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Objectives
Discuss the primary factors that contribute to ventilator-induced lung injury (VILI).
Discuss stress and strain as related to lung injury.
Describe mechanisms whereby small tidal volumes and positive end-expiratory pressure (PEEP) modify VILI.
Discuss the effect of an inappropriate ventilatory pattern on inflammatory mediator response and the translocation of cells and molecules.
Describe the proposed relationship between VILI and multiple organ dysfunction syndrome (MODS).
Discuss the clinical outcomes data to support the use of lung protective ventilatory strategies.
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Mechanical ventilation is lifesaving; it improves gas exchange, alters pulmonary mechanics, and decreases the work of the cardiopulmonary system. In spite of these beneficial effects, there are numerous potential side effects associated with mechanical ventilation, including
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Increased shunting and dead-space.
Decreased cardiac output and renal blood flow.
Increased risk of nosocomial pneumonia.
Increased intracranial pressure.
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But the concern that has received increasing attention over the past 20 years is ventilator-induced lung injury (VILI). It has become clear that the inappropriate application of mechanical ventilation can induce injury (Table 3-1) similar to acute respiratory distress syndrome (ARDS). In addition, inappropriate application of the mechanical ventilator has been implicated in the induction or extension of multiple system organ failure.
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Historically, the lung injury most associated with mechanical ventilation was barotrauma. Disruption of the alveolar capillary membrane allows air to dissect along facial planes accumulating within the pleural space or other compartments, or the development of subcutaneous emphysema. It is reasonable to assume that the higher the ventilating pressure, the greater the likelihood of barotrauma. Early reports on ARDS and asthma where unlimited peak airway pressure was applied resulted in a higher incidence of barotrauma than more recent case series where high pressure and overdistention of the lungs was avoided. No clear, specific relationship between applied pressure and barotrauma is available. However, many clinicians agree that barotrauma occurs in the lungs ventilated with high alveolar pressures and large tidal volumes (VT). The specific volume and pressure required to develop barotrauma is likely patient-specific.
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High concentrations of inhaled oxygen result in the formation of oxygen-free radicals (eg, superoxide, hydrogen peroxide, hydroxyl ion). These free radicals can cause ultrastructural changes in the lung similar to acute lung injury. In animal models, inhalation of 100% oxygen causes death within 24 to 48 hours. Human volunteers breathing 100% oxygen develop inflammatory airway changes and bronchitis within 24 hours. There are also laboratory data to suggest that former exposure to bacterial endotoxin, inflammatory mediators, and sublethal levels of oxygen (≤ 85%) protect the lung from further injury when ...