ACS (acute coronary syndrome) in patients with abnormal vital signs of chest pain, including: confusion and/or loss of consciousness, pallor, profuse sweating and cold extremities, hypotension (blood pressure <90/60 mmHg), shortness of breath or difficulty, and hypoxemia (SpO2 <90%), suggests a high-risk patient and requires immediate emergency management. While resuscitating, the cause of the disease should be actively clarified. Patients with chest pain without the above high-risk clinical features need to be alerted to the possible potential danger. In patients with chest pain whose vital signs are stable, a detailed history is the cornerstone of etiologic diagnosis. In most cases, the combination of clinical history, physical examination, and specific ancillary tests can accurately determine the cause of a patient's chest pain. It is important to emphasize that clinicians facing every case of chest pain need to prioritize fatal chest pain (Figure 1). ACS: includes ST-segment elevation myocardial infarction (STEMl), non-ST-segment elevation myocardial infarction (NSTEMI), and unstable angina (UA). The latter two types are collectively referred to as non-ST-segment elevation ACS (NSTE-ACS). 365medical.com Reprinted with permission Typical angina is located behind the sternum, with a squeezing, tightening, holding or burning sensation, etc. It may radiate to the neck, jaw, epigastric pain is located behind the sternum, with a squeezing, tightening, holding or burning sensation, etc. It may radiate to the neck, jaw, epigastric, shoulder or left forearm. It usually lasts for 2-10 min and can be relieved within 3-5 min after resting or taking nitroglycerin. Triggering factors include exertion, exercise, full meal, cold, emotional excitement, etc. The triggers and nature of UA chest pain are the same as described above, but the patient's activity tolerance decreases, or the attack occurs at rest, and the duration of chest pain is prolonged, the degree is increased, and the frequency of attacks increases. The duration of chest pain in myocardial infarction is often >30 min, which cannot be effectively relieved by nitroglycerin and may be accompanied by nausea, vomiting, profuse sweating and dyspnea. However, the symptoms may be atypical in elderly and diabetic patients, so careful differentiation is needed in clinical practice. Patients with UA generally do not have abnormal clinical signs, but a few may have heart rate changes or heart murmurs due to papillary muscle ischemia. Patients with myocardial infarction may also have no clinical signs. Some patients may present with pallor, cold and clammy skin, cyanosis, jugular venous filling and anger, hypotension, gallop rhythm, and pulmonary systolic murmur at the left edge of the sternum to be highly alert for septal perforation; some patients may have a combination of arrhythmia, bradycardia, atrioventricular block, and tachycardia, especially to be alert for ventricular tachycardia and ventricular fibrillation. ECG is an important tool for early and rapid identification of ACS, and a standard 18-lead ECG can help identify the site of myocardial ischemia. A typical NSTE-ACS ECG is characterized by at least 2 adjacent leads with ST-segment depression ≥0.1 mV or T-wave changes with dynamic changes compared with the baseline ECG. Pseudo-normalization of the original ECG T-wave inversion during the onset of symptoms is also diagnostic. Variable angina may show transient ST-segment elevation. aVR lead ST-segment elevation of more than 0.1 mV is indicative of left main or triple vascular disease. The initial ECG is normal and cannot exclude NSTE-ACS. If the chest pain persists without relief, the ECG needs to be rechecked every 5-10 min. STEMI patients with typical ECG performance in addition to V2, V3 leads, 2 or more consecutive leads after the J-point ST-segment arch dorsal upward elevation > 0.1mV; V2, V3 leads ST-segment, elevation ≥ 0.15mV in women, ≥ 0.2mV in men ≥ 40 years old, ≥ 0.25mV in men < 40 years old considered the diagnosis of STEMI. New onset of left bundle branch conduction block also suggests STEMI; electrocardiographic manifestations of T-wave elevation in ischemia-related leads suggest a hyperpolar phase of STEMI. In patients with previous combined bundle branch block, comparison of pre-morbid ECGs is important for differentiation. Myocardial injury markers are important tests to identify and diagnose ACS in patients, among which, 2 isoforms of troponin (cTn), cTnl or cTnT, are the preferred markers; creatine kinase isoenzyme (CK-MB) also has good specificity for determining myocardial necrosis. After myocardial infarction, cTn needs to be released into the blood by the myocardium after at least 2-4 h and reaches its peak at 10-24 h (Table 2). CK-MB can be used to determine recurrent myocardial infarction. It is recommended that patients with chest pain that cannot be diagnosed early be retested at an interval of 4-6 h after the initial retention of a cTn specimen to exclude myocardial infarction. It is important to emphasize here that early treatment should not be delayed in clinical practice by waiting for the patient's myocardial injury marker results. In 2012, the 3rd Global Harmonized Definition of Myocardial Infarction provided a detailed definition and classification of myocardial infarction, which is more beneficial for physicians to operate in clinical practice. Risk stratification is of great value in determining the prognosis and selecting treatment strategies for patients with ACS. patients with STEMI have the following risk factors: advanced age, female, systolic blood pressure <100 mmHg, heart rate >100 beats/min, pulmonary woven grass Killip class II-IV, atrial fibrillation, anterior wall myocardial infarction, significantly elevated cTn, history of previous myocardial infarction, diabetes mellitus, etc. predicting an increased risk of death. The risk stratification of NSTE-ACS involves more factors, as detailed in Table 3. All patients with ACS can be evaluated for their risk of death both in-hospital and out-of-hospital using the GRACE score system (Table 4).