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Hypoxic Ventilatory Response and Breathlessness Following Hypocapnic and Isocapnic Hyperventilation

Kazuo Chin; Motoharu Ohi; Hideo Kita; Naoki Otsuka; Yoshitaka Oku; Michiaki Mishima; Kenshi Kuno
Author and Funding Information

From the Department of Clinical Physiology, Chest Disease Research Institute, Kyoto University, Kyoto, Japan


1997 by the American College of Chest Physicians


Chest. 1997;112(1):154-163. doi:10.1378/chest.112.1.154
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Abstract

Study objectives: To investigate the etiology of posthyperventilation (post-HV) hypoxemia following voluntary hyperventilation (VHV), we examined the effects of hypocapnic (hypo-CO2) and isocapnic (iso-CO2) VHV on the hypoxic ventilatory response (O2-response) and on the sensation of breathlessness during the O2-response.

Methods: O2-responses and visual analog scale (VAS) scores for estimating breathlessness in 10 normal subjects during the O2-response under iso-CO2 conditions and under hypo-CO2 conditions immediately following voluntary maximal HV of 3 min duration were examined.

Results: Although there was no significant difference in the post-HV ventilation levels following hypo-CO2 vs iso-CO2 VHV, the VAS scores at the start of the O2-response following hypo-CO2 VHV (30.2±24.2 mm) were significantly higher (p<0.05) than the VAS scores at the start of the O2-response following iso-CO2 VHV (13.7±8.4 mm). However, VHV did not have a significant effect on the O2-response at 2 min after the VHV when the arterial O2 saturation (SaO2) was below 90%. The nonsteady-state hypo-CO2 induced by VHV greatly attenuated the O2-response below 90% SaO2 and VAS scores at 70% SaO2.

Conclusions: Elevated VAS scores immediately following the hypo-CO2 VHV, which might be independent of actual breathing levels, and the attenuation of the O2-response following the hypo-CO2 VHV were not due to input from lung and chest wall mechanoreceptors induced by the hyperpnea itself, but rather to the hypo-CO2 induced by hyperpnea.


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