Systemic inflammation is seen in all surgery and trauma; however, it is more profound in cardiac surgery that uses cardiopulmonary bypass (CPB). The contact of blood components with non-biological surfaces such as the pump tubing, oxygenator membranes and altered propulsion by the roller pumps is a significant factor in amplifying the inflammatory effects of CPB. While CPB is currently unavoidable in valve replacement surgery, there are choices between conventional surgery using CPB and off-pump (OP) techniques in coronary surgery, especially if reducing the extent of the systemic inflammatory response syndrome (SIRS) is an objective.
As coronary surgery accounts for over 70% of cardiac surgery, the potential for minimising the deleterious effects of the SIRS has extensive implications as it would benefit large numbers of patients. However, surgical and pharmacological strategies to prevent or minimise SIRS may have untoward consequences with respect to the completeness of revascularisation, graft patency and the degree and duration of invasive monitoring.
Evidence of Systemic Inflammation
Massive release of inflammatory markers into the circulation occurs. These include activated complement components C3a and C5a, interleukins (IL-6, IL-8 and IL-1β) and tumour necrosis factor (TNF)-α – all cytokines that promote neutrophil and monocyte mobilisation in response and directed to the sites of inflammation and perceived vascular injury. In addition, many other vasoactive mediators are released, including endothelin, histamine, prostacyclin and bradykinin.1,2 Almost invariably the concentrations of these cytokines increase by between 10- and 100-fold over baseline, with peak-level increases during CPB occurring four to 12 hours after completion of CPB before falling back to normal by between 48 and 72 hours.2
In parallel, there is organ dysfunction of varying degrees, particularly in the lungs, kidneys and central nervous and gastrointestinal systems. These parallel changes are in part attributed to the intense affects of the newly released vasoactive molecules, but may also be due to the non-pulsatile flow associated with CPB, lower mean pressures and microemboli.1–3 Inflammatory lung injury appears to be due to the effects of activated leukocytes on the pulmonary capillaries resulting in increased vascular permeability, extravascular water content and shunting. In the brain, CPB is associated with an increase in extracellular fluid, as noted on magnetic resonance imaging (MRI).4
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