A mathematical model of CO2, O2 and N2 exchange during venovenous extracorporeal membrane oxygenation
Abstract Background Venovenous extracorporeal membrane oxygenation (vv-ECMO) is an effective treatment for severe respiratory failure. The interaction between the cardiorespiratory system and the oxygenator can be explored with mathematical models. Understanding the physiology will help the clinicia...
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doaj-37ca1e84ca3147039b1182a3fce7ab6b2020-11-25T00:09:22ZengSpringerOpenIntensive Care Medicine Experimental2197-425X2018-08-016111310.1186/s40635-018-0183-4A mathematical model of CO2, O2 and N2 exchange during venovenous extracorporeal membrane oxygenationChristopher John Joyce0Kiran Shekar1David Andrew Cook2Discipline of Anaesthesiology Critical Care, University of Queensland, Ned Hanlon Building, Royal Brisbane and Women’s HospitalDiscipline of Anaesthesiology Critical Care, University of Queensland, Ned Hanlon Building, Royal Brisbane and Women’s HospitalDiscipline of Anaesthesiology Critical Care, University of Queensland, Ned Hanlon Building, Royal Brisbane and Women’s HospitalAbstract Background Venovenous extracorporeal membrane oxygenation (vv-ECMO) is an effective treatment for severe respiratory failure. The interaction between the cardiorespiratory system and the oxygenator can be explored with mathematical models. Understanding the physiology will help the clinician optimise therapy. As others have examined O2 exchange, the main focus of this study was on CO2 exchange. Methods A model of the cardiorespiratory system during vv-ECMO was developed, incorporating O2, CO2 and N2 exchange in both the lung and the oxygenator. We modelled lungs with shunt fractions varying from 0 to 1, covering the plausible range from normal lung to severe acute respiratory distress syndrome. The effects on PaCO2 of varying the input parameters for the cardiorespiratory system and for the oxygenator were examined. Results PaCO2 increased as the shunt fraction in the lung and metabolic CO2 production rose. Changes in haemoglobin and FIO2 had minimal effect on PaCO2. The effect of cardiac output on PaCO2 was variable, depending on the shunt fraction in the lung. PaCO2 decreased as extracorporeal circuit blood flow was increased, but the changes were relatively small in the range used clinically for vv-ECMO of > 2 l/min. PaCO2 decreased as gas flow to the oxygenator rose and increased with recirculation. The oxygen fraction of gas flow to the oxygenator had minimal effect on PaCO2. Conclusions This mathematical model of gas exchange during vv-ECMO found that the main determinants of PaCO2 during vv-ECMO were pulmonary shunt fraction, metabolic CO2 production, gas flow to the oxygenator and extracorporeal circuit recirculation.http://link.springer.com/article/10.1186/s40635-018-0183-4Extracorporeal membrane oxygenationECMOVenovenous ECMOExtracorporeal CO2 removalGas exchangeMathematical model |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Christopher John Joyce Kiran Shekar David Andrew Cook |
spellingShingle |
Christopher John Joyce Kiran Shekar David Andrew Cook A mathematical model of CO2, O2 and N2 exchange during venovenous extracorporeal membrane oxygenation Intensive Care Medicine Experimental Extracorporeal membrane oxygenation ECMO Venovenous ECMO Extracorporeal CO2 removal Gas exchange Mathematical model |
author_facet |
Christopher John Joyce Kiran Shekar David Andrew Cook |
author_sort |
Christopher John Joyce |
title |
A mathematical model of CO2, O2 and N2 exchange during venovenous extracorporeal membrane oxygenation |
title_short |
A mathematical model of CO2, O2 and N2 exchange during venovenous extracorporeal membrane oxygenation |
title_full |
A mathematical model of CO2, O2 and N2 exchange during venovenous extracorporeal membrane oxygenation |
title_fullStr |
A mathematical model of CO2, O2 and N2 exchange during venovenous extracorporeal membrane oxygenation |
title_full_unstemmed |
A mathematical model of CO2, O2 and N2 exchange during venovenous extracorporeal membrane oxygenation |
title_sort |
mathematical model of co2, o2 and n2 exchange during venovenous extracorporeal membrane oxygenation |
publisher |
SpringerOpen |
series |
Intensive Care Medicine Experimental |
issn |
2197-425X |
publishDate |
2018-08-01 |
description |
Abstract Background Venovenous extracorporeal membrane oxygenation (vv-ECMO) is an effective treatment for severe respiratory failure. The interaction between the cardiorespiratory system and the oxygenator can be explored with mathematical models. Understanding the physiology will help the clinician optimise therapy. As others have examined O2 exchange, the main focus of this study was on CO2 exchange. Methods A model of the cardiorespiratory system during vv-ECMO was developed, incorporating O2, CO2 and N2 exchange in both the lung and the oxygenator. We modelled lungs with shunt fractions varying from 0 to 1, covering the plausible range from normal lung to severe acute respiratory distress syndrome. The effects on PaCO2 of varying the input parameters for the cardiorespiratory system and for the oxygenator were examined. Results PaCO2 increased as the shunt fraction in the lung and metabolic CO2 production rose. Changes in haemoglobin and FIO2 had minimal effect on PaCO2. The effect of cardiac output on PaCO2 was variable, depending on the shunt fraction in the lung. PaCO2 decreased as extracorporeal circuit blood flow was increased, but the changes were relatively small in the range used clinically for vv-ECMO of > 2 l/min. PaCO2 decreased as gas flow to the oxygenator rose and increased with recirculation. The oxygen fraction of gas flow to the oxygenator had minimal effect on PaCO2. Conclusions This mathematical model of gas exchange during vv-ECMO found that the main determinants of PaCO2 during vv-ECMO were pulmonary shunt fraction, metabolic CO2 production, gas flow to the oxygenator and extracorporeal circuit recirculation. |
topic |
Extracorporeal membrane oxygenation ECMO Venovenous ECMO Extracorporeal CO2 removal Gas exchange Mathematical model |
url |
http://link.springer.com/article/10.1186/s40635-018-0183-4 |
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