Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia, Kelowna, British Columbia, Canada.
J Appl Physiol (1985). 2021 Apr 1;130(4):1171-1182. doi: 10.1152/japplphysiol.00833.2020. Epub 2021 Feb 11.
Augmented negative intrathoracic pressures (nITP) and dynamic hyperinflation (DH) are adverse breathing mechanics (ABM) associated with chronic obstructive pulmonary disease (COPD) that attenuate left ventricular (LV) preload and augment afterload. In COPD, hypertension (elevated systemic arterial load) commonly adds additional afterload to the LV. Combined ABM and hypertension may profoundly challenge ventricular-vascular coupling and attenuate stroke volume (SV), particularly if LV systolic reserve is limited. However, even in the healthy heart, the combined impact of ABM and systemic arterial loading on LV function and ventricular-vascular coupling has not been fully elucidated. Healthy volunteers (10 M/9 F, 24 ± 3 yr old) were challenged with mild (-10 cmHO nITP and 25% DH) and severe (-20 cmHO nITP and 100% DH) ABM, without and with postexercise ischemia (PEI) at each severity. LV SV, chamber geometry, end-systolic elastance (), arterial elastance (), and ventricular-vascular coupling (:) were quantified using echocardiography. Compared with resting control (58 ± 13 mL), SV decreased during mild ABM (51 ± 13 mL), mild ABM + PEI (51 ± 11 mL), severe ABM (50 ± 12 mL), and severe ABM + PEI (47 ± 11 mL) ( < 0.001); similar trends were observed for LV end-diastolic volume. The end-diastolic radius of septal curvature increased, indicating direct ventricular interaction, during severe ABM and severe ABM + PEI ( < 0.001). Compared with control (1.99 ± 0.41 mmHg/mL), increased progressively with mild ABM (2.21 ± 0.47 mmHg/mL) and severe ABM (2.50 ± 0.56 mmHg/mL); at each severity, was greater with superimposed PEI ( < 0.001). However, well-matched increases occurred, and : was unchanged throughout. ABM pose a challenge to ventricular-vascular coupling that is accentuated by superimposed PEI; however, in healthy younger adults, the LV has substantial systolic reserve to maintain coupling. In healthy younger adults, combined dynamic hyperinflation (DH) and negative intrathoracic pressures (nITP) attenuate left ventricular filling, but through different mechanisms at different severities. DH and nITP contribute to increased left ventricular afterload through mechanical effects in addition to presumed reflexive regulation, which can be further increased by elevated arterial loading. However, within this demographic, the left ventricle has substantial reserve to increase systolic performance, which matches contractility to afterload to preserve stroke volume.
增强的负胸腔内压力（nITP）和动态过度充气（DH）是与慢性阻塞性肺疾病（COPD）相关的不良呼吸力学（ABM），可减弱左心室（LV）前负荷并增加后负荷。在 COPD 中，高血压（全身动脉负荷升高）通常会给 LV 增加额外的后负荷。ABM 和高血压的联合作用可能会严重挑战心室血管耦联并减弱每搏量（SV），特别是在 LV 收缩储备有限的情况下。然而，即使在健康的心脏中，ABM 和全身动脉负荷对 LV 功能和心室血管耦联的综合影响也尚未完全阐明。健康志愿者（10 男/9 女，24 ± 3 岁）分别在轻度（-10 cmHO nITP 和 25%DH）和重度（-20 cmHO nITP 和 100%DH）ABM 下，以及在每种严重程度下进行运动后缺血（PEI）时，接受了挑战。使用超声心动图定量评估左心室 SV、腔室几何形状、收缩末期弹性（）、动脉弹性（）和心室血管耦联（：）。与静息对照（58 ± 13 mL）相比，轻度 ABM（51 ± 13 mL）、轻度 ABM+PEI（51 ± 11 mL）、重度 ABM（50 ± 12 mL）和重度 ABM+PEI（47 ± 11 mL）期间 SV 降低（<0.001）；LV 舒张末期容积也呈现出相似的趋势。在严重 ABM 和严重 ABM+PEI 期间，室间隔曲率的舒张末期半径增加，表明直接的心室相互作用（<0.001）。与对照（1.99 ± 0.41 mmHg/mL）相比，随着轻度 ABM（2.21 ± 0.47 mmHg/mL）和重度 ABM（2.50 ± 0.56 mmHg/mL），逐渐增加；在每种严重程度下，叠加 PEI 时（<0.001）更高。然而，相匹配的增加，并且：在整个过程中保持不变。ABM 对心室血管耦联构成挑战，叠加 PEI 会加剧这种挑战；然而，在健康的年轻成年人中，LV 具有很大的收缩储备来维持耦联。在健康的年轻成年人中，DH 和负胸腔内压力（nITP）联合减弱左心室充盈，但在不同严重程度下通过不同的机制。DH 和 nITP 通过机械效应除了假定的反射调节外，还会增加左心室后负荷，这可以通过升高的动脉负荷进一步增加。然而，在这一年龄段，左心室具有很大的储备来增加收缩性能，从而使收缩性与后负荷相匹配以维持每搏量。
