Since its original description, the acute respiratory distress syndrome (ARDS) has been considered to be a syndrome diffusely affecting the lung parenchyma, as usually seen on anteroposterior chest radiographs. However, CT studies have shown that lesions (seen as densities) are primarily located in the dependent lung, suggesting a non-homogeneous distribution of lung changes. Quantitative analysis of the CT scan images led us to model the ARDS lung into three compartments: the first shows normal inflation, the second is poorly inflated, and the third is non-inflated. The dimensions of the normally inflated lung, which are directly estimated from measurement of lung compliance, may be as small as 20 to 30 per cent of the dimension of a normal adult lung, and may assume the dimensions of a 'baby lung'. Ventilation-perfusion studies in ARDS are consistent with the model described; hence gas exchange is characterized by two physiological compartments, with true shunt in the non-inflated compartment and normal ventilation-perfusion in the baby lung.

Conventionally, two variables are subjected to manipulation by the clinician in order to maintain oxygenation in severe ARDS, namely fractional inspired oxygen (FiO 2) and airway pressure. Oxygen toxicity is an old concept, first described almost a century ago. It is still not known how much oxygen is safe for the diseased lung and for how long, but it is common clinical practice to keep FiO 2 as low as possible. The introduction of positive end-expiratory pressure (PEEP) allowed improvement in oxygenation in some patients, without any increase in FiO 2. In 1975 the indiscriminate use of super-PEEP revealed the ominous evidence of barotrauma as a side-effect of positive-pressure ventilation on either specific organ function or on global hemodynamics. The term barotrauma now refers not only to the occurrence of major extrapulmonary air collection, but also to all the structural changes induced by high-peak pressure and high-volume ventilation.

The PaCO 2 values are typically normal in the early stages of ARDS, but the cost of breathing to maintain these values is greatly increased. Attempts to ventilate the stiff ARDS lung with normal tidal volumes will result in high inflation pressures and specific hyperventilation of the residual healthy zones, factors that have been demonstrated to be deleterious to lung structures.

In summary, all the conventional means of maintaining adequate gas exchange are potentially harmful to the residual normal baby lung. With this in mind, the rationale for extracorporeal support is to avoid further damage to the relatively small part of the lung still available for ventilation, avoiding the need for high-pressure and high-volume ventilation by extracorporeal removal of metabolically produced CO 2.

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