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Luciano Gattinoni, MD, FRCP; Pietro Caironi, MD

JAMA. 2008;299(6):691-693.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Acute respiratory distress syndrome (ARDS) is the clinical manifestation of inflammatory lung edema originating from a variety of insults. Since its first description 40 years ago,¹ the mainstays of management have been institution of mechanical ventilation to ventilate the incompliant lungs, inspired oxygen for hypoxemia, and when hypoxemia is severe, the addition of positive end-expiratory pressure (PEEP) to increase end-expiration lung volume, which facilitates O₂ gas exchange.²

Early on, physicians recognized that the high intrathoracic pressures of mechanical ventilation caused parenchymal stress or rupture, known as barotrauma.³ However, it took several years to identify the local injury resulting from intratidal opening and closing of parts of the lung (atelectrauma)⁴ and the inflammatory reaction of the lung to nonphysiological stress (biotrauma).^5-6 Subsequently computed tomographic scanning showed that the lung fraction open to gas exchange in ARDS is small, equivalent in size to that of . . . [Full Text of this Article]

Author Affiliations: Istituto di Anestesiologia e Rianimazione, Fondazione IRCCS–Ospedale Maggiore Policlinico, Mangiagalli, e Regina Elena di Milano, Università degli Studi di Milano, Milan, Italy.

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