In excess of 20 000 tidal ventilatory cycles are undertaken daily. Ventilatory patterns that apply high transalveolar stretching forces cause or extend tissue edema and alveolar damage in experimental animals, even when alveolar rupture does not occur. Maximum alveolar pressures above 30 cmH 2O commonly produce regional overdistension in patients with acute respiratory distress syndrome. Peak tidal pressures of this magnitude cause tissue damage in experimental animals when ventilation is sustained for more than 12 to 24 h. The lung may be susceptible to edematous injury produced by high inflating pressures in both the early and late stages of acute respiratory distress syndrome. As the strong collagen infrastructure of the lung degrades, such pressures become increasingly likely to result in overt alveolar disruption (pneumothorax, pneumomediastinum, gas cyst formation) rather than edema.
Failure to maintain a certain minimum end-expiratory transalveolar pressure (i.e. total PEEP) in the early phase of acute respiratory distress syndrome may intensify pre-existing alveolar damage, particularly when high tidal volumes and inflation pressures are used. Indeed, shear forces associated with tidal collapse and reinflation of injured alveolar tissues may be responsible for an important component of ventilator-induced lung damage. The end-expiratory pressure required to avert widespread alveolar collapse varies with the regional forces applied to the lung; consequently, a higher end-expiratory pressure is required to prevent atelectasis in dependent compared with more superior regions. Similarly, a higher total PEEP is required when the chest wall is poorly compliant. Gravitational factors help to explain the strikingly dependent distribution of radiographic infiltrates at the onset of lung injury, as well as the reversal of these infiltrates and improvement of arterial oxygenation in the prone position. Total PEEP sufficient to place the tidal volume above the initial low-compliance region ( Pflex) of the static pressure-volume relationship of the respiratory system appears to attenuate the severe hemorrhagic edema otherwise induced by high ventilating pressure.
Experimentally, damaging the lung requires both high tidal pressures and failure to maintain patency of lung units tending to collapse. What recruits one area of the lung (e.g. dependent regions) is likely to overdistend others (e.g. non-dependent regions) ( Fig 1). Lung recruitment is likely to occur throughout the tidal cycle whenever alveolar pressure reaches a sufficient opening pressure during inspiration and insufficient PEEP is used to keep the same units from closing.
Fig. 1 Regional alveolar mechanics during the tidal breath in acute respiratory distress syndrome. Dependent lung units (D) may be surrounded by sufficiently high pressure to collapse at end-expiration and re-expand at some pressure achieved during the tidal cycle. Non-dependent units (ND) that are exposed to high extra-alveolar pressures may overdistend at end-inspiration, risking 'over-stretch' injury. During controlled ventilation with constant inspiratory flow, the airway pressure tracing may show indirect evidence of these phenomena if it displays segments of rapidly improving and rapidly deteriorating respiratory system compliance. (Reproduced with permission from M§ri.Di.aDd...Wh§§l.§.r.(199Z.))
Stress failure of the pulmonary capillaries with resulting extravasation of formed blood elements into the lung tissue may occur at transvascular pressures that exceed 40 to 90 mmHg, depending on animal species. Theoretically, transcapillary mechanical forces of comparable magnitude could be generated when high tidal volumes and peak static tidal pressures are used without sufficient PEEP in the setting of heterogeneous lung disease. High vascular pressure and blood flows may also be important determinants of lung injury.
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