Elliott M W, Mulvey D A, Moxham J, Green M, Branthwaite M A
Dept. of Thoracic Medicine, Royal Brompton and National Heart Hospital, London, UK.
Eur Respir J. 1991 Oct;4(9):1044-52.
The improvement in arterial blood gas tensions following assisted ventilation in chronic obstructive pulmonary disease (COPD) has usually been attributed to the relief of incipient or established respiratory muscle fatigue. The contribution of changes in the load placed upon and the drive to the respiratory muscle pump have not been evaluated. We have investigated the contribution of changes in respiratory muscle strength, the ventilatory response to CO2 and ventilatory function to changes in arterial blood gas tensions in eight patients with severe COPD completing six months domiciliary nasal intermittent positive pressure ventilation. Six patients showed a reduction and two an increase in arterial carbon dioxide tension (PaCO2), median (range) for eight patients, -0.9 kPa (-1.5 to +0.4) (p less than 0.05) and seven showed an improvement in arterial oxygen tension (PaO2), +0.7 kPa (-0.4 to +1.7) (p less than 0.05) during daytime spontaneous breathing. The reduction in PaCO2 was not related to increased inspiratory muscle strength but was correlated with a decrease in gas trapping (Spearman rank correlation coefficient (r(S)) 0.85, p less than 0.05) and in the residual volume (r(s) 0.78, p less than 0.05), suggesting reduced small airway obstruction and, therefore, a reduction in load. The change in PaCO2 also correlated with the increase in ventilation at an end-tidal CO2 of 8 kPa during rebreathing (r(s) -0.76, p less than 0.05) suggesting improved chemosensitivity to CO2. Our data do not support the hypothesis that improvements were due to the relief of muscle fatigue. We suggest that the contribution of changes in load and central drive warrant further investigation.
慢性阻塞性肺疾病（COPD）患者在辅助通气后动脉血气张力的改善通常归因于初期或已存在的呼吸肌疲劳的缓解。呼吸肌泵所承受的负荷变化及驱动变化的作用尚未得到评估。我们对8例重度COPD患者进行了研究，这些患者在家中接受了6个月的鼻间歇正压通气，研究呼吸肌力量变化、对二氧化碳的通气反应及通气功能对动脉血气张力变化的作用。8例患者中，6例动脉二氧化碳分压（PaCO2）降低，2例升高，8例患者的中位数（范围）为-0.9 kPa（-1.5至+0.4）（p<0.05）；7例患者白天自主呼吸时动脉血氧分压（PaO2）改善，为+0.7 kPa（-0.4至+1.7）（p<0.05）。PaCO2的降低与吸气肌力量增加无关，但与气体潴留减少（Spearman等级相关系数（r(S)）0.85，p<0.05）及残气量减少（r(s) 0.78，p<0.05）相关，提示小气道阻塞减轻，即负荷降低。PaCO2的变化也与重复呼吸时呼气末二氧化碳分压为8 kPa时通气增加相关（r(s) -0.76，p<0.05），提示对二氧化碳的化学敏感性改善。我们的数据不支持改善是由于肌肉疲劳缓解这一假说。我们认为负荷和中枢驱动变化的作用值得进一步研究。
