Patients undergoing cardiac surgery experience physiologic stresses from general anesthesia, thoracotomy, CPB, surgical manipulation, diaphragm dysfunction, sternotomy, postoperative pain, fluid overload, and massive transfusion. Each of these in itself may lead to pulmonary dysfunction, and acute respiratory failure (ARF) may develop. These effects may worsen clinical prognosis in the presence of preexisting risk factors including severe COPD and congestive heart failure [2–4].

Almost all patients undergoing cardiac surgery have some degree of postoperative lung dysfunction, with an incidence of about 25 %. While patients with adequate pulmonary reserve can tolerate this dysfunction well, 2–5 % of patients are at risk of developing severe lung dysfunction leading to increased morbidity, mortality, and prolonged hospitalization. Postoperative pulmonary complications such as pleural effusion (27–95 %), atelectasis (16.6–88 %), and acute respiratory distress syndrome (ARDS) (0.5–1.7 %) may occur after cardiac surgery, as cardiac surgery causes systemic inflammatory response, which causes lung injury. There are several factors affecting pathogenesis of postoperative pulmonary dysfunction after cardiac surgery and that are also related to the patient’s preoperative pulmonary status and the degree of procedural stress [2, 5].

Factors related to general anesthesia include supine position, neuromuscular block, altered chest wall compliance, acute functional residual capacity (FRC), and vital capacity (VC) reduction, which results in ventilation-perfusion mismatch and abnormal pulmonary shunt fraction. Opioids used commonly in cardiac anesthesia practice reduce hypoxic and hypercapnic ventilatory response postoperatively. As a result, a reduction of VC and FRC of lungs can lead to the onset of hypoxemia and atelectasis with increased work of breathing, which increases oxygen consumption and myocardial work [3, 5].

Postoperative ARF risk is also increased in cardiac surgery when the internal mammary artery used for grafting. Topical and systemic cooling, use of CPB, and surgical manipulations during surgery are risk factors specific to cardiac surgery. The CPB procedure allows extracorporeal maintenance of both circulation and respiration during a non-beating heart at hypothermic temperatures. It is the most likely factor for causing ARF, with two different mechanisms. Whereas interruption of ventilation results in collapsed lungs, causing atelectasis, interruption of pulmonary circulation results in pulmonary ischemia, causing release of inflammatory mediators. Systemic inflammatory response induces intrapulmonary aggregation of leukocytes and platelets, causing further impairment of gas exchange, atelectasis, and increased pulmonary shunt fraction. Because anticoagulation with heparin is essential for CPB after termination of CPB, protamine is used for reversal. Administration of protamine is also associated with systemic reactions and pulmonary hypertension. These many interrelated factors cause ARF after CPB, especially with CPB time exceeding 120 min and massive transfusion, and additional risk factors of prolonged ventilation and extubation failure postoperatively are reported. Furthermore studies report that off-pump cardiac surgery is associated with lower postoperative pulmonary complication rates [5].