The ventilatory response to carbon dioxide in high risk infants.

PURPOSE: To examine the ventilatory response to inspired carbon dioxide in infants considered to be at risk for sudden infant death syndrome or apnea. DESIGN: Clinical data measurement. SETTING: Infant apnea evaluation program of a university division of neonatology. PATIENTS: Fifty nine infants were full term characterized by the following diagnoses; siblings of infants who had died from sudden infant death syndrome (SIDS) (n = 7), apparent life threatening event (ALTE) (n = 24), apnea/cyanosis in the newborn nursery (n = 21), and controls. Sixty-nine infants were preterm and consisted of patients suffering from idiopathic apnea (n = 61), and bronchopulmonary dysplasia (n = 8). MEASUREMENTS: The ventilatory response to carbon dioxide was measured with a computerized waveform analyzer. MAIN RESULTS: Among full term infants no significant differences in the ventilatory slope in response to CO2 was seen. The range of mean slope was 19.4 +/- 7.6 in siblings of SIDS and 36 +/- 17 in control infants. Greater number of sibling of SIDS had slopes less than 20 ml/kg/min/mmHg in comparison to control infants. Sibling of SIDS had less increase in minute ventilation and inspiratory flow in response to CO2 administration in comparison to control infants. Preterm infants had similar slopes with a mean of 33 ml/kg/min/mmHg in infants with idiopathic apnea and 28 ml/kg/min/mmHg in infants with bronchopulmonary dysplasia. CONCLUSIONS: The large intragroup variability in the ventilatory response to inspired CO2, confirming previously reported data, comprises the benefit of this test. Thus, ventilatory response to CO2 administration is not useful in unselected patients at risk of SIDS or apnea.

Early onset of airway reactivity in premature infants with bronchopulmonary dysplasia.

Pulmonary function during the early development of bronchopulmonary dysplasia (BPD) in premature infants is not well understood. Furthermore, it is not known how early airway reactivity appears in BPD. During a 14-month period we studied 32 infants (mean gestational age, 27.3 wk; mean birth weight, 1.02 kg) with respiratory distress syndrome in whom BPD eventually developed. We obtained maximal expiratory flow-volume (MEFV) curves by manual inflation of the lung followed by forced deflation with a negative pressure on 64 occasions (mean postnatal age, 43.1 days). At each test MEFV curves were obtained in 3 conditions: baseline; after normal saline aerosolization with manual ventilation as a control; and after bronchodilator. Maximal expiratory flow at 25% of FVC (Vmax25) was markedly decreased at baseline and remained decreased after saline control. The FVC also was decreased in both baseline and saline control studies. After bronchodilator there was a marked (p less than 0.001) increase in Vmax25 (+214% above saline control) together with a significant (p less than 0.001) increase in FVC (+21%). Of 23 infants studied after 3 wk of postnatal age, 21 exhibited a more than 30% increase in Vmax25 above control (defined as airway reactivity). The remaining 2 infants were already receiving bronchodilator therapy. The most premature infant with demonstrable airway reactivity was 26 wk postconception, and the youngest was 12 days old. In 13 infants who were studied initially before 3 wk of age, there was a highly significant correlation (r = 0.91 p less than 0.001) between the degree of airway reactivity and the severity of respiratory disease as determined by the duration of ventilator dependence. Airway reactivity may play an important role in the development and severity of BPD.