– Previously called adult respiratory distress syndrome.
– Severe, acute lung injury involving diffuse alveolar damage, increased microvascular permeability and non cardiogenic pulmonary edema.
– Fluid builds up in the lungs and causing them to stiffen. This impairs breathing, thereby reducing the amount of O2 in the capillaries that supply the lungs.
– Alveolar capillary membrane injury lead to leakage of fluids into alveolar interstitial spaces and alteration in the capillary bed so ventilation and perfusion imbalance developed.
– Assault to the pulmonary system.
– Respiratory distress.
– Decrease lung compliance.
– Sever respiratory failure.
• Hypoxia that persists even when oxygen is administered at 100%
• Decreased pulmonary compliance
• Noncardiac-associated bilateral pulmonary edema
• Dense pulmonary infiltrates seen on x-ray
• Systemic inflammatory response is the common pathway.
• Intrinsically the alveolar-capillary membrane is injured from conditions such as sepsis and shock.
• Extrinsically the alveolar-capillary membrane is injured from conditions such as aspiration or inhalation injury.
• Fat emboli and Oxygen toxicity
• Trauma or fluid overload
– ABGs show respiratory or metabolic acidosis and hypoxemia that does not respond to increase (FiO2).
– Chest x-ray show bilateral infiltrate (early stage) and Ground-glass appearance (end stage)
– Blood culture shows infectious organism.
– Sputum study reveals the infectious organism.
– Dyspnea, tachypnea.
– Crackles, decrease breath sounds.
– Anxiety, restlessness.
• Treat the cause of ARDS.
• Oxygen therapy (FM, NC).
• Mechanical Ventilator (high PEEP without raising FiO2 to reduce risk of O2 toxicity and provide suction to remove of secretions.
• Monitor (V/S, I&O, and CVP).
• Bed rest with prone position or high fowler position to promote oxygenation and chest expansion.
• Blood and fluid therapy.
• Diuretics (Lasix) and Steroids (hydrocortisone).
• Monitor pulse oximetry, laboratory studies.