Lung injury in cardiopulmonary bypass

Acute lung injury after cardiopulmonary bypass (CPB) occurs to some degree in over a third of cases and can lead to prolonged mechanical ventilation and hospital stay. In severe cases, the mortality rate can be significant. The lungs, especially in neonates and infants, are uniquely vulnerable to injury during bypass during which the lungs have substantially diminished circulation with only bronchial artery supply, ventilation is usually discontinued and blood contact with the artificial surfaces of the bypass circuit activates a myriad of inflammatory cascades. There is activation of platelets, leukocytes, fibrinolysis and the coagulation system, kallikrein–bradykinin and complement systems. Large pools of neutrophils reside in the lungs that are immediately present to contribute to injury. Neutrophils, augmented by macrophages, marginate and then migrate into the lung to release oxygen free radicals and enzymes leading to direct lung injury. This constellation leads to increased pulmonary vascular resistance, reduced surfactant activity, atelectasis, and pulmonary edema. Heterogeneous causes of injury, including preexisting and postoperative elements, contribute together to overall lung inflammation, hypoxemia, and intrapulmonary shunting. A variety of interventions to lessen post-CPB lung injury and to manage patients with established lung injury exist though evidence for their efficacy in the cardiac surgical population is often extrapolated from experience with adult respiratory distress syndrome from other causes.