AVOIDANCE OF VENTILATOR INDUCED LUNG INJURY

Fuhrman BP

Children’s Hospital of Buffalo, Buffalo, New York, USA

 

Lung disease often progresses to acute respiratory failure.  Mechanical ventilation may then be necessary to sustain life.  It is paradoxical that mechanical ventilation may, itself, injure the lung.  Over-distension of normal lung has been shown to increase pulmonary capillary permeability and to trigger a cascade of inflammation that includes cytokine liberation, white cell accumulation, lung disruption and abnormal lung healing.  Ventilator induced lung injury (VILI) contributes to poor outcome but may be avoided. 

Lung diseases of diverse etiology may cause consolidation and atelectasis. Both processes reduce the number of normally functioning lung units.  Attempts to maintain normal ventilation may then over-distend of the few remaining functioning units.  Moreover, it has been shown that re-expansion of lung units adjacent to atelectatic segments requires excessive alveolar wall tension.  Repeated collapse and re-expansion of alveoli exacerbates VILI.  Taken together, these factors promote VILI.  In the diseased lung, VILI cannot be separated either microscopically or biochemically from the natural course of the underlying disease.  This has made VILI difficult to study in patients.

It has recently been shown that the use of small (6 ml/kg) rather than large (12 ml/kg) tidal volumes is associated with reduced mortality.  Prevention of atelectasis by high end-expiratory pressure also reduces VILI.  An approach useful in infants and children is High Frequency Oscillatory Ventilation (HFOV).  In HFOV, mean airway pressure is set high enough to prevent atelectasis and very small tidal volumes are delivered to prevent over-distension.  Partial Liquid Ventilation (PLV), gas ventilation of lung partially filled with perfluorocarbon liquid, has been show in laboratory studies to reduce lung injury.  These liquids also have anti-inflammatory effects in vitro.  The success of extracorporeal membrane oxygenation (ECMO) in neonatal lung disease may reflect a concomitant reduction in VILI.

 

 
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