Deviations from PRx-derived optimal blood pressure are associated with mortality after cardiac arrest

Aim Pressure reactivity index (PRx) provides a surrogate measurement of cerebrovascular autoregulation (CAR). We determined whether deviations from PRx-derived optimal mean arterial pressure (MAPopt) were associated with in-hospital mortality after adult cardiac arrest. Methods Retrospective analysis of post-cardiac arrest patients who had continuously recorded intracranial pressure (ICP) and MAP. PRx was calculated as a moving, linear correlation between ICP and MAP. Impaired CAR was defined as PRx ≥ 0.3. MAPopt was calculated using a multi-window weighted algorithm. The burdens of MAP < 5 mmHg below MAPopt (MAPopt-5) and > 5 mmHg above MAPopt (MAPopt + 5) were calculated by integrating the area between MAP and MAPopt-5 or MAPopt + 5 curves, respectively. Univariate logistic regression tested the association between burden of MAP < MAPopt-5 and outcome. Results Twenty-two patients were analyzed. Thirteen (59%) patients died before hospital discharge. Time (median [IQR]) between ROSC and monitoring initiation was 16 [14, 21] hours and duration of monitoring was 35 [22, 48] hours; neither differed between survivors and non-survivors. Median MAPopt was 89 [85, 97] mmHg and did not differ between survivors and non-survivors (89 [83, 94] vs. 91 [85, 105] mmHg, p = 0.64). Burden of MAP < MAPopt–5 was greater for non-survivors compared to survivors (OR 3.6 [95% CI 1.2–15.6]). Range of intact CAR (upper-lower limit) was narrower for non-survivors when compared to survivors (5 [0, 22] vs. 24 [7, 36] mmHg, p = 0.03). Conclusion A greater burden of MAP below PRx-derived MAPopt-5 was associated with mortality after cardiac arrest. Non-survivors had a narrower range of intact CAR than survivors.