Acute Lung Injury Ventilator Induced Lung Injury



        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 take place.

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 oscillation.

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 possible.


(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.