Effect of supplemental oxygen on sleep architecture and cardiorespiratory events in preterm infants.

OBJECTIVE To investigate the effect of low-flow supplemental oxygen (SupOx) on sleep architecture and cardiorespiratory events in asymptomatic preterm infants. METHODS An overnight polysomnographic evaluation was conducted prospectively in 23 premature infants who were born at 30.0 +/- 3.2 (standard deviation) weeks' gestational age and studied at 38.1 +/- 4.4 weeks' postconceptional age. Infants were free of any adverse events, including cardiorespiratory monitor alarms in the nursery for at least 1 week before the study. Infants received room air (RA) or SupOx via nasal cannula at 0.25 L/min. RESULTS Quiet sleep density was increased during SupOx (33.3 +/- 10.8% vs 26.6 +/- 10.0% total sleep time [TST] in RA), and a reciprocal decrease in active sleep density was observed (61.5 +/- 11.1% vs 68.4 +/- 9.9% TST in RA). No differences in sleep efficiency emerged (69.7 +/- 10.6% SupOx vs 69.7 +/- 8.8% RA). SupOx elicited significant decreases in apnea index (3.8 +/- 2.4 events/h vs 11.1 +/- 6.4 events/h in RA) and in the percentage of time spent in periodic breathing (1.8 +/- 2.9% vs 6.7 +/- 8.9% in RA). In addition, SupOx decreased the frequency of bradycardic events (0.3 +/- 0.8 events vs 2.5 +/- 0.03 events in RA) and improved overall oxygen saturation (98.7 +/- 1.1% vs 96.4 +/- 2.2%). No changes in alveolar ventilation, as derived from end-tidal CO2 measurements, was detected (38.6 +/- 5.8 mm Hg in SupOx vs 38.4 +/- 5.4 mm Hg in RA). CONCLUSIONS Asymptomatic preterm infants exhibit frequent and potentially clinically adverse cardiorespiratory events when assessed in the sleep laboratory. Administration of SupOx to these infants is associated with an increase in the overall duration and percentage TST spent in quiet sleep with reciprocal changes in active sleep. In addition, improvement in respiratory stability is observed with the use of low-flow SupOx, as evidenced by a decrease in apnea, periodic breathing, and bradycardia, without adverse effects on alveolar ventilation.