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ARDS for USMLE Step 2

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Acute Respiratory Distress Syndrome (ARDS) for the USMLE Step 2 Exam
ARDS is a clinical syndrome of acute respiratory failure caused by non-cardiogenic pulmonary edema and severe hypoxemia. It arises from direct or indirect injury to the alveolar-capillary barrier, leading to fluid accumulation, impaired gas exchange, and refractory hypoxemia.
Pathophysiology
ARDS results from damage to the alveolar-capillary membrane, leading to increased permeability, fluid leakage, and alveolar flooding.
  • Alveolar-Capillary Damage:
    • Inflammation causes damage to alveolar epithelial and capillary endothelial cells, increasing vascular permeability.
    • This leads to leakage of protein-rich fluid into the alveoli, causing pulmonary edema.
  • Ventilation-Perfusion (V/Q) Mismatch:
    • Fluid in the alveoli impairs gas exchange, causing V/Q mismatch and intrapulmonary shunting, which leads to refractory hypoxemia.
  • Phases of ARDS:
    • Exudative Phase (Days 1-7): Alveolar flooding, neutrophilic infiltration, and formation of hyaline membranes.
    • Proliferative Phase (Days 7-21): Alveolar repair begins, with fibroblast proliferation and resolution of some edema.
    • Fibrotic Phase (After 21 Days): Some patients progress to fibrosis and irreversible lung damage.
Etiology
ARDS occurs due to various direct or indirect lung insults. Identifying the cause is critical for management.
Direct Lung Injury
  • Pneumonia: The most common cause of ARDS, particularly bacterial and viral (e.g., COVID-19).
  • Aspiration: Inhalation of gastric contents causes chemical injury to the alveoli.
  • Pulmonary Contusion: Trauma to the lungs from blunt chest injury.
  • Inhalation Injury: Smoke or toxic gas inhalation causes direct alveolar damage.
Indirect Lung Injury
  • Sepsis: The most common non-pulmonary cause of ARDS. Systemic inflammation leads to diffuse lung injury.
  • Pancreatitis: Inflammatory mediators can cause systemic injury, affecting the lungs.
  • Transfusion-Related Acute Lung Injury (TRALI): Immune-mediated lung injury following blood transfusion.
Clinical Features
  • Symptoms:
    • Severe dyspnea: Rapid onset of shortness of breath, often requiring mechanical ventilation.
    • Tachypnea: Rapid breathing due to hypoxemia and stiff lungs.
    • Cyanosis: Hypoxemia unresponsive to supplemental oxygen.
  • Physical Exam:
    • Diffuse crackles: Indicate fluid in the alveoli.
    • Tachycardia and tachypnea: Signs of respiratory distress.
Diagnosis
ARDS is diagnosed based on the Berlin criteria, which focus on timing, imaging, and oxygenation.
Berlin Criteria
  • Timing: Onset within one week of a known clinical insult or new/worsening respiratory symptoms.
  • Chest Imaging: Bilateral opacities on chest X-ray or CT scan, not fully explained by effusion, atelectasis, or nodules.
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: 200-300 mmHg.
    • Moderate: 100-200 mmHg.
    • Severe: <100 mmHg.
Treatment
Mechanical Ventilation
Ventilation with a lung-protective strategy is the cornerstone of ARDS management.
  • Low Tidal Volume Ventilation: 4-6 mL/kg of predicted body weight to reduce ventilator-induced lung injury (VILI).
  • PEEP (Positive End-Expiratory Pressure): Prevents alveolar collapse and improves oxygenation by keeping the alveoli open during expiration.
  • Prone Positioning: Improves oxygenation in moderate to severe ARDS by redistributing blood flow and enhancing lung recruitment.
  • Permissive Hypercapnia: Allowing higher levels of CO2 to avoid ventilator-related lung injury by limiting tidal volume.
Adjunctive Therapies
  • Fluid Management: Conservative fluid strategy to prevent worsening pulmonary edema and optimize lung function.
  • Neuromuscular Blockade: May improve oxygenation and ventilator synchrony in severe cases by reducing oxygen consumption.
ECMO (Extracorporeal Membrane Oxygenation)
Considered for severe, refractory ARDS that does not respond to conventional ventilation strategies.
Key Points
  • ARDS is characterized by acute-onset hypoxemia and bilateral pulmonary infiltrates, caused by direct or indirect lung injury.
  • The pathophysiology involves diffuse alveolar damage and increased capillary permeability, leading to fluid accumulation in the alveoli and impaired gas exchange.
  • The Berlin criteria are used to diagnose ARDS, classifying severity based on the PaO2/FiO2 ratio.
  • Treatment includes lung-protective mechanical ventilation, low tidal volumes, PEEP, and prone positioning. Conservative fluid management is also essential.
  • In severe cases, ECMO is used as a salvage therapy when conventional treatment fails.

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