Abstract
(1) Background: Optimal initial oxygen (O2) concentration in preterm neonates is controversial. Our objectives were to compare the effect of delayed cord clamping with ventilation (DCCV) to early cord clamping followed by ventilation (ECCV) on O2 exposure, gas exchange, and hemodynamics in an asphyxiated preterm ovine model. (2) Methods: Asphyxiated preterm lambs (127–128 d) with heart rate <90 bpm were randomly assigned to DCCV or ECCV. In DCCV, positive pressure ventilation (PPV) was initiated with 30–60% O2 and titrated based on preductal saturations (SpO2) with an intact cord for 5 min, followed by clamping. In ECCV, the cord was clamped, and PPV was initiated. (3) Results: Fifteen asphyxiated preterm lambs were randomized to DCCV (N = 7) or ECCV (N = 8). The inspired O2 (40 ± 20% vs. 60 ± 20%, p < 0.05) and oxygen load (520 (IQR 414–530) vs. 775 (IQR 623–868), p-0.03) in the DCCV group were significantly lower than ECCV. Arterial oxygenation and carbon dioxide (PaCO2) levels were significantly lower and peak pulmonary blood flow was higher with DCCV. (4) Conclusion: In asphyxiated preterm lambs, resuscitation with an intact cord decreased O2 exposure load improved ventilation with an increase in peak pulmonary blood flow in the first 5 min.
Highlights
In the delivery room, a depressed preterm neonate often needs positive pressure ventilation (PPV) with supplemental oxygen [1]
100% O2 exposure in preterm lambs was associated with improved pulmonary blood flow and preductal SpO2, it led to supraphysiological arterial oxygenation (PaO2) that could lead to hyperoxic injury [6]
Fifteen preterm lambs were randomized to delayed cord clamping with ventilation (DCCV) (N-7) and early cord clamping followed by ventilation (ECCV) (N-8)
Summary
A depressed preterm neonate often needs positive pressure ventilation (PPV) with supplemental oxygen [1]. Inability to achieve target SpO2 by 5 min is associated with poor outcomes in preterm infants. We have shown that ventilation with 100% O2 (but not 21%), led to a decrease in PVR and increased systemic to pulmonary pressure gradient in preterm lambs [6]. Such impaired pulmonary vascular transition at birth could explain the higher mortality demonstrated by Oei et al in
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