Ventricular arrhythmias (VA) are not well treated for premature beats or sudden death. As early as the CAST trial has shown, only symptomatic treatment to suppress premature beats, ventricular premature beats are seen to decrease, but the mortality rate is seen to increase, thus changing people’s views on VA treatment, treatment is not simply to eliminate VA, but should seek to improve its overall survival rate, since then arrhythmia treatment has been on the right track. Ventricular arrhythmias can be classified in terms of ECG pattern, duration of attack, presence of organic heart disease, and prognosis, but none of them can cover all the characteristics of ventricular arrhythmias. However, in recent years it has been clear that those with combined organic heart disease, especially those with combined ischemia and cardiac insufficiency, have prognostic significance and should be used as the basis for clinical treatment. (a) Ventricular asystole Its prognostic significance should vary greatly from case to case, and should be treated by risk stratification. The prognosis is generally good for ventricular asystole without organic heart disease, even if it is a frequent ventricular asystole or a few polymorphic, paired, or cascade ventricular asystole in 24h ambulatory ECG monitoring, as determined by detailed examination and follow-up. Conventional antiarrhythmic drug therapy is not supported from the perspective of the risk-benefit ratio. Patient triggers should be removed, and sedatives or low-dose β-blockers may be used for those with stress and anxiety, with the therapeutic endpoint of symptom relief rather than a significant reduction in the number of ventricular precontractions. For some patients with many ventricular precontractions and high psychological stress that cannot be resolved temporarily, the use of class Ib or Ic antiarrhythmics may be considered for a short period of time. Patients with ventricular prophase contractions with organic heart disease, especially those with complex ventricular prophase contractions with cardiac insufficiency, have a poor prognosis and should be risk stratified based on medical history, complexity of ventricular prophase contractions, left ventricular ejection fraction, and with reference to signal-averaged electrocardiogram and rhythm variability analysis. The higher the risk, the more intensive the treatment should be. The primary disease should be treated first to control the proinflammatory factors. On this basis, β-blockers are used as starting treatment, and species with cardioselective but non-endogenous sympathomimetic effects are generally considered. The results of the CAST trial confirm that inhibition of ventricular prematureness with antiarrhythmic drugs in patients with ventricular prematureness after infarction does not necessarily improve the prognosis, especially class I antiarrhythmic drugs should not be used. Class III antiarrhythmic drugs can be used in patients with complex ventricular prematureities. A meta-analysis showed that amiodarone resulted in a significant reduction in overall mortality, especially in patients with cardiac insufficiency. The endpoint of treatment is now debated, and at least for the time being there is no longer an emphasis on the reduction of the total number of ventricular prematureities on 24h ambulatory ECG as a therapeutic goal. However, reduction in the total number of complex ventricular premature is still an acceptable target in high-risk patients. Ventricular premature should be treated acutely in the following situations: acute infarction, acute myocardial ischemia-reperfusion arrhythmias, severe heart failure, ventricular premature present after cardiopulmonary resuscitation, ventricular premature in the midst of frequent episodes of sustained ventricular tachycardia, ventricular premature produced by prolonged QT interval from various causes, and other emergencies (e.g., severe respiratory failure with hypoxemia, severe acid-base imbalance, etc.). (2), ventricular tachycardia based on organic heart disease Non-sustained ventricular tachycardia: non-sustained ventricular tachycardia occurring in patients with organic heart disease is likely to be a precursor of malignant ventricular arrhythmia, and should be carefully evaluated for prognosis and actively searched for causative factors. Intracavitary electrophysiological examination is one of the methods to evaluate the prognosis. If persistent ventricular tachycardia is not induced by electrophysiological examination, treatment should be directed at the cause and the trigger, i.e., treatment of organic heart disease and correction of triggers such as heart failure, electrolyte disturbance, digitalis toxicity, etc., based on which the application of β-blockers can help improve symptoms and prognosis. For the above treatment is not effective and ventricular tachycardia episodes are frequent and obvious symptoms can be prevented or reduced by antiarrhythmic drugs as persistent ventricular tachycardia. If electrophysiological examination can induce persistent ventricular tachycardia, it should be treated as persistent ventricular tachycardia. If the patient has left heart insufficiency or induces persistent ventricular tachycardia or ventricular fibrillation with impaired hemodynamics, a buried cardioverter-defibrillator (ICD) should be preferred. Those without the condition should be treated with medications for sustained ventricular tachycardia. Persistent ventricular tachycardia: Persistent ventricular tachycardia occurs in patients with organic heart disease and has a poor prognosis and is likely to cause sudden cardiac death. In addition to treating the underlying heart disease and carefully searching for possible precipitating factors, the ventricular tachycardia itself must be treated promptly. Common precipitating factors include cardiac insufficiency, electrolyte disturbances, digitalis toxicity, etc. The treatment of ventricular tachycardia includes termination of the attack and prevention of recurrence. (1), termination of ventricular tachycardia: immediate synchronous electrical resuscitation in the presence of hemodynamic disorders, or asynchronous resuscitation in emergency situations (such as syncope, polymorphic ventricular tachycardia or deterioration to ventricular fibrillation). Pharmacological resuscitation requires intravenous administration. Today’s published guidelines for cardiopulmonary resuscitation, treatment of chronic heart failure, and treatment of ST elevation infarction do not recommend lidocaine in aborting ventricular tachycardia and recommend amiodarone. In cases of polymorphic ventricular tachycardia with normal QT, β-blockers are given intravenously first, commonly metoprolol 5-10 mg diluted and then slowly sedated under cardiac monitoring, with immediate discontinuation of ventricular tachycardia. β-blockers are ineffective, then lidocaine or amiodarone is used. If drug therapy is ineffective, electrical cardioversion should be administered. Hemodynamically stable monomorphic ventricular tachycardia with a rhythm of 200 beats/min or less can be terminated by placing a temporary right ventricular pacing electrode and antitachycardia pacing. (2), prevention of recurrence: persistent ventricular tachycardia due to reversible or transient factors such as acute myocardial infarction, electrolyte disturbances or drugs can be excluded as a clear indication for ICD. the results of CASH and AVID trials have shown that ICD can significantly reduce the overall mortality and sudden arrhythmic death rate in such patients, and the effect is significantly better than that of antiarrhythmic drugs including amiodarone. Patients who are not eligible for ICD placement can be treated with amiodarone, and those who are ineffective or unsatisfied with amiodarone alone can be treated with beta-blockers, starting with a small dose of beta-blockers, taking care to avoid bradycardia, or sotalol or propafenone in patients with normal cardiac function. Note that sotalol has the potential to cause torsional ventricular tachycardia and should be started under inpatient conditions. If amiodarone has been used prior to administration, the right to use is required after the QT interval has returned to normal. The beta-blocker effect of sotalol is obvious and requires constant vigilance for its heart rate slowing and negative inotropic effects. Propafenone can also cause cardiac insufficiency, there are drug process to pay attention to. (c), no organic heart disease based ventricular tachycardia This type of ventricular tachycardia, also known as idiopathic ventricular tachycardia, is generally not combined with organic heart disease, the onset of the characteristic electrocardiogram patterns, according to this can be divided into: the origin of the right ventricular outflow tract (occasionally can originate in the left ventricular outflow tract) idiopathic ventricular tachycardia and left ventricular idiopathic ventricular tachycardia. After termination of the attack, electrically adjusted T-wave changes may be present during sinus rhythm. Electroconversion is recommended for prolonged episodes with hemodynamic changes. Drug treatment can be divided into: (1), treatment during the attack: for idiopathic ventricular tachycardia originating from the right ventricular outflow tract, verapamil, propafenone, β-blockers, adenosine or lidocaine can be used; for left ventricular idiopathic ventricular tachycardia, verapamil is preferred for sedation. (2), treatment to prevent recurrence: for ventricular tachycardia of right ventricular outflow, the efficiency of β-blockers is 25%-50%, and the efficiency of verapamil and Heshinshang is 25%-30%, and the combination of β-blockers and calcium antagonists can enhance the efficacy. If it is ineffective, it can be replaced with class Ic (such as propafenone, flecainide) or class Ia (such as procainamide, quinidine) drugs, which are effective for 25%-59%, and amiodarone and sotalol are effective for about 50%. For left ventricular idiopathic ventricular tachycardia, verapamil 160-320 mg/d. can be used. Idiopathic ventricular tachycardia can be radically treated with radiofrequency ablation, which has a high success rate. (d), some special types of ventricular tachycardia 1, torsional ventricular tachycardia: its episodes are often repeated, may also deteriorate into ventricular fibrillation. QT prolongation syndrome can be congenital or acquired. Acquired QT prolongation syndrome can be caused by electrolyte disorders such as hypokalemia and hypomagnesemia, and can occur in severe bradycardia, such as third-degree AV conduction block with slow ventricular escape, or by drugs such as antiarrhythmic drugs, noncompetitive antihistamines (e.g., acepromazole, triptans), and ventricular fibrillation. Asimizole), tricyclic antidepressants, etc. Therefore, the prevention and treatment of torsional ventricular tachycardia is closely related to the timely identification and management of QT prolongation. 2, for congenital long QT syndrome: (1) avoid the use of drugs that prolong the QT interval, including non-cardiovascular drugs; (2) regardless of whether there are symptoms or a family history of sudden death, β-blockers should be used, and the maximum dose that the patient can tolerate should be used. (3) cardiac pacing is effective in preventing long interval-dependent torsional ventricular tachycardia, also can prevent severe bradycardia caused by high-dose β-blockers; (4) for the survivors of cardiac arrest occurred should be placed ICD. 3, torsional ventricular tachycardia episodes of emergency treatment measures are as follows (including acquired QT prolongation syndrome): (1) find and deal with the causes of QT prolongation, such as reduced blood potassium, magnesium concentration or Drugs, etc., stop all drugs that may cause or aggravate QT prolongation; (2) when using drugs to terminate tachycardia, magnesium sulfate is preferred, the first dose of 2-5g sedation (3-5min), and then at a rate of 2-20mg/min sedation. When ineffective, lidocaine, mexiletine or phenytoin can be used; (3) the above treatment is not effective in cardiac stimulation, can shorten QT, eliminate bradycardia, prevent further aggravation of arrhythmia; (4) isoproterenol can increase the heart rate, shorten the ventricular repolarization time, help control torsional ventricular tachycardia, but may make part of the ventricular tachycardia deteriorate into ventricular fibrillation, should be used with caution, for the acquired QT It should be used with caution in patients with acquired QT prolongation syndrome and bradycardia-induced torsional ventricular tachycardia who do not have the conditions for immediate cardiac pacing. The ICD is effective in preventing sudden cardiac death, and amiodarone or (and) beta-blockers can be used after placement of the ICD. Ventricular tachycardia with very short interconnection intervals: verapamil is effective in terminating and preventing its onset, and an ICD should be placed in patients at high risk for recurrent episodes . Accelerated ventricular autonomic rhythm: an ectopic ventricular rhythm with a typical frequency of 60-110 beats/min. seen in coronary artery disease, wind heart disease, hypertension, myocarditis, dilated cardiomyopathy, digitalis overdose, cocaine use, etc. It can also occur in normal subjects and children. In acute myocardial infarction, especially during reperfusion therapy, its incidence can be more than 80%, which is a benign ectopic rhythm, mostly transient. It is usually tolerated because the frequency is not rapid. Treatment of the arrhythmia itself is usually not necessary except for the treatment of the underlying disease. Symptoms may be exacerbated in patients with pre-existing cardiac insufficiency due to loss of atrial synchronous contraction. Atropine may terminate this ectopic ventricular rhythm by increasing the sinus rate and capturing the ventricles. Selection of antiventricular arrhythmia drugs (AAD) Can be used to abort acute episodes of VA and also for the long-term prevention and treatment of VA, but no ideal AAD has been used for VA prevention and treatment so far. Therefore, those who receive AAD treatment imply that the harm caused by the arrhythmia itself to the patient outweighs the possible adverse effects of AAD application in order to have the therapeutic value of applying AAD. Not all cases of VA require treatment. In principle, persistent ventricular tachycardia, whether hemodynamically stable or unstable, should be discontinued immediately, polymorphic ventricular tachycardia, whether sustained or unsustained, should be controlled promptly, and electroshock is preferred in ventricular fibrillation. As for ventricular premature and non-sustained ventricular tachycardia, they should be treated on a case-by-case basis. In principle, Class I AAD is no longer used as a long-term prevention and treatment drug for VA in organic heart disease; Class II AAD beta-blockers can reduce the sudden death rate for the long-term prevention and treatment of chronic heart failure VA in ischemic and non-ischemic heart disease; Class III AAD has the most evidence for the application of amiodarone, which is most suitable for various organic heart diseases, regardless of the effectiveness and safety of amiodarone in aborting acute attacks or for long-term prevention and treatment. Class IV AAD calcium antagonists have no place in the prevention and treatment of VA complicated by cardiac structural abnormalities.