Effect of Increasing Blood Pressure on Brain Tissue Oxygenation in Adults After Severe Traumatic Brain Injury.

OBJECTIVES: To examine if increasing blood pressure improves brain tissue oxygenation (PbtO2) in adults with severe traumatic brain injury (TBI).

DESIGN: Retrospective review of prospectively collected data.

SETTING: Level-I trauma center teaching hospital.

PATIENTS: Included patients greater than or equal to 18 years of age and with severe (admission Glasgow Coma Scale [GCS] score < 9) TBI who had advanced neuromonitoring (intracranial blood pressure [ICP], PbtO2, and cerebral autoregulation testing).

INTERVENTIONS: The exposure was mean arterial pressure (MAP) augmentation with a vasopressor, and the primary outcome was a PbtO2 response. Cerebral hypoxia was defined as PbtO2 less than 20 mm Hg (low).

MAIN RESULTS: MAP challenge test results conducted between ICU admission days 1-3 from 93 patients (median age 31; interquartile range [IQR], 24-44 yr), 69.9% male, White (n = 69, 74.2%), median head abbreviated injury score 5 (IQR 4-5), and median admission GCS 3 (IQR 3-5) were examined. Across all 93 tests, a MAP increase of 25.7% resulted in a 34.2% cerebral perfusion pressure (CPP) increase and 16.3% PbtO2 increase (no MAP or CPP correlation with PbtO2 [both R2 = 0.00]). MAP augmentation increased ICP when cerebral autoregulation was impaired (8.9% vs. 3.8%, p = 0.06). MAP augmentation resulted in four PbtO2 responses (normal and maintained [group 1: 58.5%], normal and deteriorated [group 2: 2.2%; average 45.2% PbtO2 decrease], low and improved [group 3: 12.8%; average 44% PbtO2 increase], and low and not improved [group 4: 25.8%]). The average end-tidal carbon dioxide (ETCO2) increase of 5.9% was associated with group 2 when cerebral autoregulation was impaired (p = 0.02).

CONCLUSIONS: MAP augmentation after severe TBI resulted in four distinct PbtO2 response patterns, including PbtO2 improvement and cerebral hypoxia. Traditionally considered clinical factors were not significant, but cerebral autoregulation status and ICP responses may have moderated MAP and ETCO2 effects on PbtO2 response. Further study is needed to examine the role of MAP augmentation as a strategy to improve PbtO2 in some patients.