Abstract
Periodic breathing and apnea are common in neonates, yet the physiological mechanisms involved are not clear. A low arterial PO
2 might magnify peripheral chemoreceptor contribution to breathing, with its baseline variability inducing major changes in ventilation, leading to instability of the respiratory control system. We hypothesized that neonates: (1) would depend much more on the peripheral chemoreceptor contribution to breathing than adult subjects and (2) their baseline arterial PO
2 would sit on the steep portion of the ventilation/arterial PO
2 relationship on the adult nomogram, making breathing prone to oscillate. We analyzed data from previous polygraphic recordings in four groups of subjects: small preterm infants [SPI; postconceptional age (PCA) 33 ± 2 weeks;
n = 40], large preterm infants (LPI; PCA 36 ± 2 weeks;
n = 34), term infants (TI; PCA 42 ± 1 week;
n = 24), and adult subjects (AS; weight 63 ± 2 kg; age 29 ± 3 years,
n = 16). Peripheral chemoreceptor activity was measured by: (1) the immediate decrease in ventilation and (2) apnea time during brief inhalation of 100% O
2 (about 1 minute). We found that: (1) the immediate decrease in ventilation with 100% O
2 was more pronounced in infants than in adult subjects (38 ± 2 versus 6 ± 5%), and in infants breathing periodically versus those breathing continuously; (2) the apnea time during 100% O
2 was also significantly longer in periodic breathing infants; and (3) the TcPO
2 was much lower in infants than in adult subjects (65 ± 1 versus 93 ± 1 Torr), and also lower in periodic versus continuously breathing infants. It was located significantly to the left of values for the adult subject, on the ventilation/arterial PO
2 diagram. The data suggest that: (1) a substantial portion of baseline breathing activity early in life is maintained by increased peripheral chemoreceptor activity; and (2) neonates breathe irregularly with apneas due to the position of their arterial PO
2 values on the ventilation/arterial PO
2 diagram, in which a change in PO
2 produces a more significant change in ventilation than that observed later in life.