ARDS is an acute, diffuse, inflammatory lung injury that causes noncardiogenic pulmonary edema and severe hypoxemia. It is not a single disease but a response to a direct or indirect insult.

Mechanism

1. Inflammatory mediators and neutrophils damage the alveolar–capillary membrane, which becomes highly permeable
2. Protein-rich fluid floods the interstitium and alveoli (noncardiogenic edema — heart pressures are normal)
3. Surfactant is lost and inactivated → alveoli collapse (atelectasis), lungs become stiff (low compliance)
4. Blood passes collapsed, flooded alveoli without picking up oxygen = intrapulmonary shunt → hypoxemia refractory to increasing oxygen
5. Hyaline membranes form; later proliferation and, in some clients, fibrosis

Phases: exudative (first week — edema, hyaline membranes) → proliferative (repair) → fibrotic (in some, with long-term restriction).

Current definition — the 2024 Global Definition of ARDS

The global definition (Matthay et al., AJRCCM; online 2023, print 2024) updated the 2012 Berlin definition. It adds pulse oximetry, lung ultrasound, high-flow nasal oxygen, and a category for resource-limited settings.

Oxygenation criteria

Why SpO₂ must be ≤ 97%: above that level the oxyhemoglobin curve is flat, so SpO₂ no longer reflects PaO₂ accurately.

Worked example: a non-intubated client on HFNO 40 L/min, FiO₂ 0.50, SpO₂ 92% → S/F = 92 ÷ 0.50 = 184 (≤ 315) → meets non-intubated ARDS oxygenation criteria if the other elements are present.

• Onset usually within 24–72 hours of the insult (up to 1 week)
• Progressive dyspnea, tachypnea, increasing work of breathing
• Hypoxemia that does not improve with increasing oxygen (hallmark of shunt)
• Restlessness, anxiety, confusion; tachycardia
• Diffuse crackles (breath sounds can be surprisingly quiet early)
• On the ventilator: rising peak and plateau pressures, falling compliance
• Cyanosis late; signs of the underlying cause (sepsis, trauma, pancreatitis)

There is no drug that repairs the lung. Management supports gas exchange while preventing further ventilator-induced lung injury (VILI) and treating the cause.

Lung-protective ventilation

• Low tidal volume: about 6 mL/kg predicted body weight (range 4–8), calculated from height and sex, not actual weight
• Plateau pressure ≤ 30 cmH₂O; keep driving pressure (plateau − PEEP) low
• Adequate PEEP keeps alveoli open; higher PEEP (without prolonged recruitment maneuvers) is suggested in moderate to severe ARDS
• Permissive hypercapnia: a moderately elevated PaCO₂ and pH down to about 7.20–7.25 are accepted to avoid injurious volumes
• Oxygen target about SpO₂ 88–95% (PaO₂ 55–80 mmHg) — an ARDS-specific protective target, lower than the general 92–96%; avoid unnecessarily high FiO₂

Mechanisms of VILI

• Volutrauma — overdistension from large tidal volumes
• Barotrauma — high pressures → pneumothorax, pneumomediastinum, subcutaneous emphysema
• Atelectrauma — repeated opening and collapse of alveoli when PEEP is too low
• Biotrauma — release of inflammatory mediators that injure other organs

Prone positioning — for moderate to severe ARDS (commonly P/F < 150), at least 12–16 hours per day. It opens dorsal lung regions, improves V/Q matching and secretion drainage, and reduces mortality in severe ARDS.

Conservative fluid strategy — once shock has resolved, avoid positive fluid balance (diuretics as needed) while maintaining organ perfusion. Too much fluid worsens edema; too little harms kidneys and other organs.

Neuromuscular blocking agents (e.g., cisatracurium) — may be used for a short period early in severe ARDS to improve ventilator synchrony and lower oxygen consumption (suggested by the 2024 ATS update; the 2023 European guideline advises against routine continuous infusion). They provide no sedation or analgesia — the client must be deeply sedated first. Monitor with train-of-four, protect eyes (no blink), prevent pressure injury; prolonged use causes ICU-acquired weakness.

Corticosteroids — suggested for ARDS in the 2024 American Thoracic Society guideline update when started early (within about 14 days). Monitor glucose, infection, GI bleeding, and neuromuscular weakness.

Sedation and analgesia — light as possible, deeper when proning or paralyzed.

Rescue: venovenous ECMO in selected severe ARDS unresponsive to the above, in experienced centers. Anticoagulation → bleeding risk.

Not recommended routinely: high-frequency oscillatory ventilation, prolonged high-pressure recruitment maneuvers.

Listed in priority order.

1. Oxygenation and ventilation
   • Monitor SpO₂, ABG, P/F or S/F, ventilator pressures (peak, plateau), and breath sounds
   • Confirm protective settings (e.g., tidal volume ≈ 6 mL/kg PBW, appropriate PEEP) and monitor; do not change settings independently. A client on correct protective settings with stable gas exchange needs continued close monitoring, not escalation
   • Avoid disconnecting the ventilator circuit — loss of PEEP causes alveolar collapse and rapid desaturation; use closed (in-line) suctioning
   • Watch for barotrauma: sudden high-pressure alarm, falling SpO₂, unilateral absent breath sounds, subcutaneous emphysema, hypotension
2. Prone positioning care
   • Trained team of 4–5; secure endotracheal tube, lines, and drains; plan how to return to supine in an emergency
   • Pad face, chest, pelvis, knees; reposition head and arms regularly ("swimmer's position"); inspect face, eyes, and pressure points
   • Eye lubrication; check enteral feeding tolerance
   • Expect facial edema; watch for tube displacement and hemodynamic changes
3. Hemodynamics and fluids
   • Strict intake and output, daily weight, blood pressure, lactate, urine output (≥ 0.5 mL/kg/h)
   • Watch potassium and magnesium with diuretics
4. Sedation, analgesia, and paralysis
   • Use validated sedation and pain scales; with neuromuscular blockers ensure sedation, eye care, and train-of-four monitoring
5. Prevent complications
   • VAP bundle: head of bed 30–45° (when supine), oral care, aseptic suctioning
   • Early enteral nutrition (within 24–48 hours) — do not withhold it
   • Stress ulcer prophylaxis in high-risk clients; DVT prophylaxis; passive range of motion; turning every 2 hours when supine; early mobility when stable
6. Family support — frequent updates; ARDS has high mortality and a long recovery

(For client after recovery and for family)

• Recovery takes months; fatigue, weakness, shortness of breath, memory and concentration problems, anxiety, depression, and PTSD are common (post-intensive care syndrome)
• Follow-up with pulmonary function testing and rehabilitation
• Gradual increase in activity; pulmonary rehabilitation if offered
• Smoking cessation, vaccinations, prompt treatment of respiratory infections
• Family members may also experience stress and can be referred for support

• ARDS = increased alveolar–capillary permeability → noncardiogenic, protein-rich pulmonary edema
• Hallmark: hypoxemia refractory to oxygen (shunt)
• Most common causes: pneumonia and sepsis
• 2024 Global Definition: onset within 1 week, bilateral opacities on X-ray/CT or ultrasound, not primarily cardiac; S/F ≤ 315 (SpO₂ ≤ 97%) can replace P/F ≤ 300
• Non-intubated clients can be diagnosed if on HFNO ≥ 30 L/min or NIV/CPAP ≥ 5 cmH₂O
• Intubated severity: mild P/F 201–300, moderate 101–200, severe ≤ 100
• P/F ratio is the key oxygenation index
• Lung protection: Vt ≈ 6 mL/kg predicted body weight, plateau ≤ 30 cmH₂O, adequate PEEP, permissive hypercapnia
• VILI comes from overdistension (high volumes/pressures) and repeated collapse (too little PEEP)
• Prone positioning ≥ 12–16 h/day in moderate–severe ARDS improves oxygenation and survival
• Fluids: balance — avoid overload but maintain perfusion
• Neuromuscular blockers do not sedate; start early enteral nutrition