Objective: To confirm the hypothesis that the ventilatory response to hypoxia (VRH) may be abolished by hypocapnia.
Methods: We studied four healthy subjects during intermittent positive-pressure ventilation delivered through a nasal mask (nIPPV). Delivered minute ventilation (V̇ed) was progressively increased to lower end-tidal carbon dioxide pressure (Petco2) below the apneic threshold. Then, at different hypocapnic levels, nitrogen was added to induce falls in oxygen saturation, a hypoxic run (N2 run). For each N2 run, the reappearance of a diaphragmatic muscle activity and/or an increase in effective minute ventilation (V̇e) and/or deformations in mask-pressure tracings were considered as a VRH, whereas unchanged tracings signified absence of a VRH. For the N2 runs eliciting a VRH, the threshold response to hypoxia (TRh) was defined as the transcutaneous oxygen saturation level that corresponds to the beginning of the ventilatory changes.
Results: Thirty-seven N2 runs were performed (7 N2 runs during wakefulness and 30 N2 runs during sleep). For severe hypocapnia (Petco2 of 27.1 ± 5.2 mm Hg), no VRH was noted, whereas a VRH was observed for N2 runs performed at significantly higher Petco2 levels (Petco2 of 34.0 ± 2.1 mm Hg, p < 0.001). Deep oxygen desaturation (up to 64%) never elicited a VRH when the Petco2 level was < 29.3 mm Hg, which was considered the carbon dioxide inhibition threshold. For the 16 N2 runs inducing a VRH, no correlations were found between Petco2 and TRh and between TRh and both V̇ed and V̇e.
Conclusion: During nIPPV, VRH is highly dependent on the carbon dioxide level and can be definitely abolished for severe hypocapnia.