Objective:
The primary aim of this study was to test the feasibility of non-invasive cerebral perfusion monitoring post-arrest. We secondarily tested the association between measured autoregulation, the presence of cerebral edema, and neurological recovery.
Methods:
This was a prospective, pilot study inclusive of patients successfully resuscitated from cardiac arrest in the Emergency Department (ED). After return of spontaneous circulation, an investigator placed non-invasive, bifrontal monitoring to measure cerebral perfusion. The device uses an acousto-optic sensor to measure continuous cerebral perfusion and measurements are arbitrary units between 0-100, where 0 represents no flow (Ornim, Tel Aviv). Subjects had invasive, continuous arterial monitoring to assess mean arterial pressure (MAP). Multimodal measurements continued for 60 minutes. We calculated a Pearson coefficient between the perfusion measurements and MAP as an assessment of cerebral autoregulation, where a correlation coefficient > 0.3 indicates poor autoregulation, and a coefficient of 1 indicates completely passive cerebral perfusion to changes in MAP. Head computed tomography defined the presence of cerebral edema in the ED.
Results:
We enrolled 14 patients post-arrest with sustained return of circulation. The mean age was 55 ± 14 years, 7 were female, and 10 were African American. Six patients had pulseless electrical activity, 5 asystole, and 2 ventricular fibrillation. Bystander CPR rates were low (4 of 14, 31%). Two patients (14%) survived to hospital discharge. Cerebral perfusion was comparable between patients that survived and those that died (difference 3.1, 95% CI -14 to 8). Cerebral perfusion measurement was higher in patients with cerebral edema (difference 6.1, 95% CI 0.2 - 11.9). Autoregulation was worse in the presence of edema (0.30) compared to no edema (0.14), though this difference did not reach statistical significance (95% CI -0.7 to 0.4).
Conclusions:
In a pilot study, non-invasive post-arrest perfusion measurements plus coupling with MAP for autoregulation was feasible. Perfusion measurements were increased in the presence of cerebral edema but whether such measurements have prognostic value requires further study.
Effect of the KCa3.1 blocker, senicapoc, on cerebral edema and cardiovascular function after cardiac arrest — A randomized experimental rat study
