The pathophysiological basis of the electrocardiographic changes in pulmonary embolism (PE) is the mechanical obstruction of the pulmonary artery and its branches by emboli, combined with neurohumoral factors and hypoxia, causing pulmonary artery constriction, increased resistance to pulmonary circulation, and pulmonary hypertension. The enlargement of the right heart causes the septum to shift to the left, which impairs the function of the left ventricle and leads to a decrease in cardiac output and intra-aortic hypotension. In pulmonary embolism, the pulmonary ventilation/perfusion ratio is severely imbalanced and hyperventilation causes hypoxia and hypocapnia. The PE ECG may be normal (about 30%), but most diseased PEs have nonspecific ECG abnormalities. The latter include arrhythmias, T-wave changes and ST-segment abnormalities in V1-V4 are more common, and the SIQIIITIII sign may be present in some cases; other ECG changes include complete or incomplete right bundle branch block, pulmonary P waves, rightward deviation of the electrical axis, and cis-clockwise transposition. Pulmonary P waves are most likely caused by right atrial dilatation due to acute embolism caused by an embolus, and are present in less than 6% of patients with PE. In the evolution of pulmonary P waves in patients with PE, it was found that patients presented with sinus tachycardia and nonspecific ST-segment/T-wave changes at the time of presentation, and the time to the appearance of pulmonary P waves was approximately 6 hours. In patients with PE, Ptf-V1 is more significant and often suggests a rightward deviation of the electrical axis. SIQIIITIII signs Only about 12% of patients with acute PE initially exhibit SIQIIITIII signs, often with mild ST-segment elevation in the anterior chest leads, which suggest acute right ventricular wall hypertonia and right ventricular enlargement. QIIITIII and SI are also common, and in 73% of patients diagnosed with PE, S waves >1.5mm in lead I or R/S >1 in leads I and aVL are seen. The ST segment can be depressed or elevated in patients with ST-segment PE, and the most common change is ST-segment Mild depression, most likely related to myocardial ischemia caused by PE. T-wave inversion in the thoracic leads is a common ECG change in acute PE (about 40%) and is the best ECG predictor to identify large acute PE. The severity of acute PE may be increasing with the leftward shift of the T-wave inversion in the chest leads. The presence of T-wave disappearance in the thoracic leads, the so-called premonitory manifestation of myocardial ischemia, has the highest sensitivity and specificity for the diagnosis of PE. “Ischemic” T-wave changes have a very important positive or negative predictive value for the diagnosis of PE. The QRS axis can be left- or right-skewed, and in the Urokinase for Pulmonary Embolism Multicenter Study trial, investigators reported that left-skewed axes occurred more frequently in the study population with PE than right-skewed axes. When individual factors of combined underlying cardiopulmonary disease are taken into account, the incidence of left-axis deviation is equal to that of right-axis deviation. Right bundle branch block, including complete or incomplete right bundle branch block, occurs in approximately 25% of PEs and often disappears after normalization of right heart hemodynamic parameters. Arrhythmias have been reported to occur in 4% to 35% of patients with PE. The most common manifestation of these is sinus tachycardia. Other common arrhythmias are atrial premature beats, ventricular premature beats, atrial fibrillation, atrial flutter, and paroxysmal atrial tachycardia. Most cases of PE present with non-specific ECG abnormalities, and it is helpful to diagnose PE if the ECG changes are closely integrated with the condition. ECG changes mostly start to appear immediately after the onset of the disease, and the ECG changes in acute PE are mostly transient and variable; therefore, when PE is suspected, as in myocardial infarction, ECG review needs to be done several times a day for dynamic comparison, and it is more significant to observe dynamic changes in ECG than static abnormalities to suggest PE. In particular, it is important to observe small SI, QIII and SvI, and other changes that can help in the diagnosis of PE. Signs of right ventricular strain, such as T-wave inversion in leads V1 to V4 and new incomplete or complete right bundle branch block, are meaningful signs of right ventricular dysfunction. A new right bundle branch block is a sign of complete blockage of the main pulmonary artery. T-wave inversion in leads V1-V3 of the anterior chest leads is the most sensitive and diagnostic ECG index for determining right ventricular dysfunction in patients with acute PE, and SIQIIITIII and right bundle branch block also have good specificity, but are only moderately accurate indicators. Some domestic scholars reported that after effective thrombolytic therapy, the main changes of ECG were heart rate slowing down, left deviation of electrical axis, SI becoming shallow, QIIITIII improving, QIII becoming smaller, narrower or disappearing, right bundle branch conduction block disappearing, Svl deepening, and cis-clockwise transposition reducing or disappearing. As for the changes of T waves in the anterior chest leads, the T waves are mostly inverted and deepened. The main ECG manifestations of PE are summarized as follows: (1) SIQIIITIII or SIQIII type; (2) T-wave inversion in right thoracic leads; (3) obvious paraclonic transposition; (4) new right bundle branch block combined with sinus tachycardia; (5) right deviation of QRS electrical axis. If the ECG is normal before onset and one or more of the above ECG changes appear after onset, it is highly suggestive of PE.