To discover whether increases in inhaled O2 fraction (FIO2; up to 40%) decrease apnea via an increase in minute ventilation (VE) or a change in respiratory pattern, 15 preterm infants (birth weight 1,300 +/- 354 g, gestational age 29 +/- 2 wk, postnatal age 20 +/- 9 days) breathed 21, 25, 30, 35, and 40% O2 for 10 min in quiet sleep. A nosepiece and a flow-through system were used to measure ventilation. Alveolar PCO2, transcutaneous PO2, and sleep states were also assessed. All infants had periodic breathing with apneas greater than or equal to 3 s. With an increase in FIO2 breathing became more regular and apneas decreased (P less than 0.001). This regularization in breathing was not associated with significant changes in VE. However, the variability of VE, tidal volume, and expiratory and inspiratory times decreased significantly. The results indicate that the more regular breathing observed with small increases in FIO2 was not associated with significant changes in ventilation. The findings suggest that the increased oxygenation decreases apnea and periodicity in preterm infants, not via an increase in ventilation, but through a decrease in breath-to-breath variability of VE.

Experimentally modified breathing pattern in human subjects, by varying the inspired gas mixture or administering different neuromodulators, has been studied extensively in the past, yet unmodified breathing has not. Moreover, most data refer to infants during sleep and adults during wakefulness. We studied the baseline breathing pattern of preterm infants [n= 10; GA 30 (27–34) wk (median, range)]; term infants [n= 10; GA 40 (39–41) wk)], and adult subjects [n= 10; age 31 (17–48) y)] during quiet sleep. A flow‐through system was used to measure ventilation. We found: (i) instantaneous ventilation was 0.273 ± 0.006, 0.200 ± 0.003, and 0.135 ± 0.002 Lmin‐1.kg‐1 in preterm, term infants, and adult subjects; the coefficients of variation were 39%, 25%, and 14% (p <0.01). The greater coefficient of variation in neonates compared to adults related to increased variability in Vt (39% and 25% in preterm and term infants vs 14% in adults; p < 0.01) and f (39% and 22% vs 9%; p < 0.01). The major determinant of frequency in preterm infants was Te (81% variability), Ti varying less (25% variability); (ii) VT/Ti decreased and Ti/Ttot increased with age; (iii) the higher breath‐to‐breath variability in preterm infants was associated with larger changes in alveolar PCO2 and a larger variability in O2 saturation than later in life. We conclude: (i) the high breath‐to‐breath variability in frequency in preterm infants closely relates to variation in Te; (ii) decreased effective inspiratory timing (Ti/Ttot) in preterm infants compared with adults likely reflects their high pulmonary impedance; and (iii) greater breath‐to‐breath variability in ventilation in neonates with large variations in alveolar PCO2 and O2 saturation remains when compared with values in the sleeping adult. We speculate that high variability in Te early in life represents an effort to maintain lung volume through increased post‐inspiratory diaphragmatic activity and increased upper airway resistance in an attempt to avoid collapse due to poor chest wall recoil.

We tested the hypothesis that the immediate (< 1 min) ventilatory response to 100% O2 in preterm infants, a test of peripheral chemoreceptor activity characterized by a decrease in ventilation due to apnea, is more pronounced at lower baseline O2 concentrations. We studied 12 healthy preterm infants [birth weight 1,425 +/- 103 (SE) g; study weight 1,670 +/- 93 g; gestational age 30 +/- 1 wk; postnatal age 27 +/- 7 days] during quiet sleep. The infants inhaled 15, 21, 25, 30, 35, 40, and 45% O2 for 5 min in a randomized manner (control period), followed by 100% O2 for 2 min, and then the same initial O2 concentration again for 2 min (recovery period). A nose piece and a flow-through system were used to measure ventilation. The immediate decrease in ventilation with 100% O2 was 46% on 15% O2, 24% on 21% O2, 11% on 25% O2, 8% on 30% O2, 12% on 35% O2, and 8% on 40% O2; there was no decrease on 45% O2 (P < 0.01). The corresponding mean duration of apnea was 29 s during 15% O2, 18 s during 21% O2, 8 s during 25% O2, 9 s during 30 and 35% O2, and 3 s during 40% O2; only one infant developed a 5-s apnea during 45% O2 (P < 0.001). The findings suggest that 1) the ventilatory decrease in response to 100% O2 is dependent on the baseline oxygenation, being more pronounced the lower the baseline O2 concentration; and 2) this ventilatory decrease is entirely related to more prolonged apneas observed with lower baseline O2 concentrations. We speculate that the peripheral chemoreceptors, being so active in the small preterm infant with relatively low arterial PO2, are highly susceptible to changes in PO2, and this makes them prone to irregular or periodic breathing, especially during sleep.

Experimentally modified breathing pattern in human subjects, by varying the inspired gas mixture or administering different neuromodulators, has been studied extensively in the past, yet unmodified breathing has not. Moreover, most data refer to infants during sleep and adults during wakefulness. We studied the baseline breathing pattern of preterm infants [n = 10; GA 30 (27-34) wk (median, range)]; term infants [n = 10; GA 40 (39-41) wk)], and adult subjects [n = 10; age 31 (17-48) y)] during quiet sleep. A flow-through system was used to measure ventilation. We found: (i) instantaneous ventilation was 0.273+/-0.006, 0.200+/-0.003, and 0.135+/-0.002 L x min(-1) x kg(-1) in preterm, term infants, and adult subjects; the coefficients of variation were 39%, 25%, and 14% (p < 0.01). The greater coefficient of variation in neonates compared to adults related to increased variability in Vt (39% and 25% in preterm and term infants vs 14% in adults; p < 0.01) and f (39% and 22% vs 9%; p < 0.01). The major determinant of frequency in preterm infants was Te (81% variability), Ti varying less (25% variability); (ii) V(T)/Ti decreased and Ti/Ttot increased with age; (iii) the higher breath-to-breath variability in preterm infants was associated with larger changes in alveolar PCO2 and a larger variability in O2 saturation than later in life.

Oral breathing is an important defense mechanism, yet its prevalence and relationship to behavioral activities have not been studied in preterm infants. We tested the hypothesis that oral breathing is rare in these infants and likely to be restricted to periods of body movements. Ten healthy preterm infants (birthweight 1300 +/- 100 g [SE]; gestational age 29 +/- 1 weeks; postnatal age 36 +/- 7 days) were studied. Ventilation was measured with a nose piece and screen flowmeter. Oral breathing was detected with a carbon dioxide sampler at the mouth. Movements were classified according to intensity into type I (localized, minor signal distortion) and type II (generalized, moderate signal distortion). Oral breathing was present 10% of the time, with a mean duration of 27 +/- 3 seconds. Of 104 episodes of oral breathing, 13 (13%) occurred during type I movement, 89 (86%; p < 0.01) during type II, and 2 (2%) in the absence of movement. The delay from beginning of movements to the beginning of oral breathing was 20 +/- 3 seconds. Nasal minute ventilation decreased from 0.203 +/- 0.013 L.min-1.kg-1 during movements in the absence of oral breathing to 0.167 +/- 0.013 L.min-1.kg-1 during movements plus oral breathing (p = 0.017). In 496 type I and II movements, the prevalence of oral breathing was 21 of 165 (13%) in quiet sleep, 37 of 194 (19%) in rapid eye movement sleep, 6 of 12 (50%) in transitional sleep, and 44 of 125 (35%) in indeterminate sleep (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)