Hypercapnia increases expiratory braking in preterm infants.

In contrast to adults, newborn infants breathe from an elevated end-expiratory lung volume, determined by the interaction of airflow retardation (braking) by the diaphragm and larynx, and expiratory duration. To determine the effect of hypercapnia on this strategy, we examined changes in respiratory muscle activity and the ventilatory response to CO2 breathing in eight premature infants 33-34 wk gestational age in the first 3 postnatal days. We recorded tidal volume, airflow, and electromyograms (EMG) of the laryngeal abductor [posterior cricoarytenoid (PCA)], which abducts the vocal cords, and diaphragm during behaviorally determined quiet sleep in room air and during steady-state inhalation of 2% CO2 in air. As expected, tidal volume increased (P < 0.0005) without a change in inspiratory duration with hypercapnia. Unexpectedly, in all subjects, expiratory duration was longer during CO2 inhalation (P < 0.001), accompanied by marked changes in expiratory flow patterns consistent with increased expiratory braking. Diaphragm post-inspiratory EMG activity increased with hypercapnia (P < 0.005) with no change in baseline diaphragm or PCA EMG activity. Peak inspiratory EMG activity of the diaphragm and PCA increased with CO2 (10 and 37%, respectively; P < 0.05). We conclude that the mechanisms used to elevate end-expiratory lung volume are enhanced during hypercapnia in premature infants. This breathing strategy may be important in maintaining gas exchange in infants with lung disease.