Arterial Blood Flow by Analogue Solution of the Navier-Stokes Equation

1965 ◽  
Vol 10 (2) ◽  
pp. 271-280 ◽  
Author(s):  
I T Gabe
2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Khalid M. Saqr ◽  
Simon Tupin ◽  
Sherif Rashad ◽  
Toshiki Endo ◽  
Kuniyasu Niizuma ◽  
...  

Abstract Contemporary paradigm of peripheral and intracranial vascular hemodynamics considers physiologic blood flow to be laminar. Transition to turbulence is considered as a driving factor for numerous diseases such as atherosclerosis, stenosis and aneurysm. Recently, turbulent flow patterns were detected in intracranial aneurysm at Reynolds number below 400 both in vitro and in silico. Blood flow is multiharmonic with considerable frequency spectra and its transition to turbulence cannot be characterized by the current transition theory of monoharmonic pulsatile flow. Thus, we decided to explore the origins of such long-standing assumption of physiologic blood flow laminarity. Here, we hypothesize that the inherited dynamics of blood flow in main arteries dictate the existence of turbulence in physiologic conditions. To illustrate our hypothesis, we have used methods and tools from chaos theory, hydrodynamic stability theory and fluid dynamics to explore the existence of turbulence in physiologic blood flow. Our investigation shows that blood flow, both as described by the Navier–Stokes equation and in vivo, exhibits three major characteristics of turbulence. Womersley’s exact solution of the Navier–Stokes equation has been used with the flow waveforms from HaeMod database, to offer reproducible evidence for our findings, as well as evidence from Doppler ultrasound measurements from healthy volunteers who are some of the authors. We evidently show that physiologic blood flow is: (1) sensitive to initial conditions, (2) in global hydrodynamic instability and (3) undergoes kinetic energy cascade of non-Kolmogorov type. We propose a novel modification of the theory of vascular hemodynamics that calls for rethinking the hemodynamic–biologic links that govern physiologic and pathologic processes.


1995 ◽  
Vol 1 (3) ◽  
pp. 245-254 ◽  
Author(s):  
N. U. Ahmed

In this paper we discuss some problems arising in mathematical modeling of artificial hearts. The hydrodynamics of blood flow in an artificial heart chamber is governed by the Navier-Stokes equation, coupled with an equation of hyperbolic type subject to moving boundary conditions. The flow is induced by the motion of a diaphragm (membrane) inside the heart chamber attached to a part of the boundary and driven by a compressor (pusher plate). On one side of the diaphragm is the blood and on the other side is the compressor fluid. For a complete mathematical model it is necessary to write the equation of motion of the diaphragm and all the dynamic couplings that exist between its position, velocity and the blood flow in the heart chamber. This gives rise to a system of coupled nonlinear partial differential equations; the Navier-Stokes equation being of parabolic type and the equation for the membrane being of hyperbolic type. The system is completed by introducing all the necessary static and dynamic boundary conditions. The ultimate objective is to control the flow pattern so as to minimize hemolysis (damage to red blood cells) by optimal choice of geometry, and by optimal control of the membrane for a given geometry. The other clinical problems, such as compatibility of the material used in the construction of the heart chamber, and the membrane, are not considered in this paper. Also the dynamics of the valve is not considered here, though it is also an important element in the overall design of an artificial heart. We hope to model the valve dynamics in later paper.


2018 ◽  
Vol 7 (2) ◽  
pp. 102
Author(s):  
FATHURAHMAN MA’RUF HUDOARMA ◽  
P. H. GUNAWAN ◽  
ANIQ A. ROHMAWATI

This simulation was performed to analyze arterial blood flow using Navier-Stokes equations and LatticeBoltzmann method with Bhatnagar-Gross-Krook approach to obtain an explicit form of the LatticeBoltzmann Bhatnagar-Gross-Krook equations. Then by adding some cases of plaque on simulation domain, changes in arterial blood flow pressure can be analyzed. The area and shape of the plaque cause narrowing the artery vessels that affect the pressure and rate of blood flow dynamically. The pressure of blood flow without plaque is stable ranged from 17 to 19 Pa. While in the vessels with plaque, blood flow pressure increased significantly up to 35.145 Pa.


2013 ◽  
Vol 23 (2) ◽  
Author(s):  
Xenia Descovich ◽  
Giuseppe Pontrelli ◽  
Sauro Succi ◽  
Simone Melchionna ◽  
Manfred Bammer

Children ◽  
2021 ◽  
Vol 8 (5) ◽  
pp. 353
Author(s):  
Jayasree Nair ◽  
Lauren Davidson ◽  
Sylvia Gugino ◽  
Carmon Koenigsknecht ◽  
Justin Helman ◽  
...  

The optimal timing of cord clamping in asphyxia is not known. Our aims were to determine the effect of ventilation (sustained inflation–SI vs. positive pressure ventilation–V) with early (ECC) or delayed cord clamping (DCC) in asphyxiated near-term lambs. We hypothesized that SI with DCC improves gas exchange and hemodynamics in near-term lambs with asphyxial bradycardia. A total of 28 lambs were asphyxiated to a mean blood pressure of 22 mmHg. Lambs were randomized based on the timing of cord clamping (ECC—immediate, DCC—60 s) and mode of initial ventilation into five groups: ECC + V, ECC + SI, DCC, DCC + V and DCC + SI. The magnitude of placental transfusion was assessed using biotinylated RBC. Though an asphyxial bradycardia model, 2–3 lambs in each group were arrested. There was no difference in primary outcomes, the time to reach baseline carotid blood flow (CBF), HR ≥ 100 bpm or MBP ≥ 40 mmHg. SI reduced pulmonary (PBF) and umbilical venous (UV) blood flow without affecting CBF or umbilical arterial blood flow. A significant reduction in PBF with SI persisted for a few minutes after birth. In our model of perinatal asphyxia, an initial SI breath increased airway pressure, and reduced PBF and UV return with an intact cord. Further clinical studies evaluating the timing of cord clamping and ventilation strategy in asphyxiated infants are warranted.


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