Sudden Cardiac Arrest

Sudden Cardiac Arrest

Yuliya Krokhaleva

Marmar Vaseghi


Sudden cardiac arrest (SCA) is defined as the cessation of all mechanical activity of the heart resulting in the absence of circulation with the onset of symptoms within 1 hour preceding the otherwise unexpected event. When resuscitation is not attempted or not successful, SCA leads to sudden cardiac death (SCD). Overall survival from SCA remains poor, and out-of-hospital cardiac arrest portends a worse prognosis compared to in-hospital cardiac arrest. However, recent progress in prevention and treatment of cardiovascular diseases has been linked to improved outcomes over the years, with an increase in survival to hospital discharge after out-of-hospital cardiac arrest from 10.2% in 2006 to 12.4% in 2015 and from 28.5% in 2000 to 48.7% in 2018 after in-hospital cardiac arrest.1 Cardiovascular mortality is the leading cause of death in the United States, with SCD accounting for over half of all cases.2 Owing to its significant fatality toll, SCA has a profound impact on global public health and utilization of medical resources with far-reaching socioeconomic consequences.

Epidemiology of SCD

Over the course of the last 20 to 30 years, approximately 230,000 to 450,000 deaths per year in the United States have been attributed to SCD.2 In 2017, mortality from SCD was reported to be 379,133. The incidence of SCA tends to increase with age in both sexes. However, at any age, SCA is more common in men, who are two to three times more likely to fall victim, than women.1 The projected rate of SCA in younger subjects (less than or equal to 34 years of age) is 1 per 100,000 a year. As the population ages, the annual rate of SCA surges from the age of 35 to 75 years (1 per 1,000) and decreases after that.2

Age also affects the etiology of SCD. Autopsy studies demonstrate that younger victims (median age of 29 years) may have structurally normal hearts in up to 42% of cases, whereas older individuals (mean age 54.7 years) are found to have no structural cardiac abnormalities in only 4% of postmortem evaluations.3 In young victims, predominant causes of SCD are congenital channelopathies; inherited dilated, hypertrophic, and arrhythmogenic cardiomyopathies; and coronary artery anomalies. Other common autopsy findings include idiopathic fibrotic cardiomyopathy, obesity-associated cardiomyopathy, and hypertensive cardiomyopathy.4 Structural heart disease (SHD) is identified in the majority of older individuals with SCA, with coronary artery disease (CAD) accounting for 70% of cases.2 Other types of SHD found in 10% to 15% of instances include nonischemic cardiomyopathy (NICM), left ventricular hypertrophy (LVH), hypertrophic cardiomyopathy (HCM), arrhythmogenic right ventricular cardiomyopathy (ARVC), myocarditis, congenital coronary anomalies, and mitral valve prolapse.2 Primary arrhythmic causes include channelopathies, such as congenital long QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia (VT), Wolff-Parkinson-White (WPW) syndrome, as well as early repolarization syndrome, idiopathic VT, or ventricular fibrillation (VF). They are implicated in 1% to 2% of cases.5,6,7 Noncardiac and other unidentified etiologies account for the remaining 5% to 25% of SCA and encompass trauma, bleeding, drug overdose, pulmonary embolism, central airway obstruction, hypoxia, intracranial hemorrhage, and near-drowning. Etiologies of SCA in adults in the United States are summarized in Figure 62.1.1,2,6,7

Risk Factors Associated With SCA

Many of the risk factors for CAD and SCA are the same: hypertension, hyperlipidemia, type 2 diabetes mellitus, smoking, obesity, and a sedentary lifestyle. Most of these risk factors are treatable and/or preventable. General preventative measures tend to work on a population level but seem to have limited effects on an individual’s risk of SCA. Congestive heart failure (CHF), previous stroke or transient ischemic attack, atrial fibrillation, hypertension, diabetes mellitus, peripheral arterial disease, chronic kidney disease, obstructive sleep apnea, and chronic obstructive pulmonary disease (COPD) are independently associated with increased risk of ventricular tachyarrhythmias and SCD, particularly in patients over the age of 75 years.8 The risk of SCD in individuals with adult congenital heart disease is higher than in the general population and increases depending on the complexity of the heart defect. Eisenmenger syndrome has the highest incidence of SCA, whereas transposition of the great arteries—either after atrial switch surgery or congenitally corrected—and Fontan physiology carry moderate risk.9


SCA in a first-degree relative is a well-known risk factor for SCD. The presence of a genetic predisposition was suggested by studies that reported SCA as the first presentation of cardiac disease in several generations of families independent of other
cardiovascular risk factors. The rate of SCA or acute myocardial infarction (AMI) was reported to be 1.5- to 2-fold higher in first-degree relatives of SCD victims who had no previous history of heart disease as compared to those without a family history.10,11 Moreover, the risk of SCA in individuals with no prior history of cardiac disease was approximately 10-fold higher when there was a family history of SCD in more than one first-degree relative when compared to just one relative.11 Mutation-specific genetic testing is recommended for screening of family members of survivors of unexplained SCA to identify those with the subclinical disease who are at risk.12

Between 3% and 45% of autopsies in previously healthy children, adolescents, and adults less than 35 years of age find no anatomical or histologic pathology, and therefore, fail to determine the cause of sudden death.3,13 Common cardiac channelopathies, such as long QT syndrome, catecholaminergic polymorphic VT, and Brugada syndrome are not associated with any morphologic abnormalities on postmortem examination and can be categorized as unexplained SCD. Molecular autopsy may identify a pathologic mechanism and clarify the cause of death in in up to 27% of such cases.5 A combination of histologic and molecular autopsy examination coupled with family screening may increase the likelihood of determining the cause of SCD and help prevent it in surviving relatives.

Risk Prediction

The difference between population and individual risk is at the core of suboptimal prediction of the probability of SCA. The highest risk group is comprised of adults with underlying SHD and traditional cardiovascular risk factors, yet patients with SHD constitute a small proportion of all sudden deaths. At the same time, the overwhelming majority of SCDs occur in the general population without traditional CAD risk factors. This presents a challenging quandary of how to identify susceptible subjects at higher risk within a general population that is overall at low risk, particularly because in up to 50% of patients SCA may be the initial manifestation of cardiac disease.2 It is this group of patients who are concealed within the general population that contemporary state-of-the-art research is targeting to identify reliable predictors of SCA.

Left ventricular ejection fraction (LVEF) remains the key parameter currently used for risk stratification of SCD. Implantation of internal cardioverter defibrillators (ICDs) in patients with SHD and LVEF less than or equal to 35% provides a survival benefit.14,15 Accordingly, the presence of severe left ventricular dysfunction is the chief determinant of whether or not ICD for primary prevention of SCA is implanted. However, LVEF has limited effectiveness in providing a reliable assessment of risk, leading to both underuse and overuse of
ICDs. A small proportion of subjects with ICDs receive appropriate anti-tachycardia pacing and defibrillation therapies. Only 1% to 5% of patients with an ICD require device therapy each year, and up to 65% of patients implanted with ICDs will not receive an appropriate therapy over the 3-year period after device implantation.16 Similarly, 15% to 18% of biventricular defibrillator recipients do not require appropriate ICD therapies over a 2.4-year follow-up.17 In addition, up to 70% of all SCDs occur in individuals with LVEF greater than 35%, with half of these individuals having a normal LVEF.18 None of these subjects qualify for an ICD based on current implantation criteria. Perhaps the risk of SCD associated with LVEF less than or equal to 35% should not be viewed as a binary parameter but rather as a continuous variable over a range of values.

A number of parameters outside of LVEF have been suggested for risk stratification of SCD, but none is superior to LVEF as a predictor. Part of the challenge is that most of these parameters—both individually and in combination—predict overall cardiovascular mortality and are not specific for SCD. Moreover, the low magnitude of the predictive value (1.5- to 3-fold) of proposed non-LVEF risk factors substantially limits their clinical utility.19

The electrocardiogram (ECG) is an inexpensive and widely available test that can help detect signs of CAD and assess QRS morphology as well as QT interval. In a Spanish study of those over the age of 40 years, between 0.6% and 1.2% of individuals had ECG features that portended an increased risk of SCD, including long or short QT interval or spontaneous Brugada type 1 pattern. Moreover, when borderline ECGs were added (QT interval between normal and overtly abnormal as well as Brugada type 2 pattern), the prevalence increased to 8.3%.20 The ECG parameters associated with a higher risk of SCD are summarized in Table 62.1.19

Various imaging modalities, such as echocardiography, cardiac magnetic resonance imaging (CMR), positron emission tomography (PET), and others, allow detailed characterization of the pathologic myocardial substrate to aid in the assessment of the individual risk of SCA (see Table 62.2). The primary CMR finding associated with increased risk of SCA is the presence and extent of a left ventricular scar.21 Several echocardiographic parameters have also been linked to increased risk of SCD, ventricular tachyarrhythmias, and ICD therapies. These include the presence of LVH and abnormal longitudinal strain.21,22 The PET evidence of sympathetic denervation has
predictive value for SCA in ischemic cardiomyopathy ischemic cardiomyopathy (ICM), whereas perfusion defects and the presence of inflammation have been associated with ventricular tachyarrhythmias in cardiac sarcoidosis.23

A number of biomarkers, including C-reactive protein, B-natriuretic peptide, and nonesterified fatty acids (n-3 fatty acids), as well as decreased serum calcium level, have been linked to an increased risk of SCD in both men and women.24,25

Finally, as illustrated in Table 62.1, impaired cardiac autonomic activity, including decreased heart rate variability and heart rate turbulence as well as diminished baroreflex sensitivity, has been shown to predict not only cardiovascular mortality but also increased risk of SCA and ventricular tachyarrhythmias specifically, as reported in patients after myocardial infarction (MI) and in the setting of congenital heart disease.26 Overall, using a combination of these clinical, genetic, autonomic, imaging, and ECG parameters may provide increasingly incremental value in risk stratification for SCA compared to LVEF alone.


Historically, VT and VF were implicated in the majority of SCA events. Bradyarrhythmias, such as high-grade atrioventricular block without sufficient escape rhythm leading to asystole, are responsible for approximately 10% of cardiac arrests.2
Catecholamine surge occurring during SCA worsens ventricular tachyarrhythmias but tends to be beneficial in the setting of bradycardia, increasing the rate of the escape rhythm. Pulseless electrical activity (PEA) was the third most common mechanism of SCA. However, temporal trends show a decrease in the incidence of ventricular tachyarrhythmias and an increase in PEA and asystole as a cause of SCD.2 Reduction in arrhythmic death can be attributed to efforts targeting cardiovascular risk factors, advances in the medical treatment of CAD, and timely coronary reperfusion, as well as widespread use of ICDs. On the contrary, the rise in the incidence of PEA mirrors an increase in population aging and higher prevalence of patients with advanced heart failure.27

Ventricular tachyarrhythmias can manifest as monomorphic VT, polymorphic VT, or VF. Monomorphic VT usually occurs in the presence of a myocardial scar that has formed after a previous ischemic injury. Cardiac fibrosis, interspersed with channels of surviving myocardium within scar and border zone regions, is a typical example of the pathologic substrate. Slow electrical conduction in the border zone predisposes to the formation of reentry circuits and subsequent VT. Border zones can also serve as sites of premature ventricular complexes (PVCs) that trigger VT initiation. A rare form of monomorphic VT that utilizes right and left bundle branches or left fascicles of the electrical conduction system as a reentry circuit is called bundle branch reentry VT. It accounts for 5% to 8% of all monomorphic VTs in SHD. It is usually very rapid and tends to occur in patients with severely diseased hearts, such as those with dilated cardiomyopathy.

Polymorphic VT usually occurs in the setting of acute ischemia, inflammation, serum electrolyte abnormalities, QT interval prolongation, or autonomic nervous system imbalance. Catecholaminergic polymorphic VT is a rare disease caused by mutations in the ryanodine receptor or calsequestrin genes. It manifests as exercise- or stress-induced polymorphic VT without underlying QT prolongation.

Both monomorphic VT and polymorphic VT may accelerate and degenerate into VF. VF can also occur as the primary ventricular tachyarrhythmia. VF is characterized by chaotic multiple areas of microreentry and rotating spiral waves. Heterogeneity of depolarization and dispersion of repolarization serve as underlying conditions for VF.

Most ventricular tachyarrhythmias are initiated by a PVC trigger. In one-third of cases, it is an early PVC, falling on the T wave of the preceding QRS complex (R on T phenomenon). In two-thirds of instances, a late PVC triggers ventricular tachyarrhythmias.


As the definition of SCA suggests, patients present pulseless in a state of complete hemodynamic collapse. Patients with shockable rhythms are found to have ventricular tachyarrhythmias, whereas those with nonshockable rhythms have either asystole or PEA. Although survival after SCA is generally poor, shockable rhythms have better outcomes compared to nonshockable rhythms (25%-40% vs <5%, respectively).1 Analysis of SCA data from 648 patients from the Oregon Sudden Unexpected Death Study showed that the type of heart failure was associated with the presenting rhythm at the time of the arrest. Patients with heart failure with reduced ejection fraction with LVEF less than or equal to 40% and borderline heart failure with preserved ejection fraction with LVEF 41% to 49% were more likely (2 and 2.5 times, respectively) to present with shockable rhythms compared to those with heart failure with preserved ejection fraction with LVEF ≥50%. Only 27% of individuals with heart failure with preserved ejection fraction and cardiac arrest presented with a shockable rhythm. Individuals with heart failure with preserved ejection fraction also had the lowest rates of survival to hospital discharge of 9.9%.28

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May 8, 2022 | Posted by in CARDIOLOGY | Comments Off on Sudden Cardiac Arrest
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