Effects of epinephrine on cerebral oxygenation during cardiopulmonary resuscitation: A prospective cohort study.

Abstract

Epinephrine has been presumed to improve cerebral oxygen delivery during cardiopulmonary resuscitation (CPR), but animal and registry studies suggest that epinephrine-induced capillary vasoconstriction may decrease cerebral capillary blood flow and worsen neurological outcome. The effect of epinephrine on cerebral oxygenation (rSO₂) during CPR has not been documented in the clinical setting. rSO₂ was measured continuously using cerebral oximetry in patients with in-hospital cardiac arrest. During CPR, time event markers recorded the administration of 1mg epinephrine. rSO₂ values were analysed for a period beginning 5min before and ending 5min after the first epinephrine administration. A total of 56 epinephrine doses were analysed in 36 patients during CPR. The average rSO₂ value in the 5-min following epinephrine administration was 1.40% higher (95% CI=0.41-2.40%; P=0.0059) than in the 5-min period before epinephrine administration. However, there was no difference in the overall rate of change of rSO₂ when comparing the 5-min period before, with the 5-min period immediately after a single bolus dose of epinephrine (0.88%/min vs 1.07%/min respectively; P=0.583), There was also no difference in the changes in rSO₂ at individual 1, 2, 3, or 4-min time windows before and after a bolus dose of epinephrine (P=0.5827, 0.2371, 0.2082, and 0.6707 respectively). A bolus of 1mg epinephrine IV during CPR produced a small but clinically insignificant increase in rSO₂ in the five minutes after administration. This is the first clinical data to demonstrate the effects of epinephrine on cerebral rSO₂ during CPR.