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Acute respiratory distress syndrome (ARDS) is a diffuse inflammatory reaction of the lung to an insult and is characterized by increased pulmonary capillary permeability, lung edema, and atelectasis. The histological hallmark of ARDS is diffuse alveolar damage and its pathognomonic hyaline membranes. The associated radiographic feature is bilateral alveolar infiltrates.

The Berlin definition of ARDS published in 20121,2 has superseded the prior American-European Consensus Conference definition of 1994.3 The Berlin criteria updated the diagnostic requirements for ARDS, classified its severity based on the ratio of the arterial pressure of oxygen (PaO2) to the fraction of inspired oxygen (FiO2) (P/F ratio), and eliminated the term acute lung injury. The diagnostic criteria mandate that all of the following conditions are met before the syndrome is diagnosed: (1) In patients without known ARDS risk factors, cardiogenic or hydrostatic pulmonary edema as well as other alternative causes of bilateral pulmonary infiltrates need to be excluded; patients with a known ARDS risk factor are no longer required to undergo echocardiography or right heart catheterization to rule out cardiogenic pulmonary edema; (2) respiratory symptoms are of acute onset or are worsening significantly within 1 week prior to diagnosis; (3) imaging (either chest x-ray or computed tomography [CT]) shows bilateral alveolar infiltrates; and (4) oxygenation is impaired, the degree of which determines ARDS severity: P/F ratio greater than 200 but less than or equal to 300 defines mild, greater than 100 but less than or equal to 200 defines moderate, and 100 or less defines severe ARDS.

The incidence of ARDS is estimated to be approximately 86 cases per 100,000 person-years, which results in about 190,000 cases in the US every year.4 Both incidence and mortality are comparable to those of acute myocardial infarction.5

Acute respiratory distress syndrome is triggered by predisposing factors, with more than 60 possible insults having been identified. In clinical practice, the vast majority of cases are caused by pulmonary or extrapulmonary sepsis, aspiration, severe trauma or burns, or transfusion or drug reactions, or as a complication of hematopoietic stem cell transplantation.6,7

The pathobiology and pathophysiology of the syndrome are complex and evolving, and as a result are beyond the scope of this chapter. The reader is referred to several recent informative and well-written review articles on this topic.8-10

Low Tidal Volume Ventilation

It has been recognized for decades that mechanical ventilation is capable of causing or exacerbating lung pathology through mechanisms known collectively as ventilator-induced lung injury (VILI).11 Gross barotrauma in the form of pneumothorax is the most clinically obvious example of VILI. On a microscopic level, multiple experimental models have demonstrated that ventilation with excessive tidal volumes, so-called volutrauma, produces inflammation and changes indicative of high-permeability pulmonary edema even in healthy lungs.12...

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