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Isolated post-capillary pulmonary hypertension (Ipc-PH) occurs due to leftheart failure, which contributes to 1 out of every 9 deaths in the UnitedStates. In some patients, through unknown mechanisms, Ipc-PH transitions tocombined pre-/post-capillary PH (Cpc-PH), diagnosed by an increase in pulmonaryvascular resistance and associated with a dramatic increase in mortality. Wehypothesize that altered mechanical forces and subsequent vasoactive signalingin the pulmonary capillary bed drive the transition from Ipc-PH to Cpc-PH.However, even in a healthy pulmonary circulation, the mechanical forces in thesmallest vessels (the arterioles, venules, and capillary bed) have not beenquantitatively defined. This study is the first to examine this question via acomputational fluid dynamics model of the human pulmonary arteries, veins,arterioles, and venules. Using this model we predict temporal and spatialdynamics of cyclic stretch and wall shear stress. In the large vessels,numerical simulations show that shear stress increases coincides with largerflow and pressure. In the microvasculature, we found that as vessel radiusdecreases, shear stress increases and flow decreases. In arterioles, thiscorresponds with lower pressures; however, the venules and smaller veins havehigher pressure than larger veins. Our model provides predictions for pressure,flow, shear stress, and cyclic stretch that provides a way to analyze andinvestigate hypotheses related to disease progression in the pulmonarycirculation.

Numerical predictions of shear stress and cyclic stretch in the healthy pulmonary vasculature