Systolic Reserve Maintains Left Ventricular-Vascular Coupling When Challenged by Adverse Breathing Mechanics and Hypertension in Healthy Adults.

Augmented negative intrathoracic pressures (nITP) and dynamic hyperinflation (DH) are adverse breathing mechanics (ABM) associated with chronic obstructive pulmonary disease 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 (10M/9F, 24±3 years) were challenged with Mild (-10cmH2O nITP and 25% DH) and Severe (-20cmH2O nITP and 100% DH) ABM, without and with post-exercise ischemia (PEI) at each severity. LV SV, chamber geometry, and end-systolic elastance (Ees), arterial elastance (Ea), and ventricular-vascular coupling (Ees:Ea) were quantified using echocardiography. Compared to resting Control (58±13mL), SV decreased during Mild ABM (51±13mL), Mild ABM+PEI (51±11mL), Severe ABM (50±12mL), and Severe ABM+PEI (47±11mL) (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 to Control (1.99±0.41mmHg/mL), Ea increased progressively with Mild ABM (2.21±0.47mmHg/mL) and Severe ABM (2.50±0.56mmHg/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 reserveto maintain coupling.