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Updated: Jun 13, 2026
In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
Published on: October 27, 2020
Preserved metabolic coupling and cerebrovascular reactivity during mild hypothermia after cardiac arrest
Laurens L A Bisschops1, Cornelia W E Hoedemaekers, Koen S Simons
1Department of Intensive Care, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands. L.Bisschops@ic.umcn.nl
Objective:
Although mild hypothermia improves outcome in patients after out-of-hospital cardiac arrest, the cardiodepressive effects of hypothermia may lead to secondary brain damage. This study was performed to assess the cerebral blood flow, cerebral oxygen extraction, and cerebrovascular reactivity to changes in partial pressure of carbon dioxide in the arterial blood in comatose patients after out-of-hospital cardiac arrest treated with mild hypothermia.
Design:
Observational study.
Setting:
Tertiary care university hospital.
Patients:
Ten comatose patients after out-of-hospital cardiac arrest.
Interventions:
All patients were cooled to 32-34 degrees C for 24 hrs. Cerebrovascular reactivity to changes in carbon dioxide in the arterial blood was measured after increasing or decreasing the minute ventilation by 20%.
Measurements And Main Results:
Mean flow velocity in the middle cerebral artery and pulsatility index were measured by transcranial Doppler at 0, 3, 6, 9, 12, 18, 24, and 48 hrs after admission. Jugular bulb oxygenation was measured at the same intervals. Cerebrovascular reactivity to changes in carbon dioxide in the arterial blood was studied on admission to the intensive care unit and at 6, 12, 18, and 24 hrs by measurement of mean flow velocity in the middle cerebral artery and jugular bulb oxygenation. Mean flow velocity in the middle cerebral artery was low (30.3+/-9.5 cm/sec) on admission and remained relatively stable for the first 24 hrs. After rewarming, it increased to 67.5+/-33.0 cm/sec at 48 hrs after admission from 30.3+/-9.5 at admission (p=.009). Jugular bulb oxygenation at the start of the study was 66.2+/-8.5% and gradually increased to 82.9+/-4.9% at 48 hrs (p<.001). Regression analysis showed a significant correlation between changes in carbon dioxide in the arterial blood, mean flow velocity in the middle cerebral artery (p<.001) and jugular bulb oxygenation (p<.001). The mean percentage change in mean flow velocity in the middle cerebral artery was 3.6+/-2.9% per 1-mm Hg change of carbon dioxide in the arterial blood.
Conclusions:
The mean flow velocity in the middle cerebral artery, as a parameter of cerebral blood flow, was low during mild hypothermia, whereas cerebral oxygen extraction remained normal, suggesting decreased cerebral metabolic activity. We demonstrated that CO2 reactivity is preserved during hypothermia in these patients.
