The effects of aminophylline on the respiratory center output were studied in 14 premature infants with idiopathic apnea. The mean birth weight was 1,052 gm, and the mean gestational age was 30.2 wks. These infants had a normal expired volume per minute (VE) [291 ml/(min X kg)] and a normal esophageal pressure change per breath (4.5 cm H2O); however, their alveolar ventilation per minute (VA) was decreased [89 ml/(min X kg)], resulting in an elevated end-tidal PCO2 (PACO2) [47.8 mm Hg]. The reasons for the elevated PACO2 were the relatively large anatomical dead spaces (VD) found in these infants (3.4 ml/kg), and a decreased slope of the CO2 response curve [22.2 ml/(min X kg X mm Hg PACO2)], with a shift of the curve to the right. Oxygen consumption was normal [7.0 ml/(min X kg)]. Forty-eight hours after initiating treatment with aminophylline (2 mg/kg of body weight every 6 hr), the incidence of apneic episodes decreased from 29.7 to 4.4 per 24 hr, VA and PACO2 became normal secondary to a 33% increase in esophageal pressure change per breath, and the position of the CO2 response curve showed a significant shift to the left without change in slope. Oxygen consumption increased 20% from basal value. These findings support the hypothesis that apnea in premature infants is related to an immature respiratory center characterized by a decreased output. Aminophylline probably increases respiratory center output by lowering the threshold of the central chemoreceptor to CO2.
|Original language||English (US)|
|Number of pages||6|
|State||Published - Jan 1 1979|
ASJC Scopus subject areas
- Pediatrics, Perinatology, and Child Health