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.