Abstract
During open heart surgery the influence of a series of factors such as cardiopulmonary bypass (CPB), hypothermia, operation and anaesthesia, as well as medication and transfusion can cause a diffuse trauma in the lungs. This injury leads mostly to a postoperative interstitial pulmonary oedema and abnormal gas exchange. Substantial improvements in all of the above mentioned factors may lead to a better lung function postoperatively. By avoiding CPB, reducing its time, or by minimizing the extracorporeal surface area with the use of miniaturized circuits of CPB, beneficial effects on lung function are reported. In addition, replacement of circuit surface with biocompatible surfaces like heparin-coated, and material-independent sources of blood activation, a better postoperative lung function is observed. Meticulous myocardial protection by using hypothermia and cardioplegia methods during ischemia and reperfusion remain one of the cornerstones of postoperative lung function. The partial restoration of pulmonary artery perfusion during CPB possibly contributes to prevent pulmonary ischemia and lung dysfunction. Using medication such as corticosteroids and aprotinin, which protect the lungs during CPB, and leukocyte depletion filters for operations expected to exceed 90 minutes in CPB-time appear to be protective against the toxic impact of CPB in the lungs. The newer methods of ultrafiltration used to scavenge pro-inflammatory factors seem to be protective for the lung function. In a similar way, reducing the use of cardiotomy suction device, as well as the contact-time between free blood and pericardium, it is expected that the postoperative lung function will be improved.
Highlights
Despite the improvement in the cardiopulmonary bypass (CPB) techniques as well as the postoperative intensive care, impaired pulmonary function is a welldocumented complication of cardiopulmonary bypass, resulting in increased morbidity and mortality [1,2,3]
Whether CPB itself is directly responsible for the whole postoperative lung dysfunction is still controversial
It is indirectly suggested by some studies following off-pump coronary artery bypass, which an attenuated inflammatory response has been shown, the degree of postoperative lung dysfunction was similar with that of conventional Coronary Artery Bypass Grafting CABG [4,5]
Summary
Despite the improvement in the cardiopulmonary bypass (CPB) techniques as well as the postoperative intensive care, impaired pulmonary function is a welldocumented (by enormous experimental and clinical evidence) complication of cardiopulmonary bypass, resulting in increased morbidity and mortality [1,2,3]. Studies have shown that heparin administration a), results in a rapid release of t-PA from its body sources, which may induce fibrinolysis [79], b) causes (in vitro) inhibition of platelet function in more than 30% of patients, leading to increased postoperative blood loss [80], c) has pro-activating properties on granulocytes and platelets [81], and d), heparin after its neutralization with protamine, is inducing an activation of the complement system, action which is correlated with postoperative pulmonary shunt fraction [82] To avoid these adverse effects of heparin, some possible alternatives have been proposed. Possible ways to reduce reperfusion injury include maintenance of physiological oxygen concentration during CPB, oxygen radical scavengers administration, inhibition of xanthine oxidase by allopurinol, as well as drastic reduction of ischemia by using continuous warm blood cardioplegia techniques [99,100,101,102]
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