Chest pain is pain anywhere within the range from the head and neck to the lowest rib, related to the organs of the chest (heart, lungs, trachea, esophagus, etc.), ribs or chest muscles, and is a frequent problem for clinicians. Patients with acute chest pain are the most common group of patients in emergency medicine, accounting for about 5%-20% of patients in emergency medicine and about 20%-30% in tertiary hospitals. 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 may indicate a serious adverse prognosis, and these poor prognosis diseases, especially cardiogenic chest pain, often have a strong time-dependent nature, 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. 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 make these patients enter the green channel of emergency treatment quickly. 1. High-risk chest pain patients High-risk chest pain patients include: acute coronary syndrome, aortic coarctation, pulmonary embolism and tension pneumothorax. The medical history provided at the time of consultation, the main symptoms presented, the positive signs found on physical examination and the dynamic observation of ECG and serum myocardial damage markers are the main basis for the initial identification. 1.1, Acute coronary syndrome (ACS) Acute coronary syndromes are a group of syndromes in which coronary atherosclerotic plaque instability is the basic pathophysiological feature and acute myocardial ischemia is the common feature, 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 on the basis of atherosclerotic plaque rupture. However, coronary angioscopic studies have found that the thrombus formed at the site of ruptured UA and NSTEMI plaques 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, there are certain differences in the diagnosis and treatment of STEMI and UA/NSTEMI. History of cardiovascular disease and related risk factors, typical symptoms of chest pain and related signs, characteristic ECG and serum marker changes and dynamic evolution are the main basis for the diagnosis of acute coronary syndrome. In patients with suspected ACS, the initial evaluation should be completed within 10 minutes of the patient’s arrival in the emergency room, and the diagnosis should be established within 20 minutes: first obtain a history, physical examination, 12-lead ECG and initial cardiac marker test, and combine these findings to determine whether the patient has definite ACS. For patients with suspected ACS whose initial 12-lead ECG and cardiac marker levels are normal, repeat the ECG within 15 The cardiac marker test can be repeated 6 hours after the onset of symptoms. Third, once the diagnosis of ACS is clear, it should be treated immediately: ① nasal catheter oxygen; ② sublingual nitroglycerin (unless systolic blood pressure <90 mmHg heart rate <50 beats/min or >100 beats/min); ③ adequate analgesia, morphine or dulcolax; ④ oral aspirin 160-325 mg/dose; ⑤ classification according to whether the ST segment is elevated, and those with ST segment elevation (symptoms persist with LBBB and The possibility of immediate reperfusion therapy should be evaluated for those with ST-segment elevation (same as those with ST-segment elevation). Those with non-ST-segment elevation are not treated with thrombolysis and should be risk-stratified. (i) ST-segment elevation myocardial infarction 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. Upward elevation of the ST arch in two or more connected leads of the ECG with dynamic changes; c. Dynamic evolution of biochemical markers of myocardial necrosis (CK, CKMB, troponin, etc.). Once the diagnosis of STEMI is established, early reperfusion therapy is the key to improve ventricular function and increase survival. The goal of treatment is to open the occluded coronary artery within hours to achieve and maintain reperfusion of blood flow at the myocardial level. Once reperfusion therapy is initiated, the patient should be admitted to the CCU. (1) Reperfusion therapy includes intravenous thrombolytic therapy, direct PCI (interventional therapy), transit PCI, and easy PCI. For STEMI patients, time is the heart muscle! It is not just the concept, but to implement it in the actual treatment. Therefore, according to the conditions of your own hospital, reperfusion therapy in the shortest possible time is the key, whether it is thrombolysis, PCI, or transfer to a hospital with the conditions for PCI. (2) Intravenous thrombolysis The main advantages of intravenous thrombolysis are rapid initiation of treatment, reduced operative errors and suitability for out-of-hospital thrombolysis, which allows rapid reperfusion therapy to be given to patients when PCI is not available. The effect of thrombolysis within 3 hours of the onset of chest pain is the same as that of PCI. 30 more lives can be saved per 1000 cases within 6 hours, 20 more lives can be saved per 1000 cases from 7 to 12 hours, and there is no significant benefit for >12 hours. Therefore, fibrinolytic therapy should be initiated as early as possible. Foreign guidelines require that the time between the patient’s arrival at the emergency room and the infusion of thrombolytic drugs (door to needle) be within 30 minutes. The main intravenous thrombolytic drugs are: (1) urokinase (UK ); (2) streptokinase (SK) or recombinant streptokinase (rSK); and (3) recombinant tissue-type fibrinogen activator (rt-PA). For the clinical evaluation of these drugs: GISS-2 and ISIS-3 compared SK with t-PA and found no difference in the effect on mortality, while t-PA had a slightly higher incidence of cerebral hemorrhage. Subsequently, GUSTO compared accelerated t-PA with SK and found an advantage of accelerated t-PA in reducing mortality. (3) Direct PCI Direct PCI is a very effective method for re-establishing coronary perfusion and has been recognized as the most effective treatment for STEMI. Advantages of direct PCI: high coronary revascularization rate of more than 90%; TIMI grade 3 flow rate of up to 85%; very low reinfarction rate; no bleeding complications; few contraindications; PCI can also help physicians understand the anatomical characteristics of the patient’s coronary arteries and whether other lesions are present, providing a more visual basis for treatment. ACC/AHA guidelines for the treatment strategy of STMI are: at the onset of symptoms Patients with STMI within 12 hours or infarction with new (or presumed new) LBBB should undergo infarct-related vascular PCI.(Level of Evidence A). When cardiogenic shock occurs within 36 hours of STMI or infarction with new LBBB, revascularization should be performed within 18 hours of shock. (Level of evidence A). Direct PCI should be performed in STMI with severe heart failure or pulmonary edema (Killip class 3) within 12 hours of symptom onset (Level of Evidence B). The ACC/AHA guidelines specify that the operational criteria for direct PCI are: time from presentation to balloon dilation within 90 minutes; number of PCIs by the surgical operator exceeds 75 per year; and number of PCIs by the catheterization laboratory exceeds 200 per year, of which at least 36 are direct PCIs for STEMI with cardiac surgical support. In cases where PCI is not available, thrombolysis or transfer to a hospital that is equipped for PCI are options that should be considered. (ii) General treatment of STEMI patients Patients with STEMI should be given immediate general management such as pain relief, sedation, and oxygenation in addition to reperfusion therapy as soon as possible. At the same time, adequate antiplatelet therapy should be given: loading doses of aspirin and clopidogrel should be given as soon as possible and followed by maintenance doses. Early application of beta-blockers has been shown to reduce disability and death rates. Calcium antagonists have not been shown to reduce AMI mortality. In patients without ST-segment elevation or LBBB and without pulmonary stasis, diltiazem reduces the incidence of recurrent ischemic events, but the use of short-acting dihydropyridines increases mortality in patients with AMI. In patients with ST-segment elevation or LBBB, ACEI/ARB therapy should be initiated within hours of admission in the absence of hypotension or contraindications; ACEI/ARB therapy should be continued for CHF and EF <40%; ACEI/ARB may be discontinued after 6 weeks in the absence of complications and echocardiographic evidence of left ventricular dysfunction. Intensive statin lipid-lowering therapy is also mandatory for patients with AMI. 1.2. Unstable angina and non-ST-segment elevation myocardial infarction (UA / NSTEMI) The goal of treatment of acute coronary syndromes with non-ST-segment elevation is to stabilize the ruptured plaque lesion within hours to days so that the ruptured plaque gradually heals to a stable lesion; to manage risk factors (hypertension, hyperlipidemia, smoking and diabetes) and to prevent further plaque rupture. The diagnosis of unstable angina versus non-ST-segment elevation myocardial infarction can be made based on the history of typical angina symptoms, typical ischemic ECG changes (new or transient ST-segment depression ≥ 0.lmV, or T-wave inversion ≥ 0.2mV), and myocardial injury marker (cTnT, cTnI, or CK-MB) measurements. Risk stratification should be performed for patients with unstable angina versus non-ST-segment elevation myocardial infarction based on medical history, pain characteristics, clinical presentation, ECG and myocardial marker measurements. Treatment of unstable angina with non-ST-segment elevation myocardial infarction has two main aims: immediate relief of ischemia and prevention of serious adverse consequences (death or myocardial infarction or reinfarction). Thrombolytic therapy has been shown to be of no benefit in the management of non-ST-segment elevation acute coronary syndromes. Patients with unstable angina and non-ST-segment elevation myocardial infarction should be given early aggressive antiplatelet therapy with anticoagulation. (1) Intensive 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, GUSTO-IV-ACS found that GP IIb/IIIa receptor antagonists (abciximab) were not significantly beneficial and bleeding events were significantly increased, so the current antiplatelet therapy for ACS without ST-segment elevation has an enhanced role for ADP receptor antagonists and a diminished status for GP IIb/IIIa receptor antagonists. ② Anticoagulation therapy, heparin or low-molecular heparin must be given to UA/NSTEMI patients for anticoagulation. The status of low-molecular heparin has been established through trials such as ESSENCE, TIMI IIB and ACUTE II, and has largely replaced plain heparin in the anticoagulation of patients with acute coronary syndromes due to ease of use. Further deepening the risk stratification by 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 chest pain, positive loading test, UCGEF <0.40, hemodynamic instability, persistent ventricular tachycardia, PCI within 6 months, and post-CABG. Also, unstable angina with non-ST-segment elevation myocardial infarction should be given early intensive statin lipid-lowering therapy, and secondary prevention of coronary heart disease. 1.3. Aortic coarctation Aortic coarctation is a tear in the intima of the aorta and blood flows through the fissure into the aortic wall, causing the middle layer to peel away from the outer membrane. Later deaths. 1/3 are due to complications of the entrapment tear; the remaining 2/3 are due to other disorders. The long-term survival rate for patients who survive the acute phase with treatment is 60% at 5 years and 40% at 10 years. Clinically, they often present with tear-like pain and have a vasovagal-like reaction with shock. Sometimes the symptoms of a clamping tear are associated with an acute occluded artery such as a stroke, myocardial infarction or small bowel infarction, and the blood supply to the spinal cord is affected causing mild paralysis or paraplegia of the lower extremities and limb ischemia, and these manifestations resemble arterial embolism. Imaging tests such as aortic CT scan 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 control of blood pressure: 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. ③Control of heart rate and slowing of the rate of left ventricular contraction (dp/dt): beta-blockers are usually used. ④Interventional and surgical treatment: All acute entrapment tears of the proximal aorta (DeBakey type I and II) are indicated for surgery and should be operated as early as possible. The surgical risk is higher. deBakey type III entrapment aneurysm, interventional treatment has emerged in recent years, which is to close the entrance with a self-expanding stent with membrane to allow spontaneous formation of thrombus in its false lumen. 1.4, pulmonary embolism Acute pulmonary artery thromboembolism is an acute obstruction of pulmonary blood circulation together with the dislodgement or freeing of emboli in the systemic venous system and thrombus in the right heart lumen, with the first manifestation of 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 S1QIIITIII inversion type, characteristic change is acute right ventricular load), blood sampling for D-dimer, two-dimensional echocardiography and pulmonary enhancement spiral CT should be done in time. Treatment is based on anticoagulation, and intravenous heparin is applied to keep 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 reversible 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 anticoagulation should be used for a long time. Large pulmonary emboli with hemodynamic instability may be considered for thrombolysis, surgical retrieval, or interventional catheter fragmentation. Patients with recurrent embolism despite anticoagulation therapy or those with contraindications to anticoagulation may be considered for installation of an inferior vena cava filter. 1.5.Tension pneumothorax Pneumothorax refers to the presence of free air between the visceral layer and the wall pleura. Tension pneumothorax refers to the formation of a live valve in the injured tissue, during inspiration, the air can enter the pleural cavity through the fissure, while during expiration the live valve is reunited and the air cannot be discharged, resulting in a continuous increase of pressure in the thoracic cavity, as a result of which the lung will collapse and the mediastinum will be displaced to the opposite side, which can seriously endanger the cardiopulmonary function. Clinically, patients usually first present with sudden and severe chest pain, dyspnea, and occasionally a dry cough. The pain may radiate to the ipsilateral shoulder, contralateral chest or abdomen and may resemble acute coronary syndrome or acute abdomen. Physical signs may include a percussion drum sound, diminished or absent vocal fibrillation, and diminished motion on the affected side. Mediastinal shift may be manifested by a shift of the turbid heart sounds and apical beats to the healthy side and a marked decrease or absence of breath sounds. Chest X-ray shows partial air in the peripheral part of the lung, and the absence of lung texture can confirm the diagnosis. 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 with a tee plunger attached to a large syringe. Subsequently, thoracotomy cannulation and unilateral thoracic water-sealed drainage should be performed as soon as possible. 2. Low-risk patients with chest pain Low-risk patients with chest pain include the following diseases: (1) pericarditis; (2) lung: lobar pneumonia pulmonary hypertension, etc.; (3) digestive system diseases: reflux esophagitis, esophageal spasm, peptic ulcer, etc.; (4) pleura: pleurisy, pleural mesothelioma, lung cancer involving the pleura, etc.; (5) esophagus: esophageal pancreatic dystrophy, reflux esophagitis, etc.; (6) mediastinum: tumor; (7) diaphragm: diaphragmatic hernia. ⑧ skeletal muscle diseases: cervical spondylosis, costochondritis, muscle pain, intercostal neuralgia, spinal radiculitis, etc.; ⑨ skin: herpes zoster; ⑩ subdiaphragmatic organs: stomach, duodenum, pancreas, gallbladder; ○11 psychiatric factors (functional pain): fear, depression, cardiac neurosis, hyperventilation, etc. Consciously identifying these patients and triaging them for outpatient management can save the limited medical resources of society. It also avoids unnecessary psychological stress and financial loss to these patients and affects their quality of life.