Ventilator-Induced Lung Injury

Ventilator induced lung injury is damage to the lungs caused or worsened by mechanical ventilation. It can occur in healthy lungs, but injured lungs, such as in acute respiratory distress syndrome, are far more susceptible, because only a small fraction of lung is open and aerated (the "baby lung" of about 300 to 500 mL), which makes normal tidal volumes harmful.

Mechanisms

• Volutrauma: overdistension of aerated alveoli by excessive tidal volume (the main driver)
• Barotrauma: high airway pressure
• Atelectrauma: cyclic opening and collapse of unstable alveoli
• Biotrauma: release of inflammatory mediators from the injured lung into the circulation, leading to distant organ failure
• Oxygen toxicity: fractions of inspired oxygen above 0.6 for over 24 to 48 hours
• Patient self-inflicted lung injury: vigorous spontaneous breathing that produces large transpulmonary pressure swings

Risk markers include a tidal volume above 8 mL/kg predicted body weight, plateau pressure above 30 cmH2O, driving pressure (plateau minus positive end-expiratory pressure) above 15 cmH2O, and mechanical power above about 17 J/min. Injurious ventilation increases mortality, duration of ventilation and organ failure, and lung-protective settings lower mortality by about 9% in absolute terms in acute respiratory distress syndrome. Complications: worsening hypoxemia, air leak, multiple organ dysfunction and death.

• No specific sign. Suspect it when oxygenation worsens, compliance falls, plateau and driving pressures rise, or new infiltrates and air leak appear in a ventilated patient
• Rising oxygen requirement, tachycardia and falling blood pressure from reduced venous return
• Distant organ dysfunction: rising creatinine and liver enzymes
• Red flags: sudden desaturation, rising airway pressure, subcutaneous emphysema, and asynchrony with high effort

1. Monitoring on the ventilator:
   • Predicted body weight: men 50 + 0.91 × (height in cm - 152.4) kg, women 45.5 + 0.91 × (height in cm - 152.4) kg.
   • Tidal volume in mL/kg predicted body weight, plateau pressure (end-inspiratory pause of 0.5 seconds in a passive patient), driving pressure and static compliance.
   • Mechanical power when the ventilator reports it.
2. Esophageal manometry to estimate transpulmonary pressure when spontaneous effort is strong.
3. Imaging: chest radiograph, lung ultrasound for pneumothorax and recruitment, and CT for regional aeration when needed.
4. Arterial blood gas with PaO2 to FiO2 ratio, and echocardiography for right ventricular strain from high pressures.
5. Exclusion of other causes of worsening: pneumonia, pulmonary edema, pneumothorax, pulmonary embolism and progression of the underlying lung disease.

Differentials: progression of acute respiratory distress syndrome, ventilator-associated pneumonia, pulmonary embolism, pneumothorax, cardiogenic pulmonary edema and fluid overload.

1. Lung-protective ventilation for every patient at risk:
   • Tidal volume 6 mL/kg predicted body weight (range 4 to 8 mL/kg).
   • Plateau pressure 30 cmH2O or lower, and driving pressure 15 cmH2O or lower.
   • Respiratory rate up to 35 breaths a minute to control carbon dioxide.
   • Positive end-expiratory pressure titrated to oxygenation and compliance (usually 8 to 15 cmH2O, higher in moderate to severe disease).
2. Permissive hypercapnia: accept pH of 7.20 or higher. Give sodium bicarbonate 50 to 100 mmol IV if pH falls below 7.15 with hemodynamic instability.
3. Oxygen: lowest FiO2 to keep SpO2 at 92 to 96% (PaO2 8 to 10.7 kPa, or 60 to 80 mmHg), avoiding prolonged FiO2 above 0.6.
4. Prone positioning for at least 12 to 16 hours a day when PaO2 to FiO2 is below 150 on FiO2 of 0.6 or more and positive end-expiratory pressure of 5 cmH2O or more, with staff experienced in the maneuver.
5. Neuromuscular blockade for early severe acute respiratory distress syndrome with injurious asynchrony: cisatracurium 15 mg IV bolus, then 37.5 mg/h infusion for up to 48 hours, with train-of-four monitoring and deep sedation (propofol 1 to 3 mg/kg/h).
6. Dexamethasone 20 mg IV daily for 5 days, then 10 mg IV daily for 5 days in moderate to severe acute respiratory distress syndrome.
7. Fluid strategy: conservative fluid management once shock has resolved, with diuresis to a neutral or negative balance (furosemide 20 to 40 mg IV as needed).
8. Rescue therapies for refractory hypoxemia: recruitment maneuvers with caution, inhaled nitric oxide 5 to 20 parts per million, and venovenous extracorporeal membrane oxygenation for PaO2 to FiO2 below 80 for over 6 hours, or below 50 for over 3 hours, or pH below 7.25 with PaCO2 of 60 mmHg or more despite optimization. Extracorporeal carbon dioxide removal is used in selected centres.
9. Prevent patient self-inflicted injury: adequate analgesia and sedation, and limit large transpulmonary pressure swings.
10. Weaning: daily spontaneous breathing trials as soon as oxygenation is adequate.

Follow-up: pulmonary function tests and exercise testing at 3 to 6 months, since reduced diffusing capacity can persist. Counsel on recovery.