Coagulopathy implications using a multiscale model of traumatic bleeding matching macro- and microcirculation.

Area of Science:

• Physiology
• Biomedical Engineering
• Computational Biology

Background:

• Quantifying bleeding requires understanding coupled global and microvascular hemodynamics.
• Existing models often lack multiscale integration for dynamic bleeding rate analysis.

Purpose of the Study:

• To develop and validate a multiscale model for simulating dynamic bleeding rates.
• To quantify blood loss and wall shear rates under normal and coagulopathic conditions.

Main Methods:

• Coupled a lumped global hemodynamic model with a 24-level bifurcating vascular network.
• Incorporated shear-dependent hemostatic clot growth rates (normal and coagulopathic).
• Simulated vessel severing injuries at various scales (artery to capillary).

Main Results:

• Upstream vascular networks rapidly depressurize to mitigate blood loss.
• High wall shear rates (~10,000 s⁻¹) at wound exit drive von Willebrand factor unfolding.
• Coagulopathy led to >2L blood loss in 2h, while hemostasis limited it to <100ml within 2 min.
• Hemodilution from transcapillary refill exacerbates blood loss.

Conclusions:

• The multiscale model accurately quantifies pressure-driven blood loss and local wall shear rates.
• The model provides insights into the impact of coagulopathy and hemodilution on bleeding.
• This approach enables injury-specific bleeding rate calculations in diverse physiological states.