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Alveolar Tidal Flooding - a New Mechanism of Ventilator-Induced Lung Injury?

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A7517 - Alveolar Tidal Flooding - a New Mechanism of Ventilator-Induced Lung Injury?
Author Block: A. Tabuchi, W. M. Kuebler; Institut für Physiologie, Charité-universitätsmedizin Berlin, Berlin, Germany.
RATIONALE: While mechanical ventilation is a mainstay of therapy for ARDS, it can simultaneously trigger adverse complications, most prominently ventilator induced lung injury (VILI). This fatal association necessitates the need for optimized ventilation strategies, and thus, for a better understanding of alveolar dynamics and the mechanisms underlying alveolar epithelial injury in the mechanically ventilated, injured and edematous lung. To this end, we directly visualized alveolar dynamics in a murine model of alveolar edema by intravital microscopy. METHODS: C57bl/6 mice were anesthetized, tracheotomised, and placed in head-down right decubitus position. To model alveolar edema, phosphate buffered saline (13ml/kg b.w.) was instilled via the trachea into the dependent right lung. A thoracic window was surgically excised from the right chest wall with the animal placed in left decubitus position and the fluid-instilled upper lobe of the right lung was directly imaged by darkfield intravital microscopy. Alveolar dynamics were continuously visualized and ventilator settings were changed by stepwise increments of inspiratory plateau pressure (IPP) from 10 to 30 cmH2O in 5 cmH2O intervals at PEEP=0 (ZEEP) followed by stepwise increments of PEEP to 15 cmH2O in 1cmH2O intervals] RESULTS: Mechanical ventilation of the fluid-instilled lung caused cyclic shifts of fluid out of and back into the alveoli, a phenomenon that was accordingly termed ""alveolar tidal flooding"". Alveolar tidal flooding resulted not in structural, but functional cyclic collapse and re-opening of alveoli with cyclic shifts of air-liquid interfaces that exert excessive and deleterious shear stresses along the alveolar epithelium. Alveolar tidal flooding of fluid-filled alveoli increased in an IPP-dependent manner with an onset threshold of IPP =20 cmH2O under ZEEP. Conversely, alveolar tidal flooding at an IPP of 30 cmH2O was largely prevented by PEEP values above 10 cmH2O. CONCLUSION: Here, we identify alveolar tidal flooding as potentially injurious mechanism of mechanical ventilation in edematous lungs. Alveolar tidal flooding was prominent at low PEEP and high IPP, i.e. at high driving pressure (ΔP) and may as such contribute to the clinically established detrimental effects of high ΔP.
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