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-1) and tumour necrosis factor (TNF) - 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

Post-operative, Physiological and Haemodynamic Effects
In previous decades, patients on CPB were usually cooled to 26-28ºC and were often hypothermic and hypertensive and had high systemic vascular resistance post-operatively.⁵ These physiological reactions to cold often masked or counteracted the effects of complement activation and circulating cytokines. Contemporary perfusion at normothermia or mild hypothermia has allowed greater expression of the vasoactive mediator effects in terms of measurable physiological and haemodynamic effects, particularly with respect to temperature, systolic and mean blood pressure, systemic vascular resistance and cardiac output in the post-operative period.^6-8

Causes of Systemic Inflammatory Response Syndromes and Their Relative Contribution
Operative trauma is a potent stimulus, particularly when vascularised tissue is breached. In coronary surgery there is extensive trauma to cutaneous, subcutaneous, muscular and periosteal tissues and marrow and vascular injury (to varying extents) via sternotomy, mediastinal, internal thoracic artery and additional conduit harvesting.⁹ With specific reference to OP coronary surgery, similar patterns of substantial cytokine and vasoactive mediator release are seen, although of a lesser intensity.^2,10,11 The anti-inflammatory cytokine IL- 10 is released to similar levels in both forms of coronary surgery,¹² implying that the sternotomy, conduit harvesting, mediastinal dissection and cardiac handling are significant and possibly the most important factors. CPB, with exposure of blood to artificial surfaces and areas of endovascular trauma (aorta, right atrium), mechanical disruption of blood elements and scavenged shed blood suction, is an additional contributor. The length of CPB and surgery may also influence the degree of SIRS.^1-4,13