Thesis Defence: Lung Volumes and Their Effect on Central Hemodynamics

Jiawen Lim, supervised by Dr. Neil Eves, will defend their thesis titled “Lung Volumes and Their Effect on Central Hemodynamics” in partial fulfillment of the requirements for the degree of Master of Science in Health and Exercise Science.

An abstract for Jiawen Lim’s thesis is included below.

Defences are open to all members of the campus community as well as the general public. Registration is not required for in-person defences.

Abstract

Changes in lung volumes during breathing; at rest, exercise or in disease, alter pulmonary vascular resistance and challenge central hemodynamics. However, it is currently unknown how changes in the different components of operational lung volumes (i.e. altering end inspiratory or end expiratory lung volume [EILV, EELV] or tidal volume [Vt]) specifically modify left ventricle [LV]) function. Twenty-five healthy individuals (14:11 F:M) performed an experimental visit with measures obtained during resting breathing followed by 5 randomized breathing challenges. Each challenge was performed with controlled Vt, breathing frequency, operational lung volumes and duty cycle while 2D echocardiographic imaging of LV end diastolic (LVEDV), end systolic (LVESV) and stroke volume (LVSV) were obtained. Images were also collected for analysis of LV geometry while tissue Doppler imaging and transmitral Doppler were obtained to assess LV myocardial function and filling. Increasing EELV, with Vt at resting levels and EILV reaching critical inspiratory reserve volume (cIRV i.e.~90%TLC) decreased LVEDV (107±24 vs.102±29ml) and LVSV (66±12 vs. 63±12ml, p<0.05), compared to resting breathing. The changes in central hemodynamics with this breathing pattern were also different from increasing EILV (below cIRV) with an unchanged EELV (p<0.05). Free wall curvature increased from baseline (p=0.03) with the elevated EELV and EILV while lateral E’ and E/A ratio both decreased (p=0.001, p=0.018). Central hemodynamics were unchanged from resting breathing when increasing EILV solely through altering Vt (even when EILV reached cIRV), but lateral E’ decreased (p=0.001). During simulated exercise hyperpnea with a mild increase in EELV with EILV reaching cIRV LVEDV (102±29 vs. 93±26ml), LVESV (42±12 vs. 37±12ml) and SV (66±12 vs. 57±14ml) were reduced (p<0.05, for all) compared to baseline, but not when breathing with a similar pattern with EELV below FRC and EILV below cIRV. Lateral E’ and E/A ratio was reduced in both hyperpnea conditions (p<0.05). Our data demonstrates that increases in EILV and Vt appear to have little effect on central hemodynamics, unless EELV rises above FRC. Increasing EELV, likely reduces LVEDV through both series and direct ventricular interaction associated with external constraint of the LV, altering LV filling and relaxation.