McGill University Health Centre Research Institute, Montreal, QC, Canada.
Eur Respir J. 2010 Mar;35(3):676-80. doi: 10.1183/09031936.00120609.
This review examines 18 studies published > or =30 yrs ago. They show that the earliest manifestation of chronic obstructive pulmonary disease (COPD) is an increase in residual volume suggesting that the natural history of COPD is a progressive increase in gas trapping with a decreasing vital capacity (VC). The reduction in VC forces the forced expiratory volume in 1 s to decline with it. This is aggravated by rapid shallow breathing leading to dynamic hyperinflation. The earlier studies show that this is energetically opposite to a minimal work or force pattern and is responsible for dyspnoea and exercise limitation. This information, available for >30 yrs leads to three virtually untested hypotheses: 1) training patients to breathe slowly and deeply transiently during exercise should decrease the work of breathing, dynamic hyperinflation and improve exercise performance; 2) rapid shallow breathing is caused by alveolar and bronchial inflammation that stimulates non-myelinated vagal C-fibre afferents, which are known to cause this breathing pattern; and 3) if so, therapeutic efforts to block these afferents might restore a slow-deep pattern and be beneficial, particularly in COPD exacerbations.
这篇综述回顾了 30 年以上发表的 18 项研究。这些研究表明，慢性阻塞性肺疾病（COPD）的最早表现是残气量增加，这表明 COPD 的自然病程是气体潴留的进行性增加，导致肺活量（VC）逐渐下降。VC 的减少迫使 1 秒用力呼气量（FEV1）随之下降。这被快速浅呼吸进一步加重，导致动态过度充气。早期的研究表明，这与最小的功或力模式相反，是导致呼吸困难和运动受限的原因。这一信息已经存在了 30 多年，提出了三个几乎未经测试的假设：1）训练患者在运动期间短暂地缓慢而深地呼吸，应该会降低呼吸功、动态过度充气并改善运动表现；2）快速浅呼吸是由肺泡和支气管炎症引起的，炎症刺激非髓鞘迷走 C 纤维传入纤维，已知这些传入纤维会导致这种呼吸模式；3）如果是这样，阻断这些传入纤维的治疗努力可能会恢复缓慢-深的模式，并带来益处，特别是在 COPD 加重时。
