James Matthew D, Phillips Devin B, Domnik Nicolle J, Neder J Alberto
Respiratory Investigation Unit, Division of Respirology, Department of Medicine, Queen's University, Kingston, ON, Canada.
Respiratory Investigation Unit, Division of Respirology, Department of Medicine, Queen's University, Kingston, ON, Canada; School of Kinesiology and Health Science and Muscle Health Research Center, York University, Toronto, ON, Canada.
Respir Physiol Neurobiol. 2025 Aug-Sep;336:104423. doi: 10.1016/j.resp.2025.104423. Epub 2025 Mar 29.
Physical activity is a leading trigger of dyspnea in chronic cardiopulmonary diseases. Recently, there has been a renewed interest in uncovering the mechanisms underlying this distressing symptom. We start by articulating a conceptual framework linking cardiorespiratory abnormalities with the central perception of undesirable respiratory sensations during exercise. We specifically emphasize that exertional dyspnea ultimately reflects an imbalance between (high) demand and (low) capacity. As such, the symptom arises in the presence of a heightened inspiratory neural drive - the will to breathe - secondary to a) increased ventilatory output relative to the instantaneous ventilatory capacity (excessive breathing) and/or b) its impeded translation into the act of breathing due to constraints on tidal volume expansion (constrained breathing). In patients with chronic obstructive pulmonary disease (COPD), asthma, cystic fibrosis, and interstitial lung disease (ILD), constrained breathing assumes a more dominant role as the disease progresses. Excessive breathing due to heightened wasted ventilation in the physiological dead space is particularly important in the initial stages of COPD, while alveolar hyperventilation has a major contributory role in hypoxemic patients with ILD. Hyperventilation is also a leading driver of dyspnea in heart failure (HF) with reduced ejection fraction (EF), while high physiological dead space is the main underlying mechanism in HF with preserved EF. Similarly, wasted ventilation in poorly perfused lung tissue dominates the scene in pulmonary vascular disease. New artificial intelligence-based approaches to expose the contribution of excessive and constrained breathing may enhance the yield of cardiopulmonary exercise testing in investigating exertional dyspnea in these patients.
体力活动是慢性心肺疾病中呼吸困难的主要诱因。最近，人们对揭示这一令人痛苦症状背后的机制重新产生了兴趣。我们首先阐述一个概念框架，将心肺异常与运动期间对不良呼吸感觉的中枢感知联系起来。我们特别强调，运动性呼吸困难最终反映了（高）需求与（低）能力之间的失衡。因此，该症状出现在吸气神经驱动力增强（呼吸意愿）的情况下，这继发于以下两种情况：a）相对于瞬时通气能力，通气输出增加（过度呼吸）和/或b）由于潮气量扩张受限（受限呼吸），其转化为呼吸动作受到阻碍。在慢性阻塞性肺疾病（COPD）、哮喘、囊性纤维化和间质性肺疾病（ILD）患者中，随着疾病进展，受限呼吸起更主要的作用。在COPD的初始阶段，由于生理死腔内无效通气增加导致的过度呼吸尤为重要，而肺泡过度通气在低氧血症的ILD患者中起主要作用。在射血分数降低（EF）的心力衰竭（HF）中，过度通气也是呼吸困难的主要驱动因素，而在射血分数保留的HF中，高生理死腔是主要的潜在机制。同样，在肺血管疾病中，灌注不良的肺组织中的无效通气占主导地位。基于人工智能的新方法来揭示过度呼吸和受限呼吸的作用，可能会提高心肺运动试验在研究这些患者运动性呼吸困难中的价值。
