RSS Feeds
The Acute Respiratory Distress Syndrome
- Claude A. Piantadosi, MD; and
- David A. Schwartz, MD, MPH
- From Duke University Medical Center, Durham, North Carolina.
PHYSIOLOGY IN MEDICINE: A SERIES OF ARTICLES LINKING MEDICINE WITH SCIENCE
Co-sponsored by the American College of Physicians and the American Physiological Society
Physiology in Medicine: Dennis A. Ausiello, MD, Editor; Dale J. Benos, PhD, Deputy Editor; Francois Abboud, MD, Associate Editor; William J. Koopman, MD, Associate Editor
Annals of Internal Medicine: Paul Epstein, MD, Series Editor
Clinical Principles
Severe respiratory distress and 1 or more risk factors (including infection, aspiration, pancreatitis, and trauma)
Impaired arterial oxygenation (hypoxemia)
Bilateral pulmonary infiltrates on chest radiograph
No clinical evidence of elevated left atrial pressure (or pulmonary artery occlusion pressure of ≤ 18 mm Hg if measurements are available)
Physiologic Principles
The cardinal feature of ARDS, refractory hypoxemia, is caused by formation of protein-rich alveolar edema after damage to the integrity of the lung's alveolar-capillary barrier.
Alveolar-capillary damage in ARDS can be initiated by physical or chemical injury or by extensive activation of innate inflammatory responses. Such damage causes the lung's edema safety factor to decrease by about half, and edema develops at low capillary pressures.
Widespread alveolar flooding in ARDS impairs alveolar ventilation, excludes oxygen, and inactivates surfactant; this, in turn, decreases lung compliance, increases dispersion of ventilation and perfusion, and produces intrapulmonary shunt.
Intrapulmonary shunt is disclosed when hypoxemia does not improve despite oxygen administration; hypoxemia in ARDS does respond to positive end-expiratory pressure, which is applied carefully in accordance with strategies of lung-protective ventilation designed to avoid ventilator-associated lung injury and worsening ARDS.
The acute respiratory distress syndrome (ARDS) is defined by noncardiogenic pulmonary edema and respiratory failure in the seriously ill patient. The diagnosis is clinical, established by the development of new bilateral pulmonary infiltrates and severe hypoxemia without congestive heart failure (1). The risk for ARDS also depends on both host and etiologic factors. The most common causes are sepsis, …
Related Clinical Content
