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Apnea of prematurity: I. Lung function and regulation of breathing
Insights
Apnea of prematurity may stem from immature central breathing control. This study found infants with apnea showed decreased respiratory output and a blunted response to carbon dioxide, supporting a central regulatory disturbance hypothesis.
Area of Science:
- Neonatology
- Respiratory Physiology
Background:
- Apnea of prematurity is often attributed to immature central respiratory control.
- Understanding the underlying mechanisms is crucial for effective intervention.
Purpose of the Study:
- To investigate the hypothesis that central respiratory control immaturity causes apnea in premature infants.
- To compare respiratory parameters between premature infants with and without apnea.
Main Methods:
- Measured tidal volume, alveolar ventilation, alveolar PCO2, esophageal pressure change, and CO2 response curve slope.
- Compared these parameters in 18 premature infants with apnea and 18 matched healthy newborns.
Main Results:
- Infants with apnea exhibited significantly lower tidal volume and alveolar ventilation.
- Higher alveolar PCO2 and reduced esophageal pressure change were observed in infants with apnea.
- A significantly depressed ventilatory response to CO2 was found in the apnea group.
Conclusions:
- Findings support the hypothesis of a central disturbance in breathing regulation as the cause of apnea of prematurity.
- Decreased respiratory center output and blunted CO2 response are key indicators.
- Pulmonary mechanics and oxygenation were not different, highlighting central control as the primary issue.
Abstract:
It has been suggested that apnea of prematurity may be caused by "immaturity" of central control of breathing. To test the validity of this hypothesis tidal volume (VT), alveolar ventilation (VA), alveolar Pco2 (Paco2), esophageal pressure change, and the slope of the CO2 response curve (delta Ve [minute ventilation]/delta Paco2) were determined in 18 infants with apnea (mean of 32 episodes of more than 20 seconds duration per day) and in 18 healthy newborns used as control subjects. The infants were matched for birth weight (1,068 g v 1,065 g), gestational age (30.2 weeks v 30.2 weeks), and postnatal age (8.6 days v 8.3 days). The results were as follows: Vt (4.4 +/- 1.0 mL/kg v 5.3 +/- 1.6 mL/kg), Va (96 +/- 21 mL/kg/min v 129 +/- 33 mL/kg/min), Paco2 (45.4 +/- 8.5 mm Hg v 35.6 +/- 4.7 mm Hg), esophageal pressure change (4.5 +/- 0.9 cm H2O v 6.0 +/- 1.8 cm H2O), delta Ve/delta Paco2 (20.2 +/- 10.6 mL/min/kg/mm Hg CO2 v 40.7 +/- 19.9 mL/min/kg/mm Hg CO2). There was a significant difference between infants with and without apnea for all measurements. The results indicate a decreased respiratory center output and a depressed ventilatory response to CO2 in infants with apnea. As there was no difference between the two groups in pulmonary mechanics or oxygenation, the findings support the hypothesis that a central disturbance in regulation of breathing is the cause of apnea in these infants.