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

A comprehensive model of pulmonary gas exchange was based upon known equations and iterative mathematics.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 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.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.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. Airway dead space is increased by connecting tubes, often including a humidifying filter, and by limiting time for equilibration between airway and alveolar space [3]. In a complex relationship, dead space at the alveolar level reflects uneven ventilation/perfusion among lung compartments. Ventilated compartments with nearly zero perfusion may result from microthrombosis. Other compartments may have a broad distribution of ventilation/perfusion relationships. In a ground breaking study, West [4] showed that this impedes gas exchange by increasing alveolar dead space.In ARDS intrapulmonary shunt depends on collapsed lung units that are perfused but not ventilated. Part of venous blood thereby passes the lung without exchanging carbon dioxide and then mixes with arterial blood. Venous blood has a higher carbon dioxide content than does arterialized blood from ventilated and perfused lung units, and a shunt thereby leads to an increase in a