Kobayashi S, Nishimura M, Yamomoto M, Akiyama Y, Miyamoto K, Kawamaki Y
First Dept of Medicine, Hokkaido University School of Medicine, Sapporo, Japan.
Eur Respir J. 1996 Nov;9(11):2340-5. doi: 10.1183/09031936.96.09112340.
The purpose of this study is to examine the relationship between breathlessness and the ventilatory response to hypercapnia or hypoxia in patients with chronic obstructive pulmonary disease (COPD). Fifteen male patients (mean forced expiratory volume in one second (FEV1): 1.13 L) underwent tests to determine hyperoxic hypercapnic ventilatory response (HCVR) and isocapnic hypoxic ventilatory response (HVR) with simultaneous quantification of breathlessness by modified Borg scale. The ventilatory output was evaluated by the ratio of minute ventilation (V'E) divided by measured maximal voluntary ventilation (MVV). The magnitude of HCVR or HVR was assessed as the slope value of the V'E/MVV-end-tidal carbon dioxide pressure (PET,CO2) or arterial oxygen saturation (Sa,O2) regression line, respectively. The breathlessness during the tests was evaluated not only linearly in relation to V'E/MVV, but also at given levels of PET,CO2 or Sa,O2. The mean value of the breathlessness at two different levels of ventilation was greater during HVR than during HCVR, suggesting that hypoxia is dyspnogenic independently of ventilatory stimulation. The HCVR was inversely correlated with the breathlessness response to ventilation, while similar correlation was partly present for HVR. The HVR was positively correlated with the breathlessness at an Sa,O2 of 80%, whilst there was no such correlation between the HCVR and the breathlessness related to PET,CO2. Therefore, patients with a higher breathlessness related to increased ventilation had a lower HCVR and HVR, whilst those with a higher breathlessness with desaturation, which might include a direct influence of hypoxia, had a higher HVR. These findings suggest an interaction between ventilatory response and breathlessness during the test, which may partly include behavioural modulation of HCVR and HVR through the breathlessness in various ways, depending on the origin and nature of the sensation.
本研究的目的是探讨慢性阻塞性肺疾病（COPD）患者呼吸困难与对高碳酸血症或低氧血症的通气反应之间的关系。15名男性患者（一秒用力呼气容积（FEV1）平均值：1.13L）接受了测试，以确定高氧高碳酸通气反应（HCVR）和等碳酸低氧通气反应（HVR），同时通过改良的博格量表对呼吸困难进行量化。通气输出通过分钟通气量（V'E）除以实测最大自主通气量（MVV）的比值来评估。HCVR或HVR的大小分别被评估为V'E/MVV-呼气末二氧化碳分压（PET,CO2）或动脉血氧饱和度（Sa,O2）回归线的斜率值。测试期间的呼吸困难不仅与V'E/MVV呈线性关系进行评估，还在给定的PET,CO2或Sa,O2水平上进行评估。在HVR期间，两个不同通气水平下呼吸困难的平均值高于HCVR期间，这表明低氧血症在不依赖通气刺激的情况下会引起呼吸困难。HCVR与对通气的呼吸困难反应呈负相关，而HVR也存在部分类似的相关性。HVR与Sa,O2为80%时的呼吸困难呈正相关，而HCVR与PET,CO2相关的呼吸困难之间不存在这种相关性。因此，与通气增加相关的呼吸困难程度较高的患者HCVR和HVR较低，而与去饱和相关的呼吸困难程度较高的患者（这可能包括低氧血症的直接影响）HVR较高。这些发现表明测试期间通气反应与呼吸困难之间存在相互作用，这可能部分包括根据感觉的起源和性质，通过呼吸困难以各种方式对HCVR和HVR进行行为调节。
