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Journal Article
Research Support, Non-U.S. Gov't
Hemorrhage lowers the threshold for intra-abdominal hypertension-induced pulmonary dysfunction.
Journal of Trauma 1997 March
BACKGROUND: Intra-abdominal hypertension has been associated with pulmonary and cardiac dysfunctions. We have noted in the clinical scenario of hemorrhagic shock and resuscitation that avoidance of even moderate levels of increased intra-abdominal pressure, using prophylactic decompression, improves outcomes when compared with patients who were decompressed when intra-abdominal pressures went over 20 cm H2O. We hypothesized that prior hemorrhage and resuscitation exacerbates the cardiopulmonary dysfunction associated with intra-abdominal hypertension.
METHODS: Ten anesthetized pigs underwent placement of arterial and pulmonary artery catheters and a Silastic intra-abdominal catheter for measuring and manipulating intra-abdominal pressure. Group 1 animals (n = 5) were subjected to increasing intra-abdominal pressures at 10 mm Hg increments up to a level of 40 mm Hg. Group 2 animals (n = 5) were exposed to a severe hemorrhage and resuscitation before the increasing intra-abdominal pressure protocol.
RESULTS: Compared with baseline, hemorrhage and resuscitation caused a significant deterioration in cardiac output at intra-abdominal pressures of 10 mm Hg and above. Oxygenation was reduced at 30 and 40 mm Hg. These changes were not seen in group 1 animals. A significant difference was found between groups 1 and 2 in VT, PaCO2, and PaCO2/FIO2 ratio at an intra-abdominal pressure of 20 mm Hg. This difference was not seen at lower or higher pressures.
CONCLUSIONS: Prior hemorrhage and resuscitation caused an earlier decline in cardiopulmonary function in the setting of increased intra-abdominal pressure. These data suggest that, when interpreting intra-abdominal pressures, the clinical scenario must be considered. Prior hemorrhage and resuscitation produce the adverse consequences of intra-abdominal hypertension at lower pressures than when intra-abdominal hypertension is the only insult.
METHODS: Ten anesthetized pigs underwent placement of arterial and pulmonary artery catheters and a Silastic intra-abdominal catheter for measuring and manipulating intra-abdominal pressure. Group 1 animals (n = 5) were subjected to increasing intra-abdominal pressures at 10 mm Hg increments up to a level of 40 mm Hg. Group 2 animals (n = 5) were exposed to a severe hemorrhage and resuscitation before the increasing intra-abdominal pressure protocol.
RESULTS: Compared with baseline, hemorrhage and resuscitation caused a significant deterioration in cardiac output at intra-abdominal pressures of 10 mm Hg and above. Oxygenation was reduced at 30 and 40 mm Hg. These changes were not seen in group 1 animals. A significant difference was found between groups 1 and 2 in VT, PaCO2, and PaCO2/FIO2 ratio at an intra-abdominal pressure of 20 mm Hg. This difference was not seen at lower or higher pressures.
CONCLUSIONS: Prior hemorrhage and resuscitation caused an earlier decline in cardiopulmonary function in the setting of increased intra-abdominal pressure. These data suggest that, when interpreting intra-abdominal pressures, the clinical scenario must be considered. Prior hemorrhage and resuscitation produce the adverse consequences of intra-abdominal hypertension at lower pressures than when intra-abdominal hypertension is the only insult.
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