Thursday, 2 January 2014


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 arterial carbon dioxide tension (PaCO2). Therefore, a right-to-left shunt widens the difference between alveolar carbon dioxide tension (PaCO2) and PaCO2, which defines the alveolar dead space (see Equation 1, below). Accordingly, it contributes to the classical concept physiological dead space [5,6]. Such a shunt may reach 50% of cardiac output or more and increases the need for alveolar ventilation (V'A) and total ventilation (V'tot) [7].

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