Reasons for intracranial hypertension and hemodynamic instability during acute elevations of intra-abdominal pressure: observations in a large animal model.

In previous studies we reported that an acute elevation in intra-abdominal pressure (IAP) is responsible for the elevation in intracranial pressure (ICP) and mean blood pressure (MBP). Thus far, the reasons for the increased ICP during an acute elevation in IAP and the combined effects of increased IAP and ICP on hemodynamics have not been reported. Five large animals (swine) were studied. Each animal served as its own control. A subarachnoid screw was placed for ICP monitoring. The jugular vein, femoral vein, and femoral artery were cannulated. ICP, MBP, central venous pressure above (CVPA) and below (CVPB) the diaphragm, and PaC02 were monitored after a pneumoperitoneum with C02 was established at 5, 15, and 30 mm Hg of IAP. Cavography was performed to evaluate the morphology of the inferior vena cava at different increments of IAP. Measurements were obtained in reverse Trendelenburg (group 1), supine (group 2), and Trendelenburg (group 3) positions. Multiple regression analysis was used to examine the effects of IAP and positioning in separate models with different blood pressures as dependent variables. Increased IAP significantly increased CVPA, CVPB, ICP, and MBP. There were no changes in cerebral perfusion pressure. The change in position (from group 1 to group 3) significantly increased CVPA and decreased the CVPB. Cavograms performed on animals in the supine position with increased IAP showed a narrowing of the IVC at the level of the diaphragm. Increases in IAP will increase ICP and MBP without altering the cerebral perfusion pressure. A mechanical effect mediated by compression of the inferior vena cava at the level of the diaphragm with increased central venous pressure and decreased drainage from the lumbar plexus and central nervous system is responsible for this effect.