Hemodynamic effects of incremental dynamic hyperinflation

Abstract

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Dynamic hyperinflation (DH) is common in COPD and is often associated with exertional dyspnea. However, there is increasing evidence that DH may also impair hemodynamics via adverse cardiopulmonary interaction, though the mechanisms responsible remain unclear. As such, we examined the effect of incremental DH on left ventricular (LV) filling and ejection, and the role of direct ventricular interaction (DVI). We hypothesized that increasing DH would reduce LV end diastolic volume (LVEDV) and stroke volume (LVSV) due to DVI. 23 healthy subjects were randomly exposed to varying degrees of expiratory loading to induce DH such that end-expiratory lung volumes were increased by 25, 50, 75 and 100%, where 100% corresponded to an inspiratory reserve volume (IRV) of <0.5L. LV volumes, LV geometry, IVC collapsibility (cIVC) and LV end-systolic wall-stress (LVESWS) were assessed by tri-plane echocardiography. 25% DH reduced LVEDV (-6±5%) and LVSV (-9±8%). 50% DH elicited a similar response in LVEDV (-6±7%) and LVSV (-11±10%). 75% DH caused a larger reduction (-9±7% and -16±10%, respectively), which was associated with significant septal flattening as indicated by a 49±70% increase in the radius of septal curvature at end-diastole (RSC-ED). 100% DH caused the largest reduction in LVEDV and LVSV (-13±9% and -18±9%). 100% DH also caused the largest increase in RSC-ED (56±63%). cIVC, MAP and LV afterload (LVESWS) were unchanged at all levels of DH. Modest DH reduces LVSV due to under-filling of the LV, likely due to increased PVR. At higher levels of DH, DVI may be the primary cause of reduced LVSV, as indicated by septal flattening due to a greater relative increase in RV pressure and/or mediastinal constraint.