Abstract
Respiratory distress syndrome (RDS) is a known sequel to many acute disease processes. When the initial insult is a bacteremia, the combined effects of toxins and vasoactive substances can lead to shock. Resulting tissue hypoxia, acidemia, and vascular stasis may lead to pulmonary embolism, alterations in pulmonary capillary bed permeability, and pulmonary edema, precipitating RDS. Treatment of RDS, reversal of shock, and eradication of infection require ventilatory support, hemodynamic monitoring, and a variety of pharmacologic therapies.
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