and to evaluate challenges and strategies for autoregulatory-oriented treatment in TBI. METHODS Data including arterial blood pressure and intracranial pressure (ICP) from 362 TBI patients treated at the NIC unit, Uppsala University Hospital, Sweden, between 2008 and 2016, were retrospectively analyzed day 2 to 5. RESULTS Higher BPV was a strong predictor of both CPP deviation below and above CPPopt after multiple regression analyses. There was no other explanatory variable for CPP deviation above CPPopt, whereas also higher ICP and worse autoregulation (higher pressure reactivity index) were associated with CPP deviation below CPPopt. A higher BPV was, in turn, explained by older age, lower ICP, higher mean arterial blood pressure, and higher slow arterial blood pressure amplitude (0.018-0.067 Hz). CONCLUSION BPV was strongly associated with deviation from CPPopt. High age is a risk factor for high BPV and hence CPP insults. Our treatment protocol is focused on avoiding CPP below 60 mm Hg. It is possible that a more restrictive upper level could generate more stable blood pressure and less deviation from CPPopt.

Abstract 274: Identifying the Optimal Cerebral Perfusion Pressure Following Hypoxic-Ischemic Brain Injury

Introduction: The optimal cerebral perfusion pressure (CPP) following hypoxic-ischemic brain injury (HIBI) is currently unknown. We retrospectively analyzed intracranial monitoring data from a cohort of patients with HIBI to identify a threshold level for CPP that optimizes cerebrovascular pressure reactivity (a surrogate for CA) while limiting the risk of intracranial hypertension and brain tissue hypoxia. Hypothesis: We hypothesized that higher CPP values would be associated with improved cerebrovascular pressure reactivity. Methods: ICP, brain tissue oxygen (P bt O 2 ), MAP, and CPP (defined as MAP - ICP) were recorded continuously and time synchronized for all patients using a bedside monitor (CNS Monitor, Moberg Research). Pressure Reactivity Index (PRx) was calculated as the time varying correlation between MAP and ICP over 5 min intervals updated every minute. The degree of CA impairment (defined as % time PRx > 0.2) was plotted against MAP and CPP, respectively. The relationships between ICP and P bt O 2 versus CPP, as well as ICP and P bt O 2 versus % time PRx > 0.2, were similarly calculated. Results: We analyzed 37 patients (33 cardiac arrest, 4 prolonged hypoxia) with HIBI who underwent intracranial neuromonitoring over a 3 year period. Lower CPP values were associated with higher degrees of CA impairment. The cumulative burden of elevated PRx was significantly lower for CPP values above a cutoff of 85 mmHg compared to lower CPP values (p < 0.001, Wilcoxon rank sum test). A similar cutoff for MAP could not be identified, although lower MAP values were also associated with greater CA impairment. Intracranial hypertension (ICP > 20 mmHg) and brain hypoxia (P bt O2 < 20 mmHg) were both associated with CA impairment (p < 0.001 and p < 0.001, respectively, Wilcoxon rank sum test). Conclusions: Higher CPP and MAP values appear to be associated with improved CA after HIBI. Given that CA impairment is associated with both intracranial hypertension and brain hypoxia, our work reaffirms the notion that higher blood pressure targets may improve outcome after HIBI. The identification of a distinct CPP cutoff for CA optimization suggests that targeting CPP instead of MAP may be advantageous, although further work is required to clarify this issue.