Physiologic effects of externally applied continuous negative abdominal pressure for intra-abdominal hypertension

Background: To determine the ability of an externally applied continuous ne gative abdominal pressure device (CNAP) to reverse the effects of elevated intra-abdominal pressure on the central nervous and cardiovascular systems. Methods: Anesthetized, ventilated swine had catheters placed for measuremen t of intra-abdominal (IAP), intracranial (ICP), central venous, pulmonary a rtery, pulmonary artery occlusion, mean arterial, peak inspiratory, inferio r vena cava, and femoral vein pressures. After the animals stabilized, base line measurements were obtained. IAP was increased by incrementally in stil ling an isosmotic polyethylene glycol solution into the peritoneal cavity u ntil it was 25 mm Hg above baseline. IAP mas maintained at 25 mm Hg above b aseline for 2 hours. CNAP was then applied for 2 hours. All parameters were remeasured 30 minutes after each increase in WP, at 2 hours after attainin g maximum IAP, and lastly at 2 hours after abdominal decompression. Cardiac index was maintained near baseline by volume expansion. Results: Elevation of WP to 25 mm Hg above baseline for 2 hours caused incr eases (p < 0.05) in central venous pressure (10.3 +/- 0.9 to 15.2 +/- 1.7), inferior vena cava pressure (13.0 +/- 1.0 to 29.5 +/- 1.5), femoral vein p ressure (13.5 +/- 0.5 to 33.3 +/- 1.3), ICP (10.6 +/- 1.5 to 21.0 +/- 1.5), and peak inspiratory pressure (18.3 +/- 0.3 to 34.2 +/- 1.0). The mean art erial pressure (106.3 +/- 3.5 to 125.8 +/- 3.4), pulmonary artery pressure (24.3 +/- 2.3 to 31.3 +/- 1.7), and pulmonary artery occlusion pressure ros e (12.3 +/- 0.9 to 17.5 +/- 3.5), but not significantly. Cardiac index (3.3 +/- 0.5 to 3.4 +/- 0.4) remained essentially unchanged. CNAP significantly (p < 0.05) decreased IAP (30.7 +/- 1.3 to 18.2 +/- 1.3), central venous pr essure (15.2 +/- 1.7 to 12.4 +/- 2.1), inferior vena cava (29.5 +/- 1.5 to 19.2 +/- 1.3), and ICP (21.0 +/- 1.5 to 16.2 +/- 1.3). Pulmonary artery occ lusion pressure (17.5 +/- 3.5 to 15.0 +/- 3.1) and peak inspiratory pressur e (34.2 +/- 1.0 to 29.7 +/- 1.1) decreased, but not significantly. Conclusion: Acutely elevated IAP causes a significant increase in ICP and i mpaired cardiovascular and pulmonary function, Abdominal decompression rema ins the standard of care for abdominal compartment syndrome. However, in pa tients in whom an increased WP does not require surgical decompression, the results of this study suggest that externally applied CNAP may be of value .