Is a clinical syndrome characterized by a sudden and progressive pulmonaryedema, increasing bilateral infiltrates on chest x-ray, hypoxemia refractory to oxygensupplementation, and reduced lung compliance. These signs occur in the absence of left side failure. Patients with ARDS usually require mechanical ventilation with a higher than normal airway pressure. * PATHOPHYSIOLOGY ARDS
Occurs as a result of inflammatory trigger that initiates the release of cellular and chemical mediators, causing injury to the alveolar capillary membrane. These result in leakage of fluid into the alveolar interstitial spaces and alterations in the capillary bed. Severe ventilation-perfusion mismatching occurs in ARDS. Alveoli collapse because of the inflammatory infiltrate, blood, fluid, and surfactant dysfunction. Small airways are narrowed because of interstitial fluid and bronchial obstruction. The lung compliance becomes markedly decreased (stiff lungs), and the result is a characteristic decrease in functional residual capacity and severe hypoxemia. The blood determines to the lung or gas exchange is pumped through the non ventilated, non functioning areas of the lung, causing a shunt to develop. This means that blood is interfacing with nonfunctioning alveoli and gas exchange is markedly impaired, resulting in severe, refractory hypoxemia.
ETHOLOGIC FACTORS RELATED TO ARDS: * Aspiration (gastric secretions, drowning, hydrocarbons) * Drug ingestion and over dose * Hematological disorders (disseminated intravascular coagulopathy [DIC],massive transfusions, cardiopulmonary bypass) * Prolonged inhalation of high concentrations of oxygen, smoke or corrosive substances. * Localized infection (bacterial, fungal, viral pneumonia) * Metabolic disorders (pancreatitis, uremia) * Shock * Trauma (pulmonary contusion, multiple fractures, head injury) * Major surgery * Fat or air embolism * Systemic