Atelectasis occurs regularly during anesthesia induction and persists in the postoperative period. This may contribute to significant morbidity, delay in discharge, and additional health-care costs. It is found in almost 90 % of all patients who are anaesthetized, on average involving 10 % of total lung tissue.

During general anesthesia, lung collapse may be caused by three basic mechanisms: compression atelectasis by loss of diaphragm tone and abdominal pressure; absorption atelectasis, when less gas enters the alveolus than that removed by blood uptake; and by loss of surfactant, with a rise in surface alveolus tension [4].

In the postoperative period, pulmonary function is substantially decreased. In addition to the mechanisms that occur during induction and the intrinsic drug effect, others, such as pain, pleural opening, and diaphragm dysfunction, especially in thoracic or upper abdominal surgery, contribute to ventilation/perfusion mismatch, worsening of hypoxemia, gas exchange, and atelectasis, expressed by a restrictive syndrome (reduced vital capacity, tidal volume, and functional residual capacity) and possibly respiratory failure [5]. Diaphragm dysfunction may last from 7 to 10 days after surgery. Bed rest contributes to this scenario.