In recent years, most patients can safely undergo various surgical procedures in thoracic surgery, which is the result of paying attention to preoperative preparation, better understanding and evaluation of patients’ cardiac, pulmonary and renal functions and water, electrolyte and acid-base status, full understanding and rational application of clinical pharmacology, and improved and enhanced intraoperative and postoperative management. Intraoperative and postoperative monitoring systems and enhanced treatment wards provide effective postoperative life support for critically ill patients. After open-heart surgery, pulmonary complications are the main cause of postoperative mortality. A series of changes in the lungs occur after open-heart surgery, and pathophysiological changes in lung function occur after surgery regardless of normal or abnormal preoperative lung function, and understanding and recognizing these changes can prevent or reduce the occurrence of pulmonary complications. The first thing that is affected after open-heart surgery is the way of ventilation, with a decrease in tidal volume and an increase in the number of breaths to ensure that the ventilation per minute is not reduced. The number of physiological sighs (3 times the tidal volume) is reduced or lost, which is about 10 per hour when normal, and this voluntary deep breathing prevents alveolar atrophy and increases lung compliance. In conclusion, the result of altered ventilation after open-heart surgery results in reduced respiratory function, reduced static lung volume, reduced TV, expiratory residual volume and functional residual air volume, and these changes will affect the postoperative clinical course. Normal closed air volume allows the small airway to close and become non-functional, it is higher than the residual air volume and lower than the end-tidal point. With the reduction of functional residual air volume (ERV) after surgery, the closed air volume (CV) may reach the tidal volume (TV) range, resulting in airway closure during tidal breathing. When a patient has increased CV, decreased ERV, and abnormal lung function preoperatively, such changes can exacerbate the onset and progression of pulmonary atelectasis postoperatively. Pulmonary atelectasis may appear as a sheet or as a tiny atelectasis with normal radiographs. Increased CV in elderly and smoking patients, decreased ERV in obese patients, and abnormal CV and ERV in the presence of obstructive lung disease place these patients in a high risk group for surgery. Postoperative gas exchange abnormalities are accompanied by decreased arterial partial pressure of oxygen as a result of decreased pulmonary ventilation to perfusion ratio. Alveolar collapse causes airway closure, resulting in alveolar perfusion without ventilation, producing a functional right-to-left shunt, leading to hypoxemia, when oxygenation is ineffective. In this case, even temporary airway occlusion by secretions causes a rapid loss of oxygen distal to the obstruction. Abnormal ventilation ratios can be produced by postoperative lying still, chest pain, excessive use of pain medication, and accumulation of airway secretions. Hypoxemia is also sometimes evident after lobectomy, pneumonectomy, or even open-heart surgery without lung resection. Total lung resection increases right heart pressure and can produce hyperbaric pulmonary edema. Compression of the lung by surgery, hemodilution from excessive intraoperative and postoperative fluid infusions, decreased plasma osmolality, and hyperinflation of the residual lung in the thoracic cavity can all cause osmotic pulmonary edema.