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

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 cmH O would augment LVSV, while nITP ≥-20 cmH 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 cmH 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 cmH O, but was significantly reduced at nITP ≥-20 cmH O (-12 ± 8% and -15 ± 11% at -20 and -25 cmH 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 cmH O (P < 0.05). DVI, as indicated by a significant increase in the radius of septal curvature, occurred at nITP ≥-10 cmH O. In supine healthy humans, nITP ≤-15 cmH O does not significantly affect LV function, despite increased DVI. In contrast, nITP ≥-20 cmH O causes significant reductions in LVSV and LVEDV, which appear to be mediated by DVI and increased afterload at -25 cmH O. The impact of cIVC during nITP remains unclear.

Priming the cardiodynamic phase of pulmonary oxygen uptake through voluntary modulations of the respiratory pump at the onset of exercise

“…We speculate that the lower P oes induced by the recruitment of the inspiratory rib cage muscles in RC caused a greater accumulation of blood into the highly compliant pulmonary vasculature compared to AB and SP (Flamm et al., 1990). In support, others showed that inspiratory loading eliciting end‐inspiratory P oes below −20 cmH 2 O resulted in greater right ventricular filling, as evidenced by an increase in the radius of the septal curvature (Cheyne et al., 2018). Interestingly, this led to a decrease in left ventricular filling by direct ventricular interaction, indicated by the decrease in left ventricular SV (Cheyne et al., 2016, 2018).…”

“…In support, others showed that inspiratory loading eliciting end‐inspiratory P oes below −20 cmH 2 O resulted in greater right ventricular filling, as evidenced by an increase in the radius of the septal curvature (Cheyne et al., 2018). Interestingly, this led to a decrease in left ventricular filling by direct ventricular interaction, indicated by the decrease in left ventricular SV (Cheyne et al., 2016, 2018).…”

Mechanisms of inspiration that modulate cardiovascular control: the other side of breathing

“…As such, the impact of breathing through additional resistances as described in this review paper are in addition to this intrinsic resistance. Contrary to observations that indicate a positive influence of reduced ITP on cardiac function and circulation, there are other reports that large reductions in ITP (i.e., Ͼ20 cmH 2 O) have resulted in adverse hemodynamic effects such as increased left ventricular transmural pressure gradient or afterload (37,64,69), limited flow in the inferior vena cava (9,40,55), reduced cardiac filling (8), compromised left ventricular geometry and function (35), and lower stroke volume (7,8,80). The latter observations are associated with the physiology of individuals who create large negative "swings" in ITP during inspiration such as healthy subjects performing a sustained Mueller maneuver (5,68,69,76,77) or the pathophysiology of patients with heart failure, chronic obstructive lung disease, and asthma (5,43,58,67).…”

Hemodynamic effects of incremental lung hyperinflation

“…This study was designed and performed as an independent study but used the same subjects as a previous investigation (16). Subjects (11 men and 12 women) were 22 Ϯ 2 yr old with a body mass index of 22.4 Ϯ 2.2 kg/m 2 , forced vital capacity of 4.83 Ϯ 0.87 l [104 Ϯ 7%predicted (%pred)], forced expiratory volume in 1 s of 4.00 Ϯ 0.68 l (101 Ϯ 8%pred), total lung capacity of 5.99 Ϯ 1.00 l (97 Ϯ 7%pred), residual volume/total lung capacity of 23 Ϯ 6% (96 Ϯ 23%pred), and IC of 3.08 Ϯ 0.62 l (100 Ϯ 14%pred).…”