The term acute respiratory failure is often used synonymously with acute (formerly adult) respiratory distress syndrome (ARDS). Although ARDS may be caused by or associated with a variety of clinical conditions, most patients with this disease demonstrate similar clinical and pathologic features regardless of the cause of lung injury. Common features include: (1) a history of a preceding noxious event that served as a trigger for the subsequent development of ARDS; (2) an interval from hours to days of relatively normal lung function after the insult; and (3) the rapid onset and progression over several hours of dyspnea, severe hypoxia, diffuse bilateral pulmonary infiltration, and stiffening and noncompliance of the lungs.
Risk factors for the development of ARDS appear to be additive. The incidence of occurrence is 25% with the presence of one risk factor, 42% with the presence of two, and 85% with the presence of three. The mortality rate for ARDS remains high, ranging from 50% to 70% and often exceeds 90% when gram-negative septic shock precedes ARDS development. Events and risk factors associated with the development of ARDS include: (1) shock (septic, cardiogenic, or hypovolemic), (2) trauma, (3) pulmonary infection (e.g., with Pneumocystis carinii [jiroveci] or Escherichia coli), (4) disease states that result in the release of inflammatory mediators (e.g., extrapulmonary infections, disseminated intravascular coagulation, anaphylaxis, coronary bypass grafting, and transfusion reactions), (5) exposure to various agents (e.g., narcotics, barbiturates, and O2), (6) diseases of the central nervous system (CNS), (7) aspiration (e.g., of gastric contents or as in drowning), and (8) metabolic events (e.g., pancreatitis and uremia).
The pathophysiology of ARDS is centered around severe damage and inflammation to the alveolocapillary membrane. Irrespective of the cause of acute respiratory failure, the lung’s structural response to injury and subsequent repair occurs in a similar fashion. Although the exact mechanisms of this response and repair remain unclear, research has focused on the release of cytokines and membrane-bound phospholipids from the capillary endothelium and the activation of leukocytes and macrophages (via the complement system) within the lungs.