Effect of different levels of hyperoxia on breathing in healthy subjects

We have recently shown that breathing 50% O-2 markedly stimulates ventilation in healthy subjects if end-tidal PCO2 (PET(CO2)) is maintained. The aim of this study was to investigate a possible dose-dependent stimulation of ventilation by O-2 and to examine possible mechanisms of hyperoxic hyperventilation. In eight normal subjects ventilation was measured while they were breathing 30 and 75% O-2 for 30 min, with PET(CO2) being held constant. Acute hypercapnic ventilatory responses were also tested in these subjects. The 75% O-2 experiment was repeated without controlling PET(CO2) in 14 subjects, and in 6 subjects arterial blood gases were taken at baseline and at the end of the hyperoxia period. Minute ventilation (V over dot I) increased by 21 and 115% with 30 and 75% isocapnic hyperoxia, respectively. The 75% O-2 without any control on PET(CO2) led to a 16% increase in V over dot I, but PET(CO2) decreased by 3.6 Torr (9%). There was a linear correlation (r = 0.83) between the hypercapnic and the hyperoxic ventilatory response. In conclusion, isocapnic hyperoxia stimulates ventilation in a dose-dependent way, with V over dot I more than doubling after 30 min of 75% O-2. If isocapnia is not maintained, hyperventilation is attenuated by a decrease in arterial PCO2. There is a correlation between hyperoxic and hypercapnic ventilatory responses. On the basis of data from the literature, we concluded that the Haldane effect seems to be the major cause of hyperventilation during both isocapnic and poikilocapnic hyperoxia.