Gastrointestinal dysfunction following cardiac surgery.

Abstract

Cardiac surgery is associated with a low incidence of GI complications, but with a disproportionate mortality. A number of risk factors have become established which identify patients at risk. CPB is associated with profound reductions in mucosal blood flow. Mesenteric perfusion is altered by primary endothelial dysfunction, which may further be exacerbated by the use of vasoconstrictors during CPB; inflammatory mediators can 'prime' the mesenteric vasculature. Cardiac surgery with or without CPB is associated with increased tissue oxygen demands, particularly by the splanchnic bed. The disparity in general and regional oxygen supply and demand results in the development of mucosal hypoxia and this cannot be attributed to CPB alone. This injury is measurable by reductions in both absorptive and barrier functions of the gut. Protection may be conferred by modulating the perfusion protocol during bypass and pharmacological interventions which modify the inflammatory response to surgery.