Auckland Bioengineering Institute, The Auckland University
This a model from the article: Minimal haemodynamic system model including ventricular interaction and valve dynamics. Smith BW, Chase JG, Nokes RI, Shaw GM, Wake G. Med Eng Phys 2004 Mar;26(2):131-9 15036180 , Abstract: Characterising circulatory dysfunction and choosing a suitable treatment is often difficult and time consuming, and can result in a deterioration in patient condition, or unsuitable therapy choices. A stable minimal model of the human cardiovascular system (CVS) is developed with the ultimate specific aim of assisting medical staff for rapid, on site modelling to assist in diagnosis and treatment. Models found in the literature simulate specific areas of the CVS with limited direct usefulness to medical staff. Others model the full CVS as a closed loop system, but they were found to be very complex, difficult to solve, or unstable. This paper develops a model that uses a minimal number of governing equations with the primary goal of accurately capturing trends in the CVS dynamics in a simple, easily solved, robust model. The model is shown to have long term stability and consistency with non-specific initial conditions as a result. An "open on pressure close on flow" valve law is created to capture the effects of inertia and the resulting dynamics of blood flow through the cardiac valves. An accurate, stable solution is performed using a method that varies the number of states in the model depending on the specific phase of the cardiac cycle, better matching the real physiological conditions. Examples of results include a 9% drop in cardiac output when increasing the thoracic pressure from -4 to 0 mmHg, and an increase in blood pressure from 120/80 to 165/130 mmHg when the systemic resistance is doubled. These results show that the model adequately provides appropriate magnitudes and trends that are in agreement with existing data for a variety of physiologically verified test cases simulating human CVS function. This model was taken from the CellML repository and automatically converted to SBML. The original model was: Smith BW, Chase JG, Nokes RI, Shaw GM, Wake G. (2004) - version=1.0 The original CellML model was created by: Geoffrey Nunns gnunns1@jhu.edu The University of Auckland This model originates from BioModels Database: A Database of Annotated Published Models. It is copyright (c) 2005-2011 The BioModels.net Team. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information. In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not.. To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.