ECMO and CPB are closely related and share several similarities. Both techniques generate a biomaterial-induced inflammatory response in patients. Despite this, there are important distinctions between ECMO and CPB (Table 1), of which anyone attempting to infer from one to the other must be aware.

Table 1 Key differences between extracorporeal membrane oxygenation (ECMO) and cardiopulmonary bypass (CPB) Full size table

The most obvious distinction between ECMO and CPB is in the duration of support provided. CPB is commonly employed for only minutes to hours to facilitate a surgical procedure. Conversely, ECMO, used in patients with severe organ failure, can be prolonged for weeks to months. This difference in duration requires a different approach to anticoagulation. During CPB, loading doses of unfractionated heparin between 300 and 500 U/kg may be used [39], versus 40–80 U/kg during ECMO [40]. Upon the completion of CPB, protamine sulphate is administered to reverse the effects of heparin, a practice which is avoided during and at the conclusion of ECMO. This is an important distinction, given that the formation of protamine-heparin complexes is known to exacerbate the inflammatory response (via activation of the classical and lectin complement pathways) [41, 42].

Hypothermia is mandatory during CPB, but not commonly employed during ECMO. Likewise, haemodilution, which may also be employed during CPB, is not seen to the same degree during ECMO. Large observational studies have demonstrated an association between the lowest haematocrit recorded during CPB and post-operative mortality [43]. One suggested explanation for this is that haemodilution leads to increased neutrophil activation [44].

As part of the surgical nature of conventional CPB, cardiotomy suctioning, venting of blood and venous reservoirs are incorporated into circuits. This introduces a blood-air interface. Multiple studies have detected higher levels of pro-inflammatory cytokines in cardiotomy-suctioned blood and, in some instances, lower levels of anti-inflammatory cytokines, such as IL-10 [45–47]. The absence of an air/blood interface during ECMO may be a factor in reducing the inflammatory response.

Commonly, perfusion during CPB is non-pulsatile [48]. During VA-ECMO, depending on the residual function of the native heart, varying degrees of pulsatile flow are generated in the face of retrograde arterial perfusion by the ECMO system. This is not the case in VV-ECMO, which uses an ‘“in series configuration’, relying on the native heart for systemic perfusion [49]. Evidence from CPB suggests that pulsatile flow during extracorporeal circulation may act to reduce the inflammatory response [50]. It has been hypothesised that this may be due to the ability of pulsatile perfusion to better sustain the functional state of the microcirculation [51].

Contrary to ECMO, CPB involves inflicting an ischaemia-reperfusion injury [36]. Clamping of the aorta during surgery renders the heart, and to a large extent the lungs, ischaemic. At the completion of surgery, this clamp is removed and both organs undergo a period of reperfusion. Each phase causes a significant inflammatory reaction. In some patients this may prove significant, leading to the onset of lung ischaemia-reperfusion injury or so-called pump lung [52].

Finally, there are clear patient differences. The majority of patients undergoing CPB will have chronic disease (often severe), but are unlikely to be acutely unwell at the time of the procedure. Conversely, those undergoing ECMO are usually critically ill.