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Hypercapnia increases expiratory braking in preterm infants
E C Eichenwald1, R A Ungarelli, A R Stark
1Department of Pediatrics, Harvard Medical School, Boston, Massachusetts.
Insights
Premature infants use enhanced expiratory braking to maintain lung volume during hypercapnia. This breathing strategy may help infants with lung disease by improving gas exchange.
Area of Science:
- Neonatal Physiology
- Respiratory Control
Background:
- Newborn infants maintain elevated end-expiratory lung volume via diaphragm and laryngeal braking.
- The impact of hypercapnia on this breathing strategy in premature infants is not well understood.
Purpose of the Study:
- To investigate the effects of hypercapnia on respiratory muscle activity and ventilatory response in premature infants.
- To determine if CO2 breathing alters the mechanisms controlling end-expiratory lung volume.
Main Methods:
- Studied eight premature infants (33-34 wk gestational age) in early postnatal life.
- Recorded tidal volume, airflow, and electromyograms (EMG) of the diaphragm and posterior cricoarytenoid (PCA) muscle.
- Assessed breathing patterns in room air and during 2% CO2 inhalation.
Main Results:
- Hypercapnia increased tidal volume without altering inspiratory duration.
- Expiratory duration significantly increased with CO2, indicating enhanced expiratory braking.
- Post-inspiratory diaphragm EMG activity and peak inspiratory EMG activity of diaphragm and PCA increased with CO2.
Conclusions:
- Premature infants enhance expiratory braking mechanisms during hypercapnia.
- This augmented breathing strategy may be crucial for maintaining gas exchange in infants with respiratory conditions.
Abstract:
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.