The influence of venous admixture on alveolar dead space and carbon dioxide exchange in acute respiratory distress syndrome: computer modellingReportar como inadecuado




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Critical Care

, 12:R53

First Online: 18 April 2008Received: 04 October 2007Revised: 28 February 2008Accepted: 18 April 2008

Abstract

IntroductionAlveolar 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 VdAS-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.

MethodsA comprehensive model of pulmonary gas exchange was based upon known equations and iterative mathematics.

ResultsThe 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 VdAS-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.

ConclusionIn 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.

AbbreviationsARDSacute respiratory distress syndrome

CvCO2venous carbon dioxide content

FiO2fraction of inspired oxygen

PaCO2arterial carbon dioxide tension

PaCO2alveolar carbon dioxide tension

PcCO2partial end-capillary carbon dioxide tension

Qsblood flow to shunt

Qs-Qtshunt fraction

Qttotal cardiac output

SaO2arterial oxygen saturation

VdASalveolar dead space caused by shunt

VdAVQalveolar dead space caused by uneven ventilation-perfusion

V-Aalveolar ventilation

VtAalveolar tidal volume

V-tottotal ventilation.

Electronic supplementary materialThe online version of this article doi:10.1186-cc6872 contains supplementary material, which is available to authorized users.

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Autor: Lisbet Niklason - Johannes Eckerström - Björn Jonson

Fuente: https://link.springer.com/



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