Iatrogenic cost of mechanical ventilation

Inspired oxygen fraction

The observations that a high FiO2 (> 60 per cent) caused lung damage were mainly based on experimental studies in normal animals in which, in most cases, the delivered 100 per cent O2 was not appropriately humidified. We do not believe that there is consistent evidence that a high FiO 2 is dangerous in ALI/ARDS, as there is worldwide experience of patients who have survived treatment for days or weeks at an FiO2 of 100 per cent. It must also be remembered that, in ALI/ARDS, the lung surface exposed to high FiO2 is greatly reduced compared with normal lung, as the collapsed and consolidated regions are relatively protected.

Plateau pressure

It has been suggested that a plateau pressure of 35 cmH2O is the upper 'safe' threshold for mechanical ventilation (Slutsky 1994). However, the pressure per se is not dangerous (a diver may experience an alveolar pressure of several atmospheres!). The important factors are the transmural pressure and, probably, the pressure difference between end-expiration and end-inspiration (D Paw). As discussed above, a plateau pressure of 35 cmH2O may be associated with a wide range of transmural pressures depending, during paralysis and anesthesia, on the relationships between the lung and chest wall elastances, and in patients without paralysis (e.g. during pressure support ventilation), on the action of the respiratory muscles.

DPaw may also play a role in the lung damage. Tidal 'stretching' with D Paw = 35 cmH2O (starting from zero PEEP) is very different from that with DPaw = 15 cmH2O (starting from a PEEP of 20 cmH2O). Although no investigations have been performed in a clinical setting, there is consistent experimental evidence that a high D Pa may have a deleterious effect on lung structure. Therefore the 'safe' pressure limit of 35 cmH 2O should be evaluated considering both the transmural pressure and


Tidal volume

Tidal volumes of 10 to 15 ml/kg were used for years in ALI/ARDS; however, after consistent experimental evidence that a 'high tidal volume' may damage the lung structures, it has now been reduced to between 4 and 8 ml/kg. Standardizing the tidal volume per kilogram of weight does not seem appropriate in ALI/ARDS, where the lung gas space (the baby lung) is not related to the body weight. As the risk of an inappropriately high tidal volume is related to 'stretching', i.e. the change in tension betweeen end-expiration and end-inspiration, the tidal volume should be related to the end-expiratory lung volume.

In a normal 70-kg man, 700 ml of tidal volume (i.e. 10 ml/kg) is delivered on an end-expiratory lung volume of approximately 2500 ml. This leads to a 28 per cent increase in end-expiratory lung volume. The same tidal volume in a 70-kg man with an end-expiratory lung volume of 700 ml (moderate to severe ARDS) leads to a 100 per cent increase in end-expiratory lung volume, which is equivalent to ventilating a normal man with a tidal volume of 2500 ml.

To avoid stretching we should maintain the ratio of tidal volume to end-expiratory lung volume within the physiological range (20-30 per cent). This is impossible in severe ARDS, even with permissive hypercapnia, because of the dimensions of the baby lung.

Intratidal collapse and decollapse

The final recognized risk factor for iatrogenic lung damage is the collapse and decollapse of the dependent lung regions within the tidal volume, which may damage the lung structures. This form of barotrauma is present when compression atelectasis is dominant. In fact, during inspiration, even a low plateau pressure (20-25 cmH2O) is sufficient to open the dependent lung regions in which the 'loose' compression atelectasis is recruited. However, if the PEEP level is inadequate, the dependent lung regions collapse again at end-expiration. To avoid this, a PEEP sufficient to counteract the lung weight should be provided ( Gattinoni eL§L 1995)

Unfortunately, increasing PEEP, for a given tidal volume, leads to an increase in plateau pressure. However, if high PEEP and decreased tidal volume are used, there is a risk of development of reabsorption atelectasis. If this occurs and a 'safe' plateau pressure (< 35 cmH 2O) is being used, the transmural pressure is not sufficient to reopen the atelectasis and a progressive decrease of oxygenation may occur. A possible role of 'sigh' should be re-evaluated.

Positive end-expiratory pressure

Rather than damaging the lungs, PEEP may have a protective role. If compression atelectasis is present, PEEP acts as a force counteracting the increased lung weight and keeping open the pulmonary units which will otherwise collapse at the end of expiration. Unfortunately, the level of PEEP necessary to keep the dependent lung regions open overinflates the non-dependent lung regions. Despite this, it is possible that the protective effect of PEEP is avoidance of intratidal collapse. Moreover, PEEP may protect the lung by decreasing D Paw between inspiration and expiration, thus reducing intratidal stretching.

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