O'Donnell Denis E, Banzett Robert B, Carrieri-Kohlman Virginia, Casaburi Richard, Davenport Paul W, Gandevia Simon C, Gelb Arthur F, Mahler Donald A, Webb Katherine A
Department of Medicine, Queen's University, 102 Stuart Street, Kingston, ON, K7L 2V6 Canada.
Proc Am Thorac Soc. 2007 May;4(2):145-68. doi: 10.1513/pats.200611-159CC.
Effective management of dyspnea in chronic obstructive pulmonary disease (COPD) requires a clearer understanding of its underlying mechanisms. This roundtable reviews what is currently known about the neurophysiology of dyspnea with the aim of applying this knowledge to the clinical setting. Dyspnea is not a single sensation, having multiple qualitative descriptors. Primary sources of dyspnea include: (1) inputs from multiple somatic proprioceptive and bronchopulmonary afferents, and (2) centrally generated signals related to inspiratory motor command output or effort. Respiratory disruption that causes a mismatch between medullary respiratory motor discharge and peripheral mechanosensor afferent feedback gives rise to a distressing urge to breathe which is independent of muscular effort. Recent brain imaging studies have shown increased limbic system activation in response to various dyspneogenic stimuli and emphasize the affective dimension of this symptom. All of these mechanisms are likely instrumental in exertional dyspnea causation in COPD. Increased central motor drive (and effort) is required to increase ventilation during activity because the inspiratory muscles become acutely overloaded and functionally weakened. Abnormal dynamic ventilatory mechanics and excessive chemostimulation during exercise also result in a widening disparity between escalating central neural drive and restricted thoracic volume displacement. This neuromechanical uncoupling may form the basis for the distressing sensation of unsatisfied inspiration. Interventions that alleviate dyspnea in COPD do so by improving ventilatory mechanics, reducing central neural drive, or both-thereby partially restoring neuromechanical coupling of the respiratory system. Self-management strategies address the affective aspect of dyspnea and are essential to successful treatment.
有效管理慢性阻塞性肺疾病（COPD）中的呼吸困难需要更清楚地了解其潜在机制。本次圆桌会议回顾了目前关于呼吸困难神经生理学的已知知识，目的是将这些知识应用于临床实践。呼吸困难不是单一的感觉，有多种定性描述。呼吸困难的主要来源包括：（1）来自多个躯体本体感觉和支气管肺传入神经的输入，以及（2）与吸气运动指令输出或努力相关的中枢产生的信号。导致延髓呼吸运动放电与外周机械感受器传入反馈不匹配的呼吸紊乱会引发令人痛苦的呼吸冲动，这与肌肉努力无关。最近的脑成像研究表明，边缘系统在对各种致呼吸困难刺激的反应中激活增加，并强调了该症状的情感维度。所有这些机制可能在COPD运动性呼吸困难的病因中起作用。在活动期间增加通气需要增加中枢运动驱动（和努力），因为吸气肌会急性过载并功能减弱。运动期间异常的动态通气力学和过度的化学刺激也会导致不断升级的中枢神经驱动与受限的胸廓容积位移之间的差距扩大。这种神经机械解耦可能是未满足吸气的痛苦感觉的基础。缓解COPD中呼吸困难的干预措施是通过改善通气力学、减少中枢神经驱动或两者兼而有之——从而部分恢复呼吸系统的神经机械耦合。自我管理策略解决了呼吸困难中的情感方面，对成功治疗至关重要。
