The ECG of atrial fibrillation is characterized by the disappearance of P waves and their replacement by irregular atrial fibrillation waves, or f waves, with unequal R-R intervals, unequal QRS wave voltage, and possibly ventricular fusion waves. The clinical examination is characterized by three & unequal: unequal strength of the first heart sound, unequal heart rate and pulse, and unequal fast and slow heart rate. Atrial fibrillation is the occurrence of irregular impulses of 350 to 600 beats/min in the atria, causing uncoordinated atrial myocardial fibrillation. It is one of the more common arrhythmias in adults, and its incidence is second only to sinus arrhythmia, premature beats, and atrial tachycardia, and is 15 to 20 times higher than that of atrial flutter, and constitutes a rapid atrial arrhythmia with atrial flutter and atrial tachycardia. Atrial fibrillation is one of the better and more common arrhythmias in clinical practice, with its triggering hemodynamic disturbances and thromboembolic complications, which seriously affect the quality of life of patients. In recent years, more and more attention has been paid to the study of atrial fibrillation. P waves disappear and are replaced by atrial fibrillation waves (f waves) with irregular morphology, spacing and amplitude, frequency 350-600 beats per minute QRS wave groups are spaced & irregular, their morphology and amplitude can often be unequal. Atrial fibrillation is the occurrence of irregular impulses of 350 to 600 beats per minute in the atria, causing uncoordinated atrial myocardial fibrillation. It is one of the more common arrhythmias in adults, and its incidence is second only to sinus arrhythmia, premature beats, and atrial tachycardia, and 15 to 20 times that of atrial flutter, which together with atrial flutter and atrial tachycardia constitute rapid atrial arrhythmia. Atrial fibrillation is one of the better and more common arrhythmias in clinical practice, with its triggering hemodynamic disturbances and thromboembolic complications, which seriously affect the quality of life of patients. Atrial fibrillation is divided into paroxysmal atrial fibrillation, persistent atrial fibrillation and & atrial fibrillation. In addition to preventing thromboembolic complications, the goal of atrial fibrillation treatment remains the satisfactory control of ventricular rate, restoration of sinus rhythm and prevention of its recurrence. There are two classes of antiarrhythmic drugs used for atrial fibrillation: 1. Drugs to divert atrial fibrillation, restore sinus rhythm and prevent recurrence, including class IA (e.g. quinidine), class IC (e.g. propafenone, morethizide) and class III (amiodarone, sotalol) antiarrhythmic drugs. They mainly act on the atria to prolong the atrial induction period or slow down the intra-atrial conduction. 2. Drugs that slow down the ventricular rate, including beta-blockers, non-dihydropyridoxine calcium antagonists (verapamil and diltiazem?) and digitalis drugs. They act on the atrioventricular node to prolong the atrioventricular nodal inactivity and increase cryptic conduction. In the past, some clinicians have misinterpreted drugs that slow the ventricular rate as having the function of converting atrial fibrillation to sinus rhythm or preventing recurrence of atrial fibrillation, such as digitalis (trichothecenes, digoxin), non-dihydropyridines (verapamil and diltiazem?) and beta-blockers. Some randomized, double-blind studies have shown no significant difference between the effectiveness of resuscitation and restoration of sinus rhythm from the start of administration of quinidine compared with placebo. Quinidine has been widely used in China for the restoration of sustained atrial arrhythmia and prevention of recurrence of atrial fibrillation, but clinical studies have shown that, although effective in the treatment of atrial fibrillation, quinidine may increase morbidity and mortality.