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NEWS: Optimizing MAP After Cardiac Arrest Increases Brain Tissue Oxygenation

By Currents Editor posted 09-05-2019 10:15

  
By Sekhon MS, Gooderham P, Menon DK, et al.  The burden of brain hypoxia and optimal mean arterial pressure in patients with hypoxic ischemic brain injury after cardiac arrest.  Crit Care Med 2019; 47(7):960-969.

Reviewed by: Kyle Hobbs, MD 

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Summary

Secondary injury after cardiac arrest is a major determinant of neurologic outcome and is caused, in part, by a prolonged period of hypoperfusion (“no-reflow”) following an initial hyperemia.  Augmentation of blood pressure (MAP) may be beneficial, but optimal MAP targets and their effect on cerebral perfusion pressure (CPP) and brain tissue oxygenation (PbtO2) are unknown. 

This small, prospective interventional study conducted in a quaternary closed ICU used invasive multimodal neuromonitoring to characterize PbtO2 and its relationship to MAP, characterize cerebral autoregulation measured by pressure-reactivity index (PRx), and characterize the upper and lower limits of autoregulation. Optimal MAP was calculated, and the effect of temperature and end-tidal CO2 (EtCO2) on PbtO2 and PRx were investigated in patients with hypoxic-ischemic brain injury after cardiac arrest.  

Patients were included if time to ROSC was >10 minutes with >20 minutes of sustained circulation, post ROSC GCS < 9, and enrollment occurred within 72 hours of arrest.  Patients were excluded if they were coagulopathic, expected to undergo cardiac catheterization or to receive anticoagulant/antiplatelet therapy during the study period, treated with therapeutic hypothermia goal of < 35°C, had history of prior TBI/ICH/stroke, or if withdrawal of life-sustaining treatment was expected. 

ICP and PbtO2 monitors were inserted in the non-dominant frontal lobe through a dual lumen bolt, and jugular venous oximetry bulb catheter was placed; measured parameters included ICP, MAP, PbtO2, regional saturation of oxygen (rSO2), SjvO2, temperature and EtCO2.  Optimum MAP and lower and upper limits of autoregulation (LLA and ULA) were calculated as secondary derivatives by plotting PRx against the MAP range. Brain tissue hypoxia was defined as PbtO2 < 20 mm Hg, and dysfunctional cerebral autoregulation was defined as a PRx > 0.3. All patients underwent targeted temperature management with goal < 36°C.  

Results

Ten patients were enrolled (seven male). Initial rhythm was PEA in 9 and ventricular fibrillation in 1.  Median duration of time from arrest to insertion of neuromonitor was 15 hours; median duration of monitoring was 47 hours. The mean PbtO2 for the cohort was 23 (8) mm Hg. Thirty-eight percent of 10-minute averaged periods of time had a PbtO2 < 20. Individually, the mean percentage of time PbtO2 was < 20 was 38%. Both PbtO2 and MAP increased per hour during the monitoring period. MAP was linearly related to PbtO2 and SjvO2, but not rSO2. Overall mean PRx was 0.23 (0.27), and 48% of 10-minute averaged PRx measurements were > 0.3. Individually, median percentage of time with PRx > 0.3 was 50%. Mean optimum MAP was 89 (11), LLA 82 (8) and ULA 96 (9). Median time in which actual MAP was within 5 mm Hg of optimum MAP was 42% (range 10-78%).  PbtO2 increased as the difference (MAPDIFF) between actual MAP and optimum MAP approached 0, then leveled off as the difference went above 0 (Mean PbtO2 for MAPDIFF < -5 mm Hg was 19 (9) mm Hg; for MAPDIFF -4 to 2mm Hg, PbtO2 was 25 (9); for MAPDIFF 2-9 mm Hg, PbtO2 was 23 (10); for MAPDIFF > 9 mm Hg, PbtO2 was 26 (9)). There was no relationship between either PbtO2 or PRx and temperature or EtCO2.  PRx was 0.31 (0.19) in survivors and decreased by each hour; PRx was 0.16 (0.32) in nonsurvivors and increased each hour. 

Commentary

This study suggests that brain hypoxia post cardiac arrest is common, and augmentation of MAP to an optimum target improves brain tissue oxygenation. The degree of brain hypoxia seen in these post-arrest patients was significant (8/10 had initial PbtO2 of < 20) and responsive to MAP augmentation.  

Interestingly, both the overall calculated optimum MAP of 89 as well as the lower limit of autoregulation (82) were higher than the current post-arrest MAP recommended by current international guidelines.  Targeting individual patient’s optimum MAP (calculated with PRx) may allow for improved brain oxygenation without the complications inherent in overly aggressive blood pressure augmentation.  

The need for individualized MAP targets was seen in the current study, with marked inter-patient variability in the effect of MAP on oxygenation indices. The amount of highly detailed longitudinal data collected was a strength of this study. Limitations of the study are numerous, the most significant of which is the small sample size, limiting the ability to draw firm conclusions from the data. The majority of patients did not have intracranial monitoring placed until ~15 hours post arrest, by which time significant brain tissue hypoxia and secondary injury may have already occurred.  

While efforts were made to strictly control extraneous variables such as PaCO2, TTM and sedation, these may have also influenced cerebral blood flow, limiting the accuracy of PRx measurement. Overall, the implications of targeted MAP to improve brain tissue oxygenation are exciting, and further research is needed.     

Kyle Hobbs, MD

Clinical Neurointensivist

Intermountain Healthcare

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