Peripheral Artery Disease (P.A.D.): Vascular Hemodynamic Simulation Using a Printed Circuit Board (PCB) Design

外周动脉疾病(PAD):基于印刷电路板(PCB)设计的血管血流动力学模拟

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Abstract

BACKGROUND: Arterial stenosis produces nonlinear changes in vascular impedance that are challenging to investigate in real time using either benchtop flow phantoms or high-fidelity computational fluid dynamics (CFD) models. OBJECTIVE: This study aimed to develop and evaluate a low-cost printed circuit board (PCB) analog capable of reproducing the hemodynamic effects of progressive arterial stenosis through an R-L-C mapping of vascular mechanics. METHODS: A lumped-parameter (0D) electrical network was constructed in which voltage represented pressure, current represented flow, resistance modeled viscous losses, capacitance corresponded to vessel compliance, and inductance represented fluid inertance. A variable resistor simulated focal stenosis and was adjusted incrementally to represent progressive narrowing. Input U(in), output U(out), peak-to-peak V(pp), and mean V(avg) voltages were recorded at a driving frequency of 50 Hz. Physiological correspondence was established using the canonical relationships. R=8μlπr4, L=plπr2, C=3πr32Eh, where μ is blood viscosity, ρ is density, E is Young's modulus, and h is wall thickness. A calibration constant was applied to convert measured voltage differences into pressure differences. RESULTS: As simulated stenosis increased, the circuit exhibited a monotonic rise in U(out) and V(pp), with a precise inflection beyond mid-range narrowing-consistent with the nonlinear growth in pressure loss predicted by fluid dynamic theory. Replicate measurements yielded stable, repeatable traces with no outliers under nominal test conditions. Qualitative trends matched those of surrogate 0D and CFD analyses, showing minimal changes for mild narrowing (≤25%) and a sharp increase in pressure loss for moderate to severe stenoses (≥50%). The PCB analog uses a simplified, lumped-parameter representation driven by a fixed-frequency sinusoidal excitation and therefore does not reproduce fully characterized physiological systolic-diastolic waveforms or heart-arterial coupling. In addition, the present configuration is intended for relatively straight peripheral arterial segments and is not designed to capture the complex geometry and branching of specialized vascular beds (e.g., intracranial circulation) or strongly curved elastic vessels (e.g., the thoracic aorta). CONCLUSIONS: The PCB analog successfully reproduces the characteristic hemodynamic signatures of arterial stenosis in real time and at low cost. The model provides a valuable tool for educational and research applications, offering rapid and intuitive visualization of vascular behavior. Current accuracy reflects assumptions of Newtonian, laminar, and lumped flow; future work will refine calibration, quantify uncertainty, and benchmark results against physiological measurements and full CFD simulations.

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