  Isolated post-capillary pulmonary hypertension (Ipc-PH) occurs due to left
heart failure, which contributes to 1 out of every 9 deaths in the United
States. In some patients, through unknown mechanisms, Ipc-PH transitions to
combined pre-/post-capillary PH (Cpc-PH), diagnosed by an increase in pulmonary
vascular resistance and associated with a dramatic increase in mortality. We
hypothesize that altered mechanical forces and subsequent vasoactive signaling
in the pulmonary capillary bed drive the transition from Ipc-PH to Cpc-PH.
However, even in a healthy pulmonary circulation, the mechanical forces in the
smallest vessels (the arterioles, venules, and capillary bed) have not been
quantitatively defined. This study is the first to examine this question via a
computational fluid dynamics model of the human pulmonary arteries, veins,
arterioles, and venules. Using this model we predict temporal and spatial
dynamics of cyclic stretch and wall shear stress. In the large vessels,
numerical simulations show that shear stress increases coincides with larger
flow and pressure. In the microvasculature, we found that as vessel radius
decreases, shear stress increases and flow decreases. In arterioles, this
corresponds with lower pressures; however, the venules and smaller veins have
higher pressure than larger veins. Our model provides predictions for pressure,
flow, shear stress, and cyclic stretch that provides a way to analyze and
investigate hypotheses related to disease progression in the pulmonary
circulation.
