Electrocardiogram (ECG) has been used in clinic for more than 100 years, and surface ECG is still the most commonly used diagnostic method for AMI. This is because the body surface electrocardiogram is a non-invasive examination with simple operation and good repeatability. It can be done at the bedside and can be diagnosed in a short time. If ECG results are combined with clinical data, 70% ~ 80% AMI can be diagnosed early. In recent 10 years, some scholars have put forward some new viewpoints and indicators to diagnose AMI by comparing ECG with coronary angiography, cardiac function examination and serum biochemical markers, which has improved the ability of body surface ECG to diagnose AMI.

Before 1980s, AMI was divided into acute transmural myocardial infarction and acute subendocardial myocardial infarction, and the classification was based on whether pathological Q wave appeared in ECG. At that time, the view was that pathological Q wave reflected myocardial necrosis from epicardium to endocardium, showing transmural necrosis; If there is no pathological Q wave in ECG and only ST-T segment changes, it reflects that myocardial necrosis is limited to subendocardial myocardium.

Classification methods after the 1980s Around the 1980s, some scholars compared autopsy data with patients' ECG before their death, and found that it was neither sensitive nor specific to use pathological Q wave as the classification basis for acute transmural myocardial infarction and acute subendocardial myocardial infarction. Therefore, it has been suggested that myocardial infarction with or without pathological Q wave can be directly divided into Q wave and myocardial infarction without Q wave according to ECG.

Recently, some scholars have proposed that AMI can be divided into ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI) in the early stage according to the presence or absence of ST-segment elevation in ECG. In the early stage of AMI, only ST segment changes occur, pathological Q wave usually appears at 8 ~ 12 hours, and 14% cases appear at 72 hours. Therefore, Q-wave myocardial infarction or non-Q-wave myocardial infarction cannot be diagnosed in the early stage of AMI. It is not reliable to predict Q-wave myocardial infarction or non-Q-wave myocardial infarction according to ST segment elevation or depression. Successful thrombolytic therapy can prevent Q wave. At present, there is no pathological Q wave in the evolution of about 40% STEMI. It has guiding significance for treatment: STEMI reflects that coronary artery has thrombus occlusion and needs thrombolysis; However, NSTEMI showed that white thrombus mainly composed of platelets caused incomplete coronary artery occlusion, so antiplatelet drugs should be used, and thrombolytic therapy was harmful. Of course there are exceptions. To improve the diagnostic ability of surface ECG for AMI: According to Sgarbossa, 1 ECG recording period, 15% ~ 18% patients with acute myocardial infarction have no change, and 25% patients have atypical ECG changes. There is no change or atypical change in ECG of AMI patients, which may be due to: (1) The infarct area is too small? QV4 or Qv4 > QV5 > QV6, suggesting anterior myocardial infarction.

New diagnostic criteria of AMI and allelic Q-wave ECG (3) Progressive Q-wave: The Q-wave is small at the initial stage of onset, but it is gradually widened and/or deepened, which is called progressive Q-wave, which highly indicates myocardial infarction, but the electrode position must be fixed to exclude the influence of operational factors.

(4) Pathological Q-wave area: Although Q-wave failed to meet the standard of pathological Q-wave, Q-wave can be recorded between upper and lower ribs or left and right, reflecting the existence of pathological Q-wave area, suggesting myocardial infarction.

(5) The reverse increase of R wave in chest lead: if RV3> RV4 or RV4>RV5, it indicates that the amplitude of R wave in patients with acute chest pain caused by anterior myocardial infarction is gradually decreased. (6) It indicates the existence of myocardial infarction, and the influence of operational factors should also be excluded.

(There is a negative wave at the beginning of R wave in V4 ~ V6 leads > > 0.5 mm. Sele-Vesler thinks that it has the same diagnostic value as pathological Q wave. The new ECG classification method of ST-segment elevation myocardial infarction (STEMI) is closely related to the coronary anatomy, clinical manifestations and prognosis of patients, and also has guiding significance for treatment. Due to the influence of blood supply of Xi- Pu system, new bundle branch block often occurs, among which left anterior bundle branch block and right bundle branch block are the most common, and left bundle branch block, double branch block or Mohs II atrioventricular block can also occur. Unless effective reperfusion treatment is carried out in time, patients may have pump failure or cardiogenic shock. The 30-day mortality rate was 65438 09.6, and the 0-year mortality rate was 25.6 2. The distal end of the first perforating branch of the left anterior descending branch and the proximal end of the great oblique branch were occluded in the middle segment of the left anterior descending branch, and the st segment of leads V 1 ~ V6, I and aVL in ECG was elevated without conduction block. Myocardial necrosis was confined to the anterior segment and apical segment, and the proximal ventricular septum was not damaged. If cardiogenic shock occurs, it may be the original myocardial damage or massive bleeding and other extra-cardiac reasons. Pump failure may occur, and ventricular aneurysm complicated with apical thrombosis is also common. The 30-day mortality rate was 9.2, and the 1 year mortality rate was12.4 3. The distal left anterior descending branch of myocardial infarction was blocked, only the ST segment of lead V 1 ~ V4 was elevated, and there was no cardiogenic shock and pump failure. Thrombosis may occur due to the disappearance of apical wall motion.