The haemodynamic response to incremental increases in negative intrathoracic pressure in healthy humans

Abstract

New findings: What is the central question of this study? The haemodynamic response to incremental increases in negative intrathoracic pressure (nITP) during spontaneous breathing and the mechanisms of cardiac impairment at these levels of nITP remain unclear. What is the main finding and its importance? nITP of -20 cmH₂ O or greater reduces stroke volume in healthy, spontaneously breathing supine humans due to direct ventricular interaction and increased left ventricular afterload.

Abstract: Negative intrathoracic pressure (nITP) generally augments venous return and left ventricular (LV) stroke volume (LVSV), though large increases in nITP, commonly seen in respiratory disease, attenuate LVSV. Despite this consistent finding, the degree of nITP required to reduce LVSV and the contributions of series and direct ventricular interaction (DVI) in mediating this response remain unclear. We hypothesized that nITP ≤-15 cmH₂ O would augment LVSV, while nITP ≥-20 cmH₂ O would reduce LVSV via DVI and increased afterload. Twenty-three healthy subjects were randomly given inspiratory loads during spontaneous breathing to generate -5, -10, -15, -20 and -25 cmH₂ O. LV volumes, LV geometry, inferior vena cava collapsibility (cIVC) and LV end-systolic meridional wall-stress (LVESMWS) were assessed in the supine position using tri-plane echocardiography. LVSV remained unchanged up to -15 cmH₂ O, but was significantly reduced at nITP ≥-20 cmH₂ O (-12 ± 8% and -15 ± 11% at -20 and -25 cmH₂ O, respectively, P < 0.05) due to significant reductions in LV end-diastolic volume (LVEDV), while LV end-systolic volume was unchanged. cIVC on inspiration was significantly increased at all levels of nITP, while LVESMWS only increased at -25 cmH₂ O (P < 0.05). DVI, as indicated by a significant increase in the radius of septal curvature, occurred at nITP ≥-10 cmH₂ O. In supine healthy humans, nITP ≤-15 cmH₂ O does not significantly affect LV function, despite increased DVI. In contrast, nITP ≥-20 cmH₂ O causes significant reductions in LVSV and LVEDV, which appear to be mediated by DVI and increased afterload at -25 cmH₂ O. The impact of cIVC during nITP remains unclear.

Keywords: direct ventricular interaction; echocardiography; intrathoracic pressure.