Clinical Exercise Physiology and Respiratory Investigation Unit, Division of Respiratory and Critical Care Medicine, Dept of Medicine, Queen's University and Kingston Health Sciences Centre, Kingston, ON, Canada
Clinical Exercise Physiology and Respiratory Investigation Unit, Division of Respiratory and Critical Care Medicine, Dept of Medicine, Queen's University and Kingston Health Sciences Centre, Kingston, ON, Canada.
Eur Respir J. 2022 Nov 17;60(5). doi: 10.1183/13993003.00144-2022. Print 2022 Nov.
Increased ventilation relative to metabolic demands, indicating alveolar hyperventilation and/or increased physiological dead space (excess ventilation), is a key cause of exertional dyspnoea. Excess ventilation has assumed a prominent role in the functional assessment of patients with heart failure (HF) with reduced (HFrEF) or preserved (HFpEF) ejection fraction, pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH). We herein provide the key pieces of information to the caring physician to 1) gain unique insights into the seeds of patients' shortness of breath and 2) develop a rationale for therapeutically lessening excess ventilation to mitigate this distressing symptom. Reduced bulk oxygen transfer induced by cardiac output limitation and/or right ventricle-pulmonary arterial uncoupling increase neurochemical afferent stimulation and (largely chemo-) receptor sensitivity, leading to alveolar hyperventilation in HFrEF, PAH and small-vessel, distal CTEPH. As such, interventions geared to improve central haemodynamics and/or reduce chemosensitivity have been particularly effective in lessening their excess ventilation. In contrast, 1) high filling pressures in HFpEF and 2) impaired lung perfusion leading to ventilation/perfusion mismatch in proximal CTEPH conspire to increase physiological dead space. Accordingly, 1) decreasing pulmonary capillary pressures and 2) mechanically unclogging larger pulmonary vessels (pulmonary endarterectomy and balloon pulmonary angioplasty) have been associated with larger decrements in excess ventilation. Exercise training has a strong beneficial effect across diseases. Addressing some major unanswered questions on the link of excess ventilation with exertional dyspnoea under the modulating influence of pharmacological and nonpharmacological interventions might prove instrumental to alleviate the devastating consequences of these prevalent diseases.
相对于代谢需求而言，通气增加表明肺泡过度通气和/或生理性死腔增加（过度通气），这是运动性呼吸困难的一个关键原因。过度通气在射血分数降低（HFrEF）或保留（HFpEF）、肺动脉高压（PAH）和慢性血栓栓塞性肺动脉高压（CTEPH）的心力衰竭（HF）患者的功能评估中发挥了重要作用。我们在此为有需要的医生提供关键信息，以 1）深入了解患者呼吸困难的根源，2）制定合理的治疗方案，减少过度通气，减轻这种令人痛苦的症状。心输出量受限和/或右心室-肺动脉解偶联导致的氧气转移量减少，增加了神经化学传入刺激和（主要是化学）受体敏感性，导致 HFrEF、PAH 和小血管、远端 CTEPH 发生肺泡过度通气。因此，旨在改善中心血液动力学和/或降低化学敏感性的干预措施在减轻其过度通气方面特别有效。相比之下，1）HFpEF 中的高充盈压和 2）导致近端 CTEPH 通气/灌注不匹配的肺灌注受损，都会增加生理性死腔。因此，1）降低肺毛细血管压力和 2）通过机械方法疏通较大的肺血管（肺动脉内膜切除术和球囊肺动脉血管成形术）与过度通气的减少幅度更大有关。运动训练在各种疾病中都有很强的有益作用。在药物和非药物干预的调节影响下，解决过度通气与运动性呼吸困难之间联系的一些重大未解决问题，可能有助于减轻这些常见疾病的灾难性后果。
