Mechanisms of systemic hypertension during acute elevation of intraabdominal pressure

In previous studies we described mechanisms by which acute elevation of the intraabdominal pressure (IAP) induces intracranial hypertension (ICHTN). Here we sought to define the role of ICHTN in mediating systemic hypertension (HTN) during CO(2) pneumoperitoneum (PNP).

Six large animals (swine) were hyperventilated to buffer hypercarbia. Intracranial pressure (ICP) was monitored with a Camino intraparenchymal ICP monitoring system. A Foley catheter was introduced intracranially via a separate burr hole. At phase 1, changes in ICP, central venous pressure (CVP), and mean arterial pressure (MAP) were recorded during periods of CO(2) PNP at IAP levels of 15, 20, 25, and 30 mm Hg. At phase 2, ICHTN was produced directly by inflating the intracranial balloon to the same ICP levels that had been measured in phase 1 for each degree of IAP. CVP and MAP were recorded. Repeated measures analysis of variance was applied.

At phase 1, the mean DeltaCVP, DeltaICP, and DeltaMAP increased relative to the degree of IAP (P = 0.0001, 0.0004, and 0.024, respectively). At phase 2, the increments in DeltaMAP were significant (P = 0.024) and in the same direction and amplitude as at phase 1.

In this study, increasing the IAP with CO(2) PNP with a consequent increase of ICP and direct manipulation of the ICP produced a comparable systemic HTN. We believe that this further supports our hypothesis: Elevated IAP produces an immediate increase in the CVP, which impairs venous drainage from the central nervous system (CNS), increases the ICP, and initiates a CNS-mediated response and systemic HTN.