9/4/2023 0 Comments Barotrauma definitionHowever, the results of a recent clinical trial suggest that a higher PEEP level in association with a high volume/pressure recruitment maneuver augmented mortality incidence. The results clearly imply that the risk/benefit of those two strategies were indistinguishable when applied over a PEEP range between ~ 7–15 cmH 2O. Indeed, three major trials in this field compared the strategy of volutrauma prevention (using low PEEP and low tidal volume) with atelectrauma prevention (using high PEEP and low tidal volume). We believe that the current literature provides clues to resolving the dilemma between atelectrauma and volutrauma. The danger of this strategy is exemplified, in our opinion, by the dismal outcome of one well executed high-frequency ventilation trial where oscillations were applied at airway pressures normally associated with lung volumes close to the TLC. Indeed, the very high PEEP levels needed to achieve near complete reversal of atelectasis may lead to end-inspiratory lung volumes that approach the total capacity of the ‘baby lung’. Unfortunately, however, this mandate promotes atelectasis, prevention of which requires higher PEEP levels. There is no question that volutrauma prevention primarily requires an appropriately low tidal volume. By default, therefore, and to sharply discriminate between consequences of different ventilation strategies, the outcome measure in trials has been mortality rate. But in patients with acute respiratory distress syndrome (ARDS), VILI must be inferred from further deterioration of the lung damage already present. In animal models the different lesions due to mechanical ventilation may be easily associated with ventilator settings. Interestingly, ventilation at high PEEP did not impair gas exchange in those experiments, while hemodynamics dramatically deteriorated, in large part due to increased pulmonary resistance and right heart failure. In recent long-term experiments conducted in initially healthy prone pigs, we found that while minimal PEEP (4 cmH 2O) prevented most lesions observed at ZEEP, higher levels of PEEP inflicted damage that progressively manifested as septal rupture and alveolar hemorrhage. The presence of positive end-expiratory pressure (PEEP) may dramatically change the overall picture, depending on its level. Advancing damage leads to reduced aerated lung capacity, functionally increased elastance and impaired gas exchange. Therefore, the model of ‘high-volume’ volutrauma at ZEEP is, in reality, a mixture of volutrauma (high tidal volume) and atelectrauma (dependent atelectasis). When such large tidal volumes are applied with zero end-expiatory pressure (ZEEP), lesions occur primarily in dependent lung regions where atelectasis-associated sites for stress focusing develop during expiration. To induce volutrauma in healthy animals requires a very high tidal volume (from 20 to 40 mL/kg). Experimental models, however, do allow us to recognize the basic lesions of volutrauma and atelectrauma. Therefore, the transpulmonary pressure required in humans to reach TLC is twice that needed in pigs and three times that in rats. Indeed, the specific lung elastance, i.e., the proportionality constant between stress and strain that helps quantify the tendency for the lungs to recoil and resist deformation, is ~ 12–13 cmH 2O in man, ~ 6 cmH 2O in pigs, and ~ 4 cmH 2O in rats. Results obtained in animal experiments, however, cannot be translated directly to humans due to important species differences regarding structural tolerance. Insights into the mechanical causation of VILI are revealed when high ventilating stresses induce injury in previous healthy lungs that initially are free of possible damaging cofactors. If three of the ten cords do not elongate (in analogy to atelectasis), the remaining seven will support ~ 1430 g each (an increase in stress) and will be proportionally more stretched (an increase in strain). Each supports 1000 g (stress) and undergoes similar elongation from its resting baseline (strain). Let us assume that a load of 10 kg is sustained by 10 parallel and interconnected elastic cords that suspend it. Apart from opening and closing, these too are relevant forms of ‘atelectrauma’.Īnother important but often neglected physical amplifier of stress and strain (‘drop-out’) is rather intuitive. One consequence of microatelectasis is the generation of these stress risers, which encourage shearing stresses and also amplify the consequences of applied power to the ‘baby lung’. For injured lungs, the stress multiplier (which varies with PL) may exceed 2.0. Stress and strain amplify at interfaces between regions with different elasticity these junctions act as “stress risers”.
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