Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia, Kelowna, British Columbia, Canada.
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). 2017 Nov 1;123(5):1110-1117. doi: 10.1152/japplphysiol.01109.2016. Epub 2017 Jul 20.
Volume loading increases left ventricular (LV) stroke volume (LVSV) through series interaction, but may paradoxically reduce LVSV in the presence of large increases in right ventricular (RV) afterload because of direct ventricular interaction (DVI). RV afterload is often increased in chronic obstructive pulmonary disease (COPD) as a result of pathological changes to respiratory mechanics, namely increased negative intrathoracic pressure (nITP), dynamic lung hyperinflation (DH), and increased pulmonary vascular resistance (PVR). These hallmarks of COPD negatively impact LV hemodynamics in normovolemia. However, it is unknown how these heart-lung interactions are impacted by acute volume loading. Twenty healthy subjects (23 ± 2 yr) completed the study protocol, involving acute volume loading via 20° head-down tilt (HDT) in isolation and with ) inspiratory resistance of -20 cmHO (HDT+nITP) and ) nITP, expiratory resistance to induce DH and hypoxic-mediated increases in PVR (HDT+COPD model). LV volumes and geometry were assessed using triplane echocardiography. HDT significantly increased LVSV by 10 ± 10% through an 8 ± 6% increase in LV end-diastolic volume (LVEDV). HDT+nITP paradoxically decreased LVSV by 11 ± 12% and LVEDV by 6 ± 9% from supine baseline, or -14 ± 10% LVSV and -15 ± 13% LVEDV from HDT ( < 0.001). HDT+COPD model decreased LVSV (21 ± 10% and 28 ± 11%) and LVEDV (16 ± 10% and 22 ± 10%) from both supine and HDT, respectively ( < 0.001). Under all conditions, significant septal flattening (increased radius of septal curvature) occurred, indicating DVI. Thus, when RV afterload is increased and/or an external constraint to ventricular filling exists, acute volume loading appears to paradoxically reduce LVSV. These findings have important implications for understanding how volume status impacts cardiopulmonary interactions in COPD. Volume loading may exacerbate adverse cardiopulmonary interaction in COPD; however, the mechanisms remain unclear. We found that when negative intrathoracic pressure is increased, acute volume loading paradoxically reduces stroke volume. This reduction in stroke volume is considerably greater in a model of COPD, owing to the effects of lung hyperinflation.
容量负荷通过串联相互作用增加左心室（LV）的每搏量（LVSV），但由于直接心室相互作用（DVI），在右心室（RV）后负荷大幅增加的情况下，LVSV 可能会出现矛盾性降低。慢性阻塞性肺疾病（COPD）中，由于呼吸力学的病理变化，RV 后负荷通常会增加，具体表现为胸腔内负压（nITP）增加、动态肺过度充气（DH）和肺血管阻力（PVR）增加。这些 COPD 的特征会对正常血容量下的 LV 血流动力学产生负面影响。然而，目前尚不清楚这些心肺相互作用如何受到急性容量负荷的影响。20 名健康受试者（23±2 岁）完成了该研究方案，方案涉及通过 20°头低位倾斜（HDT）单独和与吸气阻力 -20 cmH2O（HDT+nITP）和 nITP、呼气阻力诱导 DH 和低氧介导的 PVR 增加（HDT+COPD 模型）进行急性容量负荷。使用三平面超声心动图评估 LV 容积和几何结构。HDT 通过 LV 舒张末期容积（LVEDV）增加 8±6%，使 LVSV 增加 10±10%。HDT+nITP 从仰卧位基线使 LVSV 减少 11±12%和 LVEDV 减少 6±9%，或从 HDT 使 LVSV 减少 14±10%和 LVEDV 减少 15±13%（<0.001）。HDT+COPD 模型使 LVSV（21±10%和 28±11%）和 LVEDV（16±10%和 22±10%）分别从仰卧位和 HDT 减少（<0.001）。在所有情况下，均出现明显的室间隔变平（增加室间隔曲率半径），表明存在 DVI。因此，当 RV 后负荷增加和/或存在对心室充盈的外部限制时，急性容量负荷似乎会使 LVSV 出现矛盾性减少。这些发现对于理解容量状态如何影响 COPD 中的心肺相互作用具有重要意义。容量负荷可能会使 COPD 中的不利心肺相互作用恶化；然而，其机制尚不清楚。我们发现，当胸腔内负压增加时，急性容量负荷会使每搏量出现矛盾性减少。在 COPD 模型中，这种每搏量的减少幅度要大得多，这是由于肺过度充气的影响。
