RESUMO
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 cmH2O nITP and 25% DH) and severe (-20 cmH2O nITP and 100% DH) ABM, without and with postexercise ischemia (PEI) at each severity. LV SV, chamber geometry, end-systolic elastance (Ees), arterial elastance (Ea), and ventricular-vascular coupling (Ees:Ea) 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) (P < 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 (P < 0.001). Compared with control (1.99 ± 0.41 mmHg/mL), Ea increased progressively with mild ABM (2.21 ± 0.47 mmHg/mL) and severe ABM (2.50 ± 0.56 mmHg/mL); at each severity, Ea was greater with superimposed PEI (P < 0.001). However, well-matched Ees increases occurred, and Ees:Ea 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.NEW & NOTEWORTHY 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.
