Inflammatory response to cardiac surgery and strategies to overcome it

A general activation of the immune system is observed during any operative procedure as a physiological response to the surgical trauma. Cardiopulmonary bypass may directly activate the inflammatory response by three distinct mechanisms: direct 'contact activation' of the immune system following exposure of blood to the foreign surfaces, ischaemia-reperfusion injury to vital organs and systemic endotoxaemia resulting from gut translocation of endotoxin. The inflammatory response depends upon recruitment and activation of inflammatory cells. The cellular immune response, in particular polymorphonuclear cell-endothelial adhesion, leads to widespread endothelial damage and dysfunction. Increased oxygen derived free radical activity represents a risk for myocardial and pulmonary complications. The clinical consequences of the stress response vary from a mild generalised transient response, termed the 'systemic inflammatory response syndrome,' to life threatening organ dysfunction. The introduction of the 'off-pump' coronary artery bypass graft surgery has now made it possible to differentiate the influence of cardiopulmonary bypass and surgical access on different modalities of the immune response. 'Off-pump' cardiac surgery has been found to trigger inflammatory response, lesser than 'on-pump' cardiac surgery. Researches are directed towards understanding this complex interplay of humoral and cellular mediators and develop strategies to limit the resultant organ dysfunction. Current literature on the various mediators of this inflammatory response, the role of surgical stress, the pathogenesis of the organ damage and strategies to limit / overcome this response are reviewed.