Ans. c. PCWP>18mmHgACUTE RESPIRATORY DISTRESS SYNDROMERespiratory failure with refractory hypoxemia, | lung compliance, and non-cardiogenic pulmonary edema with a PaO2 /FiO2 ratio<=300.Pathogenesis is thought to be dependent on endothelial injury. Common triggers include sepsis, pneumonia, aspiration, multiple blood transfusions, inhaled/ingested toxins, and trauma. Overall mortality is 30-40%.HISTORY/PEPresents with acute-onset (12-48 hours) tachypnea, dyspnea, and tachycardia +- fever, cyanosis, labored breathing, diffuse high-pitched rales, and hypoxemia in the setting of one of the systemic inflammatory causes or exposure.Additional Findings are as FollowsPhase 1 (acute injury): Normal physical examination; possible respiratory alkalosis.Phase 2 (6-48 hours): Hyperventilation, hypocapnia, widening A-a gradient.Phase 3: Acute respiratory failure, tachypnea, dyspnea, | lung compliance, scattered rales, and diffuse chest opacity on CXR (see Fig. 1).AP CXR showing a diffuse alveolar filling pattern deg to ARDSPhase 4: Severe hypoxemia unresponsive to therapy; | intrapulmonary shunting; metabolic and respiratory acidosis.DIAGNOSISThe criteria for ARDS diagnosis (according to the Berlin definition) are as follows:Acute onset (<1week) of respiratory distress.A PaO2 /FiO2 ratio<300with PEEP/CPAP>=5cmH2O,Bilateral pulmonary infiltrates on CXR.Respiratory failure not completely explained by heart failure.TREATMENTTreat the underlying disease and maintain adequate perfusion to prevent end-organ damage.Mechanical ventilation with low tidal volumes (4-6 cc/kg of ideal body weight) to minimize ventilator-induced lung injury,Use PEEP to recruit collapsed alveoli, and titrate PEEP and Fi02 to achieve adequate oxygenation.Goal oxygenation is PaO,>55mmHgorSaO2 >88%.