Atrioventricular block is a blockage of impulses during atrioventricular conduction. There are two types of block: incomplete and complete. The former includes first- and second-degree AV block, while the latter is also called third-degree AV block, and the block can be in the atrium, AV node, Hitchcock’s bundle and double bundle branches. In complete AV block, the temporal relationship between the atria and the ventricles is separated, and the atria lose their auxiliary pumping effect on ventricular contraction, resulting in a decrease in cardiac output. Complete AV block is more common in patients over 50 years of age, and complete AV block is more common in younger patients with transient nature. There are more male patients than female patients. The symptoms and hemodynamic changes of complete AV block depend on the degree of ventricular rate slowing and the lesion and functional status of the myocardium. In complete AV block, the temporal relationship between the atria and ventricles is separated and the auxiliary pumping of ventricular contraction by the atria is lost, resulting in a decrease in cardiac output. In congenital complete AV block, the ventricular rhythm point is often above the atrioventricular bundle bifurcation, and the ventricular rate is faster and can increase with physical activity. Myocardial function is better and cardiac output tends to increase, so these patients are often asymptomatic. In patients with acquired complete atrioventricular block, most of them may be asymptomatic at rest or may have palpitations. Palpitations, dizziness, weakness, chest tightness, and shortness of breath may be present during physical activity. If the ventricular rate is too slow, especially if the heart has significant ischemia or other lesions at the same time, or if it is complicated by extensive acute myocardial infarction or severe acute myocarditis, the symptoms may be more severe, and heart failure or shock may occur, or slow response or confusion may occur due to insufficient blood supply to the brain, which may progress to syncope (incidence up to 60%) and A-Syndrome. Due to the increase in diastolic ventricular filling volume and volume per beat, a widening of the pulse pressure difference and mild to moderate cardiac enlargement may occur. The clinical manifestations of acute myocardial infarction with complete atrioventricular block have their own characteristics: the degree of hemodynamic disturbance in acute myocardial infarction depends on the site of infarction, the rate of onset of conduction block, the site of the ventricular pacing point and the ventricular rate. In inferior wall infarction complicated by third-degree AV block, the ventricular rate is not too slow to cause clinical deterioration if it is progressively developed from first- or second-degree ventrogenic AV block. In contrast, most anterior wall infarcts complicated by third-degree AV block may present with hypotension, shock, and severe left heart failure. In both anterior and inferior wall infarcts, the sudden onset of QRS wave widening and a third-degree AV block with an excessively slow ventricular rate of less than 40 beats/min can easily induce ventricular arrest or ventricular tachycardia or ventricular fibrillation. Anterior wall myocardial infarction with complete AV block has a 2-fold higher mortality rate than inferior wall myocardial infarction. However, when inferior wall combined with right ventricular myocardial infarction is complicated by complete atrioventricular block, the rate of death increases significantly because the filling effect of the right ventricle on the left ventricle is reduced, which further decreases cardiac output and increases hemodynamic disturbances. Most of the complete AV block complicated by acute myocardial infarction is temporary, and only a few patients never recover after the infarction. Patients with slow ventricular rate and marked widening of QRS waves on ECG are particularly prone to syncope or heart failure. In patients with complete AV block, the first heart sound varies in severity and is sometimes particularly loud, like a cannonball sound, due to frequent variations in the interrelationship between atrial and ventricular systolic times. Pay attention to the causes of atrioventricular block, the presence of organic heart disease, the presence of long-term or heavy use of antiarrhythmic drugs, the presence of cardiac surgery, inflammation, electrolyte and acid-base imbalance, the presence of vagal hypertonia, carotid sinus syndrome, etc. ①Myocardial inflammation of various causes is the most common, such as rheumatic, viral myocarditis and other infections. (ii) Vagal excitation, often manifested as transient atrioventricular block. ③Drugs: such as digitalis and other antiarrhythmic drugs, most of which disappear after discontinuation of the drug, atrioventricular block. ④Various organic heart diseases such as coronary artery disease, rheumatic heart disease and cardiomyopathy. ⑤ Hyperkalemia, uremia, etc. ⑥Idiopathic conduction system fibrosis, degenerative changes, etc. (7) Trauma, atrioventricular conduction block can be caused by the accidental injury or wave of atrioventricular conduction tissue during cardiac surgery.