Definition of pulmonary stasis It is a localized venous blood stasis in the lungs, usually caused by left heart failure, where the pressure in the left heart cavity is elevated, obstructing pulmonary venous return and causing pulmonary stasis as well as interstitial B out. Clinical manifestations include shortness of breath, hypoxia, cyanosis, and coughing up large amounts of plagioid pink foamy sputum [1]. Extracorporeal circulation can be accompanied by a characteristic benign, reversible pulmonary stasis, often misdiagnosed as bronchospasm, which occurs at the beginning of extracorporeal circulation or after aortic opening and is ineffective against bronchodilators and positive inotropes, and a gradual decrease in airway pressure with a gradual reduction in flow. Incidence No reports were found in the domestic or foreign literature search. For cardiac surgery with extracorporeal circulation, the incidence is expected to be around 10-20%. Mechanism of occurrence In extracorporeal circulation, pulmonary venous blood flow is slow. There is a mismatch between the driving force causing pulmonary venous blood flow movement and the resistance to venous blood flow movement. The driving force of pulmonary venous blood flow is the mean pulmonary artery pressure-mean left atrial pressure and the resistance to pulmonary venous blood flow is the resistance of blood flow within the pulmonary veins, which is proportional to the viscosity coefficient of blood (η), proportional to the vessel length (L) and inversely proportional to the fourth power of the vessel radius (r) according to Poisson’s law: R= 8?L/πr4 [2]. During extracorporeal circulation, especially in full-flow mode, pulmonary artery pressure is relatively low, while pulmonary veins, especially small pulmonary veins, are dominated by higher resistance due to their small internal diameter, and the driving force of pulmonary venous blood is not sufficient to counteract the resistance to flow and leads to stagnation of blood in small pulmonary veins, or even quiescence of blood flow. This phenomenon can be exacerbated by the retention of gas in the pulmonary veins after opening of the right heart system, and the amount of this gas retention is also related to whether the chest cavity is opened or not. Once the transfer flow is reduced the pulmonary artery pressure increases and shows a pulsatile pressure, and the left atrial pressure changes after atrial ventricular motion, the small pulmonary venous flow starts to move, the pulmonary venous flow movement is accelerated, and the pulmonary venous stasis improves in a short period of time. Clinical manifestations The full flow of extracorporeal circulation can be accompanied by a characteristic benign, reversible pulmonary stasis, which occurs after the start of extracorporeal circulation or aortic opening, manifested as a decrease or failure to maintain the reservoir fluid level, and a gradual increase in airway pressure, with peak airway pressure reaching 30-40 cmH2O at a tidal volume of 8 ml/kg, often misdiagnosed as bronchospasm, but ineffective against bronchodilators and positive inotropes. The diagnosis is often made by mistake. Esophageal ultrasound shows ventricular filling emptiness, mitral valve and aortic valve not moving or showing a certain proportion of motion with cardiac signal, arterial blood pressure without waveform or pulsatile waveform is low, routine flow reduction can cause difficulty in stopping, while gradual reduction of flow can lead to gradual reduction of airway pressure, fluid level of blood storage tank is restored, heart filling, valve opening in equal proportion, arterial waveform is obvious, and blood pressure rises. Diagnosis and differential diagnosis Bronchospasm, left heart failure, drug allergy, increased airway secretions, perfused lung, anesthesia machine malfunction, valve sequestration and fisetin reaction. There was no history of bronchial asthma or cardiogenic asthma before surgery, no triggering factors for bronchospasm, no significant dry or wet rales on auscultation, no significant response to bronchodilators or cardiac drugs, and a time-dependent increase in airway pressure after aortic opening, no allergy-related medications or skin mucosal manifestations, and airway secretions could be slightly increased, but the process of increased airway pressure could not be improved by aspiration of secretions. There were no signs of severe hypoxemia due to massive pulmonary exudate, no anesthesia machine malfunction, gradual improvement after flow reduction and ultrasound confirmation of good valve activity. A high airway pressure shutdown and administration of fisetin can be confused with a reaction to fisetin, which can be administered after a smooth shutdown. In addition, the typical response to fisetin is a gradual increase in airway pressure after administration, which may be accompanied by a slowing of heart rate, a decrease in blood pressure, and an increase in pulmonary artery pressure, which is effective in response to positive inotropic drugs [3]. Management measures and prognosis The prognosis is generally good. The management is mainly that the anesthesiologist needs to be cognizant of this phenomenon and diagnose it in a timely manner, without using too many bronchodilators and prolonging the diversion time; the correct management should be to gradually reduce the flow and closely monitor the airway pressure, giving sufficient time for pulmonary venous venting and patiently waiting for the pulmonary arteriovenous blood flow to return to its preoperative matching pattern. Avoid overfilling the heart, maintain myocardial contractility and contraction frequency, observe the valve opening status and left ventricular filling status by ultrasound, and after the airway pressure starts to decrease and maintain for a certain period of time, continue to reduce the flow until the airway pressure returns to the basal level.