Monday, February 23, 2009

Monday February 23, 2009

Q: What happen to surfactant in ARDS?


Answer:
Normal lung expansion is accomplished by inspiratory muscle contraction generating a negative pleural pressure, which in turn, inflates the lung but lung mechanical properties resist inflation due to the inherent elasticity of lung tissue and the airway resistance. An important feature in all mammalian lungs is the presence of surface-active lining material in the alveoli, called surfactant. Surfactant greatly reduce the surface tension of the alveolar membrane and, as a consequence, allow the lung to inflate with relatively small transpulmonary pressure generations. In addition, surfactants have important anti-inflammatory properties.

Interestingly, In ARDS, the total amount of surfactant present in the lung may actually be elevated! However, type 2 cell injury in ARDS alters surfactant metabolism/recycling and the surfactant that is produced is often dysfunctional. As a consequence, surface tension in the alveoli of patients with ARDS is usually markedly elevated. This contributes to the poor compliance and ventilation-perfusion mismatch seen in ARDS. It may also be a factor in reduced host defenses with the loss of surfactant anti-inflammatory processes.

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