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The deleterious effects of mechanical ventilation on the lungs have long been referred to as barotrauma. For many years, clinicians defined barotrauma as the occurrence of air leaks resulting in the accumulation of extraalveolar air responsible for a number of manifestations, of which the most threatening is tension pneumothorax. In addition to these “macroscopic” events whose adverse consequences are usually immediately obvious, mechanical ventilation may produce more subtle physiologic and morphologic alterations, especially when it results in high airway pressures. Our knowledge of such alterations has stemmed mainly from experimental studies and has expanded considerably over recent years. Indeed, alterations in alveolar–capillary barrier integrity and release of both inflammatory and antiinflammatory mediators have been reported in animals ventilated with modalities resulting in high lung stretching. Tissue damage also may occur during mechanical ventilation when distal airways close and open repeatedly because of the movement of foam in the airway lumen or rupture of liquid menisci. The clinical relevance of these experimental findings received resounding confirmation with the results of the ARDS Network study, which showed a 22% reduction in mortality in patients with the acute respiratory distress syndrome through a simple reduction in tidal volume.1


The first comprehensive work demonstrating that mechanical ventilation may be unsafe in intact animals was performed by Webb and Tierney.2 Rats ventilated with a peak inspiratory pressure (PIP) of 30 or 45 cm H2O displayed pulmonary edema within 20 minutes to 1 hour, depending on the pressure level. Microscopic examination of the lungs disclosed moderate interstitial edema in animals ventilated with the lower peak pressure, contrasting with profuse edema and alveolar flooding in animals ventilated with the highest PIP. Other studies subsequently documented the occurrence of pulmonary edema and lung ultrastructural abnormalities3,4 after even very short periods of intermittent positive-inspiratory pressure with high PIP. Kolobow et al5 reported progressive lung injury in sheep ventilated with 50 cm H2O PIP over 48 hours, manifested as decreased pulmonary compliance and deterioration in blood oxygenation. Some of the animals died before the 48-hour end point. At autopsy, lungs exhibited congestion and severe atelectasis.


The mechanisms underlying this ventilator-induced lung injury (VILI) have been for the most part elucidated. Two main factors explain its development: the magnitude of lung overdistension and its duration. Ventilation with very high peak transalveolar pressure results in acute, rapidly fatal, permeability pulmonary edema, whereas more protracted ventilation involving alveolar distension of lesser magnitude produces a lung injury in which inflammatory phenomena may play a role. This chapter presents the current knowledge on VILI. A Medline research employing “ventilator-induced lung injury” as keywords and limited to English articles yielded approximately 1900 results up to January 2005 (when the chapter in the second edition of this book was written). A Medline search employing the same keywords yielded 3860 results when updated to December 2010, reflecting the huge scientific productivity in this field over the past 6 years. ...

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