How does human blood rheology influence arterial and cardiovascular device hemodynamics? A comprehensive review, discussion, and future directions
Abstract
Human blood is a complex biological suspension whose macroscopic flow behaviour arises from the coupled microscopic dynamics of deformable blood cells, plasma proteins, and evolving cellular microstructures. As a result, blood exhibits a range of nonlinear rheological behaviours, including shear-thinning, viscoplasticity, viscoelasticity, and thixotropy, which strongly influence its physiological and clinical hemodynamics. This review provides a comprehensive assessment of the role of blood rheology in arterial and blood-contacting cardiovascular device flows, with particular emphasis on the extent to which different rheological characteristics alter clinically relevant flow quantities and on whether the conventional Newtonian approximation remains adequate for the analysis. The underlying physical mechanisms responsible for the major rheological behaviours of blood are first discussed, followed by a critical review of the constitutive models commonly employed in hemodynamic analysis, including generalised Newtonian, viscoelastic, and thixo-elasto-viscoplastic (TEVP) ones. The effects of blood rheology on arterial flows involving stenosis, bifurcation, and aneurysm under both steady and pulsatile flow conditions are subsequently reviewed and discussed in terms of several physiologically important parameters, such as pressure drop, flow resistance, wall shear stress, flow separation, and recirculation zone. The influence of blood rheology on cardiovascular devices, including prosthetic heart valves and stents, is also reviewed, particularly regarding flow stagnation, residence time, hemolysis, and thrombosis.
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BibTeX
@misc{sasmal2026does,
title = {{How does human blood rheology influence arterial and cardiovascular device hemodynamics? A comprehensive review, discussion, and future directions}},
author = {C. Sasmal},
howpublished = {arXiv},
year = {2026},
month = sep,
doi = {10.48550/arxiv.2609.20855},
eprint = {2609.20855},
archivePrefix = {arXiv},
url = {https://arxiv.org/abs/2609.20855},
note = {CC BY 4.0},
}
RIS
TY - UNPB
TI - How does human blood rheology influence arterial and cardiovascular device hemodynamics? A comprehensive review, discussion, and future directions
AU - C. Sasmal
PY - 2026
DA - 2026/09/01
PB - arXiv
DO - 10.48550/arxiv.2609.20855
UR - https://arxiv.org/abs/2609.20855
AB - Human blood is a complex biological suspension whose macroscopic flow behaviour arises from the coupled microscopic dynamics of deformable blood cells, plasma proteins, and evolving cellular microstructures. As a result, blood exhibits a range of nonlinear rheological behaviours, including shear-thinning, viscoplasticity, viscoelasticity, and thixotropy, which strongly influence its physiological and clinical hemodynamics. This review provides a comprehensive assessment of the role of blood rheology in arterial and blood-contacting cardiovascular device flows, with particular emphasis on the extent to which different rheological characteristics alter clinically relevant flow quantities and on whether the conventional Newtonian approximation remains adequate for the analysis. The underlying physical mechanisms responsible for the major rheological behaviours of blood are first discussed, followed by a critical review of the constitutive models commonly employed in hemodynamic analysis, including generalised Newtonian, viscoelastic, and thixo-elasto-viscoplastic (TEVP) ones. The effects of blood rheology on arterial flows involving stenosis, bifurcation, and aneurysm under both steady and pulsatile flow conditions are subsequently reviewed and discussed in terms of several physiologically important parameters, such as pressure drop, flow resistance, wall shear stress, flow separation, and recirculation zone. The influence of blood rheology on cardiovascular devices, including prosthetic heart valves and stents, is also reviewed, particularly regarding flow stagnation, residence time, hemolysis, and thrombosis.
ER -