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Modern and traditional approaches combined into an effective gray-box mathematical model of full-blood acid-base
F. Ježek, J. Kofránek,
Jazyk angličtina Země Anglie, Velká Británie
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
BioMedCentral
od 2004-12-01 do 2021-12-31
BioMedCentral Open Access
od 2004
Free Medical Journals
od 2004
PubMed Central
od 2004 do 2021
Europe PubMed Central
od 2004
ProQuest Central
od 2009-01-01 do 2021-01-31
Open Access Digital Library
od 2004-01-01
Open Access Digital Library
od 2004-06-01
Open Access Digital Library
od 2004-01-01
Medline Complete (EBSCOhost)
od 2004-06-04 do 2021-12-03
Health & Medicine (ProQuest)
od 2009-01-01 do 2021-01-31
Springer Nature OA/Free Journals
od 2004-12-01 do 2021-12-31
- MeSH
- acidobazická rovnováha * fyziologie MeSH
- biologické modely * MeSH
- chemické modely * MeSH
- koncentrace vodíkových iontů MeSH
- lidé MeSH
- poruchy acidobazické rovnováhy diagnóza epidemiologie patofyziologie MeSH
- teoretické modely * MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
BACKGROUND: The acidity of human body fluids, expressed by the pH, is physiologically regulated in a narrow range, which is required for the proper function of cellular metabolism. Acid-base disorders are common especially in intensive care, and the acid-base status is one of the vital clinical signs for the patient management. Because acid-base balance is connected to many bodily processes and regulations, complex mathematical models are needed to get insight into the mixed disorders and to act accordingly. The goal of this study is to develop a full-blood acid-base model, designed to be further integrated into more complex human physiology models. RESULTS: We have developed computationally simple and robust full-blood model, yet thorough enough to cover most of the common pathologies. Thanks to its simplicity and usage of Modelica language, it is suitable to be embedded within more elaborate systems. We achieved the simplification by a combination of behavioral Siggaard-Andersen's traditional approach for erythrocyte modeling and the mechanistic Stewart's physicochemical approach for plasma modeling. The resulting model is capable of providing variations in arterial pCO2, base excess, strong ion difference, hematocrit, plasma protein, phosphates and hemodilution/hemoconcentration, but insensitive to DPG and CO concentrations. CONCLUSIONS: This study presents a straightforward unification of Siggaard-Andersen's and Stewart's acid-base models. The resulting full-blood acid-base model is designed to be a core part of a complex dynamic whole-body acid-base and gas transfer model.
Citace poskytuje Crossref.org
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- $a Ježek, Filip $u Department of Cybernetics, Faculty of Electrical Engineering, Czech Technical University in Prague, Prague, Czech Republic. filip.jezek@lf1.cuni.cz. Institute of Pathological Physiology, First Faculty of Medicine, Charles University, U nemocnice 5, 128 00, Prague 2, Czech Republic. filip.jezek@lf1.cuni.cz.
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- $a BACKGROUND: The acidity of human body fluids, expressed by the pH, is physiologically regulated in a narrow range, which is required for the proper function of cellular metabolism. Acid-base disorders are common especially in intensive care, and the acid-base status is one of the vital clinical signs for the patient management. Because acid-base balance is connected to many bodily processes and regulations, complex mathematical models are needed to get insight into the mixed disorders and to act accordingly. The goal of this study is to develop a full-blood acid-base model, designed to be further integrated into more complex human physiology models. RESULTS: We have developed computationally simple and robust full-blood model, yet thorough enough to cover most of the common pathologies. Thanks to its simplicity and usage of Modelica language, it is suitable to be embedded within more elaborate systems. We achieved the simplification by a combination of behavioral Siggaard-Andersen's traditional approach for erythrocyte modeling and the mechanistic Stewart's physicochemical approach for plasma modeling. The resulting model is capable of providing variations in arterial pCO2, base excess, strong ion difference, hematocrit, plasma protein, phosphates and hemodilution/hemoconcentration, but insensitive to DPG and CO concentrations. CONCLUSIONS: This study presents a straightforward unification of Siggaard-Andersen's and Stewart's acid-base models. The resulting full-blood acid-base model is designed to be a core part of a complex dynamic whole-body acid-base and gas transfer model.
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