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ARDS for USMLE Step 3

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Acute Respiratory Distress Syndrome (ARDS) for the USMLE Step 3 Exam
ARDS is a life-threatening condition involving acute onset of non-cardiogenic pulmonary edema, severe hypoxemia, and bilateral infiltrates. It results from damage to the alveolar-capillary membrane, leading to impaired oxygenation and respiratory failure.
Pathophysiology
ARDS is caused by widespread inflammation and injury to the alveolar-capillary membrane.
  • Alveolar-Capillary Damage:
    • Increased capillary permeability allows protein-rich fluid to leak into the alveoli, leading to non-cardiogenic pulmonary edema.
    • Neutrophilic infiltration and release of inflammatory cytokines (e.g., TNF-α, IL-6) further damage the epithelium and endothelium.
  • Impaired Gas Exchange:
    • Fluid-filled alveoli cause ventilation-perfusion (V/Q) mismatch and intrapulmonary shunting, leading to refractory hypoxemia.
  • Phases of ARDS:
    • Exudative Phase (Days 1-7): Alveolar edema, inflammation, and formation of hyaline membranes.
    • Proliferative Phase (Days 7-21): Resolution of edema, with proliferation of type II pneumocytes and fibroblasts.
    • Fibrotic Phase (After 21 Days): Some patients develop fibrosis and permanent lung damage.
Etiology
ARDS can result from a variety of direct and indirect lung injuries.
Direct Lung Injury
  • Pneumonia: The most common cause of ARDS, triggered by bacterial, viral (e.g., COVID-19), or fungal infection.
  • Aspiration of gastric contents: Causes chemical pneumonitis and alveolar damage.
  • Inhalation Injury: Smoke or toxic gas exposure leads to alveolar injury.
Indirect Lung Injury
  • Sepsis: The leading non-pulmonary cause of ARDS. Systemic inflammation damages the lungs.
  • Pancreatitis: Inflammatory mediators from the pancreas affect distant organs, including the lungs.
  • Transfusion-related Acute Lung Injury (TRALI): Occurs after blood transfusion due to immune-mediated lung injury.
Clinical Features
  • Symptoms:
    • Severe dyspnea: Acute onset of shortness of breath, requiring oxygen or mechanical ventilation.
    • Tachypnea: Rapid breathing due to hypoxemia.
    • Cyanosis: Persistent hypoxemia, often refractory to supplemental oxygen.
  • Physical Exam:
    • Diffuse crackles: On lung auscultation, indicating fluid accumulation.
    • Respiratory distress: Use of accessory muscles, tachycardia, and tachypnea.
Diagnosis
ARDS is diagnosed based on the Berlin criteria, which include timing, imaging, and oxygenation parameters.
Berlin Criteria
  • Timing: Onset within one week of a known clinical insult.
  • Chest Imaging: Bilateral opacities on chest X-ray or CT, unexplained by other causes such as pleural effusion or atelectasis.
Bilateral Opacities in Acute Respiratory Distress Syndrome
  • Origin of Edema: Respiratory failure not fully explained by cardiac failure or fluid overload.
  • Oxygenation (PaO2/FiO2 Ratio):
    • Mild ARDS: PaO2/FiO2 200-300 mmHg.
    • Moderate ARDS: PaO2/FiO2 100-200 mmHg.
    • Severe ARDS: PaO2/FiO2 < 100 mmHg.
Management
Mechanical Ventilation
Lung-protective mechanical ventilation is the mainstay of ARDS treatment.
  • Low Tidal Volume Ventilation: 4-6 mL/kg of predicted body weight to prevent ventilator-induced lung injury (VILI).
  • PEEP (Positive End-Expiratory Pressure): Maintains alveolar patency and improves oxygenation by preventing alveolar collapse.
  • Prone Positioning: Improves oxygenation in patients with moderate to severe ARDS by redistributing lung perfusion and improving lung recruitment.
  • Permissive Hypercapnia: Allowing higher CO2 levels to avoid barotrauma from high ventilatory pressures.
Adjunctive Therapies
  • Fluid Management: Conservative fluid strategy to minimize pulmonary edema and optimize oxygenation.
  • Neuromuscular Blockade: Short-term paralysis can improve oxygenation and ventilator synchrony in severe cases of ARDS.
  • ECMO (Extracorporeal Membrane Oxygenation): Used in cases of refractory ARDS unresponsive to conventional ventilation strategies.
Key Points
  • ARDS is characterized by acute respiratory failure, bilateral pulmonary infiltrates, and hypoxemia due to direct or indirect lung injury.
  • The pathophysiology involves alveolar-capillary membrane damage, leading to non-cardiogenic pulmonary edema and impaired gas exchange.
  • Diagnosis is based on the Berlin criteria, which classify ARDS by the severity of hypoxemia using the PaO2/FiO2 ratio.
  • Lung-protective ventilation (low tidal volume, PEEP) is essential for ARDS management, along with prone positioning and conservative fluid strategies.
  • ECMO is considered for severe, refractory ARDS when standard treatments fail to improve oxygenation.

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