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Pulmonary embolism is due to the embolus from the venous system or the right heart entering the pulmonary circulation, resulting in extensive embolism of the main pulmonary artery or its branches. At the same time, it is accompanied by extensive pulmonary arteriolar spasm, which obstructs the pulmonary circulation and causes the rapid rise of pulmonary artery pressure, leading to right ventricular dilatation and right heart failure. The common embolus is thrombus, and the rest are rare new biological cells, fat drops, bubbles, intravenous drug particles and even pulmonary vascular occlusion caused by the tip of the catheter.
The main causes of pulmonary embolism are blood stasis, blood hypercoagulability and vascular endothelial injury. Modern medicine believes that endothelial injury plays an important initial and continuous role in venous thrombosis. Venous endothelial injury can be caused by mechanical trauma, long-term hypoxia and immune complex deposition, which can expose collagen tissue, stimulate platelet adhesion and aggregation, and activate the blood coagulation reaction chain. Blood stasis can activate the coagulation mechanism and trigger thrombosis. The hypercoagulable state of blood is also one of the important mechanisms of thrombosis
The high-risk group of Pulmonary Embolism is the elderly people. The age at which pulmonary embolism occurs is 50 to 80 years old, and the risk increases twice every ten years. 90% of fatal pulmonary embolism occurs in patients over 50 years old. The second is thrombophlebitis and varicose veins. Thrombophlebitis and varicose veins are easy to cause venous thrombosis, which is the prime cause of pulmonary embolism.
In patients with chronic heart and lung diseases. The chronic heart and lung diseases are the main risk factors for pulmonary thromboembolism, such as rheumatic heart disease, cardiomyopathy, chronic obstructive pulmonary disease, congenital heart disease, coronary heart disease, hypertension and other patients, especially patients with atrial fibrillation and heart failure, are prone to pulmonary embolism.
At present, PE screening is mostly based on patients' clinical manifestations, arterial blood gas analysis, related biochemical indicators, electrocardiogram, etc. The above indicators have limitations in sensitivity and specificity. The diagnosis of PE needs to be based on further imaging and pulmonary ventilation/perfusion radionuclide scanning. Based on the above reasons, physicians need to constantly find more monitoring methods in clinical work, so as to find PE patients timely and accurately, and monitor them conveniently, effectively and in real time.
5.1 Application of ETCO2
As for correlation of capnography and pulmonary embolism, and circulatory function evaluation during cardiopulmonary resuscitation. It is a non-invasive, convenient, real-time and continuous monitoring means.
5.2 It is recommended to monitor ETCO2 when screening pulmonary embolism. At present, there are two main methods for screening pulmonary embolism through ETCO2 monitoring:
(1) Compare the value of ETCO2 with the value of arterial partial pressure of carbon dioxide. If ETCO2 decreases and the value of partial pressure of carbon dioxide in blood increases, it indicates that pulmonary embolism may occur.
(2) Use the volume ETCO2 to calculate the dead space ventilation ratio. If the proportion increases, pulmonary embolism may be considered. The evaluation of pulmonary embolism should be combined with other indicators such as D-dimer or WELLS score.
