Optimal release time during airway pressure release ventilation in neonatal sheep
Related Experiment Video
Updated: Aug 28, 2026

The Perinatal Asphyxiated Lamb Model: A Model for Newborn Resuscitation
Published on: August 15, 2018
1Department of Anesthesiology/Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, MD.
Objective:
To systematically investigate the effect of altering release time during airway pressure release ventilation in a neonatal animal model before and after oleic acid-induced acute lung injury.
Design:
Prospective, nonrandomized, controlled study with repeated measures.
Setting:
University research laboratory.
Subjects:
Eight neonatal sheep (aged < 7 days, weight 5.1 +/- 0.3 kg).
Interventions:
Throughout this study, airway pressure release ventilation was performed with an FIO2 of 0.21 at a frequency of 0.5 Hz (30 breaths/min) and an airway plateau pressure set to deliver tidal volumes between 10 and 15 mL/kg with a release time of 1 sec. Release time was changed in decrements of 0.2 sec starting at 1 sec and ending at 0.2 sec at 10-min intervals. Cardio-respiratory profiles were recorded at the end of each interval. The total exhaled respiratory system time constant (tau) was measured by plotting exhaled volume (integration of exhaled air flow) vs. time. Acute lung injury was induced by oleic acid infusion. The protocol was repeated with increased plateau airway pressure to maintain tidal volumes between 10 and 15 mL/kg at a release time of 1 sec.
Measurements And Main Results:
During airway pressure release ventilation at a release time of 1 sec, oleic acid-induced acute lung injury decreased dynamic lung compliance (9.9 +/- 2.2 vs. 7.5 +/- 2.0 mL/cm H2O, p < .01), the expiratory time constant (0.15 +/- 0.04 vs. 0.12 +/- 0.02 sec, p < .05), and mean arterial pressure (80 +/- 5 vs. 62 +/- 12 mm Hg, p < .01). Alveolar ventilation was maintained as long as release times were > 0.4 sec (approximately 3 tau or greater). PaO2 decreased with release times of < 0.3 sec, but the alveolar-arterial oxygen tension difference was unchanged. In this protocol, with higher plateau and mean airway pressures, oleic acid-induced acute lung injury had no effect on the relationship between release time and oxygenation or ventilation.
Conclusions:
In this neonatal laboratory model, release times that were much shorter than previously reported maintained clinically acceptable oxygenation and ventilation. The optimal duration of the release time is a function of the time constant of the respiratory system. During airway pressure release ventilation, alveolar ventilation was maintained without apparent lung volume loss with release times of between 4 tau and 10 tau.
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