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A5124 - Biological Impact of Mechanical Power at High and Low Tidal Volume in Experimental Mild Acute Respiratory Distress Syndrome
Author Block: R. Santos1, L. Maia1, M. V. de Oliveira1, C. Santos1, L. Moraes1, C. S. Samary1, E. F. Pinto1, J. Machado1, A. Carvalho1, M. Fernandes1, V. Martins1, V. Capelozzi2, T. Koch3, M. Gama de Abreu3, P. Pelosi4, P. L. Silva1, P. R. Rocco1; 1Carlos Chagas Filho Institute of Biophysics, Laboratory of Pulmonary Investigation, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil, 2Department of Pathology, University of Sao Paolo, Sao Paulo, Brazil, 3Department of Anesthesiology and Intensive Care Therapy, Dresden University of Technology, Dresden, Germany, 4Department of Surgical Sciences and Integrated Diagnostics, University of Genoa, Genoa, Italy.
RATIONALE: Mechanical power delivered from the ventilator to the lungs, which corresponds to mechanical energy over time, is associated with deterioration of lung function. While the contribution of respiratory rate (RR) to mechanical power and its impact on lung injury has been described, it is still unclear whether low and high tidal volumes (VT) result in comparable lung injury when similar levels of mechanical power are imparted. In the present study, we determined the impact of mechanical power (as obtained with low and high VT) on ventilator-induced lung injury (VILI) in a rat model of mild acute respiratory distress syndrome (ARDS). We hypothesized that VT level would still be a major determinant of the impact of mechanical ventilation on VILI even when similar levels of mechanical power are transferred from the ventilator to the lungs. METHODS: Wistar rats received Escherichia coli lipopolysaccharide intratracheally. After 24 hours, 32 rats were randomly assigned to ventilation (2 hours) with: 1) Low Power/Low VT (6 mL/kg); 2) Low Power/High VT (11 mL/kg); 3) High Power/Low VT; and 4) High Power/High VT. Mechanical power was calculated as energy (=ΔP,L2/E,L)×RR (ΔP,L=transpulmonary driving pressure; E,L=lung elastance; RR=respiratory rate), and was threefold higher in High-Power than in Low-Power groups. Eight animals were not mechanically ventilated (NV). RESULTS: Compared to Low VT, High VT increased diffuse alveolar damage (DAD) in Low-Power (p=0.0029) and High-Power groups (p=0.0058). At High VT, DAD worsened with High Power compared to Low Power (p=0.0006). Gene expressions of amphiregulin, interleukin (IL)-6, and club cell secretory protein 16 (CC16) were higher in ventilated animals than in NV. Amphiregulin and IL-6 mRNA expressions were higher in High Power/High VT than Low Power/High VT. The High Power/High VT strategy increased amphiregulin and CC16 compared to High Power/Low VT. DAD scores and gene expression of amphiregulin and CC16 correlated with power. ΔP,L best predicted variance in power, but VT best predicted variance in DAD score, E-cadherin, amphiregulin, and IL-6. CONCLUSION: In experimental mild ARDS, high power delivered by the ventilator resulted in increased VILI, even at low VT. However, the impact of high VT on VILI was greater than predicted by mechanical power calculations.