Apnea of prematurity: I. Lung function and regulation of breathing.

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.