Hypoxic Ventilatory Response to Acute and Prolonged Hypoxic Exposures in Subjects Susceptible to High-altitude Pulmonary Edema

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  • URUSHIHATA Kazuhisa
    First Department of Medicine, Shinshu University School of Medicine
  • DROMA Yunden
    First Department of Medicine, Shinshu University School of Medicine
  • ITO Michiko
    First Department of Medicine, Shinshu University School of Medicine
  • HANAOKA Masayuki
    First Department of Medicine, Shinshu University School of Medicine

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Background : The low hypoxic ventilatory response (HVR) has been suggested to be one of the pathophysiological features in high-altitude pulmonary edema (HAPE). Ventilatory responses to hypoxia vary widely depending on the length of hypoxic exposure. The pathophysiological role of HVR in the development of HAPE has not yet been well understood.<br>Methods : Isocapnic hypoxic exposure was induced to 12 Japanese HAPE susceptible subjects (HAPE-s) and 10 HAPE resistant subjects (HAPE-r) in Shinshu University at an altitude of 600 meters (m). A slope linear regression relating minute ventilation (V˙E, L/min) to oxygen saturation (SpO2, ％), V˙E＝α＊SpO2＋β, was obtained in each of the subjects of HAPE-s and HAPE-r after 10-minutes (min) and 30-min isocapnic hypoxic exposure, respectively. The slope α parameter was the ratio of change of V˙E (ΔV˙E) to change of SpO2 (ΔSpO2) and the absolute slope α value was used for evaluation of HVR. In addition, the hypoxic ventilation decline (HVD) was calculated in the later phase of hypoxic exposures.<br>Results : The HVR was significantly lower in the HAPE-s than the HAPE-r subjects at 10-min (0.29±0.18 vs 1.13±1.21, p＝0.03) and 30-min (0.16±0.09 vs 1.01±1.08, p＝0.01) hypoxic exposure. Moreover, the HVR continuously declined in the HAPE-s subjects over the prolonged hypoxic exposure from 0.29±0.18 at 10-min hypoxic exposure to 0.16±0.09 at 30-min hypoxic exposure, resulting in 29.3％ of HVD in HAPE-s, in contrast to 3.1％ of HVD in the HAPE-r subjects over the prolonged hypoxia.<br>Conclusion : The HVR was not only significantly blunted but also continuously declined in the HAPE-s over a prolonged hypoxic exposure, which contributed to the failure in acclimatization to high-altitude hypoxia.

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