Acute Respiratory Distress Syndrome (ARDS) Lecture Notes

Introduction

• Presenter: Ninja Nerds
• Topic: Acute Respiratory Distress Syndrome (ARDS)
• Section: Clinical Medicine
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Definition & Criteria

• Definition: ARDS is characterized by acute hypoxemia, bilateral pulmonary infiltrates, and non-cardiogenic pulmonary edema.
• Key Criteria (Berlin Criteria):
  • Acute hypoxemia
    • SpO2 < 90% or PaO2 < 60 mmHg
    • Developed within less than a week
  • PF ratio < 300 (PaO2/FIO2)
  • Diffuse bilateral infiltrates on chest imaging
  • Non-cardiogenic pulmonary edema (PCWP < 18 mmHg via Swan-Ganz catheter or echocardiogram)

Pathophysiology

• Initial Injury: Damage to alveolar cells (Type I and Type II cells)
  • Type I cell injury: Fluid, proteins, and immune cells fill alveoli, causing exudative phase and shunting (low V/Q mismatch)
  • Type II cell injury: Decreased surfactant leads to alveolar collapse and shunting
• V/Q Mismatch: Both alveolar filling and collapse lead to significant hypoxemia
• Primary Causes of Damage:
  • Direct Lung Injury
    • Pneumonia (e.g., SARS-CoV2)
    • Aspiration
    • Inhaled toxins (e.g., smoke inhalation)
  • Indirect Lung Injury (systemic causes)
    • Sepsis
    • Pancreatitis
    • Transfusion-Associated Lung Injury (TRALI)

Complications

• Pulmonary Hypertension:
  • Hypoxic vasoconstriction → increased PVR → increased PAP → worsened V/Q mismatch and potential right heart failure
  • Signs of right heart failure: JVD, hepatomegaly, ascites, pedal edema
• Intubation Complications:
  • Ventilator-associated pneumonia (VAP): Increased risk of infection from prolonged intubation
  • Ventilator-induced lung injury (VILI):
    • High PEEP or tidal volumes lead to alveolar rupture and pneumothorax
    • Decreased PEEP leads to alveolar de-recruitment and increased work of breathing
    • High FiO2 can cause free radical damage and V/Q mismatch

Diagnosis

• Acute Onset: Symptoms develop within one week
• PF Ratio: PaO2/FIO2 < 300
  • Severity:
    • Mild: 200-300
    • Moderate: 100-200
    • Severe: < 100
• Chest Imaging: Diffuse bilateral opacities on chest x-ray or CT
• Non-cardiogenic Origin: Confirmed through Echo or Swan-Ganz catheter showing PCWP < 18

Management

• Initial Management:
  • Sedation to sync with ventilator (Propofol, Midazolam)
  • Maintain normal volume status to avoid fluid overload
  • Low tidal volume ventilation (6 cc/kg of ideal body weight)
  • High PEEP to prevent alveolar collapse
• Advanced Management:
  • Neuromuscular blockade if PF ratio < 150 (helps to sync with ventilator and reduce respiratory effort)
  • Prone positioning if PF ratio < 150 (reduces dependent atelectasis and improves oxygenation)
  • Consider pulmonary vasodilators for refractory hypoxemia and RV dysfunction
  • VV ECMO (veno-venous extracorporeal membrane oxygenation) as a last resort if all other measures fail
• Ventilator Settings: Key Points
  • Respiratory Rate (RR) & Tidal Volume (TV): Increase RR or TV to decrease PCO2; decrease RR or TV to increase PCO2
  • PEEP & FiO2: Increase PEEP or FiO2 to increase PO2; decrease PEEP or FiO2 to decrease PO2
  • Plateau Pressure: Keep < 30 cm H2O to avoid Barotrauma
• Spontaneous Breathing Trials (SBTs):
  • Ensure underlying issue is resolved
  • Minimal FiO2 and PEEP requirements
  • Check Rapid Shallow Breathing Index (RSBI) to assess readiness for extubation

Conclusion

• Review: Diagnosing ARDS involves evaluating for acute hypoxemia, specific PF ratio, imaging for infiltrates, and ruling out cardiogenic causes.
• Management Focus: Prevent further lung injury through careful ventilator management, supportive care, and advanced therapies if necessary.
• Call to Action: Apply these principles to clinical practice for better patient outcomes.