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ARDS for USMLE Step 1

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Acute Respiratory Distress Syndrome (ARDS) for the USMLE Step 1
ARDS is a form of acute respiratory failure due to diffuse alveolar damage, resulting in non-cardiogenic pulmonary edema and severe hypoxemia. It is triggered by various direct and indirect lung injuries, causing widespread inflammation and impaired gas exchange.
Pathophysiology
ARDS results from injury to the alveolar-capillary membrane, leading to increased permeability and fluid accumulation in the alveoli. This disrupts gas exchange, causing severe hypoxemia.
  • Alveolar-Capillary Damage: Inflammation and injury to the alveoli increase capillary permeability, leading to leakage of protein-rich fluid into the alveoli (non-cardiogenic pulmonary edema).
  • Impaired Oxygen Exchange: Fluid-filled alveoli reduce ventilation, causing V/Q mismatch, shunting, and refractory hypoxemia.
  • Phases of ARDS:
    • Exudative Phase (Days 1-7): Alveolar flooding and neutrophil infiltration, leading to hyaline membrane formation and impaired oxygen diffusion.
    • Proliferative Phase (Days 7-21): Initiation of lung repair, fibroblast proliferation, and some resolution of edema.
    • Fibrotic Phase (After 21 Days): Fibrosis and lung remodeling occur in some patients, causing long-term impairment in lung function.
Causes
ARDS can be caused by direct or indirect lung injuries. Identifying the cause is essential for management.
Direct Lung Injury
  • Pneumonia: The most common cause of ARDS, caused by bacterial, viral (e.g., COVID-19), or fungal infections.
  • Aspiration: Inhalation of gastric contents leads to chemical pneumonitis and alveolar damage.
  • Inhalation Injury: Smoke or toxic gases damage the alveoli.
  • Pulmonary Contusion: Trauma to the lungs causes localized inflammation and edema.
Indirect Lung Injury
  • Sepsis: A common cause of ARDS due to the systemic release of inflammatory mediators.
  • Pancreatitis: Inflammatory mediators from the pancreas can affect the lungs.
  • Trauma: Severe trauma or shock increases the risk of ARDS.
  • Transfusion-related acute lung injury (TRALI): ARDS following blood transfusion due to recipient antibodies reacting with donor leukocytes.
Clinical Features
  • Symptoms:
    • Severe dyspnea: Rapid onset of difficulty breathing, often requiring mechanical ventilation.
    • Tachypnea: Rapid breathing due to hypoxemia and decreased lung compliance.
    • Cyanosis: Hypoxemia despite oxygen therapy.
  • Physical Exam:
    • Diffuse crackles: Heard on auscultation, indicating fluid accumulation in the lungs.
    • Tachycardia and tachypnea: Signs of respiratory distress.
Diagnosis
ARDS is diagnosed based on clinical and radiological findings. The Berlin criteria are used to confirm the diagnosis.
Berlin Criteria
  • Timing: Symptoms begin within one week of a known clinical insult.
  • Chest Imaging: Bilateral opacities on chest X-ray or CT scan that are not explained by other causes (e.g., effusion, atelectasis, or nodules).
Bilateral Opacities in Acute Respiratory Distress Syndrome
  • Origin of Edema: Pulmonary edema must not be fully explained by heart failure or fluid overload.
  • Hypoxemia (PaO2/FiO2 ratio): Severity is classified based on the ratio of PaO2 to FiO2 (fraction of inspired oxygen):
    • Mild: PaO2/FiO2 200-300 mmHg.
    • Moderate: PaO2/FiO2 100-200 mmHg.
    • Severe: PaO2/FiO2 < 100 mmHg.
Treatment
Mechanical Ventilation
The mainstay of ARDS management is supportive care, with mechanical ventilation being critical.
  • Low Tidal Volume Ventilation: 4-6 mL/kg of predicted body weight to avoid overdistension of the alveoli and ventilator-induced lung injury (VILI).
  • PEEP (Positive End-Expiratory Pressure): Used to keep alveoli open during expiration and improve oxygenation.
  • Prone Positioning: Improves oxygenation by redistributing blood flow and recruiting more alveoli, used in moderate to severe ARDS.
Adjunctive Therapies
  • Fluid Management: Conservative fluid strategies reduce pulmonary edema and improve lung function.
  • Neuromuscular Blockade: Reduces oxygen consumption and improves patient-ventilator synchrony in severe ARDS.
Key Points
  • ARDS is characterized by non-cardiogenic pulmonary edema, hypoxemia, and bilateral infiltrates on imaging, often resulting from direct or indirect lung injury.
  • The pathophysiology involves increased alveolar-capillary membrane permeability, leading to fluid leakage into the alveoli and impaired gas exchange.
  • The Berlin criteria are used to diagnose ARDS, with hypoxemia classified by the PaO2/FiO2 ratio.
  • Management focuses on lung-protective ventilation strategies, with low tidal volumes and PEEP, and adjunctive therapies such as prone positioning and conservative fluid management.
  • Identifying and treating the underlying cause, such as pneumonia or sepsis, is crucial for improving outcomes.

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