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Clinical Investigations: VENTILATORS |

Effects of Hypocapnic Hyperventilation on the Response to Hypoxia in Normal Subjects Receiving Intermittent Positive-Pressure Ventilation*

Vincent Jounieaux, MD; Veronica F. Parreira; Genevieve Aubert, MD; Myriam Dury; Pierre Delguste, PhD; Daniel O. Rodenstein, MD, PhD
Author and Funding Information

*From the Pneumology (Drs. Delguste and Rodenstein) and EEG (Dr. Aubert and Mrs. Dury) Units, Cliniques Universitaires Saint Luc, Université Catholique de Louvain, Brussels, Belgium; Pneumology Unit (Dr. Jounieaux), Center Hospitalier Universitaire Sud, Amiens, France; and University Federal of Minas Gerais (Mrs. Parreira), Belo Horizonte, Brazil.

Correspondence to: Daniel O. Rodenstein, MD, PhD, Service de Pneumologie, Cliniques Universitaires Saint Luc, Avenue Hippocrate, 10, B-1200 Bruxelles, Belgique; e-mail: rodenstein@pneu.ucl.ac.be



Chest. 2002;121(4):1141-1148. doi:10.1378/chest.121.4.1141
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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.

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