Acute Respiratory Distress Syndrome (ARDS)
Updated On: July 23, 2026
Anesthesia Implications
Lung-protective ventilation - Use low tidal volumes (about 6 mL/kg predicted body weight) with a limited plateau pressure to avoid ventilator-induced injury, and accept permissive hypercapnia as long as the pH tolerates it.
PEEP and oxygenation - Apply PEEP to recruit and keep alveoli open, and titrate FiO2 to an adequate rather than supranormal saturation. Watch for barotrauma and pneumothorax with high pressures.
Hemodynamic interaction - High intrathoracic pressure and PEEP reduce venous return; balance that against a conservative fluid strategy, since volume overload worsens the lungs.
Recruitment and positioning - Recruitment maneuvers and prone positioning improve oxygenation in severe cases; if prone, protect the pressure points, eyes, and airway.
Transport and continuity - These patients desaturate quickly off the ventilator — maintain PEEP and ventilation during every transfer and hand off the vent strategy clearly.
Severe or refractory cases - Refractory hypoxemia may need advanced rescue such as inhaled pulmonary vasodilators or ECMO; escalate early rather than chasing FiO2.
Pathophysiology
Acute respiratory distress syndrome is non-cardiogenic pulmonary edema from an inflammatory insult — sepsis, aspiration, pneumonia, trauma, pancreatitis — that increases alveolar-capillary permeability.
Protein-rich fluid floods the alveoli, surfactant is lost, and the lungs become stiff and poorly compliant with widespread V/Q mismatch and shunt, producing refractory hypoxemia. It is defined by acute onset, bilateral infiltrates, and hypoxemia not explained by cardiac failure. The injured lung is small and heterogeneous — the 'baby lung' — so conventional tidal volumes overdistend the healthier regions and cause further injury.