Cardiac Arrest (CA) refers to the sudden cessation of the heart's ability to pump blood, resulting in the interruption of systemic circulation, cessation of breathing, and loss of consciousness. Following cardiac arrest, the abrupt cessation of cerebral blood flow typically leads to loss of consciousness within approximately 10 seconds. If treatment is initiated during the critical 4-6 minute window, survival rates are relatively high; otherwise, biological death occurs, and spontaneous recovery is rare. Based on the location of occurrence, cardiac arrest is classified as out-of-hospital cardiac arrest (OHCA) or in-hospital cardiac arrest (IHCA).
Sudden Cardiac Death (SCD) refers to a natural death of cardiac origin that occurs within one hour of the onset of acute symptoms, characterized by the sudden loss of consciousness. This can occur regardless of the presence of pre-existing heart disease, and the timing and manner of death are unpredictable. Globally, approximately 4-5 million cases of SCD occur annually, with incidence increasing with age. The incidence is low in infants and children (approximately 1 per 100,000 population annually) but rises to 50 per 100,000 annually in individuals aged 50-60 years and to 200 per 100,000 annually in those over 80 years old.
Etiology
The causes of cardiac arrest are diverse and include intrinsic factors (such as cardiac and non-cardiac diseases or terminal illnesses) as well as external factors (such as trauma, drowning, or suicide). Cardiac diseases are the leading cause. The majority of SCD cases occur in patients with structural heart disease. In Western countries, approximately 80% of SCD cases are caused by coronary artery disease and its complications. Reduced left ventricular ejection fraction (LVEF) following myocardial infarction is a major risk factor for SCD. Frequent and complex ventricular premature contractions are also predictive of sudden death in survivors of myocardial infarction. Cardiomyopathies account for 5%-15% of SCD cases and are a leading cause of SCD in individuals under 35 years of age, including hypertrophic obstructive cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy. Other causes include ion channel disorders, such as long QT syndrome and Brugada syndrome.
In addition, extreme emotional stress or mental stimulation can trigger cardiac arrest by activating the sympathetic nervous system, inhibiting the vagus nerve, or affecting respiratory center regulation. These mechanisms can lead to respiratory or cardiac arrest or exacerbate pre-existing cardiovascular conditions, resulting in cardiac arrest. Examples include catecholaminergic polymorphic ventricular tachycardia and stress-induced cardiomyopathy.
Pathology
Coronary atherosclerosis is the most common pathological finding in SCD. Pathological studies indicate that acute coronary thrombosis occurs in 15%-64% of SCD cases, but only about 20% show evidence of acute myocardial infarction. Chronic myocardial infarction is also a common finding, and left ventricular hypertrophy is frequently observed in SCD cases. Left ventricular hypertrophy may coexist with acute or chronic myocardial ischemia.
Pathophysiology
The most common pathophysiological mechanism leading to cardiac arrest is ventricular tachyarrhythmias (ventricular fibrillation and ventricular tachycardia), followed by bradyarrhythmias or asystole. Less commonly, pulseless electrical activity (PEA) is observed. Ventricular tachyarrhythmias result from a series of pathophysiological abnormalities caused by interactions among coronary events, myocardial injury, metabolic disturbances, and/or alterations in autonomic nervous tone. However, the ultimate mechanisms by which these factors interact to produce fatal arrhythmias remain unclear.
Severe bradyarrhythmias and asystole occur when the sinoatrial node and/or atrioventricular node are dysfunctional, and secondary pacemaker cells fail to maintain cardiac pacing. This is often seen in severe cardiac diseases with diffuse subendocardial Purkinje fiber involvement. PEA, previously referred to as electromechanical dissociation (EMD), is a relatively rare cause of SCD and may occur in cases of ventricular rupture following acute myocardial infarction or massive pulmonary embolism.
Non-arrhythmic causes of SCD are less common and include cardiac rupture, acute obstruction of cardiac inflow or outflow tracts, and acute cardiac tamponade.
Clinical Manifestations
The clinical course of sudden cardiac death (SCD) can be divided into four stages: the prodromal phase, the terminal event phase, cardiac arrest, and biological death. The manifestations of each stage vary significantly among patients.
Prodromal Phase
In the days to months preceding sudden death, some patients may experience nonspecific symptoms such as chest pain, shortness of breath, fatigue, or palpitations. However, others may have no prodromal symptoms, with cardiac arrest occurring instantaneously.
Terminal Event Phase
This phase refers to the period between the onset of acute cardiovascular changes and the occurrence of cardiac arrest, lasting from a moment to up to one hour. The one-hour definition of SCD essentially corresponds to the duration of the terminal event phase. The clinical manifestations during this phase vary depending on the underlying cause of sudden death. Typical symptoms include severe chest pain, acute respiratory distress, sudden palpitations, or dizziness. If cardiac arrest occurs instantaneously without warning, the cause is most often cardiac in origin. In the hours or minutes preceding sudden death, changes in electrocardiographic activity are often observed, with increased heart rate and frequent ventricular ectopic beats being the most common findings. Patients who experience sudden death due to ventricular fibrillation often exhibit ventricular tachycardia beforehand. A small proportion of patients may present with circulatory failure.
Cardiac Arrest
Following cardiac arrest, cerebral blood flow decreases drastically, leading to a sudden loss of consciousness, often accompanied by localized or generalized convulsions. In the initial moments after cardiac arrest, a small amount of oxygenated blood remains in the brain, temporarily stimulating the respiratory center. This may result in intermittent, sigh-like, or short spasmodic breathing, which eventually ceases. The skin becomes pale or cyanotic, pupils dilate, and involuntary urination or defecation may occur.
Biological Death
The time from cardiac arrest to biological death depends on the nature of the underlying condition and the interval between cardiac arrest and the initiation of resuscitation. Most patients begin to experience irreversible brain damage within 4-6 minutes after cardiac arrest, progressing to biological death over the following minutes. Immediate cardiopulmonary resuscitation (CPR) and early defibrillation are critical to preventing biological death. The most common cause of death following successful cardiac resuscitation is central nervous system injury, with other frequent causes including secondary infections, low cardiac output, and recurrent arrhythmias.
Management of Cardiac Arrest
The survival rate for cardiac arrest is very low, and early initiation of CPR and defibrillation is key to successful resuscitation. CPR is divided into basic life support (BLS) and advanced life support (ALS) and is performed in the following sequence:
Recognition of Cardiac Arrest
The patient's responsiveness should be assessed, and the absence of breathing or the presence of abnormal breathing (such as gasping) should be quickly identified. Simultaneously, the presence of a pulse should be checked within 5-10 seconds. Once cardiac arrest is confirmed, basic CPR should be initiated immediately.
Calling for Help
While performing CPR, efforts should be made to activate the emergency medical services (EMS) system by calling for help or instructing someone else to do so. If available, an automated external defibrillator (AED) should be located and prepared for use.
Basic Life Support (BLS)
Once cardiac arrest is confirmed, BLS should begin immediately. The patient should be placed supine on a firm surface, and resuscitation should be performed from one side of the patient. The primary BLS measures include chest compressions (circulation), airway management (airway), and rescue breathing (breathing), collectively referred to as the CAB sequence.
Chest Compressions and Early Defibrillation
Chest compressions are the primary method of establishing artificial circulation. The mechanism of blood flow during compressions is complex and involves both the "chest pump" and "heart pump" mechanisms. Chest compressions increase intrathoracic pressure and directly compress the heart, maintaining a certain level of blood flow. When combined with rescue breathing, this ensures oxygenated blood reaches vital organs such as the heart and brain.
During chest compressions, the patient should lie flat on a hard surface, and the rescuer should kneel beside them. If compressions are performed on a bed, a hard board should be placed under the patient's back. The compression site is the lower half of the sternum, at the midpoint of the line connecting the nipples. The heel of one hand should be placed on the sternum, with the other hand placed on top, fingers interlocked. The heel of the hand should be aligned with the long axis of the sternum, and pressure should be applied using the heel of the hand, avoiding the xiphoid process. The rescuer's body should lean slightly forward, with the shoulders, elbows, and wrists aligned perpendicular to the patient's chest. The elbows should remain straight, and compressions should be performed using the weight of the rescuer's upper body. After each compression, the chest should be allowed to fully recoil, but the hands should remain in contact with the chest. The compression and relaxation phases should be of equal duration.
High-quality chest compressions emphasize rapid and forceful compressions with specific requirements for rate and depth. The recommended compression rate is 100-120 compressions per minute, with a depth of at least 5 cm for adults. For children and infants, the compression depth should be at least 1/3 of the anterior-posterior diameter of the chest (approximately 5 cm for children and 4 cm for infants). Interruptions in chest compressions should be minimized, with any necessary pauses kept under 10 seconds. Complications of chest compressions include rib fractures, hemopericardium or cardiac tamponade, pneumothorax, hemothorax, pulmonary contusion, liver or spleen lacerations, and fat embolism. Adherence to proper technique can reduce the risk of complications.
External cardiac defibrillation uses a defibrillator to deliver a high-voltage electric current through the chest wall to the heart, depolarizing myocardial cells simultaneously to terminate abnormal reentry circuits or ectopic foci causing arrhythmias, thereby restoring sinus rhythm. The key initial steps in CPR are chest compressions and early defibrillation. If an AED is available, it should be used in combination with CPR. AEDs are portable, easy to operate, and capable of automatically analyzing ECGs and guiding defibrillation, making them suitable for use by non-professionals. Rescuers should continue CPR until the AED is ready for use and apply the AED as soon as possible. Interruptions in chest compressions before and after defibrillation should be minimized, and compressions should resume immediately after each shock.
Airway Management
For patients with absent or abnormal breathing, the airway is opened after 30 chest compressions while the patient is in a supine position. Maintaining a patent airway is a critical step in successful resuscitation. If there is no cervical spine injury, the head-tilt/chin-lift maneuver can be used to open the airway. This involves placing one hand on the patient’s forehead to apply firm pressure, tilting the head backward, while using the index and middle fingers of the other hand to lift the chin. The line connecting the tip of the chin and the earlobe should be perpendicular to the ground to ensure airway patency. Foreign objects and vomitus should be cleared from the patient’s mouth, and any loose dentures should be removed.
Artificial Ventilation
After the airway is opened, two rescue breaths are performed initially, with each breath lasting more than one second to ensure sufficient tidal volume and visible chest rise. Regardless of whether chest rise is observed, chest compressions should be resumed immediately after two rescue breaths. Tracheal intubation is the best method for establishing artificial ventilation. If time or conditions do not permit intubation, alternative methods such as mouth-to-mouth, mouth-to-nose, or mouth-to-barrier device ventilation can be used. The airway must remain patent during these procedures. The rescuer pinches the patient’s nostrils closed using the thumb and index finger of the hand placed on the forehead, takes a normal breath, seals the patient’s mouth completely with their own lips, and delivers a slow breath lasting more than one second, ensuring visible chest rise. The rescuer does not need to take a deep breath before providing rescue breaths. Whether CPR is performed by one or two rescuers, the compression-to-ventilation ratio should be 30:2, alternating between compressions and ventilations. These ventilation methods are temporary measures, and tracheal intubation should be performed as soon as possible. Following intubation, ventilation with a manual resuscitator or mechanical ventilator should be initiated to provide oxygen and correct hypoxemia while avoiding hyperventilation. Unlike adult cardiac arrest, pediatric and infant cardiac arrest is often caused by various accidents, particularly asphyxiation, making artificial ventilation more critical during resuscitation. For pediatric and infant CPR, when two or more rescuers are present, the compression-to-ventilation ratio should be adjusted to 15:2.
Advanced Cardiopulmonary Resuscitation
Advanced life support (ALS) builds upon basic life support (BLS) by incorporating specialized equipment and techniques to establish more effective ventilation and circulation. Key measures include tracheal intubation for ventilation, defibrillation to restore hemodynamically stable rhythms, establishing intravenous access, and administering necessary medications to maintain restored circulation. Continuous monitoring of electrocardiography (ECG), blood pressure, pulse oximetry, and end-tidal carbon dioxide (ETCO2) levels is required, and invasive hemodynamic monitoring may be necessary when indicated.
Ventilation and Oxygenation
If spontaneous breathing does not return, tracheal intubation should be performed as early as possible to ensure adequate ventilation and correct hypoxemia. For out-of-hospital patients, ventilation is typically maintained using a mask and manual resuscitator. In-hospital patients may use a manual resuscitator with a mask until a mechanical ventilator becomes available. For adult manual resuscitators, compressing 1/2 - 2/3 of a 1-liter bag or 1/3 of a 2-liter bag is sufficient. After tracheal intubation, the ventilation rate should be standardized to one breath every 6 seconds (10 breaths per minute). Once a mechanical ventilator is available, ventilator settings should be adjusted based on blood gas analysis results.
Defibrillation, Cardioversion, and Pacing
Ventricular fibrillation (VF) is the most common arrhythmia associated with cardiac arrest. While chest compressions and artificial ventilation can partially maintain brain and cardiac function, they rarely convert VF to sinus rhythm. Restoring an effective rhythm promptly is critical for successful resuscitation. Electrical defibrillation is the most effective method for terminating VF, with the likelihood of successful resuscitation decreasing by 7-10% for every minute of delay. Early defibrillation significantly increases the chances of successful resuscitation. Defibrillation is not beneficial in cases of asystole or pulseless electrical activity (PEA).
The placement of defibrillation electrodes is crucial. The most common placement involves positioning the sternal electrode below the patient’s right clavicle and the apical electrode on the left lower lateral chest wall, aligned with the left nipple. Alternative placements include the lower chest wall along the left and right lateral axillary lines or positioning the apical electrode in its standard location while placing the other electrode on the upper left or right back. If the patient has an implanted device (e.g., a pacemaker), the electrodes should not be placed directly over the device.
For biphasic defibrillators, the initial energy level should be selected based on the manufacturer’s recommendations, typically 120-200 J. For monophasic defibrillators, the initial energy level should be set at 360 J. Subsequent defibrillation attempts should use equivalent or higher energy levels. After each defibrillation attempt, chest compressions and artificial ventilation should be resumed immediately. After five cycles of CPR (approximately two minutes), the patient’s spontaneous circulation or signs of circulation (e.g., breathing, pulse, blood pressure) should be reassessed, and further defibrillation performed if necessary.
Although defibrillation is classified as an advanced resuscitation technique, it should be performed as early as possible when conditions permit, without strict adherence to resuscitation stages.
Pacing is not recommended for patients with cardiac arrest. However, it may be considered for patients with symptomatic bradycardia. Immediate pacing should be performed for patients with severe symptoms, particularly when high-grade atrioventricular block occurs below the His bundle.
Pharmacological Treatment
Intravenous access should be established as early as possible during cardiopulmonary resuscitation (CPR) in patients experiencing cardiac arrest. Peripheral veins, such as the antecubital vein or external jugular vein, are commonly used, while central veins, including the internal jugular vein, subclavian vein, or femoral vein, may also be considered. If venous access cannot be achieved, intraosseous access may be an alternative. Certain resuscitation drugs, such as epinephrine, atropine, and lidocaine, can also be administered via the tracheal route.
Epinephrine is the first-line drug for CPR and is indicated for ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) refractory to defibrillation, as well as asystole or pulseless electrical activity (PEA). The standard dosage is 1 mg administered via intravenous push every 3-5 minutes. After each dose delivered through a peripheral vein, a 20 mL saline flush is recommended to ensure the drug reaches the heart effectively. Vasopressin can also serve as a first-line agent, though it is not recommended to be used in combination with epinephrine. Severe hypotension may be treated with norepinephrine, dopamine, or dobutamine.
Metabolic acidosis occurring during resuscitation is usually improved by optimizing ventilation and does not require aggressive bicarbonate supplementation. However, in cases of pre-existing metabolic acidosis, hyperkalemia, or overdose of tricyclic antidepressants or barbiturates, sodium bicarbonate may be administered. For patients experiencing prolonged cardiac arrest where chest compressions, defibrillation, intubation, mechanical ventilation, and vasopressor therapy are ineffective, sodium bicarbonate may also be considered. The initial dose is 1 mmol/kg, followed by half the dose every 15 minutes during ongoing CPR, with adjustments based on blood gas analysis to avoid alkalosis.
If ventricular fibrillation or pulseless ventricular tachycardia persists after two defibrillation attempts combined with CPR and epinephrine, antiarrhythmic drugs should be considered. Amiodarone is the preferred agent, though lidocaine may also be used. Magnesium sulfate is specifically indicated for torsades de pointes.
For refractory polymorphic ventricular tachycardia, torsades de pointes, rapid monomorphic ventricular tachycardia, or ventricular flutter (heart rate >260 beats per minute), as well as refractory ventricular fibrillation, intravenous beta-blockers may be attempted. Isoproterenol or ventricular pacing may be effective in terminating bradycardia and drug-induced torsades de pointes.
The management of bradyarrhythmias and asystole differs from that of ventricular fibrillation. After providing basic life support, efforts should focus on stabilizing spontaneous cardiac rhythms or initiating pacing. Simultaneously, reversible causes such as hypovolemia, hypoxemia, cardiac tamponade, and hyperkalemia should be actively identified and treated accordingly.
Following the restoration of cardiac rhythm through CPR, the priority is to maintain stable cardiac electrical activity and hemodynamic status.
Extracorporeal Cardiopulmonary Resuscitation (ECPR)
Extracorporeal cardiopulmonary resuscitation (ECPR) refers to the initiation of extracorporeal circulation using extracorporeal membrane oxygenation (ECMO) technology during CPR for patients with cardiac arrest. ECMO typically involves connecting a pump and oxygenator to the femoral artery and femoral vein to perform veno-arterial extracorporeal circulation and gas exchange. This is a complex intervention requiring a specialized team, advanced equipment, and multidisciplinary support, with significant associated costs. Considerations such as cost-effectiveness, resource allocation, and medical ethics must be carefully evaluated before implementing ECPR.
Currently, there is insufficient evidence to support the routine use of ECPR in cardiac arrest patients. However, it may be considered for patients with potentially reversible conditions under short-term support or those awaiting heart transplantation.
Post-Resuscitation Management
The restoration of spontaneous circulation following cardiac arrest marks only the beginning of the treatment process for survivors of sudden cardiac arrest. After experiencing systemic ischemic injury, patients enter a more complex phase of ischemia-reperfusion injury, which is the primary cause of in-hospital mortality following resuscitation. This condition is referred to as "post-cardiac arrest syndrome." Research has demonstrated that early intervention in this unique and complex pathophysiological state can effectively reduce mortality rates and improve patient outcomes.
The principles and measures of post-cardiopulmonary resuscitation management include maintaining effective circulation and respiratory function, particularly cerebral perfusion, preventing recurrent cardiac arrest, maintaining fluid, electrolyte, and acid-base balance, and addressing complications such as cerebral edema, acute kidney injury, and secondary infections. Among these, brain resuscitation is a key focus.
Treatment of the Primary Cause of Cardiac Arrest
A comprehensive evaluation of the cardiovascular system and related factors should be conducted to identify the cause of cardiac arrest. Reversible causes of cardiac arrest, categorized as the "5 Hs and 5 Ts," should be actively identified and treated. The "5 Hs" include hypovolemia, hypoxia, hydrogen ion (acidosis), hypokalemia, and hyperkalemia, while the "5 Ts" include tension pneumothorax, cardiac tamponade, toxins, pulmonary thrombosis, and coronary thrombosis. Acute coronary syndrome is one of the most common causes of cardiac arrest in adults. Early emergency coronary angiography and reperfusion of the infarcted vessel can significantly reduce mortality and improve prognosis.
After the restoration of spontaneous circulation, a 12- or 18-lead electrocardiogram should be performed as soon as possible to determine whether there is ST-segment elevation. For out-of-hospital cardiac arrest patients, whether conscious or comatose, who are suspected of having a cardiac cause or show ST-segment elevation on the electrocardiogram, emergency coronary angiography should be performed promptly. For patients with a suspected cardiac cause but no ST-segment elevation, emergency coronary angiography may still be considered if hemodynamic or electrical instability is present.
Maintaining Effective Circulation
Hemodynamic instability is common after cardiac arrest and may result from hypovolemia, vascular dysregulation, or cardiac dysfunction. Systolic blood pressure should be maintained at no less than 90 mmHg, and mean arterial pressure should be kept above 65 mmHg. For patients with blood pressure below the target range, volume resuscitation should be performed while monitoring cardiac function, and acidosis should be corrected based on arterial blood gas analysis. If volume resuscitation is insufficient, vasoactive drugs should be considered to maintain target blood pressure. Heart rate and rhythm should be monitored, and arrhythmias affecting hemodynamic stability should be actively managed. Bedside echocardiography can assist in identifying complications such as cardiac tamponade.
Maintaining Respiratory Function
After the restoration of spontaneous circulation, varying degrees of respiratory dysfunction may persist, and some patients may still require mechanical ventilation and oxygen therapy. Positive end-expiratory pressure (PEEP) ventilation may be beneficial for patients with respiratory failure and concurrent left heart failure, but hemodynamic stability should be assessed during its application. Oxygen concentration, PEEP, and minute ventilation should be adjusted based on arterial blood gas results and/or non-invasive monitoring.
Prevention and Management of Cerebral Hypoxia and Cerebral Edema
This process, also known as brain resuscitation, is critical for the ultimate success of cardiopulmonary resuscitation. Continuous monitoring and evaluation of neurological function should be emphasized, and active measures to protect neurological function should be implemented. For comatose patients, normal or slightly elevated mean arterial pressure should be maintained, and elevated intracranial pressure should be reduced to ensure adequate cerebral perfusion.
Key measures include:
- Therapeutic Hypothermia: Targeted temperature management is the most important strategy for protecting neurological and cardiac function. For comatose patients following resuscitation, body temperature should be lowered to 32-36°C and maintained for at least 24 hours.
- Dehydration Therapy: Osmotic diuretics combined with hypothermia can reduce cerebral edema and intracranial pressure, aiding in the recovery of brain function.
- Seizure Prevention and Management: Sedative medications can be used to control seizures caused by hypoxic brain injury, as well as shivering during the hypothermia process.
- Hyperbaric Oxygen Therapy: This approach increases blood oxygen content and diffusion, improves cerebral oxygenation, and reduces intracranial pressure.
- Promoting Early Cerebral Perfusion: Anticoagulation therapy can improve microcirculation, and calcium channel blockers can alleviate cerebral vasospasm.
Prevention and Management of Acute Kidney Injury
Acute kidney injury is more likely to occur if cardiac arrest duration is prolonged or if hypotension persists after resuscitation. Elderly patients with pre-existing kidney conditions are particularly at risk.
Effective cardiac and circulatory function should be maintained, and nephrotoxic drugs should be avoided. If oliguria or anuria persists despite the administration of furosemide, acute kidney injury should be suspected and managed accordingly.
Other Considerations
Electrolyte imbalances and acid-base disturbances should be promptly identified and corrected, and secondary infections should be prevented. For patients with absent bowel sounds or those on mechanical ventilation with impaired consciousness, a nasogastric tube should be placed, and early gastrointestinal nutrition should be initiated.
Prognosis of Cardiac Arrest
The survival-to-discharge rate for out-of-hospital cardiac arrest (OHCA) is 1.2%, while the survival-to-discharge rate for in-hospital cardiac arrest (IHCA) is 9%. For patients who achieve successful resuscitation after cardiac arrest, timely evaluation of left ventricular function is crucial. Patients with impaired left ventricular function have a higher likelihood of recurrent cardiac arrest, poorer response to antiarrhythmic drugs, and higher mortality compared to those with normal left ventricular function.
Primary ventricular fibrillation occurring in the early stages of acute myocardial infarction, which is not caused by hemodynamic abnormalities, is more likely to achieve successful defibrillation with timely intervention.
Cardiac arrest secondary to extensive acute myocardial infarction and hemodynamic instability has an immediate mortality rate as high as 59-89%. Resuscitation in such cases is often challenging, and even when successful, maintaining a stable hemodynamic state is difficult.
Prevention of Sudden Cardiac Death (SCD)
The key to preventing sudden cardiac death (SCD) lies in identifying high-risk individuals. In addition to general risk factors such as age ≥65 years, male, heart rate ≥90 beats per minute, hypertension, and diabetes, information from medical history, physical examination, electrocardiography, 24-hour Holter monitoring, and heart rate variability can be used to assess a patient’s risk of cardiac arrest.
Beta-blockers are effective in reducing the incidence of SCD in patients with structural heart disease. Amiodarone significantly reduces arrhythmia-related mortality in patients with myocardial infarction complicated by left ventricular dysfunction or arrhythmias, although it does not have a significant impact on overall mortality.
Surgical treatments for arrhythmia, such as ventricular aneurysmectomy, endocardial resection, and cryoablation under electrophysiological mapping, have limited effectiveness in preventing SCD. For patients with long QT syndrome who continue to experience syncope despite adequate beta-blocker therapy or who are unable to adhere to medication, left cervicothoracic sympathetic denervation may have some benefit in preventing SCD.
Implantable cardioverter-defibrillators (ICDs) are increasingly being used as an important measure to prevent SCD. ICDs can automatically detect ventricular fibrillation or ventricular tachycardia within seconds and perform defibrillation with a high success rate, making them the most effective method for preventing and treating SCD. For high-risk SCD patients with structural heart disease or survivors of cardiac arrest, the role of catheter-based radiofrequency ablation in preventing SCD requires further investigation.