Sudden cardiac death (SCD) refers to sudden death due to various cardiac causes. SCD can occur in patients with or without heart disease, often without any life-threatening premonitory manifestations, with sudden loss of consciousness and death within 1 hour after the onset of acute symptoms, and is a non-traumatic natural death, characterized by unexpected and rapid death. The mechanism and prevention are different from those of arrhythmic sudden death. With the clinical use of the implantable cardioverter defibrillator (ICD), the understanding of SCD has been further enhanced by its monitoring system.
SCD is an important cause of death in adults in industrialized countries due to coronary heart disease, and the incidence of SCD has been reported in the literature as 0.36 to 1.28 per 1000 per year, but sudden death without hospitalization is not counted. Therefore, the actual incidence of SCD in the population may be higher. The incidence of SCD varies widely by age, sex, and history of cardiovascular disease, and is as high as 8/1000 per year among men aged 60-69 years with a history of heart disease. 80% of out-of-hospital sudden deaths occur at home, and 15% occur on the road or in public places. The incidence of sudden cardiac death in China is 41.84/100,000, and the total number of sudden cardiac death is as high as 544,000/year, which is the highest among all countries in the world, suggesting that the task of preventing and treating sudden cardiac death in China is arduous.
Risk factors
(i) Age and gender Epidemiological analysis shows that increasing age is a risk factor for SCD. In children, 19% of all sudden deaths in the age group of 1-13 years were of cardiac origin, while in young people, SCD accounted for 30% of all sudden deaths in the age group of 14-21 years. SCD in middle-aged and older adults accounts for more than 80% to 90% of all sudden deaths, which is largely related to the increasing incidence of coronary heart disease with age, as more than 80% of SCD patients develop coronary heart disease. The incidence of SCD is higher in men than in women (approximately 4:1), and the difference in incidence between men and women between the ages of 55 and 64 years was even greater in the Framingham study (almost 7:1), because the incidence of coronary heart disease is significantly higher in men than in women in this age group.
(ii) Hypertension and left ventricular hypertrophy Hypertension is a risk factor for coronary heart disease, but the main mechanism by which hypertension causes SCD is left ventricular hypertrophy. the Framingham study showed that for every 50 g/m2 increase in left ventricular volume, the risk of SCD increased by 45%.
(iii) Hyperlipidemia Increased LDL-C is associated with all clinical types of coronary artery disease, including SCD. statin lipid-modifying drugs reduce the incidence of coronary death (including SCD) and nonfatal myocardial infarction by 30% to 40%.
(iv) Diet Many epidemiological data have confirmed that excessive intake of saturated fatty acids and low intake of unsaturated fatty acids increase the risk of coronary heart disease, but their effect on the incidence of SCD has not been directly observed. A prospective study in the United States of 20,551 men aged 40 to 84 years without a history of myocardial infarction showed that the incidence of SCD in those who ate fish at least once a week was half that of those who ate fish less than once a month.
(v) Exercise Moderate physical activity in patients with coronary artery disease helps prevent cardiac arrest and SCD, while vigorous exercise may trigger SCD and acute myocardial infarction. In adults, 11% to 17% of cardiac arrests occur during or immediately after strenuous exercise and are associated with ventricular fibrillation. This is also demonstrated during rehabilitation studies and exercise stress tests in cardiac patients, where the incidence of cardiac arrest is 1/12,000 to 1/15,000 (rehabilitation studies) and 1/200 (exercise stress tests), respectively, which is 6 times the incidence of cardiac arrest in general cardiac patients.
(vi) Alcohol consumption Excessive alcohol consumption, especially intoxication, can increase the risk of SCD, and prolonged QT interval is often found in alcoholics, who are prone to trigger ventricular tachycardia and ventricular fibrillation. However, some studies have found that moderate alcohol consumption may reduce the occurrence of SCD.
(vii) Heart rate and heart rate variability Studies have confirmed that increased heart rate is an independent risk factor for SCD, the mechanism of which is unknown and may be related to reduced vagal tone. The risk of SCD is approximately twice as high in those with impaired HRV and those with a 24-hour slowest heart rate >65 beats/min as in those with normal HRV.
(viii) Smoking Smoking is one of the triggers of SCD because it tends to increase platelet adhesion, lower the threshold for ventricular fibrillation, raise blood pressure, induce coronary artery spasm, reduce circulating oxygen-carrying capacity due to impaired carboxyhemoglobin accumulation and myoglobin utilization, and lead to nicotine-induced catecholamine release. The annual incidence of SCD was 31/1000 and 13/1000 in smokers compared to nonsmokers who smoked 20 cigarettes per day.
(ix) Mental factors Sudden changes in lifestyle, personal and social factors causing emotional excitement and isolation, and emotional depression due to overburdening of life are closely associated with SCD.
(x) Family history Family history is an important risk factor for some patients. Certain monogenic disorders such as long QT syndrome, Brugada syndrome, hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia, and catecholaminergic polymorphic ventricular tachycardia are known to predispose to SCD.
Other risk factors include intraventricular conduction block, abnormal glucose tolerance test, and obesity. Impaired left ventricular function is an important suggestive factor for SCD in men. In patients with severe heart failure, nonsustained ventricular tachycardia is an independent factor in the increased incidence of SCD.
Etiology and pathogenesis
The vast majority of people with SCD have structural cardiac abnormalities. The major cardiac structural abnormalities in adult SCD patients include coronary artery disease, hypertrophic cardiomyopathy, cardiac valve disease, myocarditis, nonatherosclerotic coronary artery anomalies, infiltrative lesions, and abnormal intracardiac channels. These structural changes in the heart underlie the development of ventricular tachyarrhythmias, which are the cause of most SCD. Some temporary functional factors, such as electrocardiographic instability, platelet aggregation, coronary artery spasm, myocardial ischemia and post-ischemic reperfusion, cause an unstable condition to occur in an abnormal previously stable cardiac structure. Certain factors such as autonomic instability, electrolyte disturbance, overexertion, emotional depression and use of ventricular arrhythmogenic drugs can trigger SCD.
Worldwide, especially in Western countries, coronary atherosclerotic heart disease is the most common structural heart abnormality causing SCD. Among all SCD in the United States, coronary atherosclerosis and its complications cause more than 80% of SCD, cardiomyopathy (hypertrophic, dilated) accounts for 10%-15%, and the remaining 5%-10% of SCD can be caused by various etiologies.
Pathophysiology
The pathophysiological changes are mainly fatal arrhythmias. 75%-80% of cardiac arrests are first recorded as ventricular fibrillation, while less than 2% are sustained ventricular tachycardia. Slow arrhythmias are most often seen in patients with severe congestive heart failure.
(i) Fatal tachyarrhythmias Chronic coronary artery disease often has a regional deficit in myocardial blood supply and thus a localized alteration of myocardial metabolic or electrolyte status. The myocardial oxygen demand increases during stress, but the diseased coronary arteries cannot increase the blood supply accordingly, leading to arrhythmias or sudden death. Alterations in vasoreactivity (coronary artery spasm or alterations in the coronary collateral circulation) can expose the myocardium to the dual hazards of temporary ischemia and reperfusion. The mechanism of coronary artery spasm has not been elucidated, but local endothelial cell lesions and changes in autonomic nervous system activity play a role. Studies suggest that platelet activation and aggregation due to endothelial cell damage and plaque rupture in chronic coronary artery lesions can lead not only to thrombosis but also to a series of biochemical changes that affect vasomotor regulation and lead to the development of ventricular fibrillation.
Rapid polymorphic ventricular tachycardia and ventricular fibrillation are characteristic arrhythmias of early ischemia and predispose to SCD, mostly due to asynchronous conduction velocities and the presence of an absolute nonresponse period around the ischemic zone, which can easily cause folding. Ventricular tachyarrhythmias also often occur during the reperfusion phase.
(The pathophysiological changes are mainly due to the inability of the lower autonomic tissues to pace in the absence of normal function of the sinus node and/or atrioventricular node. It is often caused by severe cardiac disease, diffuse subendocardial Pukenye fiber lesions, hypoxia, acidosis, shock, renal failure, trauma, hypothermia, and other systemic conditions that lead to increased extracellular K+ concentrations, partial depolarization of Pukenye cells, and decreased slope of phase 4 automatic depolarization (depressed autoregulation), leading to loss of autoregulation. This type of arrhythmia is due to the overall depression of autonomic cells, which is different from the regional lesions in acute ischemia. The suppressed autonomic cell function is particularly sensitive to tachycardia inhibition, resulting in a prolonged ventricular pause after a short bout of tachycardia. The latter leads to local hyperkalemia and acidosis, which further depresses autoregulation and eventually results in protracted ventricular arrest or ventricular fibrillation.
(iii) Autonomic nervous system and arrhythmias Sympathetic excitation tends to cause fatal arrhythmias, whereas vagal excitation has preventive and protective effects against lethal arrhythmias induced by sympathetic stimuli, as it can produce anti-adrenergic effects by inhibiting adenylate cyclase activity and reducing norepinephrine release. For example, acute myocardial infarction can cause local cardiac sympathetic and parasympathetic denervation and hypersensitivity to catecholamines, with an asynchronous shortening of the action potential time and the non-response period, which can easily trigger arrhythmias. Pre-ischemia preserves the activity of sympathetic and parasympathetic efferent fibers in the early phase of acute coronary artery occlusion and reduces the occurrence of fatal arrhythmias.
Cardiac arrest due to either of these mechanisms marks clinical death. However, from a biological point of view, the body is not really dead at this point. Because the metabolism of the body’s tissues has not yet completely stopped, the cells, the basic unit of human life, still maintain a weak life activity. If timely and appropriate resuscitation is given, there is still a possibility of survival, especially sudden death that occurs unexpectedly.
After cardiac and/or respiratory arrest, tissue blood flow is interrupted without perfusion, followed by acid-base balance and electrolyte imbalance, especially intracellular acidosis and increased extracellular K+ concentration. It was also found that when hypoxia occurs, the production of oxygen radicals increases, which combine with biofilm polyvalent unsaturated fatty acids with high affinity, causing cell membrane dysfunction, affecting membrane permeability and the activity of various enzymes, and the increase in Ca2+ inward flow increases intracellular Ca2+, eventually leading to cell death. At this point the reversible changes do unfold to an irreversible end and enter biological death.
After circulatory arrest, brain tissue reserves of adenosine triphosphate and glycogen are depleted within minutes. If the body temperature is normal, irreversible damage to brain cells can result within 8 to 10 minutes after cardiac arrest. The liver and kidneys are also more sensitive to hypoxia.
The pathophysiological process of the above-mentioned important organs occurring in hypoxia and acidosis, which are lesions of the heart and brain, can further aggravate hypoxia and acidosis, thus forming a vicious circle. The longer the time of circulatory arrest, the lower the success rate of resuscitation and the more complications. Even if the heartbeat and respiration are temporarily resuscitated successfully, the brain death can be fatal; occasionally, the life can be saved, but the disability can be caused by permanent brain damage. Therefore, every second counts in cardiac arrest.
Clinical presentation
The clinical course of SCD can be divided into 4 periods.
(i) Prodromal period Many patients have prodromal symptoms for days or weeks, or even months, before the onset of cardiac arrest, such as increased angina, shortness of breath or palpitations, easy fatigue, and other nonspecific complaints. These prodromal symptoms are not unique to SCD, but commonly precede any heart attack. Therefore, this period is more important and is key to prevention and treatment.
(ii) Onset The period of acute cardiovascular changes leading up to cardiac arrest, usually less than 1 hour. Typical manifestations include prolonged angina pectoris or chest pain of acute myocardial infarction, acute dyspnea, sudden palpitations, sustained tachycardia or dizziness. If cardiac arrest occurs instantaneously without prior warning, it is 95% cardiac in origin and has coronary artery disease. Changes in ECG activity are often seen in the hours or minutes before sudden death as seen in serial ECG recordings obtained from sudden cardiac death victims, with escalation of increased heart rate and worsening ventricular asystole being the most common. Sudden death from ventricular fibrillation is often preceded by a burst of sustained or nonsustained ventricular tachycardia. These patients with arrhythmogenic onset are mostly awake and in daily activity before the onset, and the onset period (from onset to cardiac arrest) is short. Most of the ECG abnormalities are ventricular fibrillation. Some patients with circulatory failure are already inactive or even comatose before cardiac arrest, and the onset period is long. Non-cardiac disease is often present before the terminal cardiovascular changes. Electrocardiographic abnormalities are more common in ventricular arrest than ventricular fibrillation.
(iii) Cardiac arrest The complete loss of consciousness is the characteristic feature of this period. Without immediate resuscitation, death usually occurs within a few minutes. Spontaneous reversal is rare.
Signs and symptoms of cardiac arrest appear in the following order: ① disappearance of heart sounds. ②Pulse cannot be felt and blood pressure cannot be measured. (3) Sudden loss of consciousness or short-onset convulsions. The convulsions are often generalized and occur within 10 seconds after cardiac arrest, sometimes accompanied by eye deviation. ④Breathing is intermittent, sigh-like, and stops later, mostly within 20-30 seconds after cardiac arrest. ⑤ Coma, mostly occurring 30 seconds after cardiac arrest. ⑥Dilated pupils, mostly occurring 30-60 seconds after cardiac arrest. However, this period has not yet reached biological death. If timely and appropriate resuscitation is provided, resuscitation is possible. The success rate of resuscitation depends on: (i) how late resuscitation starts, (ii) where the cardiac arrest occurs, (iii) the type of derangement of cardiac electrical activity (ventricular fibrillation, ventricular tachycardia, mechanical separation of the heart or ventricular arrest), and (iv) the clinical condition of the patient before the cardiac arrest.
(iv) Biological death The evolution from cardiac arrest to biological death depends mainly on the type of cardiac arrest electrocardiographic activity and the timeliness of cardiac resuscitation. Ventricular fibrillation or ventricular arrest has a poor prognosis if cardiopulmonary resuscitation is not given within the first 4 to 6 minutes. If CPR is not given within the first 8 minutes, there is little chance of survival, except under special circumstances such as hypothermia.
Diagnosis
The diagnosis of cardiac arrest is usually not a problem. However, rapid judgment is required. Sudden loss of consciousness and loss of carotid or femoral artery pulsations, especially heart sounds, are the most important diagnostic criteria for cardiac arrest. The skin color can be pale or a large bruise. Non-medical personnel can diagnose cardiac arrest based on loss of consciousness, absence of respiratory movements or only near-death respiratory activity, combined with loss of aortic pulsations. However, respiratory activity may persist for 1 minute or longer after the onset of arrest. Conversely, if respiratory motion is absent or there is severe wheezing while a pulse is present, this suggests a primary respiratory arrest that will lead to cardiac arrest in a very short period of time.
Treatment
Cardiac arrest is diagnosed on the basis of sudden loss of consciousness, loss of carotid or femoral pulsations, especially loss of heart sounds, absence of respiratory motion or only dying respiratory activity. Once cardiac arrest is diagnosed, immediate cardiopulmonary resuscitation (CPR), including basic life support, advanced basic life support, and post-resuscitation treatment, is indicated to maintain the vitality of the central nervous system, heart, and other vital organs until definitive treatment is given.
Basic life support refers to maintaining an open airway as well as respiratory and circulatory support. It also includes identification of SCD, resuscitation positions, and management of asphyxia.
SCD recognition begins with confirming that the rescuer, victim, and bystanders are safe. Check the victim’s response by shaking the victim’s shoulder and shouting, “Are you okay?” . If there is no response, call for help, place the victim on his or her back and open the airway by tilting the head and lifting the jaw. Keep the airway open, observe the thoracic activity, listen for breath sounds, and feel the airflow with the cheek. If breathing is normal, place them in a resuscitation position, call an ambulance, and check breathing continuously. If breathing is abnormal then perform chest compressions.
Chest compressions to check for a pulse should not exceed 10 seconds. If the patient is found to have no pulse, then chest compressions should be started immediately. To make compressions most effective, the patient should lie in a supine position on a hard surface (such as a flat surface or the ground). The rescuer should place the palm of his hand on the sternum in the middle of the chest, between both nipples, and press the other hand parallel and overlapping on the back of his hand, and make sure that the pressure does not travel to the rib cage. The body is perpendicular to the victim’s thorax, the arms are vertical, and the thorax is pressed for 4-5 cm. After each compression, the pressure is withdrawn but the hand is not separated from the thorax, and the compression frequency is about 100/min. Interruptions should be reduced during chest compressions.
Reopen the airway after 30 compressions. Keep the mouth open and lift the jaw, and after normal inspiration wrap the lips around the mouth to ensure a seal. Blow and observe thoracic elevation for 1 second, which is considered effective rescue ventilation. Leave the patient’s mouth and observe gas expulsion and thoracic retraction. Resuscitate without rechecking or interrupting resuscitation unless the patient begins to breathe normally.
Early defibrillation Early defibrillation is essential to resuscitate a patient in cardiac arrest. Resuscitators who have not witnessed an out-of-hospital cardiac arrest should perform approximately 5 cycles of CPR before checking the ECG and attempting defibrillation. a CPR cycle consists of 30 chest compressions and 2 respirations. If chest compressions are performed at a rate of 100 compressions per minute, then 5 cycles of CPR will take approximately 2 minutes. Clinical studies of out-of-hospital ventricular fibrillation cardiac arrest support CPR prior to defibrillation.
Successful defibrillation is defined as termination of ventricular fibrillation for at least 5 seconds after an electrical shock. Modern defibrillators are classified as unidirectional or bidirectional, depending on the defibrillation waveform. When using a bidirectional defibrillator, either of the two waveforms can be selected, and each waveform is effective in terminating ventricular fibrillation within a specific energy range. The first shock with a linear bidirectional waveform defibrillation should be 120J-200J, while the second and subsequent bidirectional shocks should be of the same or higher energy. Unidirectional waveform defibrillators should be selected for 200 J for the first defibrillation, and 300 J and 360 J for unsuccessful defibrillation; 360 J can also be selected for the first shock to restore rhythm as soon as possible.
Automated external defibrillators (AEDs) are intelligent, reliable computerized devices that can instruct lay first responders and medical personnel to safely defibrillate ventricular fibrillation cardiac arrests through audible and visual cues. Rescuers routinely place the defibrillator electrode plate on the anterolateral portion of the patient’s bare chest at the lateral sternal border of the sternum. The right electrode plate is placed below the patient’s right clavicle, and the left electrode plate is placed flush with the left nipple on the lower lateral part of the left chest. The energy of the first shock was 2 J/Kg and the energy of the subsequent shocks was 4 J/Kg.
Pacing therapy is not recommended for patients with cardiac arrest, while it is considered for patients with symptomatic bradycardia. It is now generally accepted that chest compressions are very important, and there is no conclusive evidence that pacing therapy is beneficial in patients in cardiac arrest, and pacing therapy is not recommended for patients in cardiac arrest with delayed chest compressions. When a pulse is present, patients with symptomatic bradycardia may be treated with percutaneous pacing or transvenous pacing.
The overall goal of advanced life support (ALS) is to adequately ventilate, redirect the rhythm to a hemodynamically effective rhythm, and maintain and support the restored circulation. Therefore, in advanced life support the patient is: intubated and well oxygenated; defibrillated, cardioverted or paced; and with intravenous access established to administer necessary medications.
After tracheal intubation, the purpose of ventilation is to correct hypoxemia. Therefore, the patient should be ventilated with oxygen rather than room air. If possible, the arterial partial pressure of oxygen should be monitored. In-hospital ventilation is usually supported by a ventilator, and out-of-hospital patients usually rely on a balloon-mask approach to maintain ventilation.
Defibrillation- cardioversion Ventricular fibrillation is the most common cause of cardiac arrest, and a key step in successful resuscitation is rapid cardioversion of the rhythm. Prompt chest compressions and artificial respiration, while maintaining vitality of the heart and brain and other vital organs, rarely convert ventricular fibrillation to normal rhythm.
The beneficial effect of epinephrine in disease treatment medication is mainly due to its alpha agonist effect, which increases coronary and cerebral perfusion pressure.
Atropine reverses cholinergic receptor-mediated slowing of heart rate and effectively relieves vagal tone, and can be applied in cardiac arrest and pulseless electrical activity.
Amiodarone. Indications: refractory VF /VT; hemodynamically stable ventricular tachycardia (VT) and other refractory tachycardias.
Lidocaine can suppress ventricular premature and post-acute myocardial infarction ventricular fibrillation. Lidocaine is generally considered only as an alternative drug in the absence of amiodarone.
Magnesium ion is effective in terminating tip-twist ventricular tachycardia caused by long QT intervals, but not in ventricular tachycardia with normal QT intervals.
Vasopressin can be used before and after cardiac arrest. Vasopressin has been used to treat vasodilatory shock, such as septicemia syndrome and infectious shock.
Norepinephrine is a naturally occurring effective vasoconstrictor and force-modifying agent.
Dopamine, a catecholamine, is commonly used in resuscitation to treat hypotension, especially in symptomatic bradycardia or after resuscitation. Combination with other drugs such as dobutamine can be a treatment option for post-resuscitation hypotension.
Dobutamine has positive inotropic effects and may be used to treat severe systolic heart failure.
Milrinone and amrinone are phosphodiesterase (PDE) inhibitors that have cardiotonic and vasodilatory effects. Phosphodiesterase inhibitors are often used in combination with catecholamines for the treatment of severe heart failure, cardiogenic shock and other patients who are not responding to catecholamines alone.
Post-resuscitation supportive therapy is important for early death caused by hemodynamic instability, multiple organ failure, and late death caused by brain injury. Post-resuscitation supportive therapy to improve the prognosis of resuscitated patients is an important component of advanced life support. Patients still have a high morbidity and mortality rate after restoration of voluntary circulation and initial stabilization. During this phase, circulatory, respiratory and neurological support should be enhanced; the reversible causes of cardiac arrest should be actively sought and treated; body temperature should be monitored and therapeutic thermoregulatory disorders and metabolic disturbances should be actively treated.
Restoring normal brain function and other organ functions is the basic goal of cardiopulmonary cerebral resuscitation. During the stage of restoration of autonomic circulation, brain tissue decreases in cerebral blood flow due to microcirculatory disorders after an initial brief period of congestion (no recurrent flow phenomenon). A normal or slightly increased mean arterial pressure should be maintained in unconscious patients to ensure ideal cerebral perfusion. Because hyperthermia and agitation can increase oxygen demand, hypothermia must be considered to treat hyperthermia. Convulsions must be controlled with anticonvulsants as soon as they are detected.
Prevention
The prevention of SCD remains an unresolved problem in modern medicine to date. The major advance in the prevention of cardiac arrest in recent years has been the identification of subjects at high risk for cardiac arrest. The risk of sudden cardiac arrest is high in coronary artery disease, especially in the acute phase of myocardial infarction, in recovery and in the chronic course thereafter. Within the first 72 hours of acute myocardial infarction, the potential risk of cardiac arrest can be as high as 15-20%. Those with a history of ventricular tachycardia or ventricular fibrillation during recovery from myocardial infarction (from day 3 to week 8) have the highest risk of sudden cardiac arrest, with a mortality rate of 50% to 80% within 6 to 12 months if treated with only general measures, 50% of which are sudden deaths. Only active intervention can improve the prognosis, and the mortality rate can be reduced to less than 15%-20% within 18 months.
1, regular medical check-ups: the elderly themselves are a high incidence of heart disease and various diseases, should regularly go to the hospital for medical check-ups. The young and middle-aged people are also prone to coronary heart disease, hypertension and other diseases due to their intense work, fast-paced life and stressful work life. Regular medical checkups and early examinations facilitate the timely detection of diseases, early treatment and reduce the risk of sudden death.
2, avoid excessive fatigue and mental tension: excessive fatigue and mental tension will put the body in a state of stress, so that the blood pressure rises, the heart burden increases, making the original heart disease aggravated. Even if there is no original organic heart disease can also trigger the occurrence of ventricular fibrillation. Therefore, everyone should make arrangements for their work and life, control the pace of work and work time, not too fast and too long.
3, quit smoking, limit alcohol, balanced diet, weight control, proper exercise, maintain good habits will reduce the occurrence of cardiovascular disease.
4, pay attention to the danger signals of over fatigue and pay attention to the precursor symptoms of the onset: long-term over fatigue will trigger some changes in the body. Such as anxiety and irritability, memory loss, inattention, insomnia and poor sleep quality, headache, dizziness and tinnitus, sexual dysfunction, hair loss and so on. When these conditions occur, the body should adjust the pace of work, proper rest, so that the body function can be restored. If it cannot be relieved, go to the hospital immediately for treatment.
5.Patients who are already suffering from coronary heart disease, hypertension and other diseases should adhere to medication treatment under the guidance of a doctor.
6.Pay attention to risk assessment of ventricular arrhythmias, including performing routine ECG, exercise stress test, ambulatory ECG, other ECG techniques (body surface signal averaged ECG, etc.), echocardiography, intracardiac electrophysiological examination, etc., to clarify the type of arrhythmia, assess the risk of SCD and make treatment decisions.
7. Pay attention to strengthening the prevention of SCD after infarction. Chronic ventricular asystole after acute myocardial infarction is a risk factor for cardiac death and sudden death, especially in those with frequent (24-hour ambulatory ECG showing ventricular asystole of 10-30 times/hour or more) ventricular asystole and short-onset, non-sustained ventricular tachycardia. LVEF, left ventricular volume, heart rate variability or pressure reflex sensitivity are useful for risk stratification of SCD after myocardial infarction, followed by frequent ventricular asystole, short-onset, nonsustained ventricular tachycardia and resting heart rate. Late ventricular potentials and intracardiac electrophysiology are not recommended routinely after myocardial infarction. Active treatment of myocardial ischemia after myocardial infarction is the main effective measure to prevent sudden death. For patients with positive exercise test and severe stenosis on coronary angiography after myocardial infarction, active interposition therapy or coronary artery bypass grafting can effectively reduce the occurrence of sudden death. The application of ICD prophylaxis in patients at high risk of SCD after myocardial infarction can significantly reduce the morbidity and mortality rate compared with conventional drug therapy. Cardiac arrest can also occur in people considered to be at low risk, and fundamental preventive measures should be devoted to the prevention of underlying heart disease and cardiac arrest triggers.