Cardiopulmonary bypass (CPB) can substantially contribute to organ dysfunction, and in particular lung, with subsequent morbidity and to peripheral vasodilatation, with the need of vasopressor agents, potentially deleterious for some organ perfusions or newly constructed bypass grafts. These clinical concerns are related to an induced inflammatory response, involving both humoral and cellular mediators. Among the former, the complement system is assumed to play a major role, although not exclusive, whereas neutrophils account for most of the cell-mediated inflammatory tissue damage. Theoretically, the systemic temperature during CPB may influence the magnitude of these inflammatory responses. It has been demonstrated that maintenance of normothermia during bypass may increase the extent of the inflammatory response to CPB over that seen under hypothermic conditions. In these latter conditions, the inflammatory mediators are also activated, but the peak levels are often delayed beyond the end of CPB. In an attempt to minimize the systemic inflammatory response to bypass and the subsequent post-perfusion syndrome, the concept of tepid CPB and cardioplegia has been developed.