ARDS is a clinical syndrome of acute respiratory failure characterized by hypoxemia and bilateral pulmonary infiltrates that cannot be fully accounted for by heart failure or fluid overload.

Epidemiology


Etiology

  • Systemic causes
  • Primary damage to the lungs
    • Pneumonia
    • Aspiration
    • Inhaled toxins
    • Drowning incidents

Tip

Sepsis is the most common cause of ARDS.


Pathophysiology

  • Tissue damage (pulmonary or extrapulmonary) → release of inflammatory mediators (e.g., interleukin-1) → inflammatory reaction → migration of neutrophils into alveoliexcessive release of neutrophilic mediators (e.g., cytokines, proteases, reactive oxygen species) → injury to alveolar capillaries and endothelial cells (diffuse alveolar damage, DAD) leading to:
    • Exudative phase: excess fluid in interstitium and on alveolar surface → pulmonary edema with normal pulmonary capillary wedge pressure (noncardiogenic pulmonary edema) → decreased lung compliance and respiratory distress
    • Hyaline membrane formation: exudation of neutrophils and protein-rich fluid into the alveolar space → formation of alveolar hyaline membranes → impaired gas exchange → hypoxemia
      • Hypoxemia → compensation through hyperventilation → respiratory alkalosis
      • Hypoxemia → chronic hypoxic pulmonary vasoconstriction → pulmonary hypertension and right-to-left pulmonary shunt (increased shunt fraction)
      • Damage to type I and type II pneumocytes → decrease in surfactant → alveolar collapse → intrapulmonary shunting
    • Organizing phase (late stage): proliferation of type II pneumocytes and infiltration of fibroblasts → progressive interstitial fibrosis

Clinical features

  • Acute dyspnea
  • Tachypnea and tachycardia
  • Cyanosis
  • Diffuse crackles

Diagnostics

Berlin criteria for ARDS

  • Acute onset: respiratory failure within one week of a known predisposing factor (e.g., sepsis, pneumonia) or worsening respiratory symptoms
  • Bilateral opacities (on chest x-ray or CT)
    • Similar appearance to pulmonary edema
    • Not sufficiently explained by pleural effusions, lobar or lung collapse, or nodules
  • Hypoxemia: PaO2/FiO2 ≤ 300 mm Hg (measured with a minimum of 5 cm H2O PEEP)
    • Mild ARDS: PaO2/FiO2 = 201–300 mm Hg
    • Moderate ARDS: PaO2/FiO2 = 101–200 mm Hg
    • Severe ARDS: PaO2/FiO2 ≤ 100 mm Hg
  • Respiratory failure cannot be fully accounted for by heart failure or fluid overload.

Mnemonic

ARDS diagnostic criteria include: Abnormal x-ray, Respiratory failure < 1 week after a known or suspected trigger, Decreased PaO2/FiO2, Should exclude CHF or fluid overload as a potential cause of respiratory distress.


Treatment