• Centro de Investigación Biomédica en Red(CIBER) de Enfermedades Respiratorias, Instituto de Salud Carlos III, Madrid, Spain. jesus.villar54@gmail.com
• Resp Care. 2011 Oct 1;56(10):1539-45.

AbstractIt has been known for decades that shock and sepsis can cause a syndrome of acute respiratory failure with characteristics of non-cardiogenic pulmonary edema. Over the years, this syndrome has been given a number of names, including congestive atelectasis, traumatic wet lung, and shock lung. In 1967 the modern counterpart to this syndrome was described and subsequently called the "acute respiratory distress syndrome" (ARDS). This syndrome results from lung injury and inflammation. As with inflammation elsewhere, ARDS is accompanied by many cellular and molecular processes, some of them specific to the syndrome, others perpetuating the syndrome, and others inactivating the by-products of inflammation. Since no specific clinical sign or diagnostic test has yet been described that identifies ARDS, its diagnosis is based on a constellation of clinical, hemodynamic, and oxygenation criteria. Current ARDS treatment is mainly supportive, since these patients frequently have coexisting conditions. Although in 1994 a new standard ARDS definition was accepted, that definition failed to standardize the measurement of the oxygenation defect and does not recognize different severities of pulmonary dysfunction. Based on current evidence there is a need for a better definition and classification system that could help us to identify ARDS patients who would be most responsive to supportive therapies and those unlikely to benefit because of the severity of their disease process. This paper examines our current understanding of ARDS and discusses why the current definition may not be the most appropriate for research and clinical practice.

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