Systemic inflammatory response during cardiopulmonary bypass and strategies

Organ dysfunction after cardiopulmonary bypass (CPB) still is a major problem in patients undergoing cardiovascular surgery. Studies have demonstrated that systemic inflammatory response (SIR) remains one of the major causes of CPB-associated organ injury. The mechanism of SIR during CPB includes the interaction of blood and artificial surface and endotoxemia. The interaction of blood and artificial surface is initiated by protein adsorption. As a result of series of chain reactions, the numerous powerful inflammatory mediators, including hormones and autacoids, are formed and released. Subsequently, the contact system, coagulation system, complement system, fibrinolysis system, and leukocytes, platelets, and endothelial cells, are all activated to participate in the interaction of blood and artificial materials. These activations of different systems and blood cells can interact and magnify each other. CPB-associated endotoxemia has been demonstrated to intensify and deteriorate SIR during CPB. SIR leads to organ injury. In clinical setting, the most common SIR-related organ damage is pulmonary dysfunction, which often is manifested by decreasing of lung compliance, rise in shunt fraction, work of breathing, and likelihood of atelectasis and pneumonia. Strategies to control CPB-related SIR have been developed, such as improvement of biocompatibility of artificial surface (new biomaterials), temporary inhibition of blood cells activation ("blood anesthesia") during CPB, and blockage of the bioactivities and effects of inflammatory mediators.