abdominal compartment syndrome

Increased IAP often coexists with sepsis in severely ill patients in the ICU, under mechanical ventilation and pharmaceutical support of the circulation with inotropes and vasoactive drugs. Both conditions have an unfavorable effect on the cardiovascular system. The purpose of this experimental study was to record the effect of increased intra-abdominal pressure on the cardiovascular system of pigs, with or without additional sepsis. Sixteen male pigs were randomly assigned in two groups A and B. In both groups, after induction to anesthesia and mechanical ventilation, the intra-abdominal pressure was increased to 25mmHg by helium insufflation in the peritoneal cavity, and that level of IAP was preserved until the end of the experiment. In Group A no other intervention apart from the increase in IAP was made, whereas in Group B, 60 minutes after the increase in IAP, 100μg/kg LPS were administered. Data were recorded after induction of anesthesia and initiation of mechanical ventilation (baseline measurement/measurement 0) and thereafter every 20 min after intra-abdominal pressure increase. The last measurement (measurement 9) was obtained immediately before release of pneumoperitoneum. Parameters measured or calculated included HR, BP(s,d,m), RVPs, PAP(s,d,m), PΑWP, CO, SV, SVR, PVR, SvO2, ETCO2. HR increased statistically significantly only in Group B, 60 minutes after the administration of LPS. BP (s, d, m) presented a significant change only in Group B, an initial increase immediately after LPS administration, followed by a decrease. CVP, RVPs and PAP (s, d, m) increased in both groups after IAP increase, whereas they presented an additional increase in Group B, after LPS administration. PΑWP changed only in Group B, after LPS administration. CO and SV were dramatically reduced in Group B, immediately after LPS administration, but gradually recovered their initial values until the end of the experiment. SVR changed only in Group B. They increased after LPS administration and then they gradually decreased. PVR increased dramatically after LPS administration and, despite gradual decrease they remained at high values until the end of the experiment. SvO2 decreased in Group B after LPS administration but gradually recovered its initial values. At the conditions of this particular experiment, the increase in intra-abdominal pressure was well tolerated by the laboratory animals. On the contrary, sepsis induction by LPS administration had an unfavorable effect on the cardiovascular system.

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