The pharmacological treatment of cardiac arrhythmias has gone through nearly a century of mileage. The author discusses the clinical application of antiarrhythmic drugs in the past hundred years as follows. In 1914, during the treatment of malaria, quinine was accidentally found to cure atrial fibrillation, and its active ingredient, quinidine, was introduced in 1918 and was formally used for the resuscitation of atrial fibrillation. In the 1960s, lidocaine was widely used, especially for its effectiveness in correcting ventricular tachycardia in patients with myocardial infarction. At the same time, the chemical synthesis of β-blockers (Jinan, Sotalol) and anti-anginal drugs (Isoptin and Amiodarone), they have a strong anti-arrhythmic effect. 1970s and synthesized the Inca amine, flucarbamate, so the development of class I anti-arrhythmic drugs reached its peak. In the early 1990s, just when people were hopeful about the prospect of arrhythmia drug therapy, a large-scale arrhythmia suppression trial (CAST for short) was conducted in the United States, and the result was a significant increase in mortality in the treatment group, which led the world to notice that anti-arrhythmic drugs also have pro-arrhythmic problems, and drug therapy may not be beneficial. A series of clinical trials later led to the realization that all antiarrhythmic drugs have different degrees of arrhythmogenic effects, including causing new arrhythmias that were not present before the drug was used (e.g., quinidine induced tip-twisting ventricular tachycardia) and worsening existing ventricular arrhythmias before the drug was used (e.g., IC drugs can make monomorphic sustained ventricular tachycardia more frequent and difficult to terminate after myocardial infarction). In addition, most antiarrhythmic drugs have the effect of reducing myocardial contractility, especially sipramine and cardioplegics, and the extracardiac organ toxicity of amiodarone cannot be ignored. Up to now, only class II drugs (beta-blockers represented by betalactam) and class III drugs (amiodarone and sotalol) have been proven to improve prognosis, and the main broad-spectrum, highly effective antiarrhythmic drugs in clinical use are cardioplegia and amiodarone. The need for and the choice of antiarrhythmic drugs in patients with arrhythmias should vary from person to person. It is important to properly assess the benefit/risk ratio of the patient after receiving the drug, and to strictly indentify the indications. Those who do not have organic heart disease and do not have obvious symptoms may not need the drug, while those with obvious symptoms prefer beta-blockers and discretionary slow-rhythm drugs, such as cardioplegia and isoptin, which have little risk of causing arrhythmias in patients with non-organic heart disease, but amiodarone, which has high organ toxicity, should not be used. In patients with myocardial infarction or chronic heart failure who develop ventricular premature or non-sustained ventricular tachycardia, the main focus is on symptomatic and symptomatic treatment to correct myocardial ischemia and heart failure. If the patient has poor cardiac function and frequent episodes of arrhythmias, amiodarone is appropriate, but cardiac rhythm equivalence that may lead to worsening prognosis should be avoided. In conclusion, anti-arrhythmic drugs should be used as much as possible, but if they are necessary, cardioplegia can be chosen for functional and amiodarone for organic.