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

• Published in: American journal of respiratory and critical care medicine 2004-02, Vol.169 (4), p.534-541
• Main Authors: Quintel, Michael, Pelosi, Paolo, Caironi, Pietro, Meinhardt, Jurgen Peter, Luecke, Thomas, Herrmann, Peter, Taccone, Paolo, Rylander, Christian, Valenza, Franco, Carlesso, Eleonora, Gattinoni, Luciano
• Format: Article
• Language: English
• Subjects: Abdomen; Abdomen - physiology; Acids; Adult; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Animals; Biological and medical sciences; chemically induced; complications; Edema; etiology; Extravascular Lung Water; Extravascular Lung Water - diagnostic imaging; Hemodynamic Processes; Hemodynamics; Intensive care medicine; Lung; Lung - diagnostic imaging; Lung - physiopathology; Lung Compliance; Lungs; Mechanics; MEDICAL AND HEALTH SCIENCES; Medical imaging; Medical sciences; MEDICIN OCH HÄLSOVETENSKAP; Oleic Acid; physiology; physiopathology; Pressure; Pulmonary arteries; Pulmonary Edema; Pulmonary Edema - diagnostic imaging; Pulmonary Edema - etiology; Pulmonary Edema - physiopathology; Pulmonary Gas Exchange; radiography; Respiratory Distress Syndrome; Respiratory Distress Syndrome, Adult - chemically induced; Respiratory Distress Syndrome, Adult - complications; Respiratory Distress Syndrome, Adult - physiopathology; Swine; Time Factors; Tomography; Tomography, X-Ray Computed; Variance analysis; X-Ray Computed
• ISSN: 1073-449X; 1535-4970
• DOI: 10.1164/rccm.200209-1060OC

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 H(2)O (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 H(2)O significantly lowered the gas content, leaving the tissue content unchanged. In OA-injured lung at aIAP 0 cm H(2)O, 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 H(2)O 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.