Multiscale hemodynamics model for the pulmonary arteries, arterioles, capillaries, venules and veins
Abstract
This study presents the first mathematical model of pulsatile hemodynamics that encompasses the complete pulmonary circulation, explicitly linking the large arteries, arterioles, capillaries, venules, and large veins. To overcome the limitations of previous models that exclude explicit capillary dynamics, we incorporate a one-dimensional structured-tree model of the pulmonary arteries and veins with a dynamic capillary sheet model. This approach establishes a recursive method for coupling the capillary sheets to the structured trees, connecting arterioles and venules in a ladder-like architecture. To evaluate the impact of incorporating this capillary structure, we compare simulated hemodynamics in a healthy control subject and a pulmonary hypertension (PH) patient. Results illustrate that including capillaries in the model significantly alters hemodynamic predictions by introducing downstream damping. In the healthy control subject, the inclusion of the capillary network attenuates pulsatile energy, yielding the expected steady venous pressure and flow profiles, whereas omitting the capillaries results in an unphysiological high pulsatility transmitting into the venous system. The structural impact of the capillaries is even more pronounced in the PH patient, where explicitly modeling the capillary bed corrects an over-prediction in peak systolic pressure in the main pulmonary artery. Furthermore, unlike the healthy control subject, the remodeled PH microvasculature fails to completely isolate the venous system from arterial pulsations. Finally, we employ parametric sensitivity analysis to investigate how specific biomechanical factors drive vascular remodeling, demonstrating the framework's capability to quantify disease progression and severity.
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BibTeX
@misc{bartolo2026multiscale,
title = {{Multiscale hemodynamics model for the pulmonary arteries, arterioles, capillaries, venules and veins}},
author = {Michelle A Bartolo and Mansoor A Haider and Nicholas A Hill and Mette S Olufsen},
howpublished = {arXiv},
year = {2026},
month = oct,
doi = {10.48550/arxiv.2607.19269},
eprint = {2607.19269},
archivePrefix = {arXiv},
url = {https://arxiv.org/abs/2607.19269},
}
RIS
TY - UNPB
TI - Multiscale hemodynamics model for the pulmonary arteries, arterioles, capillaries, venules and veins
AU - Michelle A Bartolo
AU - Mansoor A Haider
AU - Nicholas A Hill
AU - Mette S Olufsen
PY - 2026
DA - 2026/10/22
PB - arXiv
DO - 10.48550/arxiv.2607.19269
UR - https://arxiv.org/abs/2607.19269
AB - This study presents the first mathematical model of pulsatile hemodynamics that encompasses the complete pulmonary circulation, explicitly linking the large arteries, arterioles, capillaries, venules, and large veins. To overcome the limitations of previous models that exclude explicit capillary dynamics, we incorporate a one-dimensional structured-tree model of the pulmonary arteries and veins with a dynamic capillary sheet model. This approach establishes a recursive method for coupling the capillary sheets to the structured trees, connecting arterioles and venules in a ladder-like architecture. To evaluate the impact of incorporating this capillary structure, we compare simulated hemodynamics in a healthy control subject and a pulmonary hypertension (PH) patient. Results illustrate that including capillaries in the model significantly alters hemodynamic predictions by introducing downstream damping. In the healthy control subject, the inclusion of the capillary network attenuates pulsatile energy, yielding the expected steady venous pressure and flow profiles, whereas omitting the capillaries results in an unphysiological high pulsatility transmitting into the venous system. The structural impact of the capillaries is even more pronounced in the PH patient, where explicitly modeling the capillary bed corrects an over-prediction in peak systolic pressure in the main pulmonary artery. Furthermore, unlike the healthy control subject, the remodeled PH microvasculature fails to completely isolate the venous system from arterial pulsations. Finally, we employ parametric sensitivity analysis to investigate how specific biomechanical factors drive vascular remodeling, demonstrating the framework's capability to quantify disease progression and severity.
ER -