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Learning Objectives

  • The student will be able to describe the definition, prevalence, and impact of ALI and ARDS in multidisciplinary critical care medicine.

  • The student will be able to list and define the direct and indirect risk factors for ALI/ARDS, and distinguish the clinical features of ALI and ARDS.

  • The student will be able to summarize the initiating pathophysiology of ALI/ARDS, and factors that perpetuate or are associated with its nonresolution, especially ventilator-associated lung injury.

  • The student will be able to explain and defend current guidelines for the treatment and supportive care of patients with ALI/ARDS.

Acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS) represent a spectrum of respiratory failure of rapid onset characterized by diffuse, bilateral lung injury and severe hypoxemia that are caused by noncardiogenic pulmonary edema. ALI/ARDS can affect patients of any age or preexisting condition, although both predispose to worse outcomes. Respiratory failure may be initiated by pulmonary or extrapulmonary insults that increase alveolar epithelial and endothelial permeability, flood alveoli, and reduce lung compliance in a pattern reflecting an acute restrictive lung disease. Despite numerous prospective, double-blind clinical trials in patients with ALI/ARDS, the only treatment that improves survival is mechanical ventilation using a lung protective strategy in which tidal volume VT is carefully titrated to ~6 mL/kg of predicted body weight. Positive end-expiratory pressure (PEEP) ventilation is useful for alveolar recruitment in lungs that will be prone to atelectasis. Clinical vigilance must be comprehensive and anticipatory to guard against development of ventilator-associated pneumonia or worsened ALI. Although mortality can exceed 50%, survivors have a good prognosis for recovery of lung function.


ALI and ARDS affect over 190,000 patients annually in the United States and cause 75,000 deaths. They occur rapidly and show diffuse, bilateral lung injury readily evident by x-ray or CT. Patients exhibit severe hypoxemia despite use of supplemental O2, and are considered emblematic of a noncardiogenic pulmonary edema with low alveolar ventilation/perfusion ratios (V̇A/ Q̇) and abnormal physiological shunting of O2. Such acute respiratory failure usually occurs with neutrophil (PMN)-mediated lung inflammation. Pathological increases in the permeability of alveolar epithelial and endothelial cells lead to dyspnea, tachypnea, and arterial hypoxemia. These permeability defects increase efflux of proteins and fluids from blood into the alveolar interstitium and airspaces, while alveolar liquid clearance mechanisms are impaired that normally would resolve the edema. Consequently, alveolar O2 exchange deteriorates.

ALI/ARDS is complex and multiphasic. The initiating factors that may cause early lung dysfunction may differ from those that perpetuate, complicate, or delay its resolution. ALI/ARDS can be caused by pulmonary-specific mechanisms, notably severe pneumonia, aspiration of gastric contents, embolism of fat, air, or amniotic fluid, chest trauma, near-drowning, and inhalation of noxious gases. ALI/ARDS can also occur due to ...

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