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Sudden Cardiac Death
Introduction
Cardiac arrest is defined as a sudden cessation of cardiac activity resulting in hemodynamic collapse. Sudden cardiac death (SCD) is defined as death presumed to be of a cardiac cause that occurs within 1 hour of the onset of cardiac symptoms or 24 hours of last being seen healthy and alive. Autopsies may reveal a cardiac etiology, though not all SCD cases have an identifiable cause.[1] SCD may be the first presentation of cardiovascular diseases and accounts for half of cardiovascular deaths.[2] SCD has a strong association with age. Men are at a higher risk of SCD as compared to age-matched women. SCD has a low incidence in infancy, but the condition's annual incidence reaches as high as 200 per 100,000 person-years in the 8th decade of life.[3]
Coronary artery disease (CAD) is responsible for more than 75% of SCD cases in the developed world. The incidence of CAD has increased over the last few decades. However, a significant decline in cardiovascular mortality is also evident.[4] Early CAD treatment is the most effective SCD preventive method. Studies show that cardiac arrest and SCD may be the first presentation of CAD in genetically predisposed individuals. Myocardial infarction or ischemia is the typical diagnosis in these patients.[5] Early CAD identification and management of atherosclerotic cardiovascular disease (ASCVD) risk factors are the best strategies for minimizing the risk of cardiac arrest and SCD. Early cardiopulmonary resuscitation (CPR) is paramount in preventing SCD in patients with witnessed cardiac arrest.[6]
In younger individuals with inherited arrhythmias, identifying and appropriately treating the underlying condition can effectively prevent SCD. Implantable cardioverter-defibrillator (ICD) use is the only way to prevent SCD in most inherited cardiac arrhythmias.
Heart Anatomy
The human heart is a muscular organ in the thoracic cavity, slightly left of the center. The heart circulates blood, supplying oxygen and nutrients to tissues and organs. Structurally, the heart consists of 4 chambers: 2 atria and 2 ventricles. The right atrium receives deoxygenated blood returning from the body via the superior and inferior vena cavae, while the left atrium receives oxygenated blood from the lungs through the pulmonary veins. Blood flows from the atria into the ventricles through the atrioventricular valves—the tricuspid valve on the right side and mitral valve on the left. Ventricular contraction pumps blood out of the heart through the semilunar valves—the pulmonary valve on the right ventricle and aortic valve on the left ventricle—into the pulmonary artery and aorta, respectively.
The coronary arteries supply oxygen-rich blood to the heart muscle (myocardium). The left coronary artery arises from the left side of the aorta and branches into 2 main arteries. The left anterior descending artery supplies the anterior surfaces of the left ventricle and interventricular septum. The left circumflex artery supplies the left atrium and posterolateral side of the left ventricle. The right coronary artery, originating from the aorta's right side, supplies the right atrium and ventricle and part of the left ventricle's posterior wall. The coronary arteries ensure the heart receives an adequate blood supply to meet its high metabolic demands.
The cardiac conduction system comprises specialized cells that generate and transmit electrical impulses regulating the heart's rhythm and coordinating its contractions. The sinoatrial node, located in the right atrium near the entrance of the superior vena cava, serves as the heart's natural pacemaker. The electrical impulses then travel through the atria, causing them to contract and forcing blood into the ventricles. The impulses reach the atrioventricular (AV) node, situated at the junction of the atria and ventricles. The impulses are momentarily delayed in the AV node, allowing the ventricles to fill completely before contracting. From the AV node, the impulses travel through specialized conduction pathways—the bundle of His and Purkinje fibers—stimulating the ventricles to contract and pump blood to the lungs and the rest of the body.
Etiology
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Etiology
The common risk factors for SCA and SCD, as identified in population-based studies, include risk factors for ASCVD, left ventricular hypertrophy, and cardiac conduction abnormalities. Smoking directly predicts the risk of SCD. The Framingham study revealed that people who smoked had a 2.5-fold higher annual SCD incidence than those who never smoked.[7] Population-based studies showed that the risk of SCA and SCD is higher in people with structural heart diseases and ASCVD. SCD risk is relatively low in populations with lower incidences of ASCVD and structural heart diseases.[8]
The etiology varies with age, but CAD is responsible for most cases of SCD overall.[9] In young individuals, inherited cardiac arrhythmias, inherited cardiomyopathies, myocarditis, and coronary artery anomalies are the common SCD causes.[10][11] Up to half of SCD cases in the 4th decade of life arise from acute coronary syndrome (ACS).[12] Rare SCD causes include drug toxicity, coronary artery spasm, and cardiac trauma.
The literature shows that 40% to 80% of the survivors of cardiac arrest are found to have greater than 70% cross-sectional luminal stenosis in at least 1 major coronary artery. These findings vary with the age and gender of the studied population. Although less than 50% of the patients with resuscitated ventricular fibrillation have evidence of myocardial injury, autopsy studies report occlusive coronary artery thrombosis in up to 64% of the patients with SCD. Other common autopsy findings include plaque instability, fissuring, or hemorrhage, and nonobstructive coronary artery thrombosis.[13]
CAD is responsible for most SCD cases in older patients. Other SCD causes include nonischemic cardiomyopathy and valvular heart disease. Inherited arrhythmias are relatively rare in older populations.[14] SCD's cardiac causes are classified into the following groups:
Coronary Artery–Related Causes
- Myocardial infarction or ischemia
- Anomalous coronary artery origin
- Coronary spasm
- Vasculitides
- Myocardial bridging
Primary Arrhythmogenic Diseases
- Long QT syndrome (LQTS)
- Short QT syndrome (SQTS)
- Brugada syndrome
- Early repolarization syndrome
- Catecholaminergic polymorphic ventricular tachycardia (CPVT)
- Idiopathic ventricular fibrillation
- Congenital heart blocks
- Wolf-Parkinson-White syndrome
Cardiomyopathies
- Hypertrophic cardiomyopathy (HCM)
- Arrhythmogenic right ventricular cardiomyopathy (ARVC)
- Myocarditis
- Idiopathic dilated cardiomyopathy
- Noncompaction cardiomyopathy
- Infiltrative cardiomyopathy
- Restrictive cardiomyopathy
- Alcohol-related cardiomyopathy
- Peripartum cardiomyopathy
- Tokatsubo cardiomyopathy
Heart Failure
- Heart failure with reduced ejection fraction
- Heart failure with preserved ejection fraction
Valvular Heart Diseases
- Aortic stenosis
- Mitral valve prolapse
Congenital Heart Diseases
- Tetralogy of Fallot
- Transposition of great arteries
- Fontan circulation
- Ebstein anomaly
- Eisenminger syndrome
- Single ventricular physiology
- Coarctation of aorta
- Double-outlet right ventricle
- Interrupted aortic arch
- Tricuspid atresia
- Pulmonary atresia
- Total anomalous pulmonary venous connection
Miscellaneous
Epidemiology
Approximately 0.1% of the United States population experience a medical services-assessed, out-of-hospital cardiac arrest (OHCA) annually. European studies have a similar incidence, ranging from 0.04% to 0.1% of the population.[17] SCD is estimated to account for 10% to 20% of deaths in Europe, and 300,000 people are brought to the emergency department every year with OHCAs.[18] The median age in the US is between 66 and 68. Male individuals are more likely to experience SCD.[19]
Certain ethnic groups have a higher incidence of SCD than others. The literature reports a higher SCD risk in black than white people, with the difference being more pronounced among women. The reasons behind this ethnic difference include differences in income, education, and traditional risk factors for ASCVD.[20] SCD incidence rises proportionately with age, with the highest risk reported in the 8th decade of life. Overall, men have a higher SCD risk than women.[21]
Inherited cardiac arrhythmias, cardiomyopathies, and coronary artery anomalies are the major SCD causes in younger people. In contrast, CAD is the most common cause of SCD in older patients.[22][23] SCD is the leading cause of nontraumatic cause of death among young athletes. In the general population, sports-related, sudden death from any cause has an incidence of 0.5 to 2.1 per 100,000 yearly. Sports-related, sudden deaths are more frequent in elite than other student-athletes, with an incidence of 1:8,253 per year per the National Collegiate Athletic Association (NCAA). NCAA Division I male basketball players have a 1:5200 incidence of sudden death.[24][25]
SCD's circadian variation is well documented and attributed to circadian variations in the secretion of adrenaline and other hormones. SCD incidence reportedly peaks between 6 am and 12 pm. A small peak occurs during the late afternoon from ventricular fibrillation-induced OHCA. β-adrenergic blocking drugs reduce the early morning SCD peak. The reported incidence of SCD is highest on Mondays.[26]
Many individuals have SCA as their first medical encounter before SCD. Identifying people in the general population at high SCA risk facilitates primary prevention strategies and reduces the risk of SCD and SCA-associated morbidities.[27] Although limited data on the incidence of SCD exists, especially in low-middle-income countries, the global SCD incidence is reported to be as high as 100 cases per 100,000 person-year. Around 2 million SCD cases are reported each year worldwide.[28][29] This high incidence and the associated mortality and morbidity make SCA and SCD major global public health problems.
Pathophysiology
SCD mostly results from an electrical accident in the form of ventricular arrhythmias or asystole. Some patients have an anatomic and functional substrate for developing life-threatening ventricular arrhythmias or asystole. However, many have transient events in the form of myocardial ischemia or infarction, metabolic abnormalities, and drug toxicities leading to ventricular tachyarrhythmias or asystole. This reflects an interplay between the arrhythmogenic substrates and transient events perturbing myocardial hemostasis and predisposing patients to life-threatening arrhythmias, SCA, and SCD.[30]
SCD risk is highest during the first few months after a myocardial infarction due to fatal tachyarrhythmias, reinfarction, or myocardial rupture.[16] Ventricular fibrillation and tachycardia were initially identified as the most common causes of OHCA. However, recent studies show that asystole and pulseless electrical activity (PEA) are the most frequent initial rhythms in OHCAs. Approximately 50% of patients initially have asystole, and 19% to 23% have PEA as the first identifiable rhythm.[31] Blood flow to the brain slows to essentially zero immediately following OHCA, leading to death.
History and Physical
History
People with SCA present to the hospital unconscious, with no cardiac tone and respirations. Immediate resuscitation is warranted in patients in cardiorespiratory arrest, regardless of cause. Airway, breathing, circulation, disability, and exposure must be evaluated during a quick primary survey and addressed without delay. A more detailed investigation may be pursued once the patient is stable and hooked to cardiac and vital signs monitors.
On history, patients may experience palpitations, dizziness, or near-syncope before SCA. Almost half of people who had SCA report no symptoms before losing consciousness.[32] Other signs and symptoms that may be reported by a person who had SCA include the following:
- Chest pain, discomfort, tightness, pressure related to exertion
- Excessive exertional and unexplained dyspnea, fatigue, or palpitations associated with exercise
- Prior recognition of a heart murmur
- Elevated systemic blood pressure
- Sensorineural deafness, which may indicate LQTS
Relevant information that may be elicited during history-taking includes a prior history of cardiogenic or arrhythmia-related syncope or SCA and a family history of SCD or inherited cardiac arrhythmias.[33] Other information that a person who had SCA may disclose in their past medical and family history includes the following:
- Prior restriction from sports participation
- Prior physician-ordered cardiac testing
- Premature death (before age 40) in more than 1 relative attributed to heart disease
- Disability from heart disease in a close relative younger than 50
- Hypertrophic or dilated cardiomyopathy, LQTS or other ion channelopathies, Marfan syndrome, clinically significant arrhythmia, or specific knowledge of certain cardiac conditions in family members
The relevant history provides clues to certain high-risk patients. In individuals with CAD leading to cardiomyopathy and severe left ventricular systolic dysfunction, a history of syncope with a documented ventricular arrhythmia episode, New York Heart Association (NYHA) class III or IV classification, ventricular arrhythmia immediately after myocardial infarction, and previous myocardial infarctions predict high future SCA and SCD risks.[34] A family history of SCD increases the risk of SCD in those with inherited cardiac channelopathies and primary cardiomyopathies.[35]
The American Heart Association recommends cardiovascular screening for high school and collegiate athletes, with physical examination and tools evaluating personal and family history.[36]
Physical Examination
Physical examination findings in people with SCA include unresponsiveness and pulselessness. Blood pressure and cardiac tone are absent. Patients may display agonal respirations or apnea. The skin is usually cyanotic and cold to the touch. Pupils are dilated and nonreactive to light. Muscles become flaccid, with absent bladder and bowel control. Cardiac monitoring may show arrhythmias, commonly asystole, PEA, or ventricular fibrillation.
In contrast, patients with myocardial ischemia not in cardiorespiratory arrest have a range of physical findings. Diaphoresis and pallor are often present. Blood pressure may be elevated or normal, but hypotension may be a sign of cardiac decompensation. Abnormal heart sounds may be appreciated on auscultation. An S3 gallop, S4 sound, and murmurs may be signs of heart failure, which may also manifest with jugular venous distension, bilateral respiratory crackles, an abdominal fluid wave, and bipedal edema. Cardiac monitoring reveals wide rate and rhythm variations. Tachycardia, normocardia, or bradycardia may be noted. Rhythm may be normal with ST and T wave changes or outright abnormal.
Individuals with ACS often have normal neurologic function. However, ACS and stroke may cooccur, with patients exhibiting cardiac abnormalities, eg, new-onset atrial fibrillation, alongside neurologic deficits, eg, new-onset dysphonia or slurred speech. The onset of these signs must be ascertained before deciding to include neuroimaging in the cardiovascular workup. Importantly, people who survive SCA may also manifest neurologic symptoms from brain hypoxia during the arrested state.
Specific physical examination findings may point toward other potential causes of cardiac arrest. A mitral valve prolapse's mid-to-late systolic murmur, HCM's ejection systolic murmur, cyanosis, Tetralogy of Fallot right ventricular outflow murmur, and sarcoidosis' skin signs may help identify the underlying cardiac cause.
Heart murmurs should be evaluated in both supine and standing positions during the cardiovascular examination. Femoral pulses must be evaluated and compared to exclude aortic coarctation. Brachial artery blood pressure may be taken in the sitting position, preferably on both arms.[37]
Evaluation
SCA may be the first manifestation of CAD and other cardiac conditions. Full cardiac assessment is required for individuals who survive this event. Diagnostic tests should include the following:
- Electrocardiogram (ECG) to evaluate for myocardial ischemia or infarction and inherited channelopathies
- Echocardiogram to assess for preexisting heart failure, cardiomyopathies, valvular heart diseases, and congenital cardiac abnormalities
- Coronary angiography for diagnosing ASCVD, coronary artery anomalies, and coronary artery spasms
- Exercise tests in selected patients to evaluate exercise-induced ventricular arrhythmias and ischemia
- Electrophysiology testing in select groups of people to search for cardiac conduction diseases and risk stratification
- Cardiac magnetic resonance imaging (MRI) to establish the diagnosis of cardiomyopathies and assess the risk of SCD
- Genetic testing if the patient has arrhythmogenic right ventricular cardiomyopathy (ARVC), Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia (CPVT), or LQTS
- A cardiac biopsy may be considered if no other cause is found [38]
The 12-lead ECG helps in diagnosing myocardial infarction or ischemia and inherited channelopathies. Echocardiograms are the best imaging modality for evaluating heart failure, cardiomyopathy, valvular heart disease, and congenital heart disease. Coronary angiography further evaluates CAD, congenital coronary anomalies, and coronary spasms. Exercise testing is helpful for the diagnosis of ischemic heart disease, LQTS, and CPVT. Electrophysiology studies can detect suspected arrhythmia. Procainamide can provoke Brugada syndrome regardless of initial ECG findings. Cardiac MRI is recommended for tissue characterization to diagnose ARVC, sarcoidosis, and myocarditis and estimate the extent of fibrosis with late gadolinium enhancement.[39]
Genetic testing may be recommended in young patients without evidence of structural heart disease but with unexplained syncope or cardiac arrest to identify the inherited channelopathy or arrhythmogenic disorder. Genetic testing may also provide insights into the condition's prognosis and guide family members' cascade screening if a disease-causing genetic mutation is identified in the proband.[40][41]
Recent genome sequencing advances and a better understanding of inherited cardiac disorders have made genetic testing more effective in diagnosing different cardiomyopathies. Genetic testing may be used to screen asymptomatic relatives who may be carriers. Testing guides the appropriate preventive measures for those with a positive genetic mutation in the form of lifestyle modifications, medical therapy, and ongoing monitoring. Contemporary guidelines recommend genetic counseling for patients and their family members when a genetic mutation associated with an inherited arrhythmogenic cardiac disorder is identified.[42]
Treatment / Management
Initial Management
SCA's initial management is a critical and time-sensitive process aimed at restoring cardiac function and improving the chances of survival. Immediate intervention is crucial to increase the likelihood of a positive outcome. Basic (BLS) and Advanced Cardiac Life Support (ACLS) protocols must be performed by trained healthcare professionals.
Resuscitation for cardiac arrest
The initial management steps for SCA resuscitation include rapid recognition of cardiac arrest, early and effective CPR, defibrillation, postcardiac arrest care, and treatment of underlying causes. CPR with effective chest compressions and appropriate defibrillator use is paramount for treating SCD. CPR should be performed according to published BLS and ACLS algorithms (see Images. ACLS Algorithm for Asystole and PEA and ACLS Algorithm for VFib and VTach).[43] Early CPR and defibrillation and rapid arrival of emergency medical services (EMS) during cardiac arrest are the major determinants of successful resuscitation.
Strategies that may improve the chances of survival include early CPR initiation for witnessed cardiac arrest, bystander CPR, and rapid defibrillation.[44] Survival after in-hospital cardiac arrest (IHCA) is as high as 90%, especially in intensive care units where the response to ventricular fibrillation is quick. However, survival after OHCA decreases rapidly after the first few minutes from the onset of cardiac arrest. Less than 25% survive at 5 minutes, and close to zero survive 10 minutes after OHCA.[45] (A1)
Intravenous or intraosseous epinephrine every 3 to 5 minutes is an important ACLS component, improving the odds of successful resuscitation. Epinephrine's favorable effects are produced by the α-adrenergic mediated vasoconstriction, which improves coronary and cerebral perfusion pressure during CPR.[46] Amiodarone administration after at least 3 defibrillation attempts in refractory ventricular fibrillation cases increases the rate of successful resuscitation as compared to lidocaine and placebo. However, amiodarone does not improve survival to discharge compared to placebo.[47]
Procainamide administration in OHCA with a shockable rhythm does not have favorable outcomes. The drug has been associated with a higher number of shocks, longer resuscitation times, and a lower survival rate.[48] Cardiac arrest with PEA and asystole have relatively lower chances of survival than ventricular fibrillation. CPR with effective chest compression, epinephrine, and treatment of reversible etiologies is the only way of survival.[49](A1)
Postcardiac arrest care
Patients are evaluated for possible SCA causes after successful resuscitation and return of spontaneous circulation (ROSC). The initial evaluation includes an assessment of airway, hemodynamics, and neurologic status, followed by a 12-lead ECG, baseline laboratory investigations, chest radiograph, ECG, and brain imaging. Cardiac arrest results in multiorgan dysfunction. Death can also occur from shock or dysfunction of organs other than the heart. Postcardiac arrest care is complex. Thus, an interprofessional team with expertise in cardiac arrest care and dedicated postcardiac arrest treatment protocols are critical to improving survival and neurological outcomes after ROSC.[50]
ST-elevation myocardial infarction (STEMI)—diagnosed based on clinical presentation, ECG, and cardiac enzyme levels—should be managed with immediate coronary angiography followed by revascularization (see Image. ST-Elevated Myocardial Infarction on ECG). Percutaneous revascularization can be achieved safely when a postcardiac arrest angiogram reveals significant CAD. Observational studies report improved survival after successful revascularization in patients with SCA.[51] However, in the absence of STEMI, immediate coronary angiography and revascularization do not provide added benefit.[52]
Hypotension may worsen brain injury and outcomes after cardiac arrest due to decreased tissue perfusion. Maintaining systolic blood pressure above 90 mm Hg and mean arterial pressure above 65 mm Hg with proper fluid resuscitation and vasopressor therapy is recommended.[53] Avoiding hypoxia and hypoglycemia is vital in the post-cardiac arrest period, particularly in comatose patients, as these conditions can worsen tissue damage and impact long-term survival.(B2)
Targeted temperature management (32 °C to 35 °C) is recommended for at least 24 hours in patients not following commands after ROSC. Multiple studies document survival and positive neurologic outcomes when targeted temperature management is used after IHCA and OHCA, even in patients with an initially nonshockable rhythm. Fever in the postcardiac arrest period is associated with poor neurological outcomes and thus must be prevented or treated immediately.[54][55](B2)
Hypoxic brain injury is the major contributor to morbidity and mortality in survivors of OHCA and IHCA. A detailed neurological assessment and appropriate prognostication are required to avoid premature withdrawal of life-saving measures in patients who may otherwise achieve neurological recovery. Avoiding unnecessary treatment when a poor outcome is inevitable is helpful.[56] Neuroprognostication is recommended in every comatose patient after 5 days of targeted temperature management. A multimodal approach, including clinical examination, electroencephalogram, and brain imaging, is recommended for neuroprognostication, as a single test may yield false positive or false negative results.[57][58](A1)
Long-Term Management
The long-term management of patients who survive SCA focuses on reducing the risk of recurrence, improving overall prognosis, and addressing potential underlying causes or contributing factors. Patients who survive SCA face unique challenges, including the risk of recurrent arrhythmias, underlying cardiovascular disease, and psychological consequences. Therefore, a comprehensive and interprofessional approach to long-term management is crucial to optimize outcomes and enhance quality of life.
SCD prevention is critical after survival from SCA. Patients have a high risk of SCA recurrence or SCD, especially in the presence of underlying structural heart diseases and primary cardiac arrhythmias. Medical treatment has a limited role in preventing SCD. No antiarrhythmic drugs except for β-adrenergic blocking agents have documented evidence for preventing SCD.[59](A1)
However, the use of antiarrhythmic medications and heart failure therapy is essential in some patients to control arrhythmias and improve symptoms. β-blockers improve survival and reduce SCD risk in patients with left ventricular systolic dysfunction or previous acute myocardial infarction.[60][61] β-blockers, especially propranolol and nadolol, are also recommended as the first-line therapy for preventing the recurrence of arrhythmias and SCA in patients with cardiac channelopathies, eg, LQTS and catecholaminergic polymorphic ventricular tachycardia.[62](A1)
The recommended cardioprotective agents in patients with cardiomyopathy and severely reduced left ventricular systolic function include β-blockers, mineralocorticoid receptor antagonists, angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, angiotensin receptor-neprilysin inhibitors, and sodium-glucose cotransporter-2 inhibitors. These drugs have demonstrated a significant reduction in SCD rate in studies. Contemporary guidelines recommend these drugs for preventing SCD in all patients with heart failure with reduced ejection fraction, irrespective of the underlying cause of left ventricular systolic dysfunction.
Randomized trials demonstrate that ICDs effectively prevent SCD and improve survival in patients who survive SCA due to fatal arrhythmia, as compared to antiarrhythmic drugs.[63] ICD placement is advised to prevent SCD in patients who survive SCA due to ventricular tachycardia or fibrillation without an identified reversible cause. This intervention is supported by class IA recommendations in all contemporary guidelines.[64](A1)
Rehabilitation program
A significant number of patients who survive SCA experience neuropsychiatric disorders, including anxiety, depression, and posttraumatic stress after the event. Easy fatigability is another common symptom in these patients, which may occur due to physical and cognitive impairment.[65] Family members of patients who survive SCA also report significant stress and may benefit from therapy.[66]
Clinical practice guidelines recommend a structured postcardiac arrest rehabilitation program. Patients who survive SCA and their caregivers should undergo periodic, comprehensive assessments for anxiety, depression, and posttraumatic stress disorder (PTSD). Psychosocial support should also be provided to patients and their families. Individuals who survive SCA and their caregivers should receive a detailed discharge plan, including instructions regarding their daily routine.
Differential Diagnosis
The differential diagnoses of SCA and SCD include all causes of syncope and bradyarrhythmias or tachyarrhythmias, including the following:
- Acute myocardial infarction
- Aortic stenosis
- Arrhythmogenic right ventricular cardiomyopathy
- Atrioventricular block
- Brugada syndrome
- Catecholaminergic polymorphic ventricular tachycardia
- Dilated cardiomyopathy
- Ebstein anomaly
- HCM
- Idiopathic ventricular fibrillation
- LQTS
- Mitral stenosis
- Mitral valve prolapse
- Pulmonary embolism
- SQTS
- Teratology of Fallot
- Wolff-Parkinson-White syndrome
Accurately diagnosing SCA allows healthcare providers to identify underlying cardiac conditions, which may require specific management strategies to reduce the risk of recurrence. A thorough medical evaluation and diagnostic examination can help differentiate SCA and SCD from other conditions.
Prognosis
The overall survival of cardiac arrest depends on multiple factors. The global OHCA survival rate is very low. Only 22% of the patients with OHCA reach the emergency department, and only 8.8% survive until hospital discharge. The 1-year survival rate of OHCA is less than 8% in developed countries.[67] SCA survival rate may be improved with early resuscitation, bystander CPR, and defibrillator access in public places.[68][69] Periodic education of public officials and community members about the role of bystander CPR and early defibrillation is critical to improving OHCA survival rates.
Complications
SCA's complications include anoxic brain injury and multiorgan dysfunction. Mental health disorders are also reported in patients who survive SCA and their families. The literature suggests that a significant number of patients who survive cardiac arrest develop anxiety, depression, and PTSD. The incidence of depression is reported to be as high as 45%, while 6% to 15% of patients develop anxiety. PTSD is diagnosed in up to 27% of the survivors of cardiac arrest.[70]
Deterrence and Patient Education
Primary Prevention
SCA has a high mortality. Only a few patients survive OHCA despite current healthcare advances.[71] The first clinical event is almost always fatal, especially in patients who present with ventricular fibrillation. SCA's poor prognosis makes primary prevention critical, as it reduces SCD risk by identification and treatment of high-risk populations.
Primary ASCVD prevention is an effective way to prevent SCD due to myocardial infarction and ischemic cardiomyopathy.[72] Strategies for preventing myocardial infarction-related SCD include early recalculation, optimal heart failure treatment, and implantation of cardiac resynchronization therapy, especially in patients with cardiomyopathy and evidence of left ventricular dyssynchrony. Reduced ejection fraction is reported as an independent SCD predictor. Thus, an ICD is indicated for primary SCD prevention in patients with ischemic cardiomyopathy with an ejection fraction of 35% or less and heart failure symptoms on guideline-directed medical therapy.
The guidelines also recommend ICD placement for primary SCD prevention in people with nonischemic cardiomyopathy, an ejection fraction of 35% or less, and heart failure symptoms on guideline-directed medical therapy. However, ICDs should not be implanted for primary SCD prevention in those with a limited life expectancy due to noncardiac comorbidities.
Most SCD occurs in the presence of normal left ventricular systolic function, and 10% of those patients are found to have arrhythmogenic cardiac conditions. Commonly identifiable arrhythmogenic cardiac conditions include HCM, arrhythmogenic right ventricular cardiomyopathy, and inherited channelopathies. Certain features predict the future risk of ventricular arrhythmias and SCD in patients with inherited arrhythmia syndromes. These features include a family history of premature SCD in first-degree relatives, a history of recurrent syncope, and evidence of nonsustained arrhythmia.[73] In patients with arrhythmogenic cardiac conditions, the contemporary guidelines recommend ICD use for primary SCD prevention in the presence of the abovementioned features.[74]
Patients with inherited channelopathies and arrhythmogenic cardiomyopathies need to adhere to the therapy advised by their cardiologist. Patients with arrhythmia syndromes, symptomatic ventricular arrhythmias, and a family history of SCD require ICDs. Genetic testing of family members identifies asymptomatic individuals carrying a pathogenic mutation, which helps reduce the incidence. Consanguineous marriages, especially in families with inherited cardiac conditions, are reported to increase the incidence of inherited arrhythmias. Thus, genetic counseling is vital in preventing the incidence of SCD in the general population.
Secondary Prevention
Secondary SCA and SCD prevention necessitate patient adherence to long-term management strategies, as previously explained. These strategies focus on addressing underlying structural heart diseases and primary cardiac arrhythmias.
β-blockers have shown efficacy in reducing SCD risk and improving survival, especially in patients with left ventricular systolic dysfunction or previous acute myocardial infarction. Additionally, β-blockers are recommended as first-line therapy for preventing arrhythmia recurrence in patients with cardiac channelopathies. Cardioprotective agents such as β-blockers, mineralocorticoid receptor antagonists, angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, angiotensin receptor-neprilysin inhibitors, and sodium-glucose cotransporter-2 inhibitors have demonstrated significant reductions in SCD rates in patients with cardiomyopathy and severely reduced left ventricular systolic function. ICD placement is the most effective therapy for preventing SCA recurrence due to ventricular tachyarrhythmias.
Mental health issues can contribute to physiological stress responses and increase the risk of arrhythmias or other cardiac events. Providing support and interventions to address mental health concerns can play a significant role in preventing SCA recurrence.
Pearls and Other Issues
SCD refers to an unexpected and abrupt cardiac function cessation. This condition is typically caused by a sudden, life-threatening arrhythmia, disrupting the heart's ability to pump blood effectively. Rarely, the cause of SCD is unknown. Certain risk factors, such as ASCVD, a history of prior heart attack, heart failure, or family history of SCD, increase the likelihood of experiencing a sudden cardiac event. The most significant SCD risk factor is SCA survival. Prompt SCA recognition and resuscitation following BLS and ACLS guidelines are crucial for improving outcomes. Additionally, risk stratification, targeted preventive measures, and ICD use can help reduce the risk of recurrent SCA in high-risk individuals.
Enhancing Healthcare Team Outcomes
SCD and aborted SCA are major public health problems and significant burdens on the healthcare system. Vulnerable patients present with SCD as the first manifestation of the underlying cardiac conditions. CPR and proper SCA management are pivotal in prognostication. In OHCA cases, studies suggest that early SCA identification followed by bystander CPR, timely defibrillation, and early EMS arrival improve patient survival.[75]
While bystanders and EMS personnel are the first SCA responders, an interprofessional team comprising of a cardiologist, electrophysiologist, neurologist, intensive care expert, and geneticist is required to manage SCA and its complications and prevent recurrence in patients who survive the condition. Staff nurses and respiratory therapists are also vital interprofessional team members, assisting in resuscitation and postcardiac arrest care. The rehabilitation team help patients regain functional independence. Mental health professionals can help patients who survive SCA and their families address their psychosocial needs.
The American Heart Association and American College of Cardiology, in collaboration with the Heart Rhythm Society, have developed evidence-based guidelines for managing ventricular arrhythmia and preventing SCD. These guidelines, reviewed by expert committees, are grounded in an extensive literature review to inform treatment approaches for ventricular arrhythmias and inherited cardiac conditions. In cases where literature is lacking or evidence is inadequate, specialist opinion may guide therapeutic decisions.
Media
(Click Image to Enlarge)
ACLS Algorithm for Asystole and PEA. This image shows a diagram for managing asystole and PEA according to ACLS protocols.
StatPearls
(Click Image to Enlarge)
ACLS Algorithm for VFib and VTach. This image shows a diagram for managing ventricular fibrillation and ventricular tachycardia according to ACLS protocols.
StatPearls
(Click Image to Enlarge)
ST-Elevated Myocardial Infarction on Electrocardiogram. This 12-lead electrocardiogram shows ST elevation in the anterior (orange) and inferior (blue) leads. Tachycardia and anterior fascicular block are also noted. A diagnosis of ST-elevated myocardial infarction can be made, along with clinical evaluation and cardiac marker elevation.
Displaced, Public Domain, via Wikimedia Commons
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