Transcutaneous Oxygen Tension of Newborn Infants in Different Behavioral States

Publisher Website
Google Scholar
Abstract
Summary: Transcutaneous oxygen tension (tcPO2) was continuously monitored, and behavioral state was evaluated in a group of 10 normal preterm infants and 10 normal term infants. In the preterm infant group, birth weight was 1505 ± 154 g, gestational age was 32.3 ± 2.3 wk, and postnatal age was 8.4 ± 5.1 days (mean ± S.D.). In the term infant group, birth weight was 3245 ± 247 g, gestational age was 39.9 ± 0.3 wk, and postnatal age was 6.3 ± 3.4 days (mean ± S.D.). A mean tcPO2 level for each behavioral state in each infant was calculated, and a paired comparison between all states was made. In the preterm and term infant groups, mean tcPO2 levels were higher in state 1 (“quiet sleep”), state 4 (“active awake state”), and state 5 (“crying”) than during state 2 (“active sleep”). The difference (ΔtcPO2) was significant (P < 0.05). In the preterm infant group, mean tcPO2 level in state 2 was 62.9 ± 17.1 mm Hg (mean ± S.D.). Mean ΔtcPO2 in state 1 was +5.4 mm Hg (range, −0.9 to +9.2 mm Hg), mean ΔtcPO2 in state 4 was +6.8 mm Hg (range, +0.6 to +20.2 mm Hg), and in state 5 was +9.9 mm Hg (range, +5.1 to +17.5 mm Hg). In the term infant group, mean tcPO2 level in state 2 was 64.5 ± 9.6 mm Hg (mean ± S.D.). Mean ΔtcPO2 in state 1 was +5.8 mm Hg (range, −1.2 to +11.0 mm Hg), mean ΔtcPO2 in state 4 was +8.1 mm Hg (range, +2.2 to +32.3 mm Hg), and mean ΔtcPO2 in state 5 was +7.3 mm Hg (range, −1.6 to +26.5 mm Hg). There was insufficient data to evaluate tcPO2 levels during state 3 (“quiet awake state”). In the term infant group, the effect of bottle feeding on tcPO2 was also assessed. Gross alterations in tcPO2 during bottle feeding were not observed, and mean tcPO2 levels during bottle feeding (76.1 ± 8.5 mm Hg; mean ± S.D.) were not significantly different from mean tcPO2 levels found during states 1, 4, and 5. Speculation: In healthy newborn infants, crying (state 5) may be a physiologic mechanism reducing pulmonary atelectasis acquired during state 2 (“active sleep,” “REM sleep”).