The influence of venous admixture on alveolar dead space and carbon dioxide exchange in acute respiratory distress syndrome: computer modelling
(2008) In Critical Care 12(2).- Abstract
- Introduction Alveolar dead space reflects phenomena that render arterial partial pressure of carbon dioxide higher than that of mixed alveolar gas, disturbing carbon dioxide exchange. Right-to-left shunt fraction (Qs/Qt) leads to an alveolar dead space fraction (VdA(S)/VtA; where VtA is alveolar tidal volume). In acute respiratory distress syndrome, ancillary physiological disturbances may include low cardiac output, high metabolic rate, anaemia and acid-base instability. The purpose of the present study was to analyze the extent to which shunt contributes to alveolar dead space and perturbs carbon dioxide exchange in ancillary physiological disturbances. Methods A comprehensive model of pulmonary gas exchange was based upon known... (More)
- Introduction Alveolar dead space reflects phenomena that render arterial partial pressure of carbon dioxide higher than that of mixed alveolar gas, disturbing carbon dioxide exchange. Right-to-left shunt fraction (Qs/Qt) leads to an alveolar dead space fraction (VdA(S)/VtA; where VtA is alveolar tidal volume). In acute respiratory distress syndrome, ancillary physiological disturbances may include low cardiac output, high metabolic rate, anaemia and acid-base instability. The purpose of the present study was to analyze the extent to which shunt contributes to alveolar dead space and perturbs carbon dioxide exchange in ancillary physiological disturbances. Methods A comprehensive model of pulmonary gas exchange was based upon known equations and iterative mathematics. Results The alveolar dead space fraction caused by shunt increased nonlinearly with Qs/Qt and, under 'basal conditions', reached 0.21 at a Qs/Qt of 0.6. At a Qs/Qt of 0.4, reduction in cardiac output from 5 l/minute to 3 l/minute increased VdAS/VtA from 0.11 to 0.16. Metabolic acidosis further augmented the effects of shunt on VdA(S)/VtA, particularly with hyperventilation. A Qs/Qt of 0.5 may increase arterial carbon dioxide tension by about 15% to 30% if ventilation is not increased. Conclusion In acute respiratory distress syndrome, perturbation of carbon dioxide exchange caused by shunt is enhanced by ancillary disturbances such as low cardiac output, anaemia, metabolic acidosis and hyperventilation. Maintained homeostasis mitigates the effects of shunt. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1255041
- author
- Niklason, Lisbet LU ; Eckerstrom, Johannes and Jonson, Björn LU
- organization
- publishing date
- 2008
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Critical Care
- volume
- 12
- issue
- 2
- article number
- R53
- publisher
- BioMed Central (BMC)
- external identifiers
-
- wos:000257632900025
- scopus:44149125974
- ISSN
- 1364-8535
- DOI
- 10.1186/cc6872
- language
- English
- LU publication?
- yes
- id
- d17c1dd1-4f25-4ba7-9486-256d350ac160 (old id 1255041)
- date added to LUP
- 2016-04-01 11:59:54
- date last changed
- 2022-04-28 23:06:53
@article{d17c1dd1-4f25-4ba7-9486-256d350ac160,
abstract = {{Introduction Alveolar dead space reflects phenomena that render arterial partial pressure of carbon dioxide higher than that of mixed alveolar gas, disturbing carbon dioxide exchange. Right-to-left shunt fraction (Qs/Qt) leads to an alveolar dead space fraction (VdA(S)/VtA; where VtA is alveolar tidal volume). In acute respiratory distress syndrome, ancillary physiological disturbances may include low cardiac output, high metabolic rate, anaemia and acid-base instability. The purpose of the present study was to analyze the extent to which shunt contributes to alveolar dead space and perturbs carbon dioxide exchange in ancillary physiological disturbances. Methods A comprehensive model of pulmonary gas exchange was based upon known equations and iterative mathematics. Results The alveolar dead space fraction caused by shunt increased nonlinearly with Qs/Qt and, under 'basal conditions', reached 0.21 at a Qs/Qt of 0.6. At a Qs/Qt of 0.4, reduction in cardiac output from 5 l/minute to 3 l/minute increased VdAS/VtA from 0.11 to 0.16. Metabolic acidosis further augmented the effects of shunt on VdA(S)/VtA, particularly with hyperventilation. A Qs/Qt of 0.5 may increase arterial carbon dioxide tension by about 15% to 30% if ventilation is not increased. Conclusion In acute respiratory distress syndrome, perturbation of carbon dioxide exchange caused by shunt is enhanced by ancillary disturbances such as low cardiac output, anaemia, metabolic acidosis and hyperventilation. Maintained homeostasis mitigates the effects of shunt.}},
author = {{Niklason, Lisbet and Eckerstrom, Johannes and Jonson, Björn}},
issn = {{1364-8535}},
language = {{eng}},
number = {{2}},
publisher = {{BioMed Central (BMC)}},
series = {{Critical Care}},
title = {{The influence of venous admixture on alveolar dead space and carbon dioxide exchange in acute respiratory distress syndrome: computer modelling}},
url = {{http://dx.doi.org/10.1186/cc6872}},
doi = {{10.1186/cc6872}},
volume = {{12}},
year = {{2008}},
}