• Rikard Linner, Valeria Perez-de-Sa, and Doris Cunha-Goncalves.
• Department of Cardiothoracic Anaesthesia and Intensive Care, Skåne University Hospital, Lund University, Lund SE-22185, Sweden. Rikard.Linner@googlemail.com
• Resuscitation. 2012 Oct 1;83(10):1298-303.

Aim Of The StudyTo investigate the effects of early intravenous adrenaline administration on circulatory recovery, cerebral reoxygenation, and plasma catecholamine concentrations, after severe asphyxia-induced bradycardia and hypotension.MethodsOne-day-old piglets were left in apnoea until heart rate and mean arterial pressure were less than 50 min(-1) and 25 mmHg, respectively. They randomly received adrenaline, 10 μgkg(-1) (n=16) or placebo (n=15) and were resuscitated with air ventilation and, when needed, closed-chest cardiac massage (CCCM). Eight not asphyxiated animals served as time controls.ResultsCCCM was required in 13 piglets given adrenaline and in 13 given placebo. Time to return of spontaneous circulation was: 72 (66-85)s vs. 77 (64-178)s [median (quartile range)] (p=0.35). Time until cerebral regional oxygen saturation (CrSO(2)) had increased to 30% was 86 (79-152)s vs. 126 (88-309)s (p=0.30). The two groups did not differ significantly in CrSO(2), heart rate, arterial pressure, right common carotid artery blood flow, or number of survivors: 13 vs. 11 animals. Plasma concentration of adrenaline, 2.5 min after resuming ventilation, was 498 (268-868)nmoll(-1) vs. 114 (80-306)nmoll(-1) (p=0.01). Corresponding noradrenaline concentrations were 1799 (1058-4182)nmoll(-1)vs. 1385 (696-3118)nmoll(-1) (ns). In the time controls, the concentrations were 0.4 (0.2-0.6)nmoll(-1) of adrenaline and 1.8 (1.3-2.4)nmoll(-1) of noradrenaline.ConclusionThe high endogenous catecholamine levels, especially those of noradrenaline, may explain why early administered adrenaline did not significantly improve resuscitation outcome.Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.

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