Early adrenaline administration does not improve circulatory recovery during resuscitation from severe asphyxia in newborn piglets

Aim of the study

To investigate the effects of early intravenous adrenaline administration on circulatory recovery, cerebral reoxygenation, and plasma catecholamine concentrations, after severe asphyxia-induced bradycardia and hypotension.

Methods

One-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 μg kg⁻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.

Results

CCCM 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 (CrSO₂) 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 CrSO₂, 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) nmol l⁻¹vs. 114 (80–306) nmol l⁻¹ (p = 0.01). Corresponding noradrenaline concentrations were 1799 (1058–4182) nmol l⁻¹vs. 1385 (696–3118) nmol l⁻¹ (ns). In the time controls, the concentrations were 0.4 (0.2–0.6) nmol l⁻¹ of adrenaline and 1.8 (1.3–2.4) nmol l⁻¹ of noradrenaline.

Conclusion

The high endogenous catecholamine levels, especially those of noradrenaline, may explain why early administered adrenaline did not significantly improve resuscitation outcome.