ABSTRACT
Incremental improvements in cardiopulmonary bypass (CPB) technology over the last 30 years have largely eliminated CPB-associated mortality and substantially reduced its morbidity. Technological advancements have more recently focussed on ameliorating the CPBinduced systemic in ammatory response. This is triggered by the contact of blood with the nonendothelial foreign surfaces of an extracorporeal circuit and at the blood-air interface (Figure 2.1), both of which activate a number of proin ammatory pathways, including the coagulation, complement, and kallikrein-kinin systems.1 Between them, they produce a cellular response by generating active mediators, such as cytokines, which trigger leucocytes, vascular endothelial cells, and platelets, to produce systemic in ammation. Mechanical trauma induced by the CPB pump and the shearing forces
generated by cardiotomy suction also contribute to the systemic in ammatory response.2
