Ventilator induced lung injury is
caused by volutrauma and excessive use of oxygen.
Ventilator induced lung
injury occurs when the lung is directly damaged by the action of
mechanical ventilation. It is not a new concept. Macroscopic injuries
associated with the ventilation of patients with ARDS have been described
for decades: pneumothorax, pneumomediastinum, pneumoperitoneum, associated
with alveolar rupture from overdistension. The term historically applied
to this situation was “barotrauma”. This word expressed the tendency
towards alveolar overdistension when high inspiratory pressures are
applied. However the paradigm has shifted somewhat in recent years away
from pressure induced to volume induced lung injury – “volutrauma”. This
term recognizes that alveolar overdistension is more likely to occur as a
result of excessive volume, than excessive pressure.
There is a considerable body of animal evidence to support this claim. A
number of researchers have demonstrated that applying the same airway
pressure in a volume limited animal (their chests were bound to prevent
expansion), causes considerably less lung damage than when volume is not
limited. If the alveoli cannot overdistend, then they are unlikely to
become damaged (1). Moreover, if normal lungs are exposed to tidal volumes
of 10-15ml/kg, there is parenchymal inflammation, increased vascular
permeability, accumulation of fluid in the lung and alveolar space and
atelectasis. These findings are very similar to what is seen in ALI. So if
high tidal volumes injure the lung, then in patients ventilated in this
way with ALI, repair of the lungs will be slowed and resolution may not
We know, empathically, that if you inflate a balloon excessively, it
bursts. Alveoli will burst if excessive volumes inflate them. However,
there is more to ventilator induced lung injury than just overdistension.
It is believed that the phasic opening an closing of lung units causes
release of cytokines and reinforcement and amplification of the local and
systemic inflammatory response (2). Limiting the extent of volume
expansion certainly curtails this, as may the prevention of phasic opening
and closing of lung units – keeping the lungs open with PEEP. Undoubtedly,
the best way to heal an injury is to rest it, and this is also true of the
lungs(3). The less the lungs are forced to expand-collapse, the less
likely a lung injury is. The ultimate question therefore is – should we be
moving towards full tidal volume ventilation (i.e. the lungs are not
permitted to deflate at all). This can be achieved using high frequency
The other notable source of lung injury is, of course, oxygen. High FiO2
can cause lung injury by two effective mechanisms – the first is the
formation of oxygen free radicals which are cytotoxic, the second is the
problem of absorption atelectasis – as the FiO2 increases, the alveoli
that are well ventilated rapidly empty of oxygen along the concentration
gradient (into the blood), their volume falls and they are vulnerable to
collapse. It was the obsession with controlling the FiO2 that led
physicians to develop the high tidal volume strategies of the 1970s and
1980s, which we have since discovered cause lung injury in their own
right. However, it appears that an FiO2 of greater than 50% should be
considered toxic (4).
For patients with acute lung injury, the ventilation strategy is thus low
tidal volumes with a relatively fast rate, with or without more generous
PEEP has heretofore been given. For the patient who does not have ALI,
there is little evidence that any particular ventilation strategy has any
advantage. In all cases, keeping the FiO2 below 50% is appropriate where
(1) Dreyfuss D, Saumon G. Ventilator-induced lung injury: lessons from
experimental studies. Am J Respir Crit Care Med 1998; 157(1):294-323.
(2) Dreyfuss D, Saumon G. From ventilator-induced lung injury to multiple
organ dysfunction? Intensive Care Med 1998; 24(2):102-104.
(3) Marini JJ. A lung-protective approach to ventilating ARDS. Respir Care
Clin N Am 1998; 4(4):633-63, viii.
(4) Register SD, Downs JB, Stock MC, Kirby RR. Is 50% oxygen harmful? Crit
Care Med 1987; 15(6):598-601.