Comparison of two experimental ARDS models in pigs using electrical impedance tomography.

ABSTRACT

BACKGROUND: Animal trials contribute to major achievements in medical science. The so-called lavage model is frequently used to evaluate ventilation strategies in acute respiratory distress syndrome (ARDS) using electrical impedance tomography (EIT). But, the lavage model itself might have systematic impacts on EIT parameters. Therefore, we established an additional experimental model, in which ARDS is caused by intravenously administered lipopolysaccharide (LPS). In this study, we want to examine if EIT measurements provide consistent results in both experimental models or whether the pathophysiology of the model influences the findings. Overall, we want to compare both experimental models regarding clinical parameters and EIT-derived indices, namely the global inhomogeneity (GI) index and the regional ventilation delay (RVD) index. METHODS: Nineteen pigs were included in this study, allocated to the control group (CO; n = 5), lavage group (LAV; n = 7) and LPS group (LPS; n = 7). After baseline measurements and the establishment of ARDS, assessment of respiratory mechanics, hemodynamics, gas exchange and EIT recordings were performed hourly over eight hours. RESULTS: In both experimental ARDS models, EIT measurements provided reliable results. But, the GI and the RVD index did not show consistent results as compared to the CO group. Initially, GI and RVD index were higher in the LAV group but not in the LPS group as compared to the CO group. This effect disappeared during the study. Furthermore, the GI index and the RVD index were higher in the LAV group compared to the LPS group in the beginning as well. This, once again, disappeared. Clinical lung injury parameters remained more stable when using LPS. CONCLUSION: The two models showed quite different influences on the GI and RVD index. This implies, that the underlying pathophysiology affects EIT parameters and thus the findings. Hence, translation to EIT-guided clinical therapy in humans suffering from ARDS might be limited.