title: Low baseline oxygenation predisposes preterm infants to mixed apneas during inhalation of 100% oxygen.
abstract: We have shown previously that administration of 100% O2 to preterm infants induces an apnea which in about 20% of cases has an obstructive component. The obstruction occurred during the longer apneas. In the present study, we tested the hypothesis that the appearance of obstruction in longer apneas depends on the baseline oxygenation. Sixteen preterm infants were studied in quiet sleep (birthweight 1435 +/- 93 g [mean +/- SEM], study weight 1711 +/- 90 g, gestational age 30 +/- 1 weeks, and postnatal age 26 +/- 5 days) at various baseline oxygenations. A flow-through system was used to measure ventilation and alveolar gases. Respiratory efforts in the absence of flow were detected using chest and abdominal displacements or diaphragmatic electromyography. Each infant inhaled 15%, 21%, or 25% O2 for 5 minutes (control period) followed by 100% O, for 2 minutes. Baseline alveolar PO2, O2 saturation and transcutaneous PO2 increased during inhalation of 15%, 21%, and 25% O2, respectively. The immediate decrease in ventilation with 100% O2 was 52% on 15% O2, 20% on 21% O2, and 16% on 25% O2 (p < 0.001); this was associated with an apnea in all cases. The mean length of apneas during 100% O2 was 37 seconds on 15% O2, 19 seconds on 21%, and 11 seconds on 25% (p < 0.01). Twelve infants (75%) developed mixed obstructive apneas in response to 100% O2 when breathing 15% O2 during control period, three (19%) when breathing 21% O2, and none had mixed apnea when breathing 25% O2 during control period (p < 0.05). These findings suggest that lower baseline oxygenation predisposes to long mixed apneas. We speculate that the peripheral chemoreceptors, uniquely active in the small preterm infant with relatively low O2 tension, when suppressed by an increase in oxygen tension, trigger a central inhibition with loss of upper airway muscle tone. This is more pronounced when the baseline oxygen tension is lower, leading to more prolonged apnea and increased probability of obstruction.
authors.affiliation: University of Manitoba, Department of Pediatrics, Winnipeg, Canada.
authors.forename: A
authors.initials: A
authors.lastname: Zia Haider
authors.lastname: Virender Rehan
authors.forename: R
authors.initials: R
authors.lastname: Alvaro
authors.forename: S
authors.initials: S
authors.lastname: Al-Saedi
authors.forename: K
authors.initials: K
authors.lastname: Kwiatkowski
authors.forename: D
authors.initials: D
authors.lastname: Cates
authors.forename: H
authors.initials: H
authors.lastname: Rigatto
mesh_terms: D001049:Apnea / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D006801:Humans; D007231:Infant, Newborn; D007235:Infant, Premature, Diseases / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D010100:Oxygen / Q000097:blood; D010102:Oxygen Inhalation Therapy; D012890:Sleep / Q000502:physiology
chemical_list: D010100:Oxygen