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.
Highlights
Alveolar dead space reflects phenomena that render arterial partial pressure of carbon dioxide higher than that of mixed alveolar gas, disturbing carbon dioxide exchange
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
Metabolic acidosis further augmented the effects of shunt on VdAS/VtA, with hyperventilation
Summary
Alveolar dead space reflects phenomena that render arterial partial pressure of carbon dioxide higher than that of mixed alveolar gas, disturbing carbon dioxide exchange. 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. In acute respiratory distress syndrome (ARDS), dead space is often high [1,2]. This impedes gas exchange and efforts to ventilate at low tidal volume in order to provide lung protective ventilation. Dead space at the alveolar level reflects uneven ventilation/perfusion among lung compartments. In a ground breaking study, West [4] showed that this impedes gas exchange by increasing alveolar dead space
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