A mathematical model of ventilation response to inhaled carbon monoxide, based on the work of James H. Stuhmiller and Louise M. Stuhmiller [2005, JAP, 98, 2033-2044] and developed by Raymond Yakura as a final project for BIOEN 589, University of Washington.
Model number: 0214
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A comprehensive mathematical model describing the respiration, circulation, oxygen metabolism, and ventilatory control was assembled for the purpose of predicting acute ventilation changes from exposure to carbon monoxide in both humans and animals. This Dynamic Physiological Model is based on previously published work, reformulated, extended, and combined into a single model. Model parameters are determined from literature values, fitted to experimental data, or allometrically scaled between species. The model reaffirms the role of brain hypoxia on hyperventilation during carbon monoxide exposures. Improvement in the estimation of total ventilation, through a more complete knowledge of ventilation control mechanisms, and validated by animal data, will increase the accuracy of inhalation toxicology estimates. Introduction to the model: With CO acute inhalation, hyperventilation first results and followed by a subsequent ventilation depression. Hyperventilation is caused by hypoxia & increased CO2 that activates the peripheral chemoreceptors. Then, ventilation depression is caused by generation of lactic acid in the brain and by decreased brain activity. A buildup of carboxyhemoglobin with reduction in oxygen delivery to the brain leads to anaerobic glycolysis and build up of lactate. The model consists of 6 subsets: (1) RESPIRATION SYSTEM which incompasses the total ventilation and effects of dead space and humidification. (2) VENTILATION which incompasses the chemoreceptor response, brain activity response, and the combined ventilatory response (3) CIRCULATORY SYSTEM which incompasses the mass balance equations for O2, CO2 and CO, (4) BLOOD CHEMISTRY which incompasses the hemoglobin saturation, O2/CO partition, acid-base balance, and CO2 dissociation, (5) CARDIAC OUTPUT which incompasses the blood flow to the brain increases during hypoxia, (6) METABOLIC SYSTEM which incompasses the oxygen metabolism, oxygen transfer to the brain, lactic acid generation, and anaerobic limit,
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Stuhmiller, J.H. and Stuhmiller, L.M.; A mathematical model of ventilation response to inhaled carbon monoxide, 2005, Journal of Applied Physiology, 98, 2033-2044. Ba ZF et al.; Alterations in tissue oxygen consumption and extraction after trauma and hemorrhagic shock. Critical Care Medicine 28(8), 2837-2842 (2000). Duffin J et al.; A mathematical model of the chemoreflex control of ventilation. Respir Physiol 120, 13-26 (2000). Gronlund et al.; Numerical Values of Classical Haldane Coefficient. JAP 57(3), 850-859 (1984).
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