Sympathetic storm is synonymous with electrical storm, ventricular tachycardia storm, and ICD storm, and its root cause is the extreme excitation of sympathetic nerve. 2 or more spontaneous rapid ventricular tachycardia or ventricular fibrillation within 24 hours, requiring urgent treatment of clinical syndromes, is called sympathetic storm. When sympathetic nerves are overexcited, a large amount of norepinephrine is released at the end, which causes a serious loss of ion channel function in the myocardial cell membrane through cardiovascular receptors such as β. The main effects are fourfold, namely (1) enhancement of physiological and pathological ventricular myocardium with autoregulatory cell 4 phase diastolic auto-depolarizing pacing current, resulting in a significant increase in autoregulation; (2) enhancement of ventricular myocardial cell 2 phase ICa2+ inward flow, inducing trigger (2) Enhancement of ICa2+ inward flow in ventricular myocytes in phase 2, which induces triggered excitation and phase 2 refractory arrhythmias; (3) Enhancement of IK+ outflow in ventricular myocytes in phases 1 to 3, which shortens the nonstop period and predisposes to tachyarrhythmias; (4) Lowering of ventricular fibrillation threshold. These effects can cause electrical storms in hearts with a pathological basis. Sympathetic storms are clinically characterized by recurrent episodes of ventricular tachycardia and ventricular fibrillation. Normally effective antiarrhythmic drugs, including amiodarone and propafenone, may be ineffective or have poor efficacy when the internal environment is unstable. Sympathetic storms are also characterized by progressively shorter intervals between episodes of fast ventricular tachycardia and ventricular fibrillation, and increased sinus rate before each episode. Sympathetic activation can be exacerbated by the effects of electrical shock on myocardial damage and pain-causing effects, creating a vicious circle with the underlying cause and deteriorating internal environment (metabolic acidosis, electrolyte disturbances). Acute myocardial ischemia such as ACS, somatic trauma, psychological trauma, central nervous system dysfunction and injury, primary ventricular tachycardia, ventricular fibrillation, and electrical transients may lead to a dramatic increase in endogenous catecholamines several, tens, hundreds, or even thousands of times in a short period of time, resulting in extreme sympathetic activation. Sympathetic activation has a wide range of deleterious effects on ion channels. In addition, increased central sympathetic excitability can produce central arrhythmogenic effects, often manifesting as ventricular and supraventricular tachyarrhythmias and sudden death. Sympathetic activation also causes a lowering of the ventricular fibrillation threshold, predisposing patients to ventricular fibrillation. Sympathetic storms have a long and short cycle phenomenon. It often causes polymorphic, tip-twisting ventricular tachycardia and ventricular fibrillation. Sudden death occurs in more than 50% of cases with short- and long-period phenomena. Exercise and stress-induced ventricular tachycardia are associated with this phenomenon. Overdrive ventricular pacing may prevent short- and long-cycle phenomena. For the reversal and quelling of sympathetic storms, clinical practice and guidelines have clarified that β-blockers are the drug of choice, with additional causal treatment with amiodarone and massive sedation (Valium), potassium and magnesium supplementation, and correction of ischemia. β-blockers have a wide range of ion channel effects, central antiarrhythmic effects, and other specific effects that help to increase the ventricular fibrillation threshold and reduce the rate of sudden death.