Abstract
Introduction: Epinephrine has been presumed to improve cerebral oxygen delivery during CPR. Animal studies however have demonstrated that epinephrine-induced capillary vasoconstriction may actually decrease cerebral capillary blood flow and registry studies have suggested that adrenaline may actually worsen neurological outcome, The effects of epinephrine on cerebral oxygenation (rSO2) during CPR has not been documented in the clinical setting. Methods: Following ethics approval, rSO2 was measured continuously using cerebral oximetry in patients undergoing in-hospital cardiac arrest. During CPR, time event markers recorded the administration of 1mg epinephrine. rSO2% values were analysed for a 5 min window prior to and then 5 mins after the first epinephrine administration. Results: A total of 56 epinephrine doses were analyzed in 36 patients during CPR. Results are shown below. The average rSO2% in the 5 mins following epinephrine administration was 1.40% higher (95% CI=0.41-2.40%, P=0.0059) than in the 5 min period prior to epinephrine administration. After adjusting, for patients’ ROSC status, initial rhythm, hemoglobin and Charlson comorbidity index, this difference remained statistically significant (1.42% with 95% CI: 0.35-2.49%, P=0.009). There was no statistically significant difference in the gradient of rSO2% during the 5 min period immediately before (0.88) compared with immediately after (1.09) epinephrine administration. Conclusion: IV administration of 1mg epinephrine during CPR results in minimal changes to rSO2%. This is the first clinical data to demonstrate the effects of epinephrine on rSO2 and is consistent with animal studies. These results may go some way to explaining the limited effect of epinephrine on improving neurological recovery from cardiac arrest.
Published Version
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