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Published ahead of print on December 11, 2003, doi:10.1164/rccm.200209-1060OC
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American Journal of Respiratory and Critical Care Medicine Vol 169. pp. 534-541, (2004)
© 2004 American Thoracic Society

An Increase of Abdominal Pressure Increases Pulmonary Edema in Oleic Acid–induced Lung Injury

Michael Quintel, Paolo Pelosi, Pietro Caironi, Jurgen Peter Meinhardt, Thomas Luecke, Peter Herrmann, Paolo Taccone, Christian Rylander, Franco Valenza, Eleonora Carlesso and Luciano Gattinoni

Institut für Anästhesiologie und Operative Intensivmedizin, Universitätsklinikum Mannheim, Mannheim, Germany; Department of Clinical and Biological Sciences, Universita' degli Studi dell'Insubria, Ospedale di Circolo, Fondazione Macchi, Varese; Istituto di Anestesia e Rianimazione, Universita' degli Studi di Milano, Ospedale Policlinico IRCCS, Milano, Italy; and Department of Medical Sciences, Clinical Physiology, Uppsala University Hospital, Uppsala, Sweden

Correspondence and requests for reprints should be addressed to Luciano Gattinoni, M.D., F.R.C.P., Istituto di Anestesia e Rianimazione, Ospedale Maggiore Policlinico-IRCCS, Via Francesco Sforza 35, 20122 Milan, Italy. E-mail: gattinon{at}policlinico.mi.it

Increased abdominal pressure is common in intensive care unit patients. To investigate its impact on respiration and hemodynamics we applied intraabdominal pressure (aIAP) of 0 and 20 cm H2O (pneumoperitoneum) in seven pigs. The whole-lung computed tomography scan and a complete set of respiratory and hemodynamics variables were recorded both in healthy lung and after oleic acid (OA) injury. In healthy lung, aIAP 20 cm H2O significantly lowered the gas content, leaving the tissue content unchanged. In OA-injured lung at aIAP 0 cm H2O, the gas content significantly decreased compared with healthy lung. The excess tissue mass (edema) amounted to 30 ± 24% of the original tissue weight (455 ± 80 g). The edema was primarily distributed in the base regions and was not gravity dependent. Heart volume, central venous, pulmonary artery, wedge, and systemic arterial pressures significantly increased. At aIAP 20 cm H2O in OA-injured lung, the central venous and pulmonary artery pressures further increased. The gas content further decreased, and the excess tissue mass rose up to 103 ± 37% (tissue weight 905 ± 134 g), with homogeneous distribution along the cephalocaudal and sternovertebral axis. We conclude that in OA-injured lung, the increase of IAP increases the amount of edema.

Key Words: intraabdominal pressure • acute respiratory distress syndrome • pulmonary edema • lung mechanics • computed tomography scan




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