Pulmonary Function and Clinical Exercise Physiology Unit (SEFICE), Division of Respirology, Federal University of Sao Paulo, Sao Paulo, Brazil.
Division of Cardiology, Federal University of Sao Paulo, Sao Paulo, Brazil.
Eur Respir J. 2019 Apr 18;53(4). doi: 10.1183/13993003.02386-2018. Print 2019 Apr.
Impaired aerobic function is a potential mechanism of exercise intolerance in patients with combined cardiorespiratory disease. We investigated the pathophysiological and sensory consequences of a low change in oxygen uptake (Δ' )/change in work rate (ΔWR) relationship during incremental exercise in patients with coexisting chronic obstructive pulmonary disease (COPD) and systolic heart failure (HF).After clinical stabilisation, 51 COPD-HF patients performed an incremental cardiopulmonary exercise test to symptom limitation. Cardiac output was non-invasively measured (impedance cardiography) in a subset of patients (n=18).27 patients presented with Δ' /ΔWR below the lower limit of normal. Despite similar forced expiratory volume in 1 s and ejection fraction, the low Δ' /ΔWR group showed higher end-diastolic volume, lower inspiratory capacity and lower transfer factor compared to their counterparts (p<0.05). Peak WR and peak ' were ∼15% and ∼30% lower, respectively, in the former group: those findings were associated with greater symptom burden in daily life and at a given exercise intensity (leg discomfort and dyspnoea). The low Δ' /ΔWR group presented with other evidences of impaired aerobic function (sluggish ' kinetics, earlier anaerobic threshold) and cardiocirculatory performance (lower oxygen pulse, lower stroke volume and cardiac output) (p<0.05). Despite similar exertional hypoxaemia, they showed worse ventilatory inefficiency and higher operating lung volumes, which led to greater mechanical inspiratory constraints (p<0.05).Impaired aerobic function due to negative cardiopulmonary-muscular interactions is an important determinant of exercise intolerance in patients with COPD-HF. Treatment strategies to improve oxygen delivery to and/or utilisation by the peripheral muscles might prove particularly beneficial to these patients.
有氧功能受损是合并心肺疾病患者运动不耐受的潜在机制。我们研究了同时患有慢性阻塞性肺疾病(COPD)和收缩性心力衰竭(HF)的患者在递增运动中摄氧量(Δ' )/做功率(ΔWR)变化关系中低变化的病理生理和感觉后果。
在临床稳定后,51 名 COPD-HF 患者进行了递增心肺运动测试至症状限制。在一组患者(n=18)中,非侵入性测量心输出量(阻抗心动图)。27 名患者的 Δ' /ΔWR 低于正常下限。尽管 1 秒用力呼气量和射血分数相似,但低 Δ' /ΔWR 组的舒张末期容积较高,吸气量较低,转移因子较低(p<0.05)。在前一组中,峰值 WR 和峰值 '分别降低了约 15%和 30%:这些发现与日常生活和给定运动强度下更大的症状负担相关(腿部不适和呼吸困难)。低 Δ' /ΔWR 组还表现出其他有氧功能受损的证据('动力学迟缓,无氧阈值更早)和心肺循环性能下降(氧脉冲降低,每搏量和心输出量降低)(p<0.05)。尽管运动性低氧血症相似,他们表现出更差的通气效率和更高的工作肺容积,导致更大的机械吸气限制(p<0.05)。
由于心肺-肌肉相互作用的负性,有氧功能受损是 COPD-HF 患者运动不耐受的重要决定因素。改善外周肌肉供氧和/或利用的治疗策略可能对这些患者特别有益。