Chest
Volume 121, Issue 4, April 2002, Pages 1141-1148
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Clinical Investigations
VENTILATORS
Effects of Hypocapnic Hyperventilation on the Response to Hypoxia in Normal Subjects Receiving Intermittent Positive-Pressure Ventilation

https://doi.org/10.1378/chest.121.4.1141Get rights and content

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 ( V˙ed) 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 ( V˙e) 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 V˙ed and V˙e.

Conclusion

During nIPPV, VRH is highly dependent on the carbon dioxide level and can be definitely abolished for severe hypocapnia.

Section snippets

The Concept of VRH During nIPPV

In a spontaneously breathing subject, exposure to hypoxia results in a VRH defined by an increase in V˙e due to an increase in Vt and a decrease in the total duration of each breath (ie, an increase in respiratory frequency). The situation is different in a subject receiving passive mechanical ventilation with a noninvasive mode (ie, with his carbon dioxide level below the apneic threshold resulting in a silent EMGdi). When using volumetric ventilators in the controlled mode, both

Results

Forty-two N2 runs were performed: 12 N2 runs in subject 1, 7 N2 runs in subject 2, 11 N2 runs in subject 3, and 12 N2 runs in subject 4 (Table 1). Five N2 runs were discarded from the study because of instability in sleep and/or ventilation at the beginning of the run. Thirty-seven N2 runs were retained for analysis: 7 N2 runs during wakefulness, 15 N2 runs during stage 2 nonrapid eye movement (NREM) sleep, 3 N2 runs during stage 3 NREM sleep, 8 N2 runs during stage 4 NREM sleep, and 4 N2 runs

Discussion

It is well known that hypocapnia can arrest basal ventilation. Below this apneic threshold, the respiratory muscles are inhibited and spontaneous ventilation ceases. However, hypoxia, which is a potent ventilatory stimulus, is able to reactivate the respiratory muscles that are inhibited by hypocapnia. To the best of our knowledge, this study, which was performed in normal subjects receiving passive hyperventilation with nIPPV, is the first to prove that the ventilatory response to severe

References (23)

  • PH Collard et al.

    Movement arousals and sleep-related disordered breathing in adults

    Am J Respir Crit Care Med

    (1996)
  • Cited by (20)

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    Partly supported by grants 9.4547.93 and 3.4533.98 from the Belgian Fonds de la Recherche Scientifique Médicale.

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