In the past six months I have repeatedly heard of sudden deaths of patients with dilated cardiomyopathy (DCD) and other diseases with large hearts: some patients died after returning from shopping, some patients died in the middle of the night while waiting in line to register for a morning visit, some patients died while walking to a checkup, and so on. Except for the sudden ventricular fibrillation that occurred during the day in the ward, where the patient had a chance to be saved because there were many health care workers in the ward and the resuscitation was timely and there was proven experience in saving the patient, other patients passed away. This is really a pity! The literature reports that the leading causes of death in patients hospitalized with heart failure are left heart failure 59%, arrhythmias 13%, and sudden death 13%. In fact, after high-dose anti-RAS system excitatory therapy in our case, as long as they can tolerate the side effects of these drugs and take them as prescribed, then most of the patients’ cardiac function will improve, thus the death due to acute heart failure or acute exacerbation of chronic heart failure will be significantly lower. So the cause of death in patients is other causes. My personal perception is that in the past, most patients did not pass the heart failure hurdle and died of heart failure before they had a chance to have a subsequent malignant arrhythmia. However, now because of the obvious improvement of heart failure symptoms, some of the patients with dilated heart disease and others relaxed their fear of disease hazards and chose to be overactive at will (although foreign guidelines are encouraging heart failure patients to be active, I still want patients to be less active, even if their heart function has quickly recovered to class I, the so-called clinical symptom cure. Since increasing physical activity will lead to an increased load on the large heart, it will exactly counteract the therapeutic effect of our drugs. So I am asking for a gradual increase in activity only as the heart shrinks). Exertion, exertion, sweating. Vomiting, dizziness, palpitations and other symptoms occur without sufficient attention. Then the possibility of sudden death is present. Judging from the theory and years of practical experience, the most likely factors for these sudden deaths are the occurrence of hypokalemia, and excessive sympathetic excitation. In terms of the theory in the book, a potassium control of 3.5 mmol/L or more is normal. However, I think that in moderately large hearts and above, the possibility of malignant arrhythmias such as ventricular tachycardia and ventricular fibrillation increases as long as the potassium is below 4.0 mmol/L; of course, it is also possible to have frequent ventricular premature complications on top of tachyarrhythmic atrial fibrillation. The patient quickly suffers from a lack of blood supply to the brain, collapse, loss of consciousness, convulsions, coma, etc. Physiologically, low potassium causes the ventricular myocardial Purkinje fibroblast membrane to be in a hyperphase state, and the resting potential is very close to the threshold potential, so the cells are automatically depolarized by calcium ion in-flow, and the ventricular myocardium of the large heart is easily excited, leading to ventricular premature and even ventricular tachycardia and ventricular fibrillation. Therefore, I require a blood potassium level of 4.0 mmol/L or higher in general, and preferably 4.5 mmol/L or higher for short left ventricular diameters of 80 mm or more, to reduce the excitability of myocardial Purkinje fibers. When potassium-removing diuretics are used for the patient to improve cardiac function, potassium supplementation is recommended, and potassium-preserving diuretics such as spironolactone are added to prevent hypokalemia. However, note that when the blood potassium is above 5.5mmol/L, there is again a risk of slow-type arrhythmias, so potassium-preserving therapeutic measures and doses vary from person to person. For patients with ventricular arrhythmias, oral treatment such as amiodarone hydrochloride (with a slower onset of action) can reduce the chance of ventricular tachycardia and ventricular fibrillation; for patients with sympathetic excitation, oral beta-blockers can also reduce the occurrence of ventricular tachycardia and ventricular fibrillation (with a faster onset of action, but in most patients the improvement of cardiac function is slower and cardiac reversal is poorer); of course, the application of ICD ( ICDs (implantable cardioverter-defibrillators) are also useful in preventing sudden cardiac death. In addition, the patient should be careful to reduce excessive activity and to maintain blood pressure well. In case of palpitations that are different from the usual ones, it is better to go to the hospital in time with family members.