Acute Respiratory Distress Syndrome

Clinical Orientation

A 35-year-old woman is admitted with severe pancreatitis. Over 48 hours, she develops progressive hypoxemia despite increasing oxygen. Her chest X-ray shows bilateral fluffy infiltrates. Her PaO2/FiO2 ratio is 120. She is intubated. This is ARDS. This chapter answers: What mechanism links ARDS to bedside findings, tests, red flags, and nursing priorities?

What Goes Wrong?

ARDS = acute, diffuse, inflammatory lung injury → increased alveolar-capillary permeability → noncardiogenic pulmonary edema → severe hypoxemia.

The pathophysiology (three phases):

1. Exudative phase (days 1-7): Trigger (sepsis, pneumonia, trauma, pancreatitis, aspiration, transfusion, near-drowning) → systemic inflammatory response → neutrophil activation in pulmonary capillaries → damage to alveolar-capillary membrane (both endothelium and epithelium) → protein-rich fluid floods alveoli → surfactant inactivation → alveolar collapse → severe V/Q mismatch and shunt → refractory hypoxemia.

1. Proliferative phase (days 7-21): Type II alveolar cells proliferate, fibrosis begins. Some patients recover; others progress.

1. Fibrotic phase (weeks): Extensive pulmonary fibrosis → severe, prolonged respiratory failure.

Berlin Definition of ARDS:

• Acute onset (within 1 week of known clinical insult)
• Bilateral opacities on chest imaging (not explained by effusions, collapse, nodules)
• Respiratory failure not fully explained by cardiac failure or fluid overload (noncardiogenic)
• Impaired oxygenation:
  • Mild: PaO2/FiO2 200-300 (on PEEP/CPAP ≥5)
  • Moderate: PaO2/FiO2 100-200
  • Severe: PaO2/FiO2 <100

What the Nurse May See

• Progressive dyspnea and tachypnea.
• Refractory hypoxemia: SpO2 falling despite increasing FiO2. This is the hallmark — it doesn't respond to oxygen alone.
• Bilateral crackles. Eventually diffuse — not just bases like cardiogenic edema.
• Chest X-ray: Diffuse bilateral infiltrates ("white-out" in severe cases).
• Hemodynamics: PCWP normal (<18 mmHg) — distinguishes from cardiogenic pulmonary edema.

Nursing Priorities

1. Lung-protective ventilation (the ONLY proven mortality-reducing intervention):
   • Low tidal volume: 6 mL/kg predicted body weight (NOT actual weight).
   • Plateau pressure ≤30 cm H2O.
   • Permissive hypercapnia (allow PaCO2 to rise) to avoid high pressures and volumes.
   • PEEP to recruit alveoli and prevent atelectrauma.

1. Prone positioning: For moderate-severe ARDS (PaO2/FiO2 <150). Improves V/Q matching, recruits dorsal lung regions, reduces ventilator-induced lung injury. Requires team coordination, pressure-point protection.

1. Conservative fluid management: After initial resuscitation, avoid excessive fluids — they worsen pulmonary edema.

1. Treat the underlying cause: Sepsis (antibiotics, source control), pancreatitis, trauma.

1. Neuromuscular blockade: Consider in early severe ARDS to improve ventilator synchrony and reduce oxygen consumption.

1. Monitor for complications: Barotrauma (pneumothorax), ventilator-associated pneumonia, DVT/PE, ICU-acquired weakness.

Red Flags