Effects of prolonged mild hypothermia on cerebral blood flow after cardiac arrest

Abstract

Objective: The aim of the present study was to assess the cerebral blood flow and cerebral oxygen extraction in adult patients after pulseless electrical activity/asystole or resistant ventricular fibrillation who were treated with mild therapeutic hypothermia for 72 hrs.

Design: Observational study.

Setting: Tertiary care university hospital.

Patients: Ten comatose patients with return of spontaneous circulation after pulseless electrical activity/asystole or prolonged ventricular fibrillation.

Intervention: Treatment with mild therapeutic hypothermia for 72 hrs.

Measurements and main results: Mean flow velocity in the middle cerebral artery was measured by transcranial Doppler at 12, 24, 36, 48, 60, 72, 84, 96, and 108 hrs after admission. Jugular bulb oxygenation was measured at the same intervals. Mean flow velocity in the middle cerebral artery was low (26.5 (18.7-48.0) cm/sec) at admission and significantly increased to 63.9 (45.6-65.6) cm/sec at 72 hrs (p=.002). Upon rewarming, the mean flow velocity in the middle cerebral artery remained relatively constant with a mean flow velocity in the middle cerebral artery of 71.5 (56.0-78.5) at 108 hrs (p=.381). Jugular bulb oxygenation at the start of the study was 57.0 (51.0-61.3)% and gradually increased to 81.0 (78.5-88.0)% at 72 hrs (p=.003). Upon rewarming, the jugular bulb oxygenation remained constant with a jugular bulb oxygenation of 84.0 (77.3-86.3)% at 108 hrs (p=.919). There were no differences in mean flow velocity in the middle cerebral artery, pulsatility index, and jugular bulb oxygenation between survivors and nonsurvivors.

Conclusions: Temperature by itself is probably not a major determinant in regulation of cerebral blood flow after cardiac arrest. The relatively low mean flow velocity in the middle cerebral artery in combination with normal jugular bulb oxygenation values suggests a reduction in cerebral metabolic activity that may contribute to the neuroprotective effect of (prolonged) mild therapeutic hypothermia in the delayed hypoperfusion phase.