Understanding Acute Respiratory Distress Syndrome

Aug 10, 2024

Acute Respiratory Distress Syndrome (ARDS)

Introduction

  • ARDS: Acute Respiratory Distress Syndrome
  • Part of clinical medicine section
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Definition and Criteria (Berlin Criteria)

  • Acute Hypoxemia: SpO2 < 90% or PaO2 < 60 mmHg
  • PF Ratio: Must be < 300
  • Timing: Onset within less than one week
  • Imaging: Diffuse bilateral infiltrates on chest x-ray or CT scan
  • Non-Cardiogenic: Exclude cardiogenic pulmonary edema using Swan-Ganz catheter (PCWP < 18) or echocardiogram

Pathophysiology

  • Diffuse Alveolar Damage (DAD)
    • Damage to type 1 and type 2 alveolar cells and pulmonary capillaries
    • Type 1 Cell Damage: Fluid, proteins, and immune cells leak into alveolus leading to exudative phase and poor ventilation (shunt)
    • Type 2 Cell Damage: Decreased surfactant production, increased surface tension, and alveolar collapse (shunt)
  • Causes of DAD
    • Direct Lung Injury: Pneumonia, aspiration, inhaled toxins
    • Indirect Lung Injury: Sepsis, pancreatitis, transfusion-associated lung injury (TRALI)

Clinical Features

  • Symptoms: Rapid breathing, increased work of breathing, shortness of breath
  • Signs of Hypoxemia: Profound hypoxemia, respiratory distress

Complications

  • Pulmonary Hypertension
    • Hypoxic vasoconstriction, increased pulmonary vascular resistance, right heart failure
    • Signs: JVD, hepatomegaly, ascites, pedal edema
  • Ventilator-Associated Pneumonia (VAP)
    • Intubation > 2 days, bacterial colonization (Pseudomonas, MRSA)
  • Ventilator-Induced Lung Injury
    • High PEEP and tidal volumes can cause pneumothorax or pneumomediastinum
    • High tidal volumes can cause increased inflammation and worsened lung injury
    • Low PEEP can cause alveolar de-recruitment and increased work of breathing
  • Hyperoxia
    • Excessive FiO2 can cause tissue destruction and worsened V/Q mismatch due to free radicals

Diagnosis

  • Criteria
    • Acute onset < 1 week
    • PF ratio < 300
    • Diffuse bilateral infiltrates on imaging
    • Non-cardiogenic: PCWP < 18 (Swan-Ganz) or normal echo
  • Severity
    • Mild: PF ratio 200-300
    • Moderate: PF ratio 100-200
    • Severe: PF ratio < 100

Ventilator Management

  • Modes
    • CMV: Controlled mechanical ventilation for non-spontaneous breaths
    • PSV: Pressure support ventilation for spontaneous breaths
  • Adjusting Parameters
    • High PCO2: Increase respiratory rate or tidal volume
    • Low PCO2: Decrease respiratory rate or tidal volume
    • High PO2: Decrease PEEP or FiO2
    • Low PO2: Increase PEEP or FiO2
  • Key Concepts
    • PEEP: Keeps alveoli open to improve ventilation and gas exchange
    • Pip: High PIP indicates resistance in ventilator tube, low PIP indicates air leak
    • Plateau Pressures: High pressures indicate poor lung compliance (reduce tidal volume)
  • Liberation from Ventilator
    • Criteria: Resolved intubation reason, minimal FiO2 and PEEP, acceptable respiratory rate and tidal volumes

Treatment

  • Initial Management
    • Sedation (Propofol, Midazolam)
    • Maintain euvolemia
    • Low tidal volume ventilation (< 6 cc/kg ideal body weight)
    • High PEEP to prevent alveolar collapse
  • Advanced Management
    • Neuromuscular blockade: For PF ratio < 150 and failed initial measures
    • Proning: For PF ratio < 150 to reduce dependent atelectasis
    • Pulmonary vasodilators: For pulmonary hypertension and RV dysfunction
    • VV ECMO: Last resort for refractory hypoxemia