Chest pain is defined as pain anywhere within the range from the head and neck to the lowest rib, related to the organs of the chest cavity (heart, lungs, trachea, esophagus, etc.), the rib cage or the chest muscle, and is a frequent problem for clinicians. Acute chest pain has a complex etiology, different clinical manifestations, difficulty in confirming the diagnosis, and a wide variation in risk. In most cases, acute chest pain is likely to predict a serious adverse prognosis, and these poor prognosis diseases, especially cardiogenic chest pain, are often very time-dependent, and a missed diagnosis may be fatal or seriously affect the patient’s prognosis. Overseas reports show that 3% of patients diagnosed with non-cardiac chest pain in the emergency department have a malignant cardiac event within 30 d; while misdiagnosis of non-cardiac chest pain with good prognosis as severe cardiac chest pain can cause unnecessary psychological stress and economic loss and affect their quality of life. Therefore, it is very important how to correctly identify and assess chest pain. Fatal chest pains include: acute coronary syndrome, aortic coarctation, pulmonary embolism and tension pneumothorax. The medical history provided at the time of consultation, the main clinical symptoms presented, the positive signs found on examination and the dynamic observation of ECG and serum markers of myocardial injury are the main basis for the initial identification. In clinical practice, the first consulting physician must maintain a clear clinical thinking, master the classification of chest pain diseases, quickly identify patients with chest pain, eliminate low-risk patients, screen out high-risk patients and get these patients into the standardized emergency procedures quickly. Care Min, Department of Cardiology, The First Affiliated Hospital of Henan College of Traditional Chinese Medicine First consider common and easily life-threatening diseases with chest pain as the main clinical manifestation, such as ACS, aortic coarctation, pulmonary embolism and tension pneumothorax.1 Step 1: Assessment and diagnosis For patients presenting to the emergency department with acute chest pain, first immediately assess the condition and identify the fatal disease causing the chest pain.1.1 If the patient has life-threatening Signs and symptoms (including: sudden onset of syncope or dyspnea, blood pressure <90/60 mmHg, heart rate >100 beats per minute, and a large number of feet in both lungs) 1.2 Complete the first electrocardiogram and physical examination within 5 minutes (mainly noting whether the jugular veins are filling, whether the breath sounds in both lungs are consistent, and whether there are any woven woven wool in both lungs (7). 1.3 Complete blood gas analysis, myocardial biochemical markers, renal function, routine blood count, bedside chest X-ray and bedside echocardiography; 1.4 Obtain medical history (including the duration of this chest pain episode, history of previous chest pain, history of previous heart disease, history of diabetes mellitus and hypertension, and history of previous medication);2 Step 2: If no clear cause is found after the above examination, enter ACS Screening process Acute coronary syndrome (ACS) is a group of syndromes characterized by acute myocardial ischemia with the basic pathophysiological feature of coronary atherosclerotic plaque instability, including unstable angina (UA), non-ST-segment elevation myocardial infarction (NSTEMI) and ST-segment elevation myocardial infarction (STEMI). In fact, there is no clear boundary between UA to NSTEMI and then to STEMI, and they have similar pathophysiological basis as a result of secondary thrombosis based on atherosclerotic plaque rupture. However, coronary angiographic studies have found that the thrombus formed at the site of UA and NSTEMI plaque rupture is a “white” thrombus with a predominantly platelet component, whereas STEMI is a “red” thrombus with a predominantly fibrin and red blood cell component. Coronary angiography reveals that STEMI is the result of a thrombus causing occlusion of the coronary artery and interruption of blood flow, whereas UA and NSTEMI angiographic thrombi are mostly non-occlusive. Therefore, the diagnosis and treatment of STEMI and UA/NSTEMI certain differences. 2.1 Definitive diagnosis of myocardial infarction STEMI diagnosis and treatment: the diagnosis of ST-segment elevation myocardial infarction requires two or more of the following criteria: a. typical chest pain (angina) lasting more than 20 minutes; b. electrocardiogram two or more connected leads ST arch dorsal up elevation and There are dynamic changes c. Dynamic evolution of biochemical markers of myocardial necrosis (CK, CK-MB, troponin, etc.). The goal of treatment is to minimize the time to reperfusion therapy, save lives and improve prognosis, and clinical studies clearly show that for STEMI, the earlier the reperfusion, the better the prognosis. The above targets are not ideal times for reperfusion, but rather the maximum acceptable time for reperfusion. Whether thrombolytic therapy or coronary intervention (PCI) is used, both treatments are influenced by medical devices and patient factors. Studies suggest that PCI is superior to pharmacologic reperfusion. The current recommendations for early reperfusion treatment of STEMI are: if seen within 3 hours of onset, both thrombolysis and emergency PCI are options, and if seen after 3 hours of onset, emergency PCI is the recommended treatment of choice. There are many studies doing STEMI treatment process improvement, including pre-hospital completion of electrocardiogram, pre-hospital contact with the receiving hospital, pre-hospital communication with the emergency room to determine the treatment plan, and emergency room activation of the cardiac catheterization laboratory, which have been shown to significantly reduce reperfusion time. 2.2 Diagnosis and treatment of UA/NSTEMI The key to its treatment is early diagnosis of ACS, accurate risk stratification, early identification of The key to its treatment is early diagnosis of ACS, accurate risk stratification, early identification of high-risk patients, and different treatment plans according to different risk stratification. Further deepening the risk stratification and choosing whether to use early intervention strategies based on early risk stratification can significantly improve the prognosis of patients. Early intervention strategy should be used for high-risk patients with recurrent ischemic episodes despite intensive treatment, elevated troponin, ST-segment depression, signs or symptoms of cardiac insufficiency in the presence of chest pain, positive loading test, UCGEF <0.40, hemodynamic instability, persistent ventricular tachycardia, PCI within 6 months, and post-CABG. Patients with unstable angina and non-ST-segment elevation myocardial infarction should be given early and aggressive antiplatelet therapy and anticoagulation. ①Intensive antiplatelet therapy: Both the CURE and PCI-CURE trials showed that dual antiplatelet therapy with aspirin and clopidogrel reduced the occurrence of serious adverse events in patients. In contrast, the GUSTO-IV-ACS found that GP IIb/IIIa receptor antagonists (abciximab) were not significantly beneficial and that bleeding events were significantly increased, so the status of ADP receptor antagonists is now enhanced and the status of GP IIb/IIIa receptor antagonists is diminished in antiplatelet therapy for ACS without ST-segment elevation, unless the patient is in high-risk stratification ready for PCI. ② Anticoagulation therapy, heparin or low-molecular heparin must be given for anticoagulation in patients with UA/NSTEMI.3 Step 3:If ACS can be ruled out, or if severe chest pain is present at the beginning, those with a history of hypertension without evidence of ACS, or those suspected of having Marfan's syndrome, should be screened for aortic coarctation as soon as possible Aortic coarctation is a tear in the intima of the aorta, with blood flowing through the fissure into the aortic wall, causing the middle layer to break away from the The mortality rate is high, with untreated patients having an early mortality rate of 1% per hour, 75% dying within 2 weeks, and 90% dying at 3 months. The long-term survival rate is 60% at 5 years and 40% at 10 years for patients who survive the acute phase with treatment. Clinically, they often present with tear-like pain and have a vasovagal-like reaction and shock. Sometimes the symptoms of a clamping tear are associated with an acutely occluded artery such as stroke, myocardial infarction, small bowel infarction, compromised blood supply to the spinal cord causing mild paralysis or paraplegia of the lower extremities, and limb ischemia, and these manifestations resemble arterial embolism. Imaging tests such as multi-row CT scans of the aorta can establish the diagnosis. Once the diagnosis of aortic coarctation is established, pharmacological treatment should be started as soon as possible: (1) aggressive sedation and analgesic treatment; (2) rapid blood pressure control: usually a combination of sodium nitroprusside and beta-blockers. The goal is to lower the blood pressure to the lowest blood pressure level that maintains adequate cerebral, cardiac, and renal perfusion; (3) control the heart rate and slow the rate of left ventricular contraction (dp/dt): β-blockers are usually used; (4) interventional and surgical treatment: all acute entrapped tears of the proximal aorta (DeBakey types I and II) are indicated for surgery and should be operated as early as possible. Surgical risk is higher. for DeBakey type III coarctation aneurysms, the inlet is closed with a laminated self-expanding stent to allow spontaneous thrombus formation in the pseudolumen.4 Step 4 Pulmonary embolism should be screened for sudden respiratory distress with hypoxemia Acute pulmonary artery thromboembolism is an acute obstruction of pulmonary blood circulation caused by the dislodgement or freeing of emboli in the systemic venous system and thrombi in the right heart lumen that block the pulmonary vascular bed, with the first The first manifestation is hypoxemia. The common clinical manifestations of larger pulmonary embolism include severe dyspnea, increased respiration, chest pain, cyanosis, hypoxemia and even syncope. The morbidity, misdiagnosis and mortality rate in the acute phase of pulmonary embolism are quite high, with 11% sudden death within one hour of onset and 32% total mortality. Correct diagnosis and timely and effective treatment are the keys to reduce the mortality in the acute stage. When acute pulmonary embolism is suspected, electrocardiogram (its morphology is SⅠQⅢTⅢ inversion type, and the characteristic change is acute right ventricular load increase), blood sampling for D-dimer, two-dimensional echocardiography and pulmonary vascular enhancement spiral CT should be done in time. Treatment is based on anticoagulation, with application of intravenous heparin to maintain APTT at 1.5-2.5 (anti-Factor Xa activity 0.3-0.6 IU). Oral anticoagulation should be started on the first 3 days of heparin application and combined with heparin until INR reaches therapeutic levels (2.0-3.0) 2 days after discontinuation of heparin. Primary pulmonary embolism should be anticoagulated for at least 3 months if risk factors are present and for at least 6 months for idiopathic VTE. In patients with recurrent VTE or persistent risk factors (e.g., tumor) oral anticoagulants should be used for a long time. Thrombolysis, surgical retrieval or interventional catheter fragmentation may be considered in large pulmonary emboli with hemodynamic instability. Ventilator-assisted respiration should be used for those with severe hypoxemia or respiratory failure. Patients with recurrent embolism despite anticoagulation or with contraindications to anticoagulation may be considered for installation of an inferior vena cava filter. 5 Step 5 For severe dyspnea after chest trauma or coughing, a tension pneumothorax should be screened for the presence of free air between the visceral and mural pleura. Tension pneumothorax, on the other hand, refers to the formation of a live valve in the injured tissue, which allows air to pass through the fissure into the pleural cavity during inspiration, while the live valve closes during expiration and air cannot be expelled, resulting in a continuous increase in pressure in the thoracic cavity, with the result that the lung collapses and the mediastinum shifts to the opposite side, seriously endangering cardiopulmonary function. Clinically, patients usually first present with sudden and severe chest pain, dyspnea, and occasionally a dry cough, which may radiate to the ipsilateral shoulder, contralateral chest, or abdomen and may resemble acute coronary syndrome or acute abdomen. Signs may include percussion drums, diminished or absent fibrillation, decreased motion on the affected side, mediastinal shift may be manifested by turbid heart sounds and apical beats shifting to the healthy side, and markedly diminished or absent breath sounds. The diagnosis can be confirmed by a chest X-ray showing no pulmonary texture in the outer lung zone. Rapid air evacuation is a life-saving measure. A simple way to remove air is to insert a 19-gauge or larger needle into the chest and then quickly expel the air through the needle using a tee plunger attached to a large syringe. Subsequently, thoracotomy intubation and unilateral thoracic water-sealed drainage should be performed as soon as possible.6 Step 6 If neither of the above diseases can be clearly identified and the symptoms do not resolve, the patient should be kept in observation or admitted to the ward and continue to be closely observed. Patients with chest pain with a long history, recurrent episodes and not affecting daily life can be regarded as patients with low-risk chest pain and have the opportunity for further diagnosis and differential diagnosis of patients with low-risk chest pain including the following kinds of diseases: ① pericarditis; ② lung diseases: lobar pneumonia, pulmonary hypertension, etc.; ③ digestive system diseases: reflux esophagitis, esophageal spasm, peptic ulcer, etc.; ④ pleural diseases: pleurisy, pleural mesothelioma, lung cancer involving the pleura, etc.; ⑤ esophageal diseases (6) mediastinal diseases: tumors; (7) diaphragm: diaphragmatic hernia; (8) skeletal muscle diseases: cervical spondylosis, costochondritis, muscle pain, intercostal neuralgia, spinal radiculitis, etc.; (9) skin diseases: herpes zoster; (10) subdiaphragmatic organ diseases: stomach, duodenum, pancreas, gallbladder; (11) mental factors (functional pain): fear, depression, cardiac neurosis, hyperventilation, etc. Consciously identifying these patients and triaging them to outpatient management can save society's limited medical resources.