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Sudden cardiac arrest in adults: Overview

Sudden cardiac arrest in adults: Overview
Authors:
Philip J Podrid, MD, FACC
Sana M Al-Khatib, MD, MHS, FHRS
Section Editors:
Brian Olshansky, MD
Scott Manaker, MD, PhD
Deputy Editor:
Naomi F Botkin, MD
Literature review current through: May 2025. | This topic last updated: Jun 09, 2025.

INTRODUCTION — 

The abrupt cessation of cardiac activity is referred to as “sudden cardiac arrest” (SCA). If the patient is not successfully resuscitated, then it is termed sudden cardiac death (SCD). This topic provides an overview of SCA in adults. Other discussions about SCA include the following:

Assessment and management of the SCA survivors in the emergency department and intensive care unit. (See "Initial assessment and management of the adult post-cardiac arrest patient" and "Intensive care unit management of the intubated post-cardiac arrest adult patient".)

Cardiac evaluation of SCA survivors and their family members. (See "Cardiac evaluation of the survivor of sudden cardiac arrest".)

Indications for implantable cardioverter-defibrillators for the primary and secondary prevention of SCD in adults with heart failure with reduced ejection fraction (HFrEF). (See "Primary prevention of sudden cardiac death in patients with cardiomyopathy and heart failure with reduced LVEF".)

SCA in athletes. (See "Athletes: Overview of sudden cardiac death risk and sport participation" and "Screening to prevent sudden cardiac death in competitive athletes".)

SCA in patients on dialysis. (See "Evaluation of sudden cardiac arrest and sudden cardiac death in patients on dialysis".)

SCA in children. (See "Sudden cardiac arrest (SCA) and sudden cardiac death (SCD) in children".)

Psychosocial factors in SCA. (See "Psychosocial factors in sudden cardiac arrest".)

The risk and prevention of SCA in patients with cardiac conditions other than HFrEF (eg, hypertrophic cardiomyopathy, congenital long QT syndrome, arrhythmogenic right ventricular cardiomyopathy, Brugada syndrome) are discussed in related topics. (See "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation" and "Congenital long QT syndrome: Epidemiology and clinical manifestations" and "Arrhythmogenic right ventricular cardiomyopathy: Anatomy, histology, and clinical manifestations" and "Brugada syndrome: Clinical presentation, diagnosis, and evaluation".)

DEFINITIONS

Sudden cardiac arrest and sudden cardiac death – We agree with the definitions of sudden cardiac arrest (SCA) and sudden cardiac death (SCD) in the 2017 American College of Cardiology/American Heart Association/Heart Rhythm Society (ACC/AHA/HRS) guidelines [1]: "Sudden cardiac arrest is the sudden cessation of cardiac activity so that the victim becomes unresponsive, with no normal breathing and no signs of circulation. If corrective measures are not taken rapidly, this condition progresses to sudden cardiac death. Cardiac arrest should be used to signify an event that can be reversed, usually by cardiopulmonary resuscitation (CPR), administration of medications and/or defibrillation or cardioversion. SCA and SCD can result from causes other than ventricular arrhythmias, such as bradyarrhythmias, electromechanical dissociation, pulmonary embolism, intracranial hemorrhage, and aortic dissection.”

Survivors of cardiac arrest are said to have had “aborted” SCD, but the term “aborted” is sometimes implied rather than explicitly stated.

Reversible causes – Causes of SCA are sometimes described as “reversible” or “transient” if the patient’s risk of recurrent SCA is low after the precipitating condition has been treated. While many reversible causes are noncardiac in nature (eg, trauma, metabolic abnormalities), certain transient cardiac conditions (eg, acute myocardial ischemia, acute myocardial infarction, acute pericardial tamponade) can cause SCA (table 1).

Structural heart disease – The term “structural heart disease” refers to the presence of diseases of the myocardium, valves, coronary arteries, or other cardiac structures. It includes coronary artery disease (CAD), cardiomyopathies, and congenital heart disease. It does not include primary electrical conditions, often referred to as inherited channelopathies, such as long QT syndrome or Brugada syndrome.

EPIDEMIOLOGY

Incidence

Out-of-hospital cardiac arrest — Based on large data sets from the United States (US) and Europe, the annual incidence of out-of-hospital cardiac arrest (OHCA) is 84 to 88 per 100,000 population, with wide variation among states and countries [2,3]. Approximately two-thirds of individuals experiencing OHCA are male.

Rates of OHCA are sometimes reported for specific age groups, with a typical cutoff of 35 or 40 years of age:

The incidence among individuals ≥35 years of age is approximately 1 per 1000 per population year [1].

For individuals <40 years of age, the annual risk of OHCA is 4.2 to 7.8 per 100,000 person-years worldwide [4].

Death certificate reporting probably overestimates the incidence of sudden cardiac arrest (SCA) because unwitnessed deaths may be incorrectly categorized as sudden death [5,6]. In a retrospective study of 12,671 unattended out-of-hospital deaths, 40 percent of deaths attributed to cardiac arrest were not sudden or unexpected [7].

The incidence of OHCA in competitive athletes is discussed elsewhere. (See "Athletes: Overview of sudden cardiac death risk and sport participation".)

In-hospital cardiac arrest — In the US, there are approximately 292,000 adult in-hospital cardiac arrest (IHCA) events per year, with an incidence of 9.7 per 1000 hospital admissions [8]. The incidence of adult IHCA is reported as 1 to 1.6 per 1000 hospital admissions in the United Kingdom, 1.8 per 1000 admissions in Denmark, and 5.1 per 1000 admissions in Japan [9-11].

Risk factors — The following risk factors increase the likelihood of SCA in adults:

Cardiovascular disease risk factors – Because coronary artery disease (CAD) is a common cause of SCA, conditions that increase the likelihood of CAD (eg, age, male sex, diabetes mellitus, cigarette smoking, hypertension, hyperlipidemia, C-reactive protein) also increase the risk of SCA [12-14]. (See "Overview of established risk factors for cardiovascular disease".)

Family history of SCA – A family history of SCA is associated with a 1.5- to 1.8-fold increased risk of SCA [15,16]. The increase in risk is not explained by traditional cardiovascular disease risk factors that tend to aggregate in families (eg, hypercholesterolemia, hypertension, diabetes mellitus).

Psychosocial and socioeconomic factors – Observational studies have suggested that SCA is more likely in individuals who are Black, have lower socioeconomic status, or are exposed to acutely stressful situations such as earthquakes and war [17-19]. (See "Psychosocial factors in sudden cardiac arrest".)

Strenuous exercise – The risk of SCA is transiently increased during and up to 30 minutes after strenuous exercise compared with other times [20,21]. However, the actual risk during any one episode of vigorous exercise is very low (1 per 1.51 million episodes of exercise) [21]. Furthermore, the positive effect of exercise on all-cause mortality rates outweighs the risk of exercise-induced sudden cardiac death (SCD) for patients without known structural heart disease. (see "The benefits and risks of aerobic exercise").

The risk of SCA in athletes is discussed in detail elsewhere. (See "Athletes: Overview of sudden cardiac death risk and sport participation".)

Heavy alcohol consumption Heavy total alcohol consumption (ie, at least four drinks per day) may increase the risk for SCA [22]. These patients are at risk for alcoholic cardiomyopathy, which can lead to SCA.

MECHANISMS — 

The mechanisms of common cardiac and noncardiac causes of sudden cardiac arrest (SCA) are discussed below.

Cardiac conditions For most patients with cardiac conditions who present with SCA, the cause is a ventricular arrhythmia. The specific type of ventricular arrhythmia depends on the cardiac condition:

Cardiac arrest that occurs in the setting of acute myocardial infarction or myocardial ischemia is usually due to ventricular fibrillation (VF) or polymorphic ventricular tachycardia (VT) (waveform 1) but can occasionally be due to sustained monomorphic VT or complete heart block. In some patients, the rhythm may deteriorate over several minutes into asystole due to progressive metabolic derangement and loss of all electrical activity. (See "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features", section on 'Mechanisms of arrhythmogenesis'.)

Cardiac arrest due to structural heart disease (eg, cardiomyopathy) is usually caused by sustained monomorphic VT, which is a reentrant arrhythmia. (See "Ventricular arrhythmias: Overview in patients with heart failure and cardiomyopathy", section on 'Pathogenesis'.)

For patients with acquired or congenital long QT syndrome (LQTS), cardiac arrest is usually due to torsades de pointes, which is a type of polymorphic VT that occurs in individuals who have abnormalities in repolarization that manifest as QT prolongation on electrocardiography. Patients with a Brugada pattern may have VT or VF. VF may also occur in patients with Wolff-Parkinson-White syndrome. (See "Congenital long QT syndrome: Pathophysiology and genetics", section on 'Perturbations in ion channels'.)

The mechanisms of VT and VF are discussed elsewhere. (See "Reentry and the development of cardiac arrhythmias".)

Noncardiac conditions Many patients who experience cardiac arrest due to a noncardiac condition present with asystole or pulseless electrical activity. Pulseless electrical activity, also known as electromechanical dissociation, occurs when the left ventricle is unable to generate a sufficient stroke volume despite ongoing electrical activity. Pulseless electrical activity can be caused by different mechanisms, such as:

Poor myocardial contractility due to acidosis, hypoxia, or other metabolic disturbances.

Insufficient preload due to conditions that cause hypovolemia (eg, burns, hemorrhage) or vascular obstruction (eg, pulmonary embolism).

The same metabolic derangements that cause pulseless electrical activity can also lead to asystole.

ETIOLOGIES — 

There are many cardiac and noncardiac conditions that can cause sudden cardiac arrest (SCA) (table 2 and table 1).

Most common etiologies — The most commonly identified etiologies of SCA are cardiac in nature with the most common being coronary artery disease (CAD) and cardiomyopathies, including hypertrophic cardiomyopathy [7,23]. Among individuals <35 years of age who experience sudden cardiac death (SCD), 40 percent have presumed sudden arrhythmic death without structural heart disease identified on autopsy [23].

Cardiac etiologies — Cardiac etiologies of SCA include CAD, other structural heart diseases, and primary electrical abnormalities.

Coronary artery disease — Approximately 50 percent of deaths due to coronary artery disease occur suddenly [1]. Patients with atherosclerotic CAD are at risk of experiencing SCA in the setting of acute myocardial infarction or myocardial ischemia. They may also develop SCA due to sustained monomorphic ventricular tachycardia (VT) that often (but not always) originates around an area of scar caused by a prior myocardial infarction. (See "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features" and "Primary prevention of sudden cardiac death in patients with cardiomyopathy and heart failure with reduced LVEF".)

Rarely, a transmural myocardial infarction can lead to rupture of the free wall of the left ventricle, allowing blood to enter the pericardial space and causing acute pericardial tamponade. (See 'Other structural heart disease' below.)

While atherosclerotic CAD is the most common coronary condition leading to SCA, any abnormality that causes myocardial infarction or ischemia can result in SCA. Less common coronary conditions associated with SCA include coronary artery vasospasm, embolism, and dissection, and congenital anomalous coronary arteries. (See "Vasospastic angina" and "Spontaneous coronary artery dissection" and "Congenital and pediatric coronary artery abnormalities".)

Other structural heart disease — Other cardiac structural abnormalities that can cause SCA include the following:

Hypertrophic cardiomyopathy – Hypertrophic cardiomyopathy is one of the most identified cardiac abnormalities on autopsies of younger individuals with SCD. The primary mechanism by which hypertrophic cardiomyopathy can cause SCA is sustained monomorphic VT originating around areas of myocardial fibrosis. Contributing factors may include myocardial ischemia from left ventricular hypertrophy, abnormally thick walls of coronary arteries, and left ventricular outflow tract obstruction. (See "Hypertrophic cardiomyopathy: Management of ventricular arrhythmias and sudden cardiac death risk".)

Arrhythmogenic right ventricular cardiomyopathy – Arrhythmogenic right ventricular cardiomyopathy causes sustained monomorphic VT originating in the RV. SCA is often the first presentation of the disease. (See "Arrhythmogenic right ventricular cardiomyopathy: Anatomy, histology, and clinical manifestations", section on 'Sudden cardiac death'.)

Dilated cardiomyopathy – Dilated cardiomyopathy can be idiopathic, inherited (eg, familial dilated cardiomyopathy such as lamin cardiomyopathy), or acquired (ie, secondary to virus, toxin, or medication). Dilated cardiomyopathy increases the risk of SCA due to ventricular arrhythmias. (See "Familial dilated cardiomyopathy: Prevalence, diagnosis and treatment" and "Primary prevention of sudden cardiac death in patients with cardiomyopathy and heart failure with reduced LVEF".)

Myocarditis Myocarditis can develop due to a variety of infectious and noninfectious causes. Patients with myocarditis are at risk of SCA, which is usually due to ventricular arrhythmias; however, in some cases (eg, Lyme carditis), SCA can be caused by complete heart block. (See "Clinical manifestations and diagnosis of myocarditis in adults", section on 'Sudden cardiac death'.)

Infiltrative cardiomyopathy – Infiltrative cardiomyopathies such as cardiac sarcoidosis and cardiac amyloidosis can cause SCA due to ventricular arrhythmias or heart block. (See "Management and prognosis of cardiac sarcoidosis", section on 'Arrhythmias and conduction system disease' and "Cardiac amyloidosis: Treatment and prognosis", section on 'Sudden death prevention'.)

Valvular heart disease – Patients with severe aortic valve stenosis are at risk of SCA. While the mechanism of SCA in these patients is uncertain, ventricular arrhythmias resulting from severe left ventricular hypertrophy and subendocardial ischemia likely play a major role. A subset of patients with mitral valve prolapse appear to be at risk of SCA due to ventricular arrhythmias. (See "Clinical manifestations and diagnosis of aortic stenosis in adults", section on 'Sudden cardiac death' and "Mitral valve prolapse: Overview of complications and their management", section on 'Subgroups at risk for SCD'.)

Congenital heart disease – Certain patients with complex congenital heart disease are at risk of SCA due to ventricular arrhythmias during adulthood. (See "Tetralogy of Fallot (TOF): Long-term complications and follow-up after repair", section on 'Arrhythmias and sudden cardiac death'.)

Acute pericardial tamponade – The rapid accumulation of fluid within the pericardial space can lead to impaired cardiac filling and SCA. (See "Cardiac tamponade".)

Primary electrical causes — Several primary electrical conditions can cause SCA. Some of these conditions are known as inherited channelopathies; those are listed here in order of decreasing prevalence:

Congenital long QT syndrome – Congenital long QT syndrome (LQTS) is the most common inherited channelopathy. It can cause a type of polymorphic VT called “torsades de pointes” that can lead to SCA. (See "Congenital long QT syndrome: Epidemiology and clinical manifestations", section on 'Polymorphic VT/torsades de pointes' and "Acquired long QT syndrome: Clinical manifestations, diagnosis, and management", section on 'Patients with acute TdP'.)

Brugada syndrome – Brugada syndrome is an autosomal dominant genetic disorder that causes ventricular arrhythmias (typically ventricular fibrillation) and SCA. Factors associated with ventricular arrhythmias include fever, cocaine, alcohol intoxication, and sodium channel-blockers such as flecainide and procainamide. (See "Brugada syndrome: Clinical presentation, diagnosis, and evaluation", section on 'Sudden cardiac arrest and/or death'.)

Catecholaminergic polymorphic VT – Catecholaminergic polymorphic VT is a rare condition associated with several pathogenic genetic variants. Patients with catecholaminergic polymorphic VT can experience SCA. (See "Catecholaminergic polymorphic ventricular tachycardia".)

Early repolarization syndrome (ie, idiopathic VF) – While early repolarization is a common finding on the electrocardiogram in young, healthy individuals, in rare cases, early repolarization appears to be associated with idiopathic VF. (See "Early repolarization", section on 'Arrhythmic risk'.)

Congenital short QT syndrome – Congenital short QT syndrome is a rare inherited channelopathy associated with SCA due to polymorphic VT. (See "Short QT syndrome", section on 'Cellular basis of arrhythmogenesis'.)

Other electrical etiologies — Noninherited electrical disorders include the following:

Acquired long QT syndrome – Acquired LQTS is more common than congenital LQTS, and is usually due QT-prolonging medications. This condition can lead to torsade de pointes that, in turn, can cause SCA. (See "Acquired long QT syndrome: Definitions, pathophysiology, and causes".)

Complete heart block – Complete heart block does not usually cause cardiac arrest. However, in rare cases, patients may experience SCA. (See "Acquired third-degree (complete) atrioventricular block", section on 'Clinical presentation'.)

Wolff-Parkinson-White syndrome – In Wolff-Parkinson-White syndrome, there is an accessory pathway allowing conduction to bypass the atrioventricular node. If atrial fibrillation occurs and there is a rapid ventricular rate due to rapid conduction down the pathway, this can lead to VF and SCA. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis", section on 'Ventricular fibrillation and sudden death'.)

Commotio cordis – Commotio cordis, which is one of the most common causes of SCA during athletic events, occurs when there is a blow to the chest by a hard projectile (ie, ball) or high-energy physical contact (eg, tackle during football) that occurs during a critical period of repolarization (ie, R-on-T premature ventricular complex). (See "Commotio cordis", section on 'Mechanism'.)

Noncardiac etiologies — There are many noncardiac causes of SCA (table 2 and table 1). Some of the more common etiologies include opioid overdose, pulmonary embolism, and upper airway obstruction. The initial assessment and management of SCA survivors include the identification and treatment of noncardiac conditions that cause SCA. (See "Initial assessment and management of the adult post-cardiac arrest patient", section on 'Identifying and treating reversible causes of cardiac arrest'.)

EVALUATION AND MANAGEMENT — 

The initial evaluation and management of survivors of sudden cardiac arrest (SCA) generally take place in the emergency department (for out-of-hospital cardiac arrest [OHCA]) or the intensive care unit (for in-hospital cardiac arrest [IHCA]). An overview of our approach is as follows:

We provide initial stabilization and treat any reversible causes. (See "Initial assessment and management of the adult post-cardiac arrest patient".)

For those who require care in the intensive care unit, we provide general critical care management. Individuals who remain unconscious and unresponsive after resuscitation are at risk for hypoxic-ischemic brain injury and should receive active temperature control for the prevention of this complication. (See "Intensive care unit management of the intubated post-cardiac arrest adult patient".)

Individuals who have experienced SCA are at risk for recurrence unless a reversible cause has been identified and treated. For patients who do not have a reversible cause, the presumed etiology of the SCA is ventricular arrhythmia. We take the following steps for these patients:

We evaluate the patient for cardiac causes of SCA (table 2). Depending on the results of those tests, evaluation of first-degree family members may be indicated. As examples, family members of individuals with hypertrophic cardiomyopathy, congenital long QT syndrome (LQTS), or Brugada syndrome should be evaluated for that condition. (See "Cardiac evaluation of the survivor of sudden cardiac arrest".)

We implant an implantable cardioverter-defibrillator (ICD) in most of these patients, regardless of whether a cardiac cause of the arrest has been found. Recommendations for patients who have specific cardiac conditions are discussed elsewhere, including patients with the following diagnoses:

-Heart failure with reduced ejection fraction (HFrEF). (See "Primary prevention of sudden cardiac death in patients with cardiomyopathy and heart failure with reduced LVEF".)

-Hypertrophic cardiomyopathy. (See "Hypertrophic cardiomyopathy: Management of ventricular arrhythmias and sudden cardiac death risk", section on 'Secondary prevention'.)

-Congenital LQTS. (See "Congenital long QT syndrome: Treatment", section on 'Implantable cardioverter-defibrillator'.)

-Brugada syndrome. (See "Brugada syndrome or pattern: Management and approach to screening of relatives", section on 'Initial therapy with implantable cardioverter-defibrillator'.)

For patients in whom a cause of SCA cannot be determined, we recommend placement of an ICD.

We do not usually implant ICDs in patients with hypoxic-ischemic brain injury because these patients have a poor neurologic prognosis.

Survivors of SCA are at risk for recurrent SCA. In an observational study of 924 patients with OHCA (excluding individuals with likely noncardiac etiologies) who survived to hospital discharge, at least 10 percent experienced recurrent SCA [24].

ICDs deliver antitachycardia therapy (eg, antitachycardia pacing and shocks) to treat ventricular fibrillation (VF) and ventricular tachycardia (VT). The ICD does not prevent arrhythmia but treats it when it occurs. Randomized trials have studied the utility of ICDs for the secondary and primary prevention of SCA. In a meta-analysis of four trials including 1926 patients with HFrEF who experienced resuscitated SCA or hemodynamically significant VT, patients who were randomly assigned to receive ICDs had lower rates of all-cause mortality (relative risk [RR] 0.75, 95% CI 0.64-0.87) and SCA (hazard ratio [HR] 0.50, 95% CI 0.34-0.62) compared with those who received antiarrhythmic drug therapy [25]. In a meta-analysis of five trials including 3130 patients with HFrEF who were at risk for SCD due to ventricular arrhythmias, those who were randomly assigned to receive ICDs had lower rates of all-cause mortality (RR 0.66, 95% CI 0.46-0.96) compared with those assigned to antiarrhythmic medication or conventional therapy.

Although these trials evaluated ICDs in patients with HFrEF, the benefit of ICDs is likely the same in patients without structural heart disease. In a registry study including 200 patients with unexplained cardiac arrest without known coronary artery disease (CAD), repolarization syndromes, or left ventricular dysfunction, advanced testing determined a diagnosis in approximately 40 percent of patients [26]. There was no difference in ICD implantation rates in patients with and without a diagnosis, with 155 patients in the overall study receiving ICDs. The rate of experiencing an appropriate shock in ICD recipients was 3.9 percent after one year and 10.4 percent after three years, with similar rates of ICD events in patients with and without a diagnosis.

ICDs are discussed in detail elsewhere. (See "Implantable cardioverter-defibrillators: Overview of indications, components, and functions" and "Implantable cardioverter-defibrillators: Choosing a device and system descriptions".)

OUTCOMES

Survival after OHCA — The survival of patients experiencing out-of-hospital cardiac arrest (OHCA) is discussed below. The outcomes of sudden cardiac death (SCD) in competitive athletes and neurologic outcomes after cardiac arrest are addressed separately. (See "Athletes: Overview of sudden cardiac death risk and sport participation" and "Hypoxic-ischemic brain injury in adults: Evaluation and prognosis".)

Mortality data — Most registries and observational studies report data on short-term survival (ie, survival until hospital discharge). In a meta-analysis of 141 studies of patients with OHCA who received cardiopulmonary resuscitation (CPR), the pooled rate of survival to hospital discharge was 8.8 percent [27]. Survival was higher in those who had a witnessed cardiac arrest and received bystander CPR. In the 2022 CARES registry, which included 147,736 patients with nontraumatic OHCA treated by emergency medical services (EMS), survival to hospital discharge was 9.3 percent, with significant variation among states (5.5 to 15.4 percent) [2]. Survival to hospital discharge with good functional status (ie, neurologically intact) was 7.5 percent. In the EuReCa ONE study of 10,682 individuals with OHCA, 10.3 percent survived to hospital discharge or for at least 30 days after OHCA, with a range of 1.1 to 30.8 percent among participating countries [3].

Long-term survival data are also available. In a meta-analysis of 21 studies including 11,800 patients with OHCA who survived until hospital discharge, the median survival time was five years; 64 percent of patients survived for at least 10 years [28]. Patients with a shockable initial rhythm had a lower risk of mortality compared with those who had a nonshockable rhythm (HR 0.30, 95% CI 0.23-0.39).

Survival after OHCA may be improving. In a meta-analysis of 141 studies of patients with OHCA who received CPR, one-year survival increased from 8 percent in 2000 to 2009 to 13.3 percent in 2010 to 2019 [27]. The improvement in survival is likely due to increased availability of automated external defibrillators (AEDs) and initiatives to educate the public in bystander CPR techniques. In the 2022 CARES registry, 40 percent of individuals with OHCA had bystander CPR, while public AEDs were used in 11.3 percent of cases [2].

Factors predicting outcomes — Several factors have been shown to predict outcomes after OHCA, including patient-specific characteristics, type of cardiac arrest, aspects of prehospital care, and the use of active temperature control:

Patient characteristics Several patient characteristics are associated with increased mortality after OHCA. These include the following:

Age – Older age is associated with worse survival after OHCA [29-31].

Sex – Some studies have reported higher mortality rates for female adults. However, this finding is confounded by the increased prevalence of risk factors that predict mortality (eg, older age, nonshockable rhythm) in female compared with male individuals who experience OHCA [2]. In addition, studies have shown that female individuals are less likely than male individuals to receive bystander CPR [32,33].

Socioeconomic factors – Studies in the United States have reported worse outcomes in adults who identify as Black compared with those who do not [34-36]. This finding is likely due to socioeconomic and health care disparities. In the 2022 CARES registry, Black and Hispanic individuals had lower rates of bystander CPR than other racial and ethnic groups [2,37]. Rates of CPR and AED use correlated with neighborhood median household income.

Comorbidities – Patients with preexisting comorbidities (eg, heart failure, prior myocardial infarction, diabetes, cancer, Alzheimer’s disease, more than two chronic illnesses) have a lower rate of survival to hospital discharge after ventricular fibrillation (VF) arrest compared with those who do not have comorbidities [38].

Cardiac arrest characteristics

Witnessed event – Individuals who have a witnessed OHCA are more likely to survive than those whose arrest is unwitnessed [39] because resuscitation can be provided sooner to those whose arrest is witnessed.

Type of rhythm – Adults who experience OHCA due to a shockable rhythm (ie, VF, ventricular tachycardia [VT]) have a lower mortality than those who have a nonshockable rhythm (ie, asystole, pulseless electrical activity). Survival of those with a nonshockable rhythm is poor; in a cohort study of 35,843 individuals with OHCA and asystole, only 1.4 percent survived until 30 days after discharge, and only 0.2 percent survived with a favorable neurologic status [40].

Duration of CPR – Patients who require CPR for <5 minutes are more likely to survive than those who require prolonged CPR.

Resuscitation Early resuscitation with good-quality CPR and defibrillation (if indicated) is critical to survival after OHCA.

Bystander CPR – Early CPR is associated with improved survival after OHCA [41-45]. Because many bystanders are reluctant to perform rescue breathing on strangers, chest compression-only CPR has been studied as an alternative to standard CPR. Not only does chest compression-only CPR increase the likelihood that individuals with OHCA will receive any CPR at all; chest compression-only CPR may lead to better outcomes compared with standard CPR. In a meta-analysis of three trials comparing chest compression-only bystander CPR with standard bystander CPR, individuals randomly assigned to chest compression-only CPR had a slightly improved chance of survival (14 versus 12 percent, risk ratio [RR] 1.22, 95% CI 1.01-1.46) [46].

Quality of CPR – The quality of CPR depends on the compression rate, compression depth, chest recoil, and percentage of time chest compression is administered. CPR quality impacts survival. In a meta-analysis of 10 studies including 4722 patients, individuals were more likely to survive cardiac arrest if they received deeper chest compressions and had compression rates between 85 and 100 compressions per minute, compared with shallower and slower compression rates [47]. (See "Adult basic life support (BLS) for health care providers", section on 'Performance of excellent chest compressions'.)

AEDs – For patients in cardiac arrest due to a shockable rhythm, survival declines by approximately 10 percent for each minute without defibrillation [48-50]. Early defibrillation with an AED by a bystander is associated with improved survival after OHCA. In an observational study of 4115 individuals with witnessed OHCA who had a shockable rhythm, those who were shocked with an AED by a bystander were more likely to survive (66.5 versus 43 percent, p<0.001) and be discharged from the hospital with a favorable neurologic outcome (57.1 versus 32.7 percent, p<0.001) than those who were initially shocked by EMS [51]. AEDs are discussed elsewhere. (See "Automated external defibrillators".)

Prehospital care by EMS

Advanced Cardiac Life Support (ACLS) versus Basic Life Support (BLS) – Adults with OHCA who receive Advanced Cardiovascular Life Support (ACLS) in the prehospital setting have better survival than those who receive Basic Life Support (BLS) [52].

Route of medication administration – Vascular access for the administration of medications in the setting of cardiac arrest may be obtained either intravenously or intraosseously. Observational studies comparing these forms of vascular access suggested that initial intravenous access was associated with higher rates of return of spontaneous circulation, survival, and favorable neurologic outcomes [53-56]. However, three randomized trials demonstrated comparable rates of survival and favorable neurologic outcomes with either intravenous and intraosseous access [57-59].

Active temperature control – Active control of core body temperature for at least 72 hours has been shown to improve outcomes after cardiac arrest. Initial trials demonstrated reduced mortality and a greater likelihood of favorable neurologic outcome with active temperature control to hypothermic temperatures (32 to 34°C) compared with no active temperature control [60,61]. Subsequent trials found similar outcomes with targeted hypothermia and targeted normothermia [62]. Active temperature control is routinely used for survivors of cardiac arrest who do not initially have purposeful neurologic activity on examination. (See "Intensive care unit management of the intubated post-cardiac arrest adult patient", section on 'Active temperature control' and "Hypoxic-ischemic brain injury in adults: Evaluation and prognosis".)

Other prognostic factors – Other predictors of poor prognosis include persistent coma after resuscitation, hypotension, cardiogenic shock, pneumonia, acute kidney injury, acidemia, and elevated serum lactate.

Risk scores — Two clinical risk scores have been developed to predict survival after OHCA:

The NULL-PLEASE score was retrospectively validated in a single-center cohort of 547 patients with OHCA between 2013 and 2016 [63]. The following 10 components were each assigned one point:

Nonshockable rhythm

Unwitnessed arrest

Long no-flow period (no bystander CPR)

Long low-flow period (>30 minutes before return of spontaneous circulation)

pH (arterial) <7.2

Lactate >7 mmol/L

End-stage kidney disease on dialysis

Age ≥85 years

Ongoing CPR on arrival to hospital

Extracardiac cause

Patients with ≥5 points on the NULL-PLEASE score had a greater than threefold risk of mortality compared with patients with a score of 0 to 4 (odds ratio [OR] 3.3, 95% CI 2.3-4.9). The score components that were individually associated with worse outcomes were long low-flow period and age ≥85 years.

The CREST score (from 0 to 5), derived from 638 patients and validated in 318 patients who experienced out-of-hospital cardiac arrest and were enrolled in the International Cardiac Arrest Registry (INTCAR), stratifies patients on risk of circulatory death following return of spontaneous circulation [64].

Coronary artery disease (CAD; preexisting)

Rhythm nonshockable

Ejection fraction <30 percent

Shock at presentation

Time (ischemic time prior to return of spontaneous circulation ) >25 minutes

The risk of circulatory death increased with every additional point, from 10 percent mortality (for CREST score of 0) up to 50 percent mortality (for CREST score of 5).

Survival after IHCA

Survival after IHCA – Outcomes after in-hospital cardiac arrest (IHCA) are poor but appear to be improving. In a meta-analysis of 40 studies including data from 1985 to 2018, the pooled one-year survival after IHCA was 13.4 percent [65]. There was a modest improvement in survival over time (10-year odds ratio [OR] 1.7, 95% CI 1.04-2.76).

Factors predicting outcomes after IHCA – Factors that predict outcomes after IHCA include the following:

Patient characteristics – Patient characteristics associated with improved survival after IHCA include younger age, normal baseline neurologic function, and having few medical comorbidities [66].

Timing – Survival is lower when arrest occurs during off-hours (ie, nights and weekends) than on-hours [67].

Location – Patients on cardiac wards who experience IHCA are more likely to survive than those on noncardiac wards [65].

Cardiac arrest characteristics – Having a witnessed arrest, an initial shockable rhythm, and early defibrillation are associated with improved survival in IHCA, similar to OHCA [68,69]. Resuscitation duration ≥10 minutes and being unmonitored are associated with worse survival [69].

Number of arrests – Patients with multiple resuscitations involving CPR have a lower likelihood of survival than those who have a single arrest [70].

Quality of resuscitation – The following hospital practices are associated with improved survival after IHCA [71]:

-Monitoring for interruptions in chest compressions

-Reviewing cardiac arrest cases monthly or quarterly

-Having a hospital resuscitation champion

-Having a resuscitation team with diverse team members, clear roles and responsibilities, and in-depth mock codes [72]

Risk score to predict survival after IHCA The GO-FAR score predicts the likelihood of survival with good neurologic function after IHCA based on 13 clinical variables. This score, which can be calculated using the GO-FAR calculator, was derived and validated using data on 51,240 patients in 366 United States hospitals that were participating in the Get With The Guidelines-Resuscitation registry from 2007 to 2009 [73]. Patients were divided into the following groups based on likelihood of survival to discharge with good neurologic status:

Very low likelihood of survival (<1 percent chance) – Score of 24 or greater

Low likelihood of survival (1 to 3 percent chance) – Score 14 to 23

Average likelihood of survival (>3 to 15 percent chance) – Score -5 to 13

Higher-than-average likelihood of survival (>15 percent chance) – Score -15 to -6

A subsequent prospective registry study of 62,131 patients with IHCA between 2010 and 2016 validated the ability of the GO-FAR score to predict survival; in this study, survival rates were slightly higher, likely related to ongoing improvements in postresuscitation care [74]. The GO-FAR score appears to be an effective aid for patients and/or caregivers to better understand the likely goals and outcomes of care. (See "Communication in the ICU: Holding a meeting with families and caregivers of adult patients", section on 'Sharing clinical information'.)

INFORMATION FOR PATIENTS — 

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Sudden cardiac arrest (The Basics)")

SUMMARY AND RECOMMENDATIONS

Definition – Sudden cardiac arrest (SCA) refers to the sudden cessation of cardiac activity. SCA will progress to sudden cardiac death (SCD) if corrective measures are not taken rapidly. (See 'Definitions' above.)

Incidence – The annual incidence of out-of-hospital cardiac arrest (OHCA) among adults is approximately 84 to 88 per 100,000 population, with wide variation among countries and states. Among adults ≥35 years of age, the annual incidence is approximately 1 per 1000 individuals. For in-hospital cardiac arrest (IHCA), the incidence ranges from 1 to 9.7 per 1000 hospital admissions. (See 'Epidemiology' above.)

Mechanisms – SCA due to a cardiac condition is usually arrhythmic in nature (ie, ventricular fibrillation [VF], ventricular tachycardia [VT]). Most patients who have SCA due to a noncardiac condition present with a nonshockable rhythm (ie, asystole, pulseless electrical activity). (See 'Mechanisms' above.)

Etiologies A variety of cardiac and noncardiac conditions can cause SCA (table 2 and table 1).

Cardiac conditions

-Coronary artery disease (CAD) is the most common cardiac condition causing SCA. (See 'Coronary artery disease' above.)

-Other cardiac structural abnormalities that can cause SCA include hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, dilated cardiomyopathy, myocarditis, infiltrative cardiomyopathy, valvular heart disease, and congenital heart disease. (See 'Other structural heart disease' above.)

-Primary electrical causes of SCA include congenital and acquired long QT syndrome (LQTS), Brugada syndrome, Wolff-Parkinson-White syndrome, and several rare conditions. (See 'Primary electrical causes' above.)

Noncardiac conditions – There are many noncardiac conditions that can cause SCA including trauma, opioid overdose, pulmonary embolism, and upper airway obstruction. (See 'Noncardiac etiologies' above.)

Evaluation and management – Patients with SCA require initial stabilization, identification and treatment of reversible causes, general critical care management, and active temperature control to preserve neurologic function.

SCA survivors who do not have a reversible cause of SCA identified are at risk for recurrence. Most of these patients should undergo ICD implantation, including patients who have specific cardiac conditions (heart failure with reduced ejection fraction [HFrEF, hypertrophic cardiomyopathy, congenital LQTS, Brugada syndrome, etc). For patients in whom a cause of SCA cannot be determined after evaluation, we recommend implantation of an ICD (Grade 1B). (See 'Evaluation and management' above.)

Outcomes

Out-of-hospital arrest

-Approximately 9 percent of individuals with OHCA survive to hospital discharge, with wide variation among states and countries. (See 'Mortality data' above.)

-Factors predicting worse outcomes after OHCA include older age, female sex, Black race, preexisting comorbidities, unwitnessed event, nonshockable rhythm, prolonged arrest, lack of bystander cardiopulmonary resuscitation (CPR), poor quality CPR, and lack of automated external defibrillator availability. Active temperature control is associated with improved survival. (See 'Factors predicting outcomes' above.)

-Risk scores can be used to predict outcomes after OHCA. (See 'Risk scores' above.)

In-hospital arrest

-The one-year survival after IHCA is approximately 13 percent. Factors predicting worse outcomes after IHCA include older age, baseline comorbidities, arrest during off-hours, arrest on a noncardiac ward, unwitnessed arrest, nonshockable rhythm, resuscitation ≥10 minutes, and multiple cardiac arrests. Certain hospital practices are associated with improved survival. A risk score is available for outcome prediction. (See 'Survival after IHCA' above.)

ACKNOWLEDGMENT — 

The UpToDate editorial staff acknowledges David Siscovick, MD, who contributed to earlier versions of this topic review.

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Topic 963 Version 41.0

References

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