Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota.
J Appl Physiol (1985). 2019 Sep 1;127(3):691-697. doi: 10.1152/japplphysiol.00877.2018. Epub 2019 Jul 11.
It is unknown whether central hemodynamics are impaired during exercise in chronic obstructive pulmonary disease (COPD) patients. We hypothesized that, at a similar absolute V̇o during exercise, COPD patients would have a lower stroke volume and cardiac output compared with healthy controls. Furthermore, we hypothesized that greater static hyperinflation [ratio of inspiratory capacity to total lung capacity (IC/TLC)] and expiratory intrathoracic pressure would be significantly related to the lower cardiac output and stroke volume responses in COPD patients. Clinically stable COPD ( = 13; FEV/FVC: 52 ± 13%) and controls ( = 10) performed constant workload submaximal exercise at an absolute V̇o of ~1.3 L/min. During exercise, inspiratory capacity maneuvers were performed to determine operating lung volumes and cardiac output (via open-circuit acetylene rebreathe technique) and esophageal pressure were measured. At similar absolute V̇o during exercise ( = 0.81), COPD had lower cardiac output than controls (COPD: 11.0 ± 1.6 vs. control: 12.2 ± 1.2 L/min, = 0.03) due to a lower stroke volume (COPD: 107 ± 13 vs. control: 119 ± 19 mL, = 0.04). The heart rate response during exercise was not different between groups ( = 0.66). FEV (%predicted) and IC/TLC were positively related to stroke volume ( = 0.68, = 0.01 and = 0.77, < 0.01). Last, esophageal pressure-time integral during inspiration was positively related to cardiac output ( = 0.56, = 0.047). These data demonstrate that COPD patients have attenuated cardiac output and stroke volume responses during exercise compared with control. Furthermore, these data suggest that the COPD patients with the most severe hyperinflation and more negative inspiratory intrathoracic pressures have the most impaired central hemodynamic responses. Chronic obstructive pulmonary disease leads to cardiac structural changes and pulmonary derangements that impact the integrative response to exercise. However, it is unknown whether these pathophysiological alterations influence the cardiac response during exercise. Herein, we demonstrate that COPD patients exhibit impaired central hemodynamics during exercise that are worsened with greater hyperinflation.
在慢性阻塞性肺疾病（COPD）患者的运动过程中，中心血液动力学是否受损尚不清楚。我们假设，在运动过程中相同的绝对 V̇o 下，COPD 患者的每搏量和心输出量会低于健康对照组。此外，我们还假设更大的静态过度充气[吸气容量与总肺容量之比（IC/TLC）]和呼气胸内压与 COPD 患者心输出量和每搏量反应降低有显著关系。13 例临床稳定的 COPD 患者（FEV/FVC：52 ± 13%）和 10 例对照组完成了绝对 V̇o 约为 1.3 L/min 的亚最大负荷恒功运动。运动过程中，通过开路乙炔再呼吸技术进行吸气容量操作以确定工作肺容量和心输出量，同时测量食管压力。在运动过程中（ = 0.81），COPD 患者的绝对 V̇o 相似，但心输出量低于对照组（COPD：11.0 ± 1.6 对对照组：12.2 ± 1.2 L/min， = 0.03），这是由于每搏量较低（COPD：107 ± 13 对对照组：119 ± 19 mL， = 0.04）。两组间运动时心率反应无差异（ = 0.66）。FEV（%预测值）和 IC/TLC 与每搏量呈正相关（ = 0.68， = 0.01 和 = 0.77， < 0.01）。最后，吸气时食管压力时间积分与心输出量呈正相关（ = 0.56， = 0.047）。这些数据表明，与对照组相比，COPD 患者在运动过程中心输出量和每搏量反应减弱。此外，这些数据表明，过度充气和更负的吸气胸内压最严重的 COPD 患者中心血液动力学反应受损最严重。慢性阻塞性肺疾病导致心脏结构改变和肺部紊乱，影响对运动的整合反应。然而，尚不清楚这些病理生理改变是否会影响运动时的心脏反应。在此，我们证明 COPD 患者在运动过程中存在中心血液动力学障碍，随着过度充气的加重而恶化。
