Cerebral oxygenation during inductionof therapeutic hypothermia after cardiac arrest

Abstract

Introduction Induced mild hypothermia (32 to 34°C) improves survival and neurological outcome after CA. Near-infrared spectroscopy (NIRS) measures cerebral tissue oxygen saturation (SctO2 ). As of today, no data are available on SctO2 monitoring during therapeutic hypothermia (TH). Therefore, SctO2 was measured in this study during the fi rst 36 hours after CA. Methods After IRB approval, data were collected from 23 patients. Cold saline (30 ml/kg) was administered as soon as possible after hospital admission. TH (33°C) was induced by endovascular or surface cooling and maintained for 24 hours. All patients were sedated (propofol/ remifentanil) for the duration of TH. NIRS sensors were bilaterally applied to the frontotemporal area before start of TH. Patients were monitored during induction, maintenance and recovery of TH. Results Of 23 patients, 11 patients did not survive until hospital discharge due to post-ischemic brain damage. Twelve patients survived until hospital discharge, of whom eight without any neurological impairment. Temperature at admission was 34.6°C (±0.5°C). Patients reached the target temperature of 33°C, 4 hours after induction of TH. Two patients died during maintenance of TH due to refractory hemodynamic shock. In all patients, SctO2 values started above 65%. Two and a half hours after induction of TH, SctO2 values decreased with 9% (±3%). The decrease in cerebral oxygenation during induction of TH was not associated with a major change in hemodynamic parameters (MAP before induction of TH: 79 mmHg ± 19; at 33°C: 82 mmHg ± 9), nor with a major change in systemic oxygenation (SpO2 before TH: 99% ± 1; at 33°C: 97% ± 3). In patients who survived until hospital discharge, SctO2 returned to baseline values, 3.5 hours after induction of TH, before the target temperature of 33°C was reached. In patients who did not survive the hospital stay, SctO2 remained lower than baseline values until the target temperature was reached. In these nonsurvivors, SctO2 values did only return to baseline values during maintenance of TH (10 hours after induction of TH). During maintenance of TH and rewarming (0.3°C), no further signifi cant changes in SctO2 values were observed. Conclusion Noninvasive monitoring revealed a decrease in cerebral oxygenation during induction of mild hypothermia in patients after cardiac arrest. We observed a diff erence in oxygenation between hospital survivors and nonsurvivors.