An increased alveolar-arterial Po2 difference and a decrease in functional residual capacity are common intraoperatively and postoperatively. There is an associated increase in ventilation/perfusion maldistribution and in intrapulmonary shunt, and this may occur without roentgenographic evidence of atelectasis. The intraoperative mechanism is a function of general anesthesia and is corrected within the first few hours after most types of peripheral surgery. Postoperative hypoxemia is most exaggerated in the elderly, the obese, those with preoperative cardiopulmonary disease, and after operations on the upper abdomen and thorax. After these procedures, arterial Po2 does not return to normal until after the second postoperative day. Anesthetic technique and intraoperative maneuvers do not influence this postoperative course, but regional analgesia is more effective than narcotics for maintaining postoperative pulmonary function. Low concentrations of supplementary O2 are usually effective in maintaining a normal arterial PO2 and should be administered routinely to those at hazard postoperatively, combined with a vigorous nursing “stir-up” regimen.