Neural Drive and Ventilatory Strategy of Breathing in Normal Children, and in Patients with Cystic Fibrosis and Asthma

Abstract

The drive and performance of breathing during hypercapnia, isocapnic hypoxia, and transient hyperoxia were studied in 20 normal children (mean age 12.3 years), in ten children with asthma, and in ten children with cystic fibrosis (CF) matched by sex and age. These latter two groups of patients had had obstructive respiratory symptoms since infancy and their pulmonary disease was of moderate severity as documented by their pulmonary function studies. During hypercapnia, normal children had a linear increase in minute ventilation (delta VE), in tidal volume (delta VT) and in the inspiratory drive (VT/Ti). The drive of breathing was evaluated by the occlusion pressure (P0.1) at functional residual capacity. The P0.1 response to PaCO2 was linear. Patients with asthma and CF showed a blunted ventilatory response (delta VE, delta VT, VT/Ti) to Co2 but a normal response in P0.1. In normal subjects, the test of isocarbic hypoxia demonstrated an exponential type of increase in delta VE, delta VT, and P0.1 as PAO2 decreased from 110 to 40 torr. With severe hypoxia (PAO2 less than 50 torr), children with CF (but not asthmatic patients) experienced a paradoxical decrease in delta VE while the drive (P0.1) remained above normal in both groups of patients. Finally, the transient O2 inhalation test caused a decrease in VE of 26%, 21%, an 34%, respectively, in normal subjects, in asthmatic children, and in children with CF. It is concluded that the CO2 and O2 drive of normal children resembles that described for adults and that the CO2 and O2 command of breathing is normal in children with asthma and CF. However, the ventilatory response in children with chronic obstructive pulmonary disease is subnormal probably due to the impairment of the respiratory mechanics. Finally the respiratory depression induced by severe hypoxia in children with CF is unexplained, but it may reflect the high dependency of their respiratory muscle on oxygen supply.