Objective To study the feasibility of lung ultrasound (LUS) in prone position and to compare it with supine position in neonates with respiratory distress. Study Design Neonates ≥ 29 weeks of gestational age with respiratory distress requiring respiratory support within first 12 hours of life were enrolled prospectively. First LUS (fLUS) was done in the position infant was nursed (supine or prone), infant’s position changed, a second LUS (sLUS) was performed immediately and a third LUS (tLUS) was done 1 to 2 hours later. Primary outcome was the comparison of LUS scores (LUSsc) between fLUS and sLUS. Results Sixty-four neonates were enrolled. Common respiratory diagnoses were transient tachypnea of newborn (TTN; 53%) and respiratory distress syndrome (RDS; 41%). LUSsc was different between fLUS and sLUS (fLUSsc 6 [interquatile range: 4, 7] vs. sLUSsc 7 [4, 10], p < 0.001), while there was no difference between the fLUS and tLUS (fLUSsc 6 [4, 7] vs. tLUSsc 5 [3, 7], p = 0.43). Subgroup analysis confirmed similar findings in neonates with TTN, while in babies with RDS, all the three LUSsc were similar. Conclusion LUS is feasible in prone position in neonates. LUS scores were higher immediately after a change in position but were similar to baseline 1 hour after the change in position.

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.

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The timing and magnitude of airway narrowing in central apneas is unknown. We have developed a method of apnea classification that relies on the transmission of cardiac airflow oscillation to indicate airway patency. Using a theoretical model, we showed that the amplitude of the cardiac airflow oscillation is proportional to airway diameter for small lumens. While in the majority of central apneas the amplitude of the cardiac airflow oscillation remains nearly constant, in a subset of events the waveform decreases with time, suggesting airway narrowing. We hypothesized that this is not a random occurrence but reflects a critical period of airway instability during central apnea. To test this hypothesis we studied 41 preterm infants. Of 4,456 central apneas, 585 had a decrease in the amplitude of the cardiac oscillation. The amplitude of the cardiac airflow oscillation during an apnea was recorded to provide a dynamic measure of changes in airway diameter with time. To allow for comparisons between patients the amplitude of each cardiac airflow oscillation was expressed as a proportion of the maximum amplitude observed in each infant. We then compared the amplitude at multiple successive 0.5 s intervals with the amplitude of the cardiac airflow oscillation observed at the apnea outset using ANOVA. We found a significant decrease in cardiac airflow oscillation after only 1 s irrespective of the apnea duration (3 to 16 s). We conclude that airway narrowing during central apnea is not a random occurrence but appears shortly after the onset of the apnea. We speculate that the phenomenon is secondary to passive airway relaxation.

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