The influence of venous admixture on alveolar dead space and CO2 exchange in ARDS: computer modelling. Critical care (London, England) [Crit Care] Journal article | | Title | The influence of venous admixture on alveolar dead space and CO2 exchange in ARDS: computer modelling. | | Author(s) | Niklason L, Eckerstrom J, Jonson B | | Source | Crit Care 2008 Apr 18; 12(2):R53. | | Abstract | ABSTRACT:
INTRODUCTION: Alveolar dead space reflects phenomena rendering arterial partial pressure of CO2 higher than that of mixed alveolar gas disturbing CO2 exchange. Right to left shunt fraction (Qs/Qt) leads to an alveolar dead space fraction (VdAS/VtA) where VtA is alveolar tidal volume. In the acute respiratory distress syndrome (ARDS), ancillary physiological disturbances may be low cardiac output, high metabolic rate, anaemia and acid base instability. The purpose of the study was to analyze to what extent shunt contributes to alveolar dead space and perturbs CO2 exchange at 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 reached at 'basal conditions' 0.21 at Qs/Qt of 0.6. At Qs/Qt of 0.4, reduction of cardiac output from 5 to 3 l/min increased VdAS/VtA from 0.11 to 0.16. Metabolic acidosis further augmented effects of shunt on VdAS/VtA, particularly at hyperventilation. A Qs/Qt of 0.5 may increase arterial PCO2 by about 15 to 30% if ventilation is not increased.
CONCLUSION: In ARDS, perturbation of CO2 exchange caused by shunt is enhanced by ancillary disturbances like low cardiac output, anaemia, metabolic acidosis and hyperventilation. Maintained homeostasis mitigates effects of shunt. | | Language | ENG | | Pub Type(s) | JOURNAL ARTICLE
| | PubMed ID | 18423016 |
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