Profile of Alveolar Gases during Periodic and Regular Breathing in Preterm Infants

Abstract

To determine the changes in alveolar PCO₂ (P_ACO₂) and PO₂ (P_AO₂) during periodic and regular breathing epochs in the same infants, we studied 11 preterm infants during quiet sleep (birth weight 1,630 ± 94 g; gestational age 31 ± 1 weeks; postnatal age 32 ± 3 days). A total of 94 breathing/apneic cycles were analyzed and compared with regular periods. During periodic and regular breathing epochs, there were negative correlations of P_AO₂ on P_ACO₂. Short (5 s) and long ( > 5 s) apneas for individual infants occurred along the regression line for that infant. There was not a single overall critical P_ACO₂ below which apnea occurred, but for individual infants the P_ACO₂ and the P_ACO₂ of the breath preceding apnea varied within a limited range. Apneas occurred in clusters of P_ACO₂ and P_AO₂ along the average regression line of P_AO₂ on P_ACO₂. Analysis of the data showed that apnea occurred at the lowest P_ACO₂ and highest P_AO₂ levels if allowance was made for circulation time. During apnea, ‘the best fit’ for the increase in P_ACO₂ and the decrease in P_AO₂ was linear, rather than logarithmic. The findings suggest the following. (1) There is not a single overall critical level of P_ACO₂ for apnea to occur, but in a given infant this level varies within a limited range. This indicates that these infants are likely breathing near the apnea threshold. (2) Short and long apneas appear to occur randomly along the regression of P_AO₂ on P_ACO₂ for a particular infant. (3) The changes in alveolar gases are linear during apnea. The data are consistent with the idea that each infant has an optimum narrow range of P_ACO₂ and P_AO₂ values in which apnea occurs.

Quantification of periodic breathing in premature infants

“…AOP begins within 1–2 days after birth and usually resolves between 36 and 42 weeks postmenstrual age (Eichenwald, Aina & Stark 1997), whereas PB typically starts after the first week and often persists beyond NICU discharge, for up to several months past term-corrected age (Wilkinson et al 1995). The timing of onset of PB coincides with the time that peripheral arterial chemoreceptors, silenced at birth with the acute rise in blood oxygen levels, become highly sensitive to small fluctuations in blood gases (Pereira et al 1995, Khan et al 2005). PB typically includes apneic pauses of less than 10 seconds and may entrain only small or no decline in heart rate and oxygen saturation (Poets, Southall 1991, Razi, DeLauter & Pandit 2002), rarely low enough to reach the threshold to trigger bedside monitor alarms, whereas AOP is often prolonged and associated with significant bradycardia and oxygen desaturation (Finer et al 2006).…”

“…Peripheral chemoreceptors are desensitized at birth, with the acute increase in blood oxygen content during fetal to neonatal transition, then are gradually reset by about one week of age at which time PB emerges (Barrington, Finer 1990). Hypersensitivity of chemoreceptors to changes in blood oxygen and carbon dioxide levels leads to self-sustained oscillations between breathing and apneic pauses, especially during quiet sleep (Pereira et al 1995, Rigatto 2003). …”

Clinical associations with immature breathing in preterm infants: part 2—periodic breathing

“…In a study of preterm and term neonates, the difference between apneic and eupneic CO 2 thresholds was about 1 Torr, in contrast to adults with a difference of about 3.5 Torr, which might partially account for neonates’ tendency to oscillate between apnea and breathing. ( 33 , 36 )…”