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Acute respiratory distress syndrome

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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

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 alveoli → excessive 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 c
    • 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

  1. Address Underlying Cause: Identify and treat the precipitating event (e.g., empiric Abx for sepsis, source control).
  2. Ventilation Strategy (LTVV):
    • Low Tidal Volumes (6 mL/kg of Ideal Body Weight [IBW]) to prevent volutrauma. c
      • The “Baby Lung” Concept: In ARDS, large portions of the lung are consolidated, fluid-filled, and non-functional. The remaining aerated lung is small.
      • Preventing Volutrauma: Standard tidal volumes (10–12 mL/kg) would over-distend and tear this limited, functional lung tissue (volutrauma), worsening inflammation (biotrauma). 6 mL/kg IBW safely ventilates the small remaining aerated lung.
    • Permissive Hypercapnia: Accept respiratory acidosis (pH ≥ 7.20) to maintain low tidal volumes.
      • Acidosis > Lung Destruction: Clinical trials (e.g., ARDSNet) showed that mild respiratory acidosis (pH 7.20) is well-tolerated by the body and is far less harmful than the physical trauma of trying to blow off using high, damaging tidal volumes.
    • Target Plateau Pressure: < 30 cm H2O to prevent barotrauma.
  3. Oxygenation Strategy (High PEEP):
    • Set high PEEP to prevent alveolar collapse (atelectrauma) and recruit alveoli.
    • Target SpO2: 88–95% (or PaO2 55–80 mmHg) to avoid oxygen toxicity from high FiO2.
  4. Refractory Hypoxemia Management:
    • Prone Positioning: First-line for moderate-to-severe ARDS (PaO2/FiO2 < 150 mmHg). Done ≥ 16 hrs/day to improve V/Q matching and decrease ventilator-induced lung injury (VILI).
    • Neuromuscular Blockade (NMB): Cisatracurium infusion to reduce patient-ventilator dyssynchrony.
    • Fluid Restriction: Conservative fluid management strategy (keep pt dry) to minimize pulmonary edema.
    • ECMO: Veno-venous (VV-ECMO) for severe, refractory cases when conventional strategies fail.

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