BACKGROUND: The abdominal compartment syndrome and its repercussion on hemodynamic and central nervous system repercussions were studied experimentally in an animal model. METHODS: Eigth dogs were operated under general anesthesia. Intracranial pressure(ICP), mean arterial pressure(MAP), cerebral perfusion pressure(CPP), central venous pressure(CVP) and cardiac output(CO) were studied. Baseline measurements were obtained, and then an abdominal pucture was performed in order to raise the IAP by air insufflations. The IAP was initially increased to 10cmH2O and further elevated by increments of 10cmH2O. All parameters were measured after a 15 minute stabilization period of each pressure increase. When the abdominal pressure reached 40cmH2O, all parameters were measured again and decompression of the abdominal cavity was carried on. Final measurements were then obtained. RESULTS: The increase of IAP caused the following physiologic changes: ICP progressively increase; initial MAP increase until 20cmH2O IAP and decrease at 40cmH2O; initial CPP increased until 10cmH2O intra-abdominal pressure and progressively decreased beyond 30cmH2O; CVP progressive increase; CO decrease beyond 30cmH2O. ICP, MAP, CPP, CVP and CO returned to near baseline level after abdominal surgical decompression. CONCLUSION: The progressive increase of IAP is associated with several hemodynamic and central nervous system changes, that returned to near initial values after abdominal cavity surgical decompression.
Wounds and injuries; Pos-operative complications; Experimental surgery; Intracranial pressure; Perfusion; Cardiac output
