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Sudden Death: Death Be Not Proud

4.00 Contact Hours
  • 0% complete
A score of 80% correct answers on a test is required to successfully complete any course and attain a certificate of completion.
Author:    Pamela Downey (MSN, ARNP)


The purpose of this continuing education course is to enable the participants to understand the cardiac and non-cardiac causes of SCA/SCD and to recognize the importance of appropriate management of survivors of SCA/SCD. Primary and secondary prevention of another SCA/SCD experience will be discussed, as well as, factors which influence the outcome of such an event.


Upon completion of this course, the participant will be able to:

  1. Differentiate between the terms sudden cardiac arrest (SCA) and sudden cardiac death (SCD).
  2. Familiarize acronyms with their meanings pertaining to SCA/SCD.
  3. Describe the epidemiology of and risk factors contributing to SCA/SCD.
  4. Relate the etiology of SCA/SCD in terms of structural heart disease, the absence of structural heart disease and other acute triggers.
  5. Describe the management issues relevant for survivors of SCA/SCD.
  6. Describe the initial evaluation of SCA/SCD survivors immediately after resuscitation.
  7. Discuss the history and physical examination, laboratory testing and ECG results of SCA/SCD survivors.
  8. Discriminate between the evaluation for structural heart disease and primary electrical disease and relevance of evaluating family members.
  9. Compare and contrast primary versus secondary prevention of SCA/SCD.
  10. Discuss the prognosis for survivors of SCA/SCD.
  11. Describe the outcomes following SCA/SCD according to etiology.
  12. Relate the factors affecting out-of-hospital versus in-hospital SCA/SCD outcomes.


Sudden cardiac arrest (SCA) and sudden cardiac death (SCD) refer to the sudden cessation of cardiac activity with hemodynamic collapse, typically due to sustained ventricular tachycardia (VT)/ventricular fibrillation (VF). These events mostly occur in patients with structural heart disease (that may not have been previously diagnosed), particularly coronary heart disease (CHD).

The event is referred to as SCA (or aborted SCD) if an intervention (e.g., defibrillation) or spontaneous reversion restores circulation, and the event is called SCD if the patient dies.1 However, the use of SCD to describe both fatal and nonfatal cardiac arrest persists by convention.

The specific causes of SCA vary with the population studied and patient age. SCA most commonly results from hemodynamic collapse due to VF in the setting of structural heart disease.2

The outcome following SCA depends upon numerous factors including the underlying cause and the rapidity of resuscitation.

Most individuals suffering from SCA become unconscious within seconds to minutes as a result of insufficient cerebral blood flow. There are usually no premonitory symptoms. If symptoms are present, they are nonspecific and include chest discomfort, palpitations, shortness of breath, and weakness.

Helpful Acronyms

SCA = Sudden cardiac arrest

SCD = Sudden cardiac death

Abnormal Cardiac Rhythms
AFAtrial fibrillationPVCPremature ventricular contraction
AVAtrioventricular blockSQTSShort QT syndrome
CPVTCatechaminergic polymorphic ventricular tachycardiaSVTSupraventricular tachycardia
LQTSLong QT syndromeVFVentricular fibrillation
NSVTNonsustained ventricular tachycardiaVTVentricular tachycardia
PEAPulseless electrical activityWPW Wolff-Parkinson-White
Cardiac/Noncardiac Diagnoses
ACSAcute coronary syndromeMIMyocardial infartion
ARVCArrhythmogenic right ventricularSTEMIST elevation MI
CHDCoronary heart diseaseNSTEMINon-ST elevation MI
CHFCongestive hear failure PTSDPosttraumatic stress disorder
CVDCardiovascular diseaseSIDSSudden infant death syndrome
HCMHypertrophic cardiomyopathySUDEPSudden unexplained death in epilepsy
HFHeart failureSUNDSSudden unexplained nocturnal death syndrome
Cardiac Interventions/Management
ACEAngiotensin-converting enzymeEMIElectromagnetic interference
AEDAutomated external difibrillatorEPElectrophysiologic
CABGCoronary artery bypass graftESUElectrosurgery unit
CCBCalcium channel blockerETTExercise tolerance testing
CMRCardiac magnetic resonance imagingICDImplantable cardioverter-defibrillator
CRPC-reactive proteinLVEFLeft ventricular carioverter-defibrillator
CRTCardiac resynchronization therapyMRIMagnetic resonance imaging
CRT-DCardiac resynchronization therapy defibrillatorPCIPercutaneous coronary intervention
DFTDefibrillation threshold testingS-ICDSubcutaneous coronary intervention
ECT ElectrocardiogramWCDWearable cardioverter-defibrillator
EMSEmergency medical servicesAHAAmerican Heart Association
BLSBasic life supportHRSHeart Rhythm Society
ALSAdvanced life supportLVLeft ventricular
CARESCardiac Arrest Registry to Enhance SurvivalPAPosteroanterior
ACCAmerican College of CardiologyIVIntravenous


Various criteria have been used to define SCA and SCD in the medical literature.3 Difficulties in deriving a specific definition include the following:

  • Events are witnessed in only two-thirds of cases, making the diagnosis difficult to establish in many instances.
  • It is not possible to restrict the definition of SCA to documented cases of VF since the cardiac rhythm at clinical presentation is unknown in many cases.
  • The duration of symptoms prior to SCA generally defines the suddenness of death. However, the duration of symptoms is unknown in approximately one-third of cases.

For these reasons, operational criteria for SCA and SCD have been proposed that do not rely upon the cardiac rhythm at the time of the event. These operational criteria focus on the out-of-hospital occurrence of a presumed sudden pulseless condition and the absence of evidence of a noncardiac condition (e.g., central airway obstruction, intracranial hemorrhage, pulmonary embolism, etc.) as the cause of cardiac arrest.

The 2006 ACC/AHA/HRS established data standards for electrophysiology including definitions to guide documentation in research and clinical practice.

The following definitions of SCA and SCD were presented:

"SCA 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 death. Cardiac arrest should be used to signify an event that is reversed, usually by CPR and/or defibrillation or cardioversion, or cardiac pacing. Sudden cardiac death should not be used to describe events that are not fatal.1"

The terms SCA and SCD as defined in the 2006 ACC/AHA/HRS will be used throughout this course. However, many continue to use SCD to describe both fatal and nonfatal cardiac arrest.


Death certificate data suggest that SCD accounts for approximately 15% of the total mortality in the United States and other industrialized countries.4 However, death certificate data may overestimate the prevalence of SCD.5,6 In a prospective evaluation of deaths in one county in Oregon, SCD was implicated in 5.6% of annual mortality.5

In absolute terms, the estimated number of SCDs in the United States in 1999 was approximately 450,000.7 Despite advances in the treatment of heart disease, the outcome of patients experiencing SCA remains poor, although the prognosis varies significantly according to the initial rhythm.

A number of factors increase the risk of experiencing SCA.4,6,8 The incidence of SCA increases:

  • Dramatically with age in both men and women8,9
    • During a 38-year follow-up of subjects in the Framingham Heart Study, the annual incidence of sudden death increased with age in both men and women. However, at each age, the incidence of sudden death is higher in men than women.
  • Dramatically with sex
    • Men are two to three times more likely to experience SCA than women.
    • Nearly one-half of women who experienced SCD did not have prior clinically-recognized CHD.8,10
  • With underlying cardiac disease
    • During a 38-year follow-up of subjects in the Framingham Heart Study, the annual incidence of SCD in both men and women was related to the clinical manifestations of CHD. SCD was highest in those with a myocardial infarction, intermediate in those with angina and no prior infarction, and lowest in those without overt CHD.8
    • The magnitude of the influence of underlying cardiac disease on the risk of SCA is illustrated by the following observations:
      • The risk of SCA is increased 6- to 10-fold in the presence of clinically recognized heart disease, and two- to four-fold in the presence of CHD risk factors.6,10
      • SCD is the mechanism of death in over 60% of patients with known CHD.4,7,11
      • SCA is the initial clinical manifestation of CHD in approximately 15% of patients.11,12,13


SCA usually occurs in individuals with some form of underlying structural heart disease, most notably CHD.

Coronary Heart Disease (CHD)

Sixty-five to 70% of all SCDs are attributable to CHD.7,14 However, the frequency of CHD is much lower in SCDs occurring under the age of 30 to 40 (e.g., 24% under the age of 30 in a review of SCDs in the United States in 1999, and 8% series of autopsies in military recruits).7,14

These observations were largely made from analyses of all reported SCDs in the United States using the diagnosis on the death certificate, which is of uncertain accuracy. A similar frequency of CHD was noted in a study of 84 consecutive survivors of out-of-hospital cardiac arrest.15 Immediate coronary angiography revealed clinically significant coronary disease in 60 (71%) of the patients, 40 of whom (48% of all patients) had an occluded coronary artery. The absence of an occluded coronary artery in the other 20 patients does not preclude an ACS (or ischemia) since absence of occlusion on early angiography is seen in 60 to 85% of patients with a NSTEMI ACS and in up to 28% of patients with a STEMI.

Although not specifically mentioned in most of these studies, heart failure (HF) is a relatively common cause of SCD. SCD accounts for 30 to 50% of deaths in patients with HF,16 and the incidence of SCD appears to be increased during periods of worsening HF symptoms.17 Although the risk of both arrhythmic and nonarrhythmic death can be reduced with appropriate chronic HF therapy, the SCD risk remains elevated. Thus, virtually all SCD survivors with HF receive an implantable cardioverter-defibrillator (ICD).

Examples of CHD (ischemic heart disease) include the following:

  • Coronary artery disease with myocardial infarction or angina
  • Coronary artery embolism
  • Nonartherogenic coronary artery disease (arteritis, dissection, congenital coronary artery anomalies)
  • Coronary artery spasm

Other Structural Heart Disease (Nonischemic Heart Disease)

Other forms of structural heart disease, both acquired and hereditary, account for approximately 10% of cases of out-of-hospital SCA.4,7,14 The frequency is much higher in subjects under the age of 30 (over 35% in a review of SCDs in the United States in 1999, and over 40% in a series of autopsies in military recruits).7,14

Examples of such disorders include the following:

  • Acute pericardial tamponade
  • Acute myocardial rupture
  • Aortic dissection
  • Congenital coronary artery anomalies
  • HF and cardiomyopathy in which SCD is responsible for approximately one-third of deaths.
  • Dilated cardiomyopathy
  • Hypertrophic cardiomyopathy
  • Arrhythmogenic right ventricular dysplasia/arrhythmogenic right ventricular cardiomyopathy (ARVC)
  • Left ventricular hypertrophy due to hypertension or other causes
  • Myocarditis
  • Mitral valve prolapse

No Structural Heart Disease

In different reports, approximately 10 to 12% of cases of SCA among subjects under age 45 occur in the absence of structural heart disease.18,19 while a lower value of about 5% has been described when older patients are included.5,20,26

Several major diseases must be considered as possible causes of SCD in patients without evidence of structural heart disease.21 Many of these disorders are familial and therefore are associated with an increased risk of SCD in first-degree relatives.

Brugada Syndrome

  • The Brugada syndrome is characterized by the electrocardiographic (ECG) findings of right bundle branch block and ST-segment elevation in leads V1 to V3 and an increased risk of SCD.
  • Brugada syndrome is due to a functional abnormality in repolarization. There may be some overlap with an early subclinical manifestation of ARVC.
  • The Brugada syndrome occurs in families, with genetic transmission consistent with autosomal dominant inheritance with variable penetrance. Mutations in the cardiac sodium channel gene, SCN5A, have been found in several families.
  • A sudden unexpected nocturnal death syndrome (SUNDS) has also been described in young, apparently healthy males from Southeast Asia. This disorder is closely related and indeed may be the same as Brugada syndrome since a majority of affected patients have the ECG manifestations of the Brugada syndrome and the same mutations in the sodium channel gene.
  • Different mutations of the same SCN5A gene have been found in a number of cardiac disorders, including the long QT syndrome, and a unique allele found in African Americans, Y1102.

Commotio Cordis (Chest Wall Trauma)

  • Commotio cordis is defined as SCD secondary to a relatively innocent chest wall impact due to VF. Affected patients have no underlying heart disease and there is no structural damage to the chest wall, thoracic cavity, or the heart.
  • Early defibrillation of commotio victims is lifesaving, despite historical evidence that resuscitation may be more difficult in commotio cordis than in other forms of SCD.

Early Repolarization Syndrome

  • Early repolarization pattern on an ECG is common.
  • Studies have shown a higher frequency of early repolarization in SCA survivors without apparent heart disease.22 These survivors tended to have increased incidences of recurrent VF compared with those SCA survivors with normal hearts and no early repolarization.
  • Early repolarization in the inferior and lateral leads is associated with an increased risk of SCA. However, large population studies continue to describe a 5 to 10% incidence of early repolarization, and when found in the absence of a SCA it is thought to be benign.23
  • Early repolarization ECG pattern is especially common in athletes, and in these individuals it is generally benign.24 An expert consensus panel does not recommend any specific treatment for those with early repolarization without SCA.25

Familial SCD of Uncertain Cause

  • A family history of SCD in the absence of apparent structural heart disease is associated with an increased risk for primary SCD.26-28
  • It has been estimated that the adjusted relative risk for SCD, compared with controls, is 1.6 to 1.8 in individuals without apparent structural heart disease in whom a first-degree relative had SCD.26,27
  • The absolute increase in risk is quite small since primary SCD is rare in the general population. The increase in risk is incompletely understood.
    • Some of these families have an inherited cardiac disease, as illustrated in a report in which 147 first-degree relatives of 32 patients with SCD underwent a detailed cardiac assessment.36 Seven (22%) of the 32 families had an inherited cardiac disease, including four with LQTS, one with myotonic dystrophy, and one with hypertrophic cardiomyopathy.
    • Genome-wide association studies have demonstrated an increased risk with several loci.29

Idiopathic VF (Primary Electrical Disease)

  • If all of the above disorders are excluded, and the heart is structurally normal, the diagnosis of primary electrical disease is made.20,21,30 More commonly referred to as idiopathic VF, this entity is estimated to account for 5% of cases of SCD.20
  • In a review of 54 published cases with presumed idiopathic VF, the mean age was 36 years with a male-to-female ratio of 2.5-to-1.30 A history of syncope preceded the episode of VF in 25%. In a meta-analysis of 639 patients with idiopathic VF from 23 studies, among whom 80% had an ICD for secondary prevention, 31% of patients had recurrent ventricular arrhythmias over a mean follow-up of five years.31

Long QT Syndrome (LQTS)

  • Long QT can be primary (genetic/inherited), i.e., Long QT Syndrome (LQTS) or secondary (acquired). It may be associated with a specific form of polymorphic VT called torsades de pointes. Among patients with inherited LQTS, the precipitating factors and prognosis vary with the genetic abnormality.
  • The majority of secondary causes of a prolonged QT interval result from an interaction with a drug/electrolyte which interferes with an ion channel involved in repolarization, the same ion channels involved in the LQTS. Most of the pharmaceutical agents which increase the QT interval are prescription drugs such as antipsychotics, anti-emetics, quinolones, antiarrhythmics, and methadone.32

Short QT Syndrome (SQTS)

  • SQTS is an extremely rare inherited channelopathy associated with markedly shortened QT intervals and SCD in individuals with a structurally normal heart.
  • In contrast to LQTS, ion channel defects associated with SQTS lead to abnormal abbreviation of repolarization, predisposing affected individuals to a risk of atrial and ventricular arrhythmias.

Polymorphic Ventricular Tachycardia with Normal QT Interval

  • Polymorphic VT with a normal QT interval is largely caused by:
    • Acute cardiac ischemia or
    • Catecholaminergic polymorphic VT (CPVT)
  • Ischemia is the cause in the majority of these patients necessitating prompt evaluation for cardiac ischemia.
  • In those without cardiac ischemia, CPVT, an inherited channelopathy, may be the cause.
    • Affected patients typically present with life-threatening VT or VF occurring during emotional or physical stress, with syncope often being the first manifestation of the disease.
    • Although sporadic cases occur, this is a largely familial disease. The majority of known cases are due to mutations in the cardiac ryanodine receptor, which is the cardiac sarcoplasmic calcium release channel. One report suggested that this disorder may account for at least one in seven cases of sudden unexplained death.33

Third Degree (Complete) AV Block

  • Third Degree AV Block is defined as a blockage which occurs in the AV junction where no atrial impulses reach the ventricles.
  • The potential etiologies of third-degree AV block are similar to lesser degrees of AV block and include reversible causes:
    • Pathologic causes include:
      • Cardiomyopathy (e.g., amyloidosis, sarcoidosis)
      • Endocarditis with abscess formation
      • Hyperkalemia
      • Hypervagotonia
      • Infiltrative malignancies
      • Myocardial ischemia (acute or chronic) involving the conduction system
      • Myocarditis (e.g., Lyme disease)
      • Neuromuscular diseases
    • Iatrogenic causes include:
      • Medication-related (AV nodal blocking medications)
      • Post-cardiac surgery
      • Post-catheter ablation
      • Post-transcatheter aortic valve implantation
    • Idiopathic causes include:
      • Progressive cardiac conduction disease with myocardial fibrosis and/or sclerosis that affects the conduction system.

VF Secondary to Premature Ventricular Contractions (PVCs)

Short coupled PVCs have been described as a trigger of VF.34 Generally these arise from the Purkinje fibers, but PVCs from papillary muscles have also been described to trigger VF. Ablation of these triggering PVCs may eliminate recurrent episodes of VF.35

Wolff-Parkinson-White (WPW) Syndrome and other Forms of Supraventricular Tachycardia (SVT)

  • Both WPW syndrome and, very rarely, other forms of SVT can cause SCD.
  • The frequency with which this occurs was assessed in a report of 290 patients with aborted SCD. The mechanism was an arrhythmia associated with the WPW syndrome in 2.1% and atrial fibrillation (AF) with a rapid ventricular response which was the most common.36 A similar incidence of preexcitation (3.6%) was noted in a report of 273 children and young adults with SCD.37
  • Most patients who have been resuscitated from VF secondary to preexcitation have a previous history of syncope, atrioventricular reciprocating tachycardia, and/or AF.38 However, preexcitation and arrhythmias have been previously undiagnosed in up to 25% of such patients.39,40
  • Among patients with WPW syndrome who survive an episode of SCD, ablation of the accessory pathway is the treatment of choice.

Noncardiac Disease

Fifteen to 25% of cardiac arrests are noncardiac in origin.21,41

Noncardiac disease triggers for SCA/SCD include:

  • Autonomic nervous system activation
  • Bleeding
  • Central airway obstruction
  • Drug intoxication
  • Electrolyte disturbances (particularly hypokalemia and hypomagnesemia)
  • Intracranial hemorrhage
  • Ischemia
  • Near-drowning
  • Pickwickian syndrome
  • Pulmonary embolism
  • Proarrhythmic effect of some antiarrhythmic drugs
  • Psychosocial factors
  • Sudden infant death syndrome (SIDS)
  • Sudden unexplained death in epilepsy (SUDEP)
  • Trauma

Warning Symptoms

"Warning" symptoms may precede the SCA event in a large number of individuals, but symptoms may be unrecognized or minimized by them thus limiting the discovery of the symptoms especially in those who do not survive the event. In addition, individuals who have SCA and are often resuscitated have retrograde amnesia and thus do not remember events or symptoms that may have been present.

In a community-based study of 839 individuals with SCA between 2002 and 2012 in whom symptom assessment could be ascertained (either from the surviving patient or from family members, witnesses at the scene of the event, or medical records from the four weeks leading up to the event), results showed42:

  • 430 patients (51%) were identified as having warning symptoms within four weeks preceding their SCA.
  • Eighty percent of patients experienced symptoms at least one hour before SCA, with 34% having symptoms more than 24 hours before SCA.
  • Chest pain (46%) and dyspnea (18%) were the most common symptoms, with women more likely to have experienced dyspnea than chest pain (31% versus 24%).

Recommendations from this study proposed that patients with symptoms concerning for cardiac disease, particularly new or unstable symptoms, should seek prompt medical care for potentially life-saving evaluation and treatment.

As symptoms are nonspecific and may reflect benign conditions, and as these symptoms may not necessarily occur before all episodes of SCA (insensitive), their presence may not be of value in helping offset or prevent episodes. A causal or temporal relationship between symptoms and SCD has not been established.

Risk Factors

A number of clinical characteristics and other factors are associated with an increased risk of SCA among individuals without prior clinically recognized heart disease.26,43-47 Most risk factors for CHD are also risk factors for SCA. These include10,26,27,43,44,48:

  • A family history of premature CHD and SCA
  • Cigarette smoking
  • Diabetes mellitus
  • Dyslipidemia
  • History of myocardial infarction
  • Hypertension
  • Obesity
  • Physical inactivity

Cigarette Smoking

Current cigarette smoking and the number of cigarettes smoked per day among current smokers are strongly related to the risk of SCA in patients with CHD. For example:

  • Among 101,018 women followed for 30 years in the Nurses' Health Study, current smokers had a significantly greater risk of SCD than women who had never smoked.49
  • There was an increased risk even among those women who smoked 1 to 14 cigarettes per day.
  • For women in this study who stopped smoking, the risk of SCD declined over time in a linear fashion. These women had the same risk of SCD as women who never smoked 20 years after quitting.

Based upon the observations that the risk of SCA is particularly high among current smokers and declines rapidly after stopping smoking, smoking cessation should be viewed as a critical component of efforts to reduce the risk of SCA, as well as, a multitude of other complications.


The risk of SCA is transiently increased during and up to 30 minutes after strenuous exercise compared to other times.44,50 However, the actual risk during any one episode of vigorous exercise is very low (1 per 1.51 million episodes of exercise).50 Furthermore, the magnitude of the transient increase in risk during acute exercise is lower among men who are regular exercisers compared with men for whom exercise is unusual.44,50

The small transient increase in risk during exercise is outweighed by a reduction in the risk of SCA at other times.43,51 Regular exercise is associated with a lower resting heart rate and increased heart rate variability, characteristics associated with a reduced risk of SCD.

One exception to the lower overall risk associated with intensive exercise occurs in patients with certain, often unrecognized underlying heart diseases. Examples include hypertrophic cardiomyopathy, anomalous coronary artery of wrong sinus origin, myocarditis, and ARVC.26,52

Family History of SCA

A family history of SCA, either alone or with myocardial infarction, is associated with a 1.5 to 1.8-fold increased risk of SCA.26,27 The increase in risk is not explained by traditional risk factors that tend to aggregate in families, such as hypercholesterolemia, hypertension, diabetes mellitus, and obesity.

The magnitude of the increase in risk associated with the presence of a family history is modest compared to the two- to five-fold increase in risk associated with other modifiable risk factors such as physical inactivity and current cigarette smoking. Few studies have examined potential gene-environment interactions related to the risk of SCD. Nevertheless, it is likely that interactions of mutations or polymorphisms in specific genes and environmental factors influence this risk.

Serum C-Reactive Protein (CRP)

Chronic inflammation, as manifested in part by higher serum concentrations of CRP, has been implicated as a risk factor for a variety of cardiovascular diseases (including ACS and stroke). Elevated serum CRP is also associated with an increased risk of SCA.54

Excess Alcohol Intake

Moderate alcohol intake (e.g., one to two drinks per day, and avoidance of binge drinking) may decrease the risk of SCD.55 In comparison, heavy alcohol consumption (six or more drinks per day) or binge drinking increases the risk for SCD.55,56

Psychosocial Factors

Clinical observations have suggested a possible relation between acutely stressful situations and the risk of SCA. Major disasters, such as earthquakes and war, result in a rapid transient increase in the rate of SCA in populations.45,46 The level of educational attainment and social support from others may alter the risk associated with stressful life events.


Excessive caffeine intake has been investigated as a potential risk factor for SCA.57 In the limited data available, no significant association between caffeine intake and SCA has been found.

Fatty Acids

Elevated plasma nonesterified fatty acid (free fatty acid) concentrations were associated with ventricular arrhythmias and SCD after a myocardial infarction.58 However, nonesterified fatty acids were not associated with SCD in the Cardiovascular Health Study, a population-based cohort of older adults.59 In addition, in a population-based case-control study among individuals without prior clinically recognized heart disease, SCA cases had higher concentrations of trans isomers of linoleic acid in red blood cell membranes.60 In contrast, higher dietary intake and higher levels of long-chain n-3 polyunsaturated fatty acids (eicosapentaenoic acid and docosahexaenoic acid) in plasma and the red blood cell membrane are associated with a lower risk of SCD.47,61-63


Management issues for survivors of SCA include the following:

  • Identification and treatment of acute reversible causes
  • Evaluation for structural heart disease
  • An evaluation for primary electrical diseases in patients without obvious arrhythmic triggers or cardiac structural abnormalities
  • Neurologic and psychologic assessment
  • Evaluation of family members in selected patients with a suspected or confirmed hereditary syndrome

Initial Evaluation

The evaluation begins immediately after resuscitation. The highest priority is to exclude any obvious reversible factors that may have led to the event (Table 1).

Table 1: Treatable Conditions Associated with Cardiac Arrest
ConditionCommon Associated Clinical Setting64
AcidosisDiabetes, diarrhea, drug overdose, renal dysfunction, sepsis, shock
AnemiaGastrointestinal bleeding, nutritional deficiencies, recent trauma
Cardiac TamponadePost-cardiac surgery, malignancy, post-myocardial infarction, pericarditis, trauma
HyperkalemiaDrug overdose, renal dysfunction, hemolysis, excessive potassium intake, rhabdomyolysis, major soft tissue injury, tumor lysis syndrome
Hypokalemia*Alcohol abuse, diabetes mellitus, diuretics, drug overdose, profound gastrointestinal losses
HypothermiaAlcohol intoxication, significant burns, drowning, drug overdose, elderly patient, endocrine disease, environmental exposure, spinal cord disease, trauma
HypovolemiaSignificant burns, diabetes, gastrointestinal losses, hemorrhage, malignancy, sepsis, trauma
HypoxiaUpper airway obstruction, hypoventilation (CNS** dysfunction, neuromuscular disease), pulmonary disease
Myocardial InfarctionCardiac arrest
PoisoningHistory of alcohol or drug abuse, altered mental status, classic toxidrome (e.g., sympathomimetic), occupational exposure, psychiatric disease
Pulmonary EmbolismImmobilized patient, recent surgical procedure (e.g., orthopedic), peripartum, risk factors for thromboembolic disease, recent trauma, presentation consistent with acute pulmonary embolism
Tension PneumothoraxCentral venous catheter, mechanical ventilation, pulmonary disease (e.g., asthma, chronic obstructive pulmonary disease), thoracentesis, thoracic trauma

* Hypomagnesemia should be assumed in the setting of hypokalemia, and both should be treated.

**CNS: central nervous system.

History and Physical Examination

  • The patient (if conscious) and family should be questioned, with particular attention to the following:
    • Prior diagnoses of heart disease
    • Use of any medications, especially antiarrhythmic drugs, diuretics, and drugs that might produce LQTS
    • Ingestion of toxins or illicit drugs
    • Antecedent symptoms, especially evidence of ischemia
    • Antecedent stressful events or activities
  • A coherent history may not be obtainable since the cardiac arrest is frequently unwitnessed and, in addition, the patient resuscitated from VF often has retrograde amnesia and is unable to remember what occurred prior to the cardiac arrest.

Laboratory Testing

  • Immediate evaluation should include standard laboratory testing to exclude electrolyte abnormalities and, in many cases, an arterial blood gas to exclude acidosis. Any reversible metabolic abnormalities should be identified and corrected, particularly hypokalemia and hypomagnesemia which can predispose to ventricular tachyarrhythmias.65,66
  • Two important limitations should be considered when interpreting the test results:
  1. Electrolyte abnormalities during and shortly after resuscitation may be secondary to cardiac arrest and hypoperfusion rather than a cause of SCD.67
  2. Electrolyte abnormalities by themselves are usually insufficient to cause SCD. Clinical settings that increase the proarrhythmic effect of hypokalemia and hypomagnesemia include acute myocardial infarction, overt HF, and LQTS.68
  • It is potentially hazardous to ascribe a cardiac arrest to an electrolyte or metabolic derangement alone, unless there is compelling evidence of an association. Mistaken attribution of a major arrhythmia to an innocent or merely potentiating laboratory abnormality can place the patient at high risk if appropriate therapy to prevent recurrent SCD is delayed or not given. Importantly, electrolyte and pH abnormalities may be secondary to the arrhythmia itself.
  • This risk was illustrated in a review of 169 patients treated with an ICD for sustained ventricular arrhythmia in whom the plasma potassium concentration was measured on the day of the arrhythmia.69 The likelihood of a recurrent sustained ventricular arrhythmia was 82% at five years. The long-term risk was similar in patients with low, normal, and high plasma potassium concentrations at presentation.

Electrocardiogram (ECG)

  • An ECG can reveal evidence of both acute abnormalities and chronic conditions. It should be part of the immediate evaluation and repeated as necessary once the patient's cardiac, hemodynamic, and metabolic condition stabilizes.70 The ECG should be evaluated for evidence of the following:
    • Ongoing ischemia or prior myocardial infarction
    • Conduction system disease, including bundle branch block, second-degree heart block, and third-degree heart block
  • Less common abnormalities that also may be evident include:
    • ARVC suggested by VT or ventricular ectopy with a left bundle branch block configuration and an inferior axis. In addition, abnormalities of the baseline QRS may be present, including an epsilon wave in the right precordial leads
    • Brugada syndrome, evidenced by a pseudo-RBBB and persistent ST segment elevation in V1 to V3
    • Hypertrophic cardiomyopathy
    • LQTS, possibly with torsades de pointes
    • WPW syndrome, evidenced by a short PR interval and a slurred QRS complex upstroke

Evaluation for Structural Heart Disease

Excluding patients with an obvious noncardiac etiology (e.g., trauma, hemorrhage, pulmonary embolus, etc.), structural heart disease is present in up to 90% of patients with SCD.4,5,7,15,18,20,41

All survivors of SCD should undergo a complete cardiac examination to determine the nature and extent of underlying heart disease. The initial history, physical examination, and laboratory tests may provide evidence of one of these disorders, but further testing is usually necessary to confirm a diagnosis.

The standard evaluation typically includes:

  • ECG
  • Cardiac catheterization with coronary angiography
  • Echocardiography

In the appropriate clinical setting, coronary angiography and echocardiography may be part of an urgent initial evaluation.

In selected patients, cardiac magnetic resonance imaging (MRI) and, rarely, myocardial biopsy are performed.

Coronary Angiography

  • Coronary angiography is performed in most survivors of SCD for one of two indications:
  1. Management of an ACS
    • SCD may be the presenting manifestation of an ACS. Among patients with an ACS, malignant arrhythmias are significantly more common in the setting of an acute ST elevation MI (STEMI) but are also seen in approximately 2% of patients with a non-ST elevation MI (NSTEMI). In patients with an ACS and ischemia, the arrhythmia is usually polymorphic VT, rapid ventricular flutter, or VF.
    • Any patient with evidence of a confirmed or suspected STEMI or NSTEMI following resuscitation from SCD should undergo urgent cardiac catheterization and primary percutaneous coronary intervention (PCI) or in some cases surgical revascularization as appropriate.
    • Patients who experience SCD during the first 48 hours after a STEMI have a higher in-hospital mortality compared with STEMI patients who do not experience sustained VT or VF. However, among patients who survive to hospital discharge, there is little or no difference in mortality at one to two years.
  2. Diagnosis of chronic CHD
    • Diagnostic angiography
      • In SCD survivors without an ACS, angiography is still considered to exclude stable, chronic CHD, which is the leading cause of SCD.70 Malignant arrhythmias and SCD occur in such patients, usually those who have had a prior infarction with residual myocardial scarring. In contrast to patients with an ACS, the culprit arrhythmia is usually scar-related monomorphic VT, which is not the result of ischemia. However, monomorphic VT can ultimately degenerate to VF, particularly if the arrhythmia induces ischemia. Because SCD may be the first clinical evidence of chronic CHD, most SCD survivors undergo diagnostic angiography prior to discharge.
  • Even for patients arriving at the hospital in refractory VT/VF who are receiving ongoing CPR, immediate coronary angiography appears beneficial in a carefully selected group of patients (18 to 75 years of age with VT/VF as initial rhythm who received three shocks and amiodarone loading dose and who can be in the catheterization lab in <30 minutes post-arrest).71
  • Diagnostic coronary angiography may not be necessary for selected patients without signs or symptoms of CHD if another clear cause for SCD is identified (e.g., LQTS, WPW, Brugada, HCM, left ventricular noncompaction, or ARVC).
  • Angiography is suggested in younger patients without an apparent cause for SCD in whom angiography may also detect an anomalous origin of a coronary artery. Among competitive athletes under age 35, anomalous origin of a coronary artery was present in 13% of SCD survivors in one series.63
  • Patients with stable CHD who experience an episode of primary SCD without evidence of simultaneous ischemia are at high risk for recurrent malignant arrhythmias, even after percutaneous or surgical revascularization.72-75 As a result, such patients are treated with an ICD.


  • Echocardiography can detect abnormalities that suggest or confirm the diagnosis of many of the important causes of SCD. Since global left ventricular dysfunction due to myocardial stunning can be induced by cardiac arrest and cardiopulmonary resuscitation, evaluation of left ventricular function should be performed at least 48 hours after resuscitation.76
  • Potential causes of SCD that can be detected with echocardiography include the following:
    • Aortic stenosis
    • ARVC
    • CHD – Left ventricular dysfunction with wall motion abnormalities suggest prior myocardial infarction. Dyskinetic wall motion is consistent with an aneurysm.
    • Dilated cardiomyopathy
    • HCM

Cardiac Magnetic Resonance Imaging (CMR)

  • CMR is indicated for selected patients in whom a diagnosis is uncertain after the above evaluation.
  • CMR is useful in the evaluation of the following disorders:
    • ARVC
    • Cardiac amyloidosis
    • Cardiac sarcoidosis
    • Congenital heart disease, including anomalous origin of coronary arteries
    • Dilated cardiomyopathy
    • HCM
    • Myocarditis
  • The utility of CMR angiography as an alternative to invasive coronary angiography is not well defined. Alternatively, cardiac computed tomography angiography may be used to assess both congenital and acquired coronary abnormalities.

Evaluation for Primary Electrical Diseases

General Issues

  • Approximately 5 to 10% of SCD survivors have no evidence of a noncardiac etiology or of structural heart disease after the above evaluation. Such patients are considered to have a primary electrical disorder.
  • The majority of these patients do not actually have "normal" hearts, but historically diagnostic tools have been unable to identify the structural or functional derangement. In the past, the etiology of many of these deaths was unknown and termed "idiopathic." Subsequent discoveries have identified the cause of death in many of these patients.5,29,77 As understanding of the mechanisms of primary electrical disorders has improved, so have diagnostic capabilities, with important benefits for both the victims of SCD and their families.
  • These disorders are often detected by characteristic changes on an ECG.
  • Several of the disorders that cause SCD in the absence of structural heart disease are due to abnormalities of cardiac ion channels, including the following:
    • Brugada syndrome
    • CPVT
    • LQTS
    • SQTS
  • Disorders associated with SCD that are not due to ion channel abnormalities include:
    • WPW syndrome
    • Commotio cordis
  • Patients without evidence of any of the above structural or electrical abnormalities are said to have idiopathic VF or primary electrical disease.
  • Identification of a primary electrical disorder in a SCD survivor has two important benefits:
  1. Directing medical treatment to prevent arrhythmia recurrence (e.g., beta blockers for CPVT). Although medical therapy alone is now uncommon in SCD survivors, adjunctive medical therapy can be useful to reduce the frequency of ICD shocks.
  2. Guiding the evaluation and management of family members

Electrophysiologic (EP) Study

  • EP testing is not usually performed in patients with an established etiology of SCD. However, an EP study can be valuable in those whose initial evaluation reveals no etiology, and in selected patients with a previously identified disorder.
  • In SCD survivors with an apparently normal heart, EP testing may reveal the following:
    • Abnormalities of atrioventricular conduction
      • The presence of severe conducting system disease suggests that a serious bradyarrhythmia may have contributed to the SCD event.
      • These patients, though, typically present with syncope rather than SCD.
      • Furthermore, even when conduction disease is identified, VT/VF may be the real culprit and ventricular stimulation to induce ventricular arrhythmias may be warranted.
    • An accessory pathway in patients with WPW syndrome
      • An accessory pathway can result in rapid conduction of a supraventricular arrhythmia, primarily AF, producing a very rapid ventricular rate that can degenerate to VF.
      • Such patients usually have evidence of preexcitation on their ECG. If preexcitation is evident on an ECG in a survivor of SCD, EP study and ablation of the accessory pathway are usually indicated.
    • Inducible ventricular arrhythmias
      • VT and VF may be induced in patients with a number of underlying cardiac abnormalities. The prognostic value of inducible arrhythmias is best established in patients with prior myocardial infarction and reduced left ventricular (LV) systolic function.
      • There is evidence that inducible VF, particularly when repeatedly induced with nonaggressive protocols, suggests the diagnosis of idiopathic VF and may predict recurrent arrhythmic events.30,78
      • In a review of the literature, 69% of patients with idiopathic VF had a sustained ventricular tachyarrhythmia induced with a nonaggressive protocol. The induced arrhythmia was generally polymorphic in configuration and poorly tolerated.30
      • In some other conditions it is not clear that inducible VT or VF has prognostic significance (e.g., Brugada syndrome, infiltrative diseases, HCM. Furthermore, aggressive stimulation protocols can induce polymorphic VT or VF in some individuals without cardiac disease. Thus, inducible arrhythmias can be a nonspecific finding. For this reason, the significance of inducible ventricular arrhythmias in patients with apparently normal hearts is unclear. On the other hand, the absence of inducible VT/VF may not preclude ICD implantation since lack of inducibility does not predict low risk.
    • Myocardial scar
      • Substrate mapping may identify areas of scar indicating abnormal substrate and a predisposition to ventricular arrhythmias. These abnormalities are more commonly seen in patients with CHD, HCM, ARVC, or infiltrative diseases, but also occur in some cases of idiopathic VF.79
      • In addition, some patients with idiopathic VF have other electrophysiologic abnormalities, including areas of slow conduction, regionally delayed repolarization, or dispersion in repolarization.80
    • Supraventricular arrhythmias
      • Patients in whom VT or VF was not well documented at the time of SCD may have another culprit arrhythmia, usually a SVT. In such patients, SVT may be inducible during EP study.81

Exercise Testing

  • Exercise testing is not usually part of the CHD evaluation in SCD survivors since most undergo coronary angiography. However, the provocation of ischemia with exercise, independently of coronary anatomy, is of importance in the evaluation of the SCD survivor. Although angiography alone does not prove a causal relationship to SCD or the presence of ischemia, the observation that revascularization appears to improve outcomes15,73,75 means that a negative exercise test in a patient with significant coronary disease on angiography is not likely to affect the decision on revascularization. Also, of great importance is the provocation of VT or VF in these patients, which would predict a higher recurrence rate. It is also a target for adjunctive antiarrhythmic therapy in addition to an ICD. While VT (which is often scar mediated and provoked by catecholamines) may be provoked during exercise, VF most commonly occurs after exercise in the recovery period (when ischemia is more common).
  • In patients with apparently normal hearts, exercise testing can assist in the diagnosis of LQTS and CPVT.70 It is also useful in patients with WPW pattern as the resolution of the delta wave with exercise generally correlates with low likelihood of a rapid ventricular rate with AF which is the etiology for VF and SCD in these patients.

Ambulatory Monitoring

  • In patients without a clear etiology for SCD, ambulatory monitoring may reveal recurrent sustained or nonsustained arrhythmias. However, most patients without an established diagnosis will have an ICD placed prior to discharge, and the memory features in these devices may preclude the need for ambulatory monitoring.

Pharmacologic Challenge

  • Some of the primary electrical disorders may still be present despite no evidence of abnormalities on any of the proceeding tests. ECG abnormalities may be intermittent or latent, and genetic testing is not yet comprehensive enough to exclude all possible disorders.
  • Investigators have evaluated the role of pharmacologic challenge to elicit diagnostic ECG changes or arrhythmias in selected SCD survivors. One report included 18 SCD survivors with no evidence of structural heart disease.82 All patients had a normal ECG, echocardiogram, coronary angiography, and CMR. Patients were infused with epinephrine (0.05 to 0.5 microg/kg per minute) and then procainamide (1 g over 30 minutes). Epinephrine was intended to induce CPVT and procainamide to induce the characteristic ECG abnormalities of Brugada syndrome.
  • The following findings were noted:
    • Ten patients were diagnosed with CPVT based upon an abnormal response to an epinephrine infusion (frequent or polymorphic ventricular ectopy, nonsustained VT, or sustained VT). Four of these patients had ventricular ectopy during exercise testing, but none had sustained or nonsustained VT.
    • Two patients were diagnosed with Brugada syndrome.
    • Six patients were left with a diagnosis of idiopathic VF.
    • Among 55 family members who were tested, eight affected members from one family were diagnosed with CPVT, and one relative was diagnosed with Brugada syndrome.
  • In summary, two-thirds of patients whose standard evaluation provided no etiology for SCD had a diagnosis established with pharmacologic provocative testing. This allowed for the addition of appropriate adjunctive therapy (beta blockers for CPVT) and the identification of nine additional affected family members.

Minor Cardiac Abnormalities Not Associated with SCD

  • During the course of the cardiac evaluation, minor cardiac abnormalities are often detected that do not have a clear causal relationship to SCD. These findings do not preclude the diagnosis of idiopathic VF. However, their severity must be considered, and monitoring is warranted since these disorders may be the initial manifestations of an underlying structural heart disease that will become clinically apparent at a later date.20
    • Examples of such disorders which do not exclude idiopathic VF are:
      • First degree atrioventricular (AV) block
      • Transient second-degree Mobitz type II AV block without bradycardia
      • Isolated bundle branch block

Evaluation of Family Members

  • Some causes of SCD are familial, including a genetic predisposition to premature CHD, and the risk of cardiovascular disease appears significantly higher in first- and second-degree relatives of the SCD victims, particularly young victims.
    • In a nationwide Danish study from 2000 to 2006, 470 victims of SCD were identified who were 35 years of age or younger.83 Among a cohort of 3,073 first- and second-degree relatives of the SCD victims who were followed for up to 11 years, CVD was significantly more likely to be present than in the general population. In contrast, among relatives of elderly (> 60 years of age) victims of SCD, there was no difference in the rates of CVD compared with the general population.
  • A general cardiologic evaluation of first- and second-degree relatives of victims of unexplained SCD can yield the diagnosis of a heritable disease in up to 40% of families as illustrated by the following observations.28,84,85
    • In a study of 32 families of victims of unexplained SCD, a general cardiologic evaluation (ECG, echocardiogram, Holter monitor and, less commonly, stress testing) was completed in 107 first-degree relatives.28 Seven families (22%) were diagnosed with a heritable disease: four with LQTS, one with nonstructural cardiac disease, one with myotonic dystrophy, and one with HCM.
    • These findings were extended in a second report that evaluated 43 families with 183 surviving first- and second-degree relatives of victims of unexplained SCD at age ≤40.84 Careful history identified 26 additional cases of unexplained SCD at age ≤40. Cardiology evaluation included ECG, echocardiogram, exercise tolerance testing (ETT), and measurement of serum lipids. Additional testing, as indicated, included a flecainide challenge for suspected Brugada syndrome or cardiac MR for suspected ARVC.
  • When a clinical diagnosis was established, genetic testing for the suspected disease was performed. Where a genetic abnormality was confirmed, additional screening was done in another 150 family members. The following findings were noted:
    • A heritable disease was identified in 17 families (40%): five with CPVT, four with LQTS, two with Brugada syndrome, one with Brugada/LQTS, three with ARVC, one with HCM, and one with familial hypercholesterolemia. Genetic analysis confirmed the diagnosis in 10 families.
    • An average of 8.9 asymptomatic carriers per family was identified, many through the secondary genetic analysis.
    • Identification of a specific disease was more likely if ≥2 unexplained SCD events occurred in the family, and if more family members underwent evaluation.
    • The increased yield in the second study may reflect the more extensive evaluation, including ETT, and the inclusion of more family members.
  • Consistent with these findings, it has been recommended that first-degree family members of patients with SCD in the absence of structural heart disease be informed of the potentially increased risk and that an assessment should be offered at a center with experience in the diagnosis and management of inherited cardiac diseases.21 Routine genetic screening for inherited disorders is not feasible although, in the presence of an identifiable condition, the genetic evaluation of family members may be undertaken at some centers.

Neurologic and Psychologic Assessment

SCD survivors who have been resuscitated should be given a complete neurologic examination to establish the nature and extent of impairment resulting from the arrest. The physical examination, rather than imaging studies or other testing, is the most useful way of elucidating the patient's degree of neurologic function, mental impairment, and of determining prognosis.

A 2004 meta-analysis of 11 studies found that the following clinical signs predicted a poor clinical outcome following cardiac arrest with 97% specificity86:

  • Absence of pupillary light response after 24 hours
  • Absence of corneal reflex after 24 hours
  • Absent motor responses to pain after 24 hours
  • Absent motor responses after 72 hours

Equally important is an assessment of the patient's psychologic state. Posttraumatic stress disorder (PTSD) may occur in SCD survivors. This was suggested in a study of 143 patients who had been resuscitated and discharged with no, or only moderate neurologic disability.87 All patients completed a self-rating questionnaire at a mean of 45 months after cardiac arrest: 39 (27%) fulfilled criteria for PTSD.

Primary Prevention

The optimal approach to the primary prevention of SCA varies among the following categories:

  • General population
  • Patients surviving an acute MI
  • Patients with HF and cardiomyopathy
  • Patients with one of the congenital disorders associated with an increased risk of SCA (e.g., Brugada syndrome, congenital LQTS, WPW).

General Population

There are two approaches to reduce the risk of SCA in the general population:

  1. Screening and risk stratification to identify individuals who may benefit from specific interventions (e.g., stress testing, screening ECGs).
    • Among populations already known to be at an elevated risk of SCA (e.g., individuals with a prior MI), further risk stratification with a variety of tests can identify subgroups that benefit from specific therapies, such as an ICD.
    • However, in the general population without known CVD, there is no evidence that routine screening with any test (e.g., 12-lead ECG, exercise stress testing, or Holter monitoring) effectively identifies populations at an increased risk of SCA.
    • With regard to risk stratification of the general population, the following has been suggested:
      • Screening for risk factors for CVD according to standard guidelines.
      • Screening for CHD as appropriate in selected patients, according to standard guidelines.
      • Routine additional testing for the purpose of SCA risk stratification is not recommended.
  2. Interventions that may be expected to reduce the risk of SCA in any individual (e.g., smoking cessation or other lifestyle modifications). Such interventions generally target the underlying disorders that predispose to SCA.
    • Many of the traditional risk factors associated with the development of CHD are also associated with SCA.
    • Management of these risk factors may reduce the incidence of SCA in the general public. Such interventions include:
      • Effective treatment of hypercholesterolemia
      • Effective treatment of hypertension
      • Adoption of a heart-healthy diet
        • Fish Intake and Fish Oil
          • In observational studies of populations at low cardiovascular risk, greater dietary fatty fish intake was associated with lower cardiac mortality.47,62,63,88,89 This benefit is due in part to a reduced risk of SCD. Based upon these results, subsequent randomized trials evaluated the benefit of fish oil supplements in various high-risk populations.90,91
          • For most individuals, there is little evidence that the pharmacologic doses of n-3 polyunsaturated fatty acids found in fish oil supplements (approximately 10 to 20 times the nutritional dose from fish) provide more protection than the intake of one to two servings of fatty fish (e.g., salmon) per week.
            • The pharmacologic use of fish oils supplements should be restricted to individuals with refractory hypertriglyceridemia along with the periodic monitoring of apolipoprotein B levels.
      • Regular exercise
        • There are no data from long-term exercise intervention trials among apparently healthy individuals that focus upon major disease endpoints. Nevertheless, regular exercise should be encouraged for the primary prevention of CHD and SCA.
        • Although there is a small transient increase in risk during and shortly after strenuous exercise, there is an overall reduction in SCD among exercisers compared with sedentary men.43,44,51,92
        • It is unclear if more exercise (higher intensity or longer duration) is better than less (non-strenuous physical activity, such as walking for exercise 30 minutes most days).
        • Patients should be advised to pay attention to potential symptoms of CHD, even if they have engaged in regular exercise without limitations for an extended period of time.
        • Patients with known heart disease should be encouraged to engage in regular exercise in a supervised setting such as a cardiac rehabilitation program.
      • Smoking cessation
      • Moderation of alcohol consumption
        • Excess alcohol intake increases the risk of SCA, while light-to-moderate alcohol consumption (i.e., ≤2 drinks per day) is associated with a lower risk of CAD and cardiovascular mortality.55,56
        • It is reasonable to expect that moderate alcohol intake will also reduce SCA.
        • This effect was documented by the Physicians Health Study, which evaluated 21,537 men who were free of known CVD.66 Compared to men who rarely or never drank, those who had two to four drinks per week or five to six drinks per week had a significantly reduced risk for SCD.
      • Effective treatment of diabetes
    • These interventions are generally in agreement with guidelines published in 2001 by a task force of the European Society of Cardiology.93
    • There is no definitive evidence that risk factor reduction in the general population lowers the rate of SCA. However, a number of studies have demonstrated that interventions to treat risk factors can lower total cardiovascular and coronary mortality. Since the majority of CHD mortality is due to SCD, these results suggest that interventions to reduce risk factors will reduce SCD rates as well.
      • A multifactorial, controlled, randomized trial from the Belgian component of the World Health Organization evaluated the effect of efforts aimed at reducing serum cholesterol (via dietary changes), increasing physical activity, and controlling smoking, hypertension, and weight (in those who were overweight) on risk factors and mortality.94 Compared to the control group, the intervention group had significant reductions in the incidence of CHD and coronary mortality.

Post Myocardial Infarction

Patients with HF and LV systolic dysfunction, regardless of the etiology, are at an increased risk of SCA.

  • Primary prevention with an ICD is recommended in selected patients with either ischemic or nonischemic cardiomyopathy.
  • In addition, as with patients with CHD, standard medical therapies for HF (beta blockers, ACE inhibitors or angiotensin II receptor blockers, and aldosterone inhibitors such as spironolactone

Counseling Patients and Families

Given the mounting evidence related to the primary prevention of SCA, it now is clear that primary care providers can influence the occurrence of these events. There are clinical recommendations for those at risk of SCA that are likely to reduce risk.

Secondary Prevention

Implantable Cardioverter-Defibrillator (ICD) Therapy

An ICD is the preferred therapeutic modality in most survivors of SCA. The ICD does not prevent the recurrence of malignant ventricular arrhythmias, but it effectively terminates these arrhythmias when they do recur.

ICD patients who have frequent arrhythmia recurrences and device discharges may benefit from adjunctive therapies, such as antiarrhythmic drugs or catheter ablation.


  • The main indications for the use of an ICD can be divided into two groups95,96:
    1. Secondary Prevention
      • Implantation of an ICD is recommended for the secondary prevention of SCD due to life-threatening VT/VF in the following settings95:
        • Patients with a prior episode of resuscitated VT/VF or sustained hemodynamically unstable VT in whom a completely reversible cause cannot be identified. This includes patients with a variety of underlying heart diseases and those with idiopathic VT/VF and congenital LQTS, but not patients who have VT/VF limited to the first 48 hours after an acute MI.
        • Patients with episodes of spontaneous sustained VT in the presence of heart disease (valvular, ischemic, hypertrophic, dilated, or infiltrative cardiomyopathies) and other settings (e.g., channelopathies).
        • A key issue is the prevention of total mortality (not arrhythmic or sudden death). Simply correcting VT/VF may not improve overall mortality. Therefore, patient selection for ICD implantation should consider both the known risk of SCD due to VT/VF for a specific condition and the risk of total mortality from underlying medical conditions as well.
    2. Primary Prevention
      • Implantation of an ICD is recommended for the primary prevention of SCD due to life-threatening VT/VF in patients who have received optimal medical management (including the use of beta blockers and angiotensin-converting enzyme [ACE] inhibitors) yet remain at high risk of SCD, including95:
        • Patients with a prior MI (at least 40 days ago) and left ventricular ejection fraction (LVEF) ≤30%.
        • Patients with cardiomyopathy, New York Heart Association (NYHA) functional class II to III (Table 2), and LVEF ≤35%.
Table 2: NYHA Classifications of Cardiovascular Disability97,98
ClassNYHA Functional ClassificationSpecific Activity Scale
IPatients with cardiac disease but without resulting limitations of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea, or anginal pain.Patients can perform to completion any activity requiring ≥7 metabolic equivalents, e.g., can carry 24 lb. up eight steps; do outdoor work (shovel snow, spade soil); do recreational activities (skiing, basketball, squash, handball, jog/walk 5 mph).
IIPatients with cardiac disease resulting in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain.Patients can perform to completion any activity requiring ≥5 metabolic equivalents, e.g., have sexual intercourse without stopping, garden, rake, weed, roller skate, dance fox trot, walk at 4 mph on level ground, but cannot and do not perform to completion activities requiring ≥7 metabolic equivalents.
IIIPatients with cardiac disease resulting in marked limitation of physical activity. They are comfortable at rest. Less than ordinary physical activity causes fatigue, palpitation, dyspnea, or anginal pain.Patients can perform to completion any activity requiring ≥2 metabolic equivalents, e.g., shower without stopping, strip and make bed, clean windows, walk 2.5 mph, bowl, play golf, dress without stopping, but cannot and do not perform to completion any activities requiring >5 metabolic equivalents.
IVPatients with cardiac disease resulting in inability to carry on any physical activity without discomfort. Symptoms of cardiac insufficiency or of the anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort is increased.Patients cannot or do not perform to completion activities requiring >2 metabolic equivalents. Cannot carry out activities listed above (specific activity scale III).
  • Patients with nonischemic cardiomyopathy generally require optimal medical therapy for three months with documentation of persistent LVEF ≤35% at that time.
    • Some patients with HF who are candidates for an ICD also have an intraventricular conduction delay (≥120 milliseconds) and are candidates for cardiac resynchronization therapy (CRT) with a biventricular pacemaker. Such patients could be treated with a device with combined ICD and biventricular pacing functions (cardiac resynchronization therapy-defibrillator [CRT-D]).
  • Patients with syncope who have structural heart disease and inducible sustained VT or VT going to VF on electrophysiology study.
  • Select patients with certain underlying disorders who are deemed to be at high risk for life-threatening VT/VF. These patients include:
    • Patients with congenital LQTS who have recurrent symptoms and/or torsades de pointes despite therapy with beta blockers or other high-risk patients.
    • High-risk patients with HCM or ARVC.
    • High-risk patients with Brugada syndrome, CPVT, and other channelopathies.

Contraindications to ICD Therapy

  • ICD therapy is not recommended in the following settings95:
    • Patients with ventricular tachyarrhythmias due to a completely reversible disorder in the absence of structural heart disease (e.g., electrolyte imbalance, drugs, or trauma).
    • Patients who do not have a reasonable expectation of survival with an acceptable functional status for at least one year, even if they otherwise meet ICD implantation criteria.
    • Patients with incessant VT or VF in whom other therapies (e.g., catheter ablation) should be considered first.
    • Patients with severe psychiatric illnesses that may be aggravated by device implantation. In clinical practice, this situation is very rarely encountered and may apply more to primary prevention than secondary prevention settings.
    • Patients with NYHA Class IV HF that is refractory to optimal medical treatment who are not candidates for cardiac transplantation or CRT.
    • Patients with syncope without inducible ventricular tachyarrhythmias and without structural heart disease.
    • Patients with VF or VT amenable to surgical or catheter ablation in whom the risk of SCD is normalized after successful ablation (e.g., atrial arrhythmias associated with the WPW syndrome, RV or LV outflow tract VT, idiopathic VT, or fascicular VT in the absence of structural heart disease).
    • ICD implantation should be delayed in patients with active infections or other acute medical issues. If necessary, the patient can be bridged with a wearable cardioverter-defibrillator (WCD) until ICD implantation can be carried out.

Elements of the ICD

  • The ICD system is comprised of the following elements (Picture 1)99:
    • Pacing/sensing electrodes
      • Pacing and sensing functions require a pair of electrodes. Contemporary pacemakers and defibrillators usually use leads with two electrodes on the ventricular lead: the distal electrode at the tip of the lead and a second electrode in the shape of a ring, several millimeters back from the tip (i.e., true bipolar leads). These bipolar leads provide accurate sensing, with high amplitude, narrow electrograms. Some ICD leads utilize integrated bipolar sensing in which the bipole consists of a single tip electrode and the distal shocking coil electrode. In addition to improved sensing capabilities, bipolar leads reduce the risk of extraneous interference, which could lead to inappropriate device function (e.g., inappropriate shocks delivered due to sensing of muscular activity).
    • Defibrillation electrode
      • The defibrillation function of the electrodes requires a relatively large surface area and positioning of the lead to maximize the density of current flow through the ventricular myocardium. Contemporary ICD systems use a "coil" of wire that extends along the ventricular lead as the primary defibrillation electrode. Thus, a single transvenous lead can accomplish all pacing, sensing, and defibrillation functions.
      • Additional defibrillation electrodes improve defibrillation efficacy and reduce the defibrillation threshold. Most contemporary ICD systems have two or three defibrillation electrodes. Along with the distal coil in the RV on the transvenous lead, some ICD leads have a second defibrillation coil proximal to the RV coil. In addition, with "active can" technology, the metal housing of the ICD serves as one of the shocking electrodes. This configuration requires that the pulse generator be implanted in the pectoral region. The active can and transvenous lead systems can be combined to achieve adequate defibrillation thresholds (minimum energy required for successful defibrillation, which should generally be 10 joules less than the maximum output of the device).
      • There are three types of pacing offered by current transvenous systems.
        • Single-chamber systems have only an RV lead.
        • Dual-chamber systems have right atrial (RA) and RV leads.
        • CRT, also called biventricular systems, have RA, RV, and LV leads, or in some patients with permanent atrial fibrillation, RV and LV leads.
    • Pulse generator
      • The pulse generator contains the sensing circuitry, as well as, the high voltage capacitors and battery.
      • Placement:
        • The development of small pulse generators (e.g., thickness ≤15 mm) has permitted placement in the infraclavicular region of the anterior chest wall in nearly all patients.100 The majority are placed in a:
          • Prepectoral (i.e., subcutaneous) position
          • Subpectoral position is advantageous. For most patients with the pulse generator in this location, the impulses generated are transmitted to the myocardium via transvenous leads. Epicardial systems are still available and may be necessary as a result of anatomical limitations to placing a transvenous lead(s). Additionally, a subcutaneous ICD (S-ICD) system is now available in which the pulse generator is placed overlying the left lower lateral ribs.
          • A pulse generator will last for five or more years in most patients, with one study suggesting that devices implanted after 2002 have significantly longer battery lives (5.6 versus 4.9 years).101 Single-chamber ICDs implanted since 2002 had the longest battery life (mean 6.7 years). Current devices are expected to last even longer.102

Implantable Cardioverter Defibrillator

Implantable Cardioverter Defibrillator (ICD)
When the ICD senses an abnormal heart rhythm, it delivers an electrical shock to reset the heart to a normal rhythm.


  • Prior to implanting an ICD, the healthcare provider must determine the optimal position for placement of the leads and the pulse generator. Most current ICD systems utilize one or two transvenous leads placed via the axillary, subclavian, or cephalic vein, with attachment to a pulse generator in the subcutaneous tissue in the infraclavicular anterior chest wall. In more recent years, there has been a trend toward single coils rather than dual coils, which were favored earlier in the era of transvenous ICD systems. The rationale for this is that a proximal coil is rarely needed for defibrillation and that single-coil leads are less difficult to extract in the future if lead removal is necessary. An additional defibrillation lead can be placed in the azygos vein, coronary sinus, or subcutaneous tissue if necessary.
  • Choosing the optimal pulse generator location
    • Modern devices are small enough to be implanted in the pectoral region of the anterior chest wall, either subcutaneously or submuscularly, similar to a pacemaker implantation.
    • Transvenous devices placed in the pectoral region are associated with fewer perioperative complications, shorter procedure time, shorter hospital stays, lower hospitalization costs, and lower total costs.103-105
    • Although implantation on the left side is preferred, a right-sided implant can be performed.106,107 The left pectoral position is usually chosen for two reasons: defibrillation energy requirement is usually lower on the left because of the location of the heart in the left chest, and there is a small risk of arm swelling due to venous occlusion, which would impact fewer people on the left as the majority of patients are right handed.
    • Additionally, a S-ICD system is available that allows for defibrillation (though no backup pacing or antitachycardia pacing) without the insertion of a transvenous lead. The pulse generator for the S-ICD system is implanted in a subcutaneous pocket in the left lateral, mid-axillary thoracic position.
  • Choosing the optimal lead placement
    • In most new ICD implantations, the lead with the pace/sense electrodes is placed transvenously, with the distal electrode positioned on the RV apical endocardium. RV septal lead placement is also an option. In rare cases, usually due to limitations of the venous anatomy and/or a high risk of bacteremia and endovascular infection, the pace/sense electrodes are placed on the epicardium during surgery. The electrodes should record a ventricular electrogram of at least 5 mV. These signals should be sufficiently large for detection of VT and VF.
    • Dual-chamber ICDs have an additional lead with another pair of pace/sense electrodes in the right atrium for atrial sensing and pacing.108
    • An S-ICD has been developed with no leads placed in the heart. The subcutaneous lead, which toward its terminal end contains an 8-cm shocking coil electrode, is tunneled from the pulse generator in the left axilla to a position along the left parasternal margin. The S-ICD can sense VT/VF and deliver therapeutic shocks but cannot deliver antitachycardia pacing or pacing for bradycardias.

Defibrillation Threshold (DFT) testing

  • DFT testing has historically been performed at the time of device implantation, although the necessity for this evaluation with the current generation of devices has been questioned.109-115
  • DFT testing is generally performed in patients receiving an S-ICD.
  • DFT testing is not required and can be omitted in patients undergoing a left pectoral transvenous ICD implantation with a RV apical lead that is functioning appropriately.
  • DFT testing is reasonable in patients undergoing a right pectoral ICD implantation or ICD pulse generator changes (on either right or left side). The rationale for testing right-sided implants is that defibrillation may be more difficult with a right pectoral pulse generator, given the fact that the heart lies in the left chest. For generator changes, there may be concerns about the integrity of the chronic leads.
  • DFT testing should not be performed in patients with a documented nonchronic cardiac thrombus, atrial fibrillation/flutter without adequate anticoagulation, severe aortic stenosis, unstable angina, recent stroke or transient ischemic attack, or hemodynamic instability. Additionally, many centers avoid DFT testing in patients with very low LVEFs (<15%) or severe pulmonary hypertension.
  • Some electrophysiologists feel that universally omitting DFT testing might compromise the safety within certain subsets of patients, especially those patients with high DFTs who would benefit from a higher energy device and/or additional leads.
  • A distinction should be made, however, between DFT testing at initial implantation and at the time of generator replacement. DFT testing at the time of generator replacement is useful in subsets of patients with leads that have a hazard alert or in patients at higher risk of DFT changes (e.g., obese patients, patients with HF symptoms, patients on amiodarone, etc.).116
  • Early ICD systems frequently required lead system adjustment at the time of implantation in order to achieve an adequate safety margin (arbitrarily set at 10 joules or greater). As technology improved, thresholds were substantially reduced.117 As a result, it is now unusual for the standard triad defibrillation system (two shock coils and an active can) to require modification at the time of implantation. Data regarding DFT testing on the more modern single-coil systems are limited since the available cohort and registry data predate the development of single-coil systems. On average, omitting the proximal coil in a single-coil system likely increases the DFT a few joules, which usually does not impact the safety margin but could be significant in some patients.
  • Several studies have illustrated the impact of DFT testing at the time of ICD implantation with the current generation of devices, generally showing no significant difference in outcomes.112-115,118,119 In a systematic review and meta-analysis of 13 studies involving 9,740 patients undergoing initial ICD implantation, there was no significant difference in mortality or adverse outcomes between patients with and without DFT testing.120

Periprocedural Monitoring

  • Nearly all patients who undergo ICD implantation will have the device placed using local anesthesia at the site of the pulse generator insertion, with intravenous sedation provided for patients who experience significant anxiety or pain by nurse anesthetists and/or anesthesiologists.
  • Following ICD implantation:
    • A posteroanterior (PA) and lateral chest x-ray should be obtained to establish the position of the pulse generator and the associated lead(s) and to exclude any apparent complications, including pneumothorax and lead dislodgment.
    • Patients should also have a 12-lead ECG recorded during pacing to document the ECG appearance of the QRS complex.


  • There are a variety of potential complications associated with ICDs, both at and around the time of implantation, as well as, long-term over the life of the patient and his/her device.
  • Periprocedural complications include:
    • Bleeding
    • Cardiac perforation
    • Infection
    • Perioperative mortality (rare)
    • Shoulder related problems including:
      • Decreased shoulder mobility
      • Pain
      • Reduced function
      • Insertion tendonitis
  • Long-term complications include:
    • Lead-related problems
      • Increased defibrillation threshold
      • Infection
      • Lead failure (resulting in failure to pace, failure to shock, or inappropriate shocks)
      • Tricuspid valve damage
      • Venous thrombosis
    • Pulse generator complications
      • Electronic circuit damage
      • Electromagnetic interference
      • Skin erosion due to the size and weight of the generator and infection of the pulse generator pocket
      • Twiddler’s Syndrome-a condition in which twisting or rotating of the pulse generator within its pocket results in lead dislodgement and device malfunction.
    • Arrhythmia-related problems
      • Appropriate shocks which can have an adverse effect on quality of life, including emotional problems and driving restrictions.
      • Inappropriate shocks
      • "Phantom" shocks
    • Miscellaneous complications
      • HF
      • Quality of life -The ICD is often associated with deleterious psychosocial effects, with as many as 50% of recipients reporting elevated levels of anxiety and depression resulting from the fear of receiving a shock, device failure, decrease in physical activity, and negative lifestyle changes (such as the inability to drive or to return to work).121-129 Some patients develop severe psychiatric problems after receiving appropriate shocks.130

Reuse of Explanted ICD

  • Many ICD pulse generators have useful battery life remaining at the time of a patient's death or when the ICD is explanted due to infection or device upgrade.
  • Because of concerns regarding the transmission of infectious disease from patient to patient, and because of the lack of data regarding device reliability when used in such a fashion, reuse of explanted ICDs has not been approved by any governing or regulatory body.
  • However, due to the large numbers of patients in resource-limited settings who have indications for an ICD but are unable to afford the device, there is a potential for compassionate reuse of ICDs if sterility and reliability can be assured.
  • From a single-center cohort of 81 indigent patients with indications for an ICD who received 106 explanted ICD pulse generators (cleaned and sterilized using a protocol involving hydrogen peroxide, povidone-iodine, and ethylene oxide gas) with a projected battery life of three or more years, the following findings were reported131:
    • Appropriate ICD therapy (shocks or antitachycardia pacing) in 64 out of 106 devices (60%)
    • Mean time to subsequent ICD replacement 1,287 days
    • No infectious complications
    • One lead dislodgement and one lead fracture.

ICD Functions

  • ECG monitoring and storage
    • Contemporary ICDs have more extensive storage and monitoring capacities, thereby allowing more expedient patient management, often without requiring a face-to-face visit. Some examples include:
      • Recording and display of stored electrograms from tachyarrhythmia events thus allowing for the detection of "silent" or asymptomatic arrhythmias where management of the patient is likely to change (e.g., AF).
      • Telemetry capabilities that permit easier analysis when patients receive shocks.
      • Remote monitoring capabilities via telephone or internet that allow healthcare providers to review ICD parameters and events without requiring the patient to come to the office or hospital.
  • Antitachycardia pacing
    • VT, particularly reentrant VT associated with scar from a prior MI, can sometimes be terminated by pacing the ventricle at a rate slightly faster than the tachycardia. When a paced impulse enters the reentrant circuit during a tachycardia, it can depolarize a segment of the circuit, leaving that segment refractory when the reentrant wave returns, thus terminating the tachycardia.
    • Antitachycardia pacing, or overdrive pacing, refers to the delivery of short bursts (e.g., eight beats) of rapid ventricular pacing to terminate VT. Although a variety of algorithms exist, antitachycardia pacing is usually programmed to be delivered at a rate that is slightly faster (e.g., at a cycle length 10 to 12% shorter) than the rate of the detected tachycardia.
    • S-ICDs cannot pace for bradycardia or for antitachycardic pacing.
    • Though employed substantially less frequently, antitachycardia pacing can also terminate some atrial tachyarrhythmias, and these features have been incorporated in some contemporary ICD systems.
  • Cardioversion/defibrillation
    • A shock that is synchronized to be delivered at the peak of the R wave is referred to as cardioversion.
    • Because VT is an organized electrical rhythm, the delivery of an electrical shock during the vulnerable period of repolarization can cause VT to degenerate into VF.
    • Synchronized cardioversion prevents shock delivery during the vulnerable period. Although ICDs can be programmed to deliver synchronized shocks at a range of energies up to the maximum output of the device (usually 30 to 35 joules), synchronized cardioversion can often terminate VT with relatively low energy (e.g., 10 joules or less).
    • An unsynchronized shock (i.e., a shock delivered randomly during the cardiac cycle) is referred to as defibrillation. Healthcare providers can program ICDs to deliver unsynchronized shocks for very rapid ventricular arrhythmias (e.g., heart rate greater than 200 beats/min). Because VF is not an organized rhythm, synchronized cardioversion is neither possible nor necessary. Similarly, it can be difficult to synchronize with very rapid VTs, and such rapid rhythms are unlikely to be hemodynamically tolerated.
    • ICDs are typically programmed to deliver synchronized shocks at energies approaching the maximum output of the device (usually 30 to 35 joules).
  • Bradycardia pacing
    • All contemporary transvenous ICDs are capable of pacing although, S-ICDs cannot deliver pacing therapies.
    • Many patients with an ICD have a conventional indication for cardiac pacing.132
    • Separate ICDs and pacemakers can produce device-to-device interactions, particularly with older models, potentially resulting in inappropriate shocks and underdetection of VT/VF.133-136
    • With rare exceptions, patients should have only one transvenous or epicardial device, although the combined use of a leadless pacemaker with an S-ICD is under investigation.
    • Generally, however, when a patient with a pacemaker develops an indication for ICD implantation, the pacemaker is removed and replaced with an ICD.
    • For patients with known AV block or sinus node dysfunction, or those who are receiving LV pacing as part of CRT, the device will be programmed accordingly.
    • For those without pre-existing AV block or sinus node dysfunction and who presumably do not require regular ventricular pacing, the ICD will typically be programmed to minimize the amount of pacing provided (e.g., pace only for intrinsic rates less than 40 beats/min).
    • In addition to the usual indications for pacing, the ability to provide pacing also protects against bradyarrhythmias that can follow a tachycardia or shock, and also against ventricular arrhythmias that are bradycardia-dependent.137 Because of the unique physiology following a ventricular tachyarrhythmia and device shock, ICDs allow for distinct post-shock pacing programming (usually at higher outputs).
  • Cardiac resynchronization therapy (CRT)
    • CRT, which utilizes biventricular pacing, is an effective treatment for symptomatic HF in some patients with LV dyssynchrony.
    • CRT is currently recommended in patients with advanced HF (usually NYHA class III or IV), severe systolic dysfunction (LV ejection fraction ≤35%), and intraventricular conduction delay (QRS >120 milliseconds).
    • The evidence of benefit is greatest in patients with left bundle branch block and a QRS duration >150 milliseconds.
    • Pacing of the LV is most frequently achieved by transvenous insertion of an electrode into a cardiac vein via the coronary sinus.
    • Surgical placement of an epicardial lead is also an option in patients following failed efforts at transvenous lead placement, or in patients undergoing cardiac surgery for another reason.
    • Improvement in HF can reduce the frequency of ventricular arrhythmias, raising the possibility that biventricular pacing may have an adjunctive role with an ICD by reducing the need for ICD therapy.
  • Perioperative ICD functioning
    • During surgical procedures, the function of ICDs may be affected by electromagnetic interference (EMI), most commonly due to use of an electrosurgery unit (ESU).
    • ICDs with integrated bipolar sensing configuration may be more susceptible to EMI than those with true bipolar sensing.
    • Very rarely, direct damage from cautery to the ICD may alter its ability to deliver pacing or shocks or reset the ICD to an alternate or backup mode. The much more common concern is that the device might misinterpret the cautery as tachyarrhythmia, leading to withholding of bradycardia pacing and perhaps inappropriate ICD shocks.

Wearable Cardioverter-Defibrillator (WCD)

  • Some patients who are at risk for SCD do not meet established criteria for implantation of an ICD or may require only short-term protection (such as patients awaiting subsequent ICD insertion or cardiac transplantation).
  • In such settings, a wearable WCD may be preferable to either ICD insertion or bystander resuscitation

Subcutaneous ICD (S-ICD)

  • Some patients who are at risk for SCD and require an ICD will have compelling reasons for avoiding the indwelling transvenous leads associated with a standard ICD (e.g., other indwelling leads or catheters, high risk for systemic infection, relatively young age at implant with numerous device implants anticipated over a lifetime, etc.). 
  • An entirely S-ICD has been developed that can provide an effective alternative means of defibrillation, albeit without some of the standard capabilities of a traditional transvenous ICD (i.e., no antitachycardia pacing or backup bradycardia pacing). 

Antiarrhythmic Drugs

  • Nearly all survivors of SCA without a reversible cause should be evaluated for placement of an ICD. Because an ICD treats but does not prevent arrhythmias, patients who have arrhythmias with symptoms or device discharges may require adjunctive antiarrhythmic therapy.
  • In addition to ICD therapy for survivors of SCA, there are three main indications for concomitant antiarrhythmic drug therapy138-140:
    1. To reduce the frequency of ventricular arrhythmias in patients with frequent ICD shocks. In one analysis, the occurrence of frequent ICD shocks was the primary reason for adding an antiarrhythmic drug (64%).140
    2. To suppress supraventricular arrhythmias that may cause symptoms or interfere with ICD function, potentially resulting in "inappropriate" shocks.
      • "Inappropriate" shocks result from non-life-threatening arrhythmias which meet the programmed parameters for ICD therapy, primarily based upon rate (e.g., AF with a rapid ventricular response exceeding the programmed threshold for delivering a shock).
      • "Inappropriate" shocks have been reported in up to 29% of ICD patients and can have a substantial impact on the patient’s quality of life.141
        • These shocks are caused by a variety of arrhythmias including sinus tachycardia, AF, and NSVT.141-142
        • More sophisticated programming features of current-generation ICDs may allow the device to ignore clinically unimportant and non-life-threatening arrhythmias rather than delivering an unnecessary shock.
    3. To reduce the ventricular rate of VT so that it is better tolerated hemodynamically and/or more amenable to termination by anti-tachycardia pacing or low energy cardioversion.

Indications for Pharmacologic Therapy

  • Nearly all survivors of SCA without a reversible cause should be evaluated for placement of an ICD. Because an ICD treats but does not prevent arrhythmias, patients who have arrhythmias with symptoms or device discharges may require adjunctive antiarrhythmic therapy.
  • In addition to ICD therapy for survivors of SCA, there are three main indications for concomitant antiarrhythmic drug therapy138-140:
    1. To reduce the frequency of ventricular arrhythmias in patients with frequent ICD shocks. In one analysis, the occurrence of frequent ICD shocks was the primary reason for adding an antiarrhythmic drug (64%).140
    2. To suppress supraventricular arrhythmias that may cause symptoms or interfere with ICD function, potentially resulting in "inappropriate" shocks.
      • "Inappropriate" shocks result from non-life-threatening arrhythmias which meet the programmed parameters for ICD therapy, primarily based upon rate (e.g., AF with a rapid ventricular response exceeding the programmed threshold for delivering a shock). 
      • "Inappropriate" shocks have been reported in up to 29% of ICD patients and can have a substantial impact on the patient’s quality of life.141
        • These shocks are caused by a variety of arrhythmias including sinus tachycardia, AF, and NSVT.141-142
        • More sophisticated programming features of current-generation ICDs may allow the device to ignore clinically unimportant and non-life-threatening arrhythmias rather than delivering an unnecessary shock.
    3. To reduce the ventricular rate of VT so that it is better tolerated hemodynamically and/or more amenable to termination by anti-tachycardia pacing or low energy cardioversion.

Choice of Pharmacologic Therapy

  • Medications used to manage cardiac arrhythmias (Table 3):
Table 3: Medications Used to Mange Cardiac Arrhythmias
Medications used to slow fast cardiac rhythms or stabilize irregular rhythms are known as antiarrhythmics. Antiarrhythmic medications are divided into classes by their primary mode of action.

  • Class I agents: Sodium channel blockers that slow electrical conduction in the heart tissue. They are primarily used to treat rapid heart rhythms originating in the ventricles.

Class I agents are subdivided into:

Ia – Quinidine, Procainamide, Disopyramide

Ib – Lidocaine, Tocainide, Mexiletine, Phenytoin

Ic – Flecainide, Propafenone, Ecainide, Moricizine

  • Class II agents: Beta blockers that reduce heart workload by blocking certain hormones that bind with beta receptors in the heart. This makes it harder for a rapid heartbeat to be triggered.

Class II agents include:

Metoprolol, Propranolol, Esmolol, Atenolol

  • Class III agents: Potassium channel blockers which slow the use of potassium in heart cells.

Class III agents include:

Amiodarone, Sotalol, Azimilide, Bretylium, Cloflium, Dofetilide, Tedisamil, Ibutilide, Sematilide

  • Class IV agents: Calcium channel blockers (CCBs) decrease the contraction of the heart and dilate (widen) the arteries thus slowing overall heart rate.

Class IV agents include:

Verapamil, Diltiazem

  • Class V agents: A category for those medications which fail to fit into other class descriptions.

Class V agents include:

Magnesium, Digitalis (digoxin), Adenosine

  • For patients with an ICD who require adjunctive antiarrhythmic therapy due to ongoing arrhythmias, treatment with the combination of amiodarone plus a beta blocker is recommended rather than treatment with amiodarone alone or other antiarrhythmic agents. On occasion, therapy with mexiletine or sotalol may be useful.
  • In general, the class I antiarrhythmic drugs are not used as the majority of patients with SCA have structural heart disease, and these drugs are not recommended in these patients.
  • Pharmacologic therapy, in the form of beta blockers and antiarrhythmic medications, can be helpful in controlling arrhythmias in survivors of SCA.
    • Virtually all patients who have survived SCA should be considered for beta-blocker therapy. However, due to the efficacy of the ICD in treating sustained ventricular tachyarrhythmias and improving mortality, antiarrhythmic drugs are generally reserved for use in select patients as adjunctive therapy, or as primary therapy when an ICD is not indicated or refused by the patient.

Empiric Versus Guided Pharmacologic Therapy

  • Empiric pharmacologic therapy for SCA survivors, primarily with beta blockers and/or an antiarrhythmic drug, is an effective approach for survivors of SCA who have refused ICD placement or are not candidates for an ICD.
  • Beta blockers have some efficacy with relatively few side effects, while for most patients amiodarone is the most efficacious antiarrhythmic drug for preventing recurrent ventricular arrhythmias.
  • In current practice, however, when pharmacologic therapy is administered to a patient with or without (because of refusal or noncandidacy for) an ICD, empiric treatment with beta blockers and/or amiodarone is the preferred approach.
    • Other antiarrhythmic drugs (for example mexiletine or sotalol) are considered if there is recurrent arrhythmia despite therapy with amiodarone and/or a beta blocker.

Beta Blockers

  • Nearly all patients who have survived SCA should receive a beta blocker as part of their therapy.
  • Beta blockers are not generally considered to be adequate monotherapy and should be used in conjunction with an antiarrhythmic drug for most patients resuscitated from SCA due to VT or VF. However, the associated anti-adrenergic effects of beta blockers may be effective at reducing both arrhythmias and SCA when no specific antiarrhythmic treatment is given.
    • In an analysis from the AVID trial, patients who were discharged from the hospital on a beta blocker had a mortality reduction compared with those patients not receiving a beta blocker.143
  • Most SCA survivors will have multiple indications for a beta blocker (e.g., post-myocardial infarction, HF, etc.) from which they derive clinical benefit.
    • Beta-blockers reduce the incidence of sudden death and total mortality in patients with a recent myocardial infarction and in those with symptomatic HF or congenital LQTS.
    • Even in the absence of any additional indications, beta blockers should be used as part of the medical regimen following SCA due to VT/VF.
  • Beta blockers can potentiate the effects of class I antiarrhythmic drugs by preventing the effect of sympathetic stimulation on reversing the depressant effect on slowing conduction. They can also potentiate the action of class III antiarrhythmic drugs by preventing the sympathetic effect on shortening repolarization.

Antiarrhythmic Drugs

  • Amiodarone is the most effective for preventing recurrent ventricular tachyarrhythmias, although mexiletine, sotalol, and dofetilide are also useful in reducing recurrent ventricular arrhythmias.
    • Empiric therapy with amiodarone is preferred for treatment immediately following SCA in patients with recurrent ventricular tachyarrhythmias, as well as, for those who have refused (or are not candidates for) ICD placement.144
    • Following stabilization of the patient, if there are concerns about potential toxicity related to amiodarone, particularly for anticipated long-term use, mexiletine, sotalol, or dofetilide may be considered


  • Several clinical trials and systematic reviews have evaluated the efficacy of antiarrhythmic drugs as adjuvant therapy in ICD patients.142,145-150 There were significant differences in trial methodologies, which limit direct comparisons. Amiodarone has generally been the most effective antiarrhythmic drug for preventing ventricular arrhythmias (and associated ICD shocks).
    • In one systematic review which included eight randomized trials involving 1,889 patients, there was significant heterogeneity among the trials. Key findings included:149
      • Amiodarone in combination with a beta blocker significantly reduced the incidence of shocks compared with the beta blocker alone.
      • Sotalol reduced the incidence of ICD shocks when compared with a placebo. There was also a trend toward fewer shocks in patients treated with sotalol versus another beta blocker.
      • Treatment with either azimilide or dofetilide resulted in nonsignificant trends towards reduction in total ICD shocks compared with placebo. However, the incidence of appropriate ICD therapies (shocks plus antitachycardia pacing) was significantly reduced by azimilide.
    • In a second systematic review of 17 randomized trials involving 5,875 patients, patients taking an antiarrhythmic drug had significantly fewer ICD shocks compared with those not on an antiarrhythmic.151 However, the reduction in shocks seen in patients receiving an antiarrhythmic drug was not associated with improved survival.
    • In the OPTIC trial, a multicenter trial that randomized 412 patients with an ICD to treatment with a beta blocker alone, a beta blocker plus amiodarone, or sotalol alone, the rate of any ICD shock at one year was significantly lower with amiodarone plus a beta blocker than with sotalol or a beta blocker alone.145 There was a trend toward fewer total ICD shocks in the sotalol group compared with beta blockers alone. However, sotalol had no significant effect compared with a beta blocker alone in reducing the incidence of appropriate shocks or antitachycardia pacing.
      • Another major advantage of amiodarone is a very low frequency of proarrhythmia. Although amiodarone can markedly prolong the QT interval, torsades de pointes is rare. Caution is necessary when amiodarone is given with other drugs that can prolong the QT interval or therapy is complicated by hypokalemia or hypomagnesemia.


  • When patients are started on an antiarrhythmic drug, a baseline ECG should be obtained prior to drug initiation and then serial ECGs obtained for the first two to three days, particularly to monitor heart rate and assess for any significant QT interval prolongation.
  • Amiodarone
    • The initial dosing of amiodarone will vary depending on the route (IV or oral), as well as, the clinical situation:
      • For patients with electrical storm or incessant VT, amiodarone IV (150 mg IV push, followed by 1 mg/minute IV infusion for six hours, followed by 0.5 mg/min IV infusion for 18 additional hours) is the initial antiarrhythmic agent.
      • For patients who have been on IV therapy for more than two weeks, maintenance oral amiodarone at a dose of 200 to 400 mg/day is begun.
      • For patients who have been on IV therapy for one to two weeks, an intermediate maintenance oral amiodarone dose of 400 to 800 mg/day is begun. This should be continued until a total loading dose of 10 to 15 grams has been received, then the dose should be reduced to the usual maintenance dose of 200 to 400 mg/day. As oral amiodarone is only approximately 50% bioavailable, a total of 20 to 30 grams needs to be administered.
      • For patients who have been on IV therapy for one week or less, a full oral amiodarone loading dose of 400 to 1200 mg/day (typically in two divided doses) is started. This should be continued until a total loading dose of 10 to 15 grams has been received (and a total of 20 to 30 grams administered due to the reduced oral bioavailability), then the dose should be reduced to the usual maintenance dose of 200 to 400 mg/day.
  • Sotalol
    • Sotalol is not universally available in intravenous form. Bradycardic and proarrhythmic events can occur after the initiation of sotalol therapy and with each upward dosing adjustment. As a result, sotalol should be initiated and doses increased in a hospital with facilities for cardiac rhythm monitoring and assessment.
    • Sotalol is started at a dose of 80 mg twice daily, with dose adjustments at three-day intervals once steady-state plasma concentrations have been achieved and the QT interval has been reviewed on an ECG. Patients with renal insufficiency require a modification of the dosing interval.
  • Dofetilide
    • Dofetilide is only available in oral form and is not universally available in all countries.
  • Mexiletine
    • Mexiletine, which is a lidocaine-like antiarrhythmic drug, is only available for oral use.
    • It is often used with or without amiodarone for treating patients with an ICD who have ventricular arrhythmias that are of concern.
    • The usual dose is 200 to 400 mg po three times daily.

Treatment of Breakthrough Arrhythmias

  • Patients who have recurrent, or breakthrough, arrhythmias resulting in repeat ICD shocks or SCA in spite of therapy with a beta blocker and/or antiarrhythmic drug represent a significant clinical challenge. As with the occurrence of any ventricular arrhythmia, any identifiable reversible causes (e.g., myocardial ischemia, electrolyte disturbances, etc.) should be corrected.
  • In the absence of any reversible causes, treatment should be approached as follows:
    • For patients who are taking only a beta blocker, an antiarrhythmic drug, ideally amiodarone, should be added.
    • For patients who are taking only an antiarrhythmic drug, a beta blocker should be added.
    • For patients who are taking both a beta blocker and an antiarrhythmic drug, treatment options include:
      • Upward titration of either or both existing drugs or
      • Discontinuation of the current antiarrhythmic drug in favor of an alternative antiarrhythmic drug
      • It is preferred first to increase the dose of the beta blocker and the current antiarrhythmic drug to the maximum recommended dose (or maximum tolerated dose if side effects arise). If this approach is ineffective and the patient continues to have recurrent ventricular arrhythmias and shocks, the current antiarrhythmic drug should be stopped, and treatment initiated with another agent.
      • Another important option for patients with a recurrent arrhythmia despite amiodarone and a beta blocker is the addition of a class I antiarrhythmic agent that does not alter the QT interval (i.e., mexiletine or propafenone).

Impact on ICD Therapies

  • The primary goal of using beta blockers and/or antiarrhythmic drugs in patients with an ICD is to minimize the frequency of recurrent ventricular arrhythmias, thereby decreasing the likelihood of the patient receiving additional ICD shocks.
  • Beyond reducing the likelihood of ICD shocks, however, antiarrhythmic drug therapy may impact the efficacy of ICD therapies by potentially altering defibrillation thresholds and by slowing the ventricular rates of any recurrent sustained tachyarrhythmias.

Alterations in Defibrillation Thresholds (DFTs)

  • Any antiarrhythmic drug can potentially alter the DFT, although the effect has been most pronounced with amiodarone and its major metabolite desethylamiodarone, which increase the DFT in a dose-dependent fashion.152-154
  • DFT testing has historically been performed at the time of ICD implantation, although the routine necessity for this evaluation with the current generation of ICDs has been questioned. However, repeat DFT testing may be warranted after the initiation of amiodarone if there is concern about rising DFT thresholds (as may occur in certain clinical situations, including AF, hypertension, and left ventricular hypertrophy).
  • In the report on the efficacy of routine ICD testing discussed above, 71 patients had an ICD test due to the initiation or dose-adjustment of an antiarrhythmic drug (primarily amiodarone or sotalol), and the ICD failed to defibrillate only two patients.155
  • The role of ICD testing after the initiation of antiarrhythmic therapy was more directly assessed in a substudy of the OPTIC trial, in which 94 patients underwent serial ICD testing to determine the impact of each of three drug regimens (beta blockers, amiodarone plus a beta blocker, and sotalol) on DFTs.156 At a mean follow-up of 60 days after drug initiation, the mean DFT decreased from baseline in the patients assigned to beta blockers or sotalol (8.8 to 7.1 and 8.1 to 7.2 joules, respectively), while among patients taking amiodarone there was a nonsignificant increase in the mean DFT from 8.5 to 9.8 joules. Given the relatively small number of patients in each arm of this study, the small mean increase in DFT does not preclude the possibility that there may be a larger increase in some patients. Thus, the necessity for ICD testing after the initiation of antiarrhythmic drugs, primarily amiodarone, remains uncertain.

VT Rate Slowing

  • In patients receiving chronic antiarrhythmic drug therapy, the rate of recurrent VT is often slower than the rate seen during the index arrhythmia. This slower ventricular rate can have both positive and negative impacts on the delivery of ICD therapy:
    • Antitachycardia pacing is often more effective for the treatment of VT with a slower ventricular rate. When antitachycardia pacing effectively terminates the VT, the ICD does not deliver a shock, and many patients will have no knowledge of the event.
    • Slower ventricular rates during VT may result in the VT falling below the previously defined rate thresholds for the ICD to detect and treat the arrhythmia. As a result, if no ICD programming changes are made, and the VT is hemodynamically significant (i.e., resulting in syncope, palpitations, chest pain, dyspnea, or even SCA), the patient may not receive an appropriately-indicated therapy.
    • Consequently, it is common practice to lower the VT detection cutoff when initiating antiarrhythmic drug therapy, with the specific detection threshold individualized based on the specific data available from prior events in the individual patient.

Prognosis And Outcomes Following Sudden Cardiac Arrest

Despite advances in the treatment of heart disease, the outcome of patients experiencing SCA remains poor.157-160 For example:

  • A report analyzed outcomes for over 12,000 patients treated by EMS personnel in Seattle over 24 years. Survival to hospital discharge for those treated between 1998 and 2001 was not significantly better than for those treated between 1977 and 1981 (15.7% versus 17.5%). In contrast, the long-term outcome among patients who survive until hospital discharge following SCA appears to be improving.157
  • Among a nationwide cohort of 547,153 patients in Japan with out-of-hospital SCA between 2005 and 2009, survival to hospital discharge with favorable neurologic status improved approximately twofold in several groups over the five-year period (from 1.6% to 2.8% among all patients with out-of-hospital SCA, from 2.1% to 4.3% among bystander-witnessed SCA, and from 9.8% to 20.6% among bystander-witnessed SCA with VF as the initial rhythm).158 However, in spite of this doubling of neurologically favorable survival, overall survival following SCA remains poor.
  • Among 70,027 U.S. patients prospectively enrolled in the CARES registry following out-of-hospital SCA between 2005 and 2012, survival to hospital discharge improved significantly from 5.7% in 2005 to 8.3% in 2012.159 Improvements were also noted in pre-hospital survival and neurologic function at hospital discharge.
  • In a Canadian study of 34,291 patients who arrived at the hospital alive following out-of-hospital cardiac arrest between 2002 and 2011, survival at both 30-day and one-year increased significantly between 2002 and 2011 (from 7.7% to 11.8% for one-year survival).160
  • Similarly, among a cohort of 6,999 Australian patients with out-of-hospital SCA resuscitated by EMS between 2010 and 2012, 851 patients (12.2%) survived for at least one year, with more than half of patients reporting good neurologic recovery and functional status at one year.161

The reasons for the continued poor survival of patients with SCA are uncertain.157 Although some aspects of acute resuscitation have improved over time (increased bystander CPR and shortened time to defibrillation), these positive trends have been off-set by adverse trends in clinical features of patients presenting with SCA (such as increasing age and decreasing proportion presenting with VF).157,162 In addition, the response times of both BLS and ALS services have increased, possibly as a result of population growth and urbanization.163

Marked regional differences in the incidence and outcome of SCA have been observed. In a prospective observational study of 10 North American regions, the adjusted incidence of EMS-treated out-of-hospital SCA ranged from 40.3% to 86.7% (median 52.1%) per 100,000 census population while known survival to discharge ranged from 3.0% to 16.3% (median 8.4%).164 The adjusted incidence of VF ranged from 9.3% to 19.0% (median 12.6%) per 100,000 census population while known survival to discharge ranged from 7.7% to 39.9% (median 22%). These regional differences highlight the importance of local health care and EMS systems to SCA outcomes. A pilot study comparing the feasibility of EMS transport to a regional cardiac arrest center (with increased transit time) versus transport to the closest hospital suggested no difference in 30-day mortality or major adverse cardiac events, results which should be considered hypothesis-generating for larger scale studies.165

Neurologic Prognosis Following SCA

Survivors of SCA have variable susceptibility to hypoxic-ischemic brain injury, depending on the duration of circulatory arrest, extent of resuscitation efforts, and underlying comorbidities.

Outcome According To Etiology

There is an association between the mechanism of SCA and the outcome of initial resuscitation.


When the initial observed rhythm is asystole (even if preceded by VT or VF), the likelihood of successful resuscitation is low. Only 10% of patients with out-of-hospital arrests and initial asystole survive until hospital admission and only 0 to 2% until hospital discharge.166-168 The poor outcome in patients with asystole or bradycardia due to a very slow idioventricular rhythm probably reflects the prolonged duration of the cardiac arrest (usually more than four minutes) and the presence of severe, irreversible myocardial damage.

Factors associated with successful resuscitation of patients presenting with asystole include167,169:

  • No further need for treatment with atropine for a bradyarrhythmia after initial resuscitation
  • Shorter arrival time of EMS personnel
  • Witnessed arrest
  • Younger patient age

Pulseless Electrical Activity (PEA)

Patients who have SCA due to PEA (also called electrical-mechanical dissociation) also have a poor outcome. In one study of 150 such patients, 23% were resuscitated and survived to hospital admission while only 11% survived until hospital discharge.170

Ventricular Tachyarrhythmia

The outcome is much better when the initial rhythm is a sustained ventricular tachyarrhythmia. The most frequent etiology is VF. Approximately 25% to 40% of patients with SCA caused by VF survive until hospital discharge.157,171,172 In the Seattle series cited above of over 12,000 EMS-treated patients with SCA, 38% had witnessed VF.157 Patients with witnessed VF had a significantly greater likelihood of surviving to hospital discharge than those with other rhythms (34% versus 6%).

Acute MI or myocardial ischemia is the underlying cause of VF for many of the patients who survive to hospital discharge. In a series of 79 such patients from the Mayo Clinic, 47% had an acute MI, while in a series of 47 such patients from the Netherlands, 51% had an acute MI.171,172

Survival is approximately 65% to 70% in patients who present with hemodynamically unstable VT.173 The prognosis may be better in patients found in monomorphic VT because of the potential for some systemic perfusion during this more organized arrhythmia. In addition, patients with VT tend to have a lower incidence of a previous infarction and a higher ejection fraction when compared with those with VF.174

SCA due to Noncardiac Causes

As many as one-third of cases of SCA are due to noncardiac causes.179,198 Trauma, nontraumatic bleeding, intoxication, near drowning, and pulmonary embolism are the most common noncardiac etiologies. In one series, 40% of such patients were successfully resuscitated and hospitalized, but only 11% were discharged from the hospital, and only 6% were neurologically intact or had a mild disability.

Factors Affecting Out-Of-Hospital SCA Outcome

Despite the efforts of emergency personnel, resuscitation from out-of-hospital SCA is successful in only one-third of patients, and only about 10% of all patients are ultimately discharged from the hospital, many of whom are neurologically impaired.159,160,162-179

The cause of death in-hospital is most often noncardiac, usually anoxic encephalopathy or respiratory complications from long-term ventilator dependence. Only about 10% of patients die primarily from recurrent arrhythmia, while approximately 30% die primarily from a low cardiac output or cardiogenic shock as the consequence of mechanical failure. Recurrence of severe arrhythmia in the hospital is associated with a poorer outcome.180

In addition to later initiation of CPR and the presence of asystole or PEA (electromechanical dissociation)166-168,170 there are a number of other factors that are associated with a decreased likelihood of survival with neurologic function intact following out-of-hospital SCA172,181-184:

  • Absence of any vital signs
  • Alzheimer disease
  • Cancer
  • Cerebrovascular accident with severe neurologic deficit
  • History of cardiac disease
  • History of more than two chronic diseases
  • Prolonged CPR more than five minutes
  • Sepsis

There are also several poor prognostic features in patients with SCA who survive until admission:

  • History of class III or IV HF
  • Hypotension
  • Need for intubation
  • Need for vasopressors
  • Older age
  • Persistent coma after CPR
  • Pneumonia
  • Renal failure after CPR

VF Duration

VF in the human heart rarely, if ever terminates spontaneously, and survival is therefore dependent upon the prompt delivery of effective CPR. Electrical defibrillation is the only way to reestablish organized electrical activity and myocardial contraction.

Increasing duration of VF has two major adverse effects:

  1. VF reduces the ability to terminate the arrhythmia and
  2. If VF continues for more than four minutes, irreversible damage to the central nervous system and other organs begins.185-187 Consequently, the longer the duration of the cardiac arrest, the lower the likelihood of resuscitation or survival with or without neurologic impairment even if CPR is successful.

It has been suggested that without CPR, survival from a cardiac arrest caused by VF declines by approximately 10% for each minute without defibrillation, and after more than 12 minutes without CPR, the survival rate is only 2% to 5%.188-190

Time to Resuscitation

These observations constitute the rationale for attempts to provide more rapid resuscitation in patients with out-of-hospital SCA. One approach is optimizing the EMS system within a community to reduce the response interval to less than eight minutes.191

However, the response times of both BLS and ALS services have actually increased, possibly as a result of population growth and urbanization. In the Seattle series of over 12,000 EMS-treated patients, the BLS response interval increased from 3.8 to 5.1 minutes between 1977 and 2001, and the ALS response interval increased from 8.4 to 9.0 minutes.157

Thus, bystander CPR and even defibrillation have been recommended and have been implemented in some settings. Such interventions permit more rapid responses than those provided by BLS or ALS personnel, with better survival as a result. In the Seattle series, the odds ratio for survival to discharge for patients who received bystander CPR to those who did not was 1.85.157

Bystander CPR

The administration of CPR by a layperson bystander (bystander CPR or bystander-initiated CPR) is an important factor in determining patient outcome after out-of-hospital SCA. Survival after SCA is greater among those who have bystander CPR when compared with those who initially receive more delayed CPR from EMS personnel. In addition to improved survival, early restoration or improvement in circulation is associated with better neurologic function among survivors.192-194

For adults with sudden out-of-hospital SCA, compression-only bystander CPR (without rescue breathing) appears to have equal or possibly greater efficacy compared with standard bystander CPR (compressions plus rescue breathing). The 2010 AHA Guidelines for CPR recommended that bystanders perform compression-only CPR to provide high-quality chest compressions prior to the arrival of emergency personnel.195,196

The importance of bystander CPR and support for compression-only bystander CPR comes from a combination of retrospective and prospective studies. An initial report from the Seattle Heart Watch program in the late 1970s evaluated 109 consecutive patients resuscitated at the scene by a bystander trained in CPR and compared their outcomes with those of 207 patients who initially received CPR from EMS personnel.197 There was no difference between the two groups in the percentage of patients resuscitated at the scene and admitted alive to the hospital (67% versus 61%), but the percentage discharged alive was significantly higher among those with bystander CPR (43% versus 22%). The most important reason for the improvement in survival in this study was that earlier CPR and prompt defibrillation were associated with less damage to the central nervous system. More patients with bystander CPR were conscious at the time of hospital admission (50% versus 9%), and more regained consciousness by the end of hospitalization (81% versus 52%).

These observations were subsequently confirmed in larger studies.193,194,198-202

  • In a nationwide study of out-of-hospital cardiac arrest in Japan between 2005 and 2012, during which time the number of out-of-hospital cardiac arrests grew by 33% (n = 17,882 in 2005 compared with n = 23,797 in 2012), rates of bystander CPR increased (from 39% to 51%), and recipients of bystander CPR had a significantly greater chance of neurologically intact survival (8.4% versus 4.1% without bystander CPR).193 Early defibrillation by bystanders was also associated with significantly greater odds of surviving neurologically intact.
  • In a cohort of 19,468 individuals with out-of-hospital cardiac arrest in Denmark between 2001 and 2010 which was not witnessed by EMS personnel (from the nationwide Danish Cardiac Arrest Registry), the frequency of bystander CPR increased from 21% in 2001 to 45% in 2010, with a corresponding significant increase in survival at 30 days (3.5% to 10.8%) and one year (2.9% to 10.2%).201
  • In a subsequent study from the Danish Cardiac Arrest Registry, which included 2,855 persons with out-of-hospital cardiac arrest in Denmark between 2001 and 2012 (including 2,084 with arrests not witnessed by EMS personnel) and who survived at least 30 days, the frequency of bystander CPR increased from 67% in 2001 to 81% in 2012 among 30-day survivors.203 Over one year of follow-up post-arrest, bystander CPR was associated with significantly lower risks of brain damage or nursing home admission, as well as, lower risk of all-cause mortality.
  • In a nationwide cohort of 30,381 witnessed cardiac arrests in Sweden between 1990 and 2011, 15,512 patients (51.1%) received bystander CPR prior to the arrival of emergency personnel.202 Individuals receiving bystander CPR prior to the arrival of emergency personnel had a significantly greater 30-day survival (10.5% versus 4% without early CPR).

Despite the benefits of bystander CPR, it is not always performed. Reasons for this include204:

  • The bystander's lack of CPR training.
  • The bystander's concerns about possible transmission of disease while performing rescue breathing.
  • Neighborhood demographics (racial composition and income level) also appear to be a factor in the rates of performance of bystander CPR.
    • In an analysis of 14,225 patients with cardiac arrest in 29 U.S. sites participating in CARES, bystander CPR was significantly more likely to be performed:
      • In higher-income (above 40,000 USD per year), predominantly (>80%) white neighborhoods than in higher-income, predominantly (>80%) black neighborhoods or lower-income (less than 40,000 USD per year) neighborhoods of any racial mix (mostly white, mostly black, or integrated).205

Interventions that appear to improve the rate of bystander CPR include verbal encouragement and instruction in CPR by EMS dispatchers, and public campaigns to promote the delivery of bystander CPR204:

  • In a series of over 12,000 EMS-treated patients from Seattle, bystanders not trained in CPR were given instructions by telephone from the EMS dispatcher. The proportion of patients receiving bystander CPR increased from 27% to 50%, almost entirely as a result of the implementation of dispatcher-assisted CPR in that interval.157
  • A prospective observational study of 4,400 adults with out-of-hospital SCD noted a rise in the delivery of bystander CPR from 28% to 40% over the course of a five-year public campaign to encourage bystander compression-only CPR.206

Chest Compression-Only CPR

Bystander CPR with only chest compressions results in improved survival to hospital discharge, compared with chest compressions with interruptions for rescue breathing, with an absolute improvement in mortality of 2.4%.207

Initial observational studies that evaluated the delivery of compression-only CPR versus standard CPR including rescue breathing found no significant differences in survival or long-term neurologic function between the two groups, suggesting that compression-only CPR could be safely delivered.206,208-210 The trends toward improved survival to discharge with compression-only CPR became statistically significant when the results of the three trials (thereby increasing the number of patients) were combined in a meta-analysis (14% versus 12% in the standard CPR group).211,212

In a nationwide study of Japanese out-of-hospital cardiac arrest victims between 2005 and 2012, chest compression-only CPR resulted in improvements in the number of SCA victims receiving bystander CPR, as well as, the number of patients surviving with favorable neurological outcomes.213 These findings hold promise for improving the delivery of bystander CPR. Further data are required to determine if bystander-delivered compression-only CPR (rather than standard CPR) will translate into better neurologic outcomes for patients with out-of-hospital cardiac arrest.

Automated Mechanical CPR Devices

Several automated devices that deliver chest compressions have been developed in an attempt to improve upon chest compressions delivered by humans, as well as, to allow rescuers to perform other interventions simultaneously. While a 2013 meta-analysis of 12 studies (only 3 of which were randomized clinical trials) suggested higher rates of return of spontaneous circulation when an automated device was used, subsequent randomized trials showed no significant differences in survival between the mechanical CPR and manual CPR groups.

Timing of Defibrillation

The standard of care for resuscitation from VF has been defibrillation as soon as possible. In the Seattle series of over 12,000 EMS-treated patients, 4,546 had witnessed VF. For these patients, the defibrillation response interval was significantly correlated with survival to hospital discharge (odds ratio 0.88 for every one-minute increase in response time).157 Subsequent studies have shown similar benefits, with earlier defibrillation being associated with improved survival.193,198,214

Despite these findings, it has been suggested that outcomes may be improved by performing CPR before defibrillation, at least in patients in whom defibrillation is delayed for more than four to five minutes.215,216 An initial report from Seattle compared outcomes in two time periods: when an initial shock was given as soon as possible and subsequently, when the initial shock was delayed until 90 seconds of CPR had been performed.215 Survival to hospital discharge was significantly increased with routine CPR before defibrillation, primarily in patients in whom the initial response interval was four minutes or longer (27% versus 17% without prior CPR).

However, in the largest study to date comparing shorter versus longer periods of initial CPR prior to defibrillation in 9,933 patients with SCA, patients were randomly assigned to receive 30 to 60 seconds versus 180 seconds of CPR prior to cardiac rhythm analysis and defibrillation (if indicated).217 There was no significant difference in the primary endpoint of survival to hospital discharge with satisfactory functional status (5.9% in both groups).

For patients with SCA and ventricular tachyarrhythmia, early defibrillation and CPR should be performed as recommended in the 2010 ACLS guidelines.

Automated External Defibrillators (AEDs)

The use of AEDs by early responders is another approach to more rapid resuscitation. In most but not all studies, AEDs have been found to improve survival after out-of-hospital cardiac arrest.

Predictive Value of BLS and ALS Rules

Two termination of resuscitation rules have been proposed by the OPALS study group for use by EMS personnel. The rule for BLS providers equipped with AEDs includes the following three criteria218:

  1. Event not witnessed by EMS personnel
  2. No AED used or manual shock applied in out-of-hospital setting
  3. No return of spontaneous circulation in out-of-hospital setting

The ALS rule includes the BLS criteria, as well as, two additional criteria219:

  1. Arrest not witnessed by bystander
  2. No bystander-administered CPR

Validation of the predictive value of the BLS and ALS termination rules was performed with data from a retrospective cohort study that included 5,505 adults with out-of-hospital SCA.220 The overall rate of survival to hospital discharge was 7%. Of 2,592 patients (47%) who met BLS criteria for termination of resuscitation efforts, only 5 survived to hospital discharge. Of 1,192 patients (22%) who met ALS criteria, none survived to hospital discharge.

However, the validity of these termination rules may be reduced with improvements in EMS and post-resuscitation care. One potential target for understanding and ameliorating current limitations to post-arrest care is the observed marked regional variation in prognosis following SCA.

Adequacy of CPR

The adequacy of CPR delivered to a victim of cardiac arrest and outcomes related to resuscitation efforts may depend on a variety of factors (e.g., rate and depth of chest compressions, amount of time without performing chest compressions while performing other tasks such as defibrillation, etc.). The AHA 2010 Guidelines for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care emphasized early defibrillation (when available) and high-quality chest compressions (rate at least 100 per minute, depth of 2 inches or more) with minimal interruptions.196

The effect of CPR quality has been evaluated in several studies221-223 :

  • In a 2013, systematic review and meta-analysis which included 10 studies (4,722 patients total, 4,516 of whom experienced out-of-hospital cardiac arrest), individuals surviving cardiac arrest were significantly more likely than non-survivors to have received deeper chest compressions and have had compression rates between 85 and 100 compressions per minute (compared with shallower and slower compression rates).221
  • In a study of 3,098 patients with out-of-hospital cardiac arrest, return of spontaneous circulation was highest at a rate of 125 compressions per minute.222 However, higher chest compression rates were not significantly associated with survival to hospital discharge.

End-tidal carbon dioxide levels have an excellent correlation with very low cardiac outputs when measured after at least 10 minutes of CPR and may provide prognostic information, suggesting that the cardiac output maintained during CPR is a determinant of outcome.

Body Temperature

An increase in body temperature is associated with unfavorable functional neurologic recovery after successful CPR. The increase in temperature may be neurally-mediated and can exacerbate the degree of neural injury associated with brain ischemia. For the highest temperature within 48 hours, each degree Celsius higher than 37ºC increases the risk of an unfavorable neurologic recovery.224

On the other hand, the induction of mild to moderate hypothermia (target temperature 32 to 34ºC for 24 hours) may be beneficial in patients successfully resuscitated after a cardiac arrest, although studies have shown variable outcomes.

Prehospital ACLS

The incremental benefit of deploying EMS personnel trained in ACLS interventions (intubation, insertion of intravenous lines, and intravenous medication administration) on survival after cardiac arrest probably depends upon the quality of other prehospital services.

  • In the OPALS study, ACLS interventions were added to an optimized EMS program of rapid defibrillation. No improvement in the rate of survival for out-of-hospital cardiac arrest was observed with addition of an ACLS program.198
  • In a retrospective report from Queensland with an EMS program not optimized for early defibrillation, the presence of ACLS-skilled EMS personnel was associated with improved survival for out-of-hospital cardiac arrest.225

Effect of Older Age

The risk of SCA increases with age with older age being associated with poorer survival in some, but not all, studies of out-of-hospital cardiac arrests157,226-230:

  • In one study of 5,882 patients who experienced an out-of-hospital cardiac arrest, 22% were >80 years of age. Compared with patients <80 years of age, octogenarians and nonoctogenarians had a lower rate of hospital discharge (9.4% and 4.4% versus 19% for those <80). The discharge rate was higher in those with VF or pulseless VT as the initial rhythm. Very old patients still had poorer survival (24% and 17% versus 36%), but age was a weaker predictor than the initial rhythm.231
  • In the Seattle series of over 12,000 EMS-treated patients, every one-year increase in age was associated with a lower likelihood of survival to hospital discharge for all patients and for those with witnessed VF.157
  • In a study of 36,605 patients ages 70 years or older enrolled in a Swedish registry between 1990 and 2013 following SCA, 30-day survival was significantly higher in patients ages 70 to 79 years (6.7%) compared with patients ages 80 to 89 years (4.4%) and those over 90 years of age (2.4%).230

Effect of Gender

The incidence of SCA is greater in men than in women.157,232 The effect of gender on outcome has been examined in multiple cohorts, with the following findings232-234:

  • Men are more likely than women to have VF or VT as an initial rhythm.
  • Men are more likely than women to have a witnessed arrest.
  • Men have a higher one-month survival than women following SCA, due to the higher likelihood of VF/VT as their presenting rhythm.
  • When considering only patients with VF/VT as the initial rhythm, women have a greater survival with favorable neurologic outcome.

Effect of Comorbidities

The impact of preexisting chronic conditions on the outcome of out-of-hospital SCA was evaluated in a series of 1,043 SCA victims in King County, Washington in the United States.235 There was a statistically significant reduction in the probability of survival to hospital discharge with increasing numbers of chronic conditions, such as:

  • CHF
  • Diabetes
  • Hypertension
  • Prior myocardial infarction

The impact of comorbidities was more prominent with longer EMS response intervals.

Long-Term Outcome

The reported long-term survival of resuscitated SCD survivors is variable and may depend upon multiple factors:

  • In patients with out-of-hospital VF, was early defibrillation achieved?
  • Do the data come from randomized trials, in which many, often sicker, patients are excluded, or from community-based observations?
  • Was the patient treated with early revascularization, antiarrhythmic drugs, or an ICD?
  • Does the patient have other risk factors, particularly a reduced LVEF?
  • Do patients with seemingly transient or reversible causes of SCA have a better prognosis?
  • Did the episode of SCA begin as VF or VT?

The potential effect of successful early defibrillation on long-term outcome following out-of-hospital cardiac arrest due to VF was assessed in a population-based study of 200 patients. Over 70% of these patients survived until hospital admission, and 40% of these patients were discharged with mild or absent neurologic impairment. Among these 79 patients, 43 underwent coronary revascularization and 35 received an ICD, 13 of whom had subsequent shocks for VT or VF. The expected five-year survival of the study population (79%) was the same as that of age-, sex-, and disease-matched controls who did not have out-of-hospital cardiac arrest, but significantly lower than age- and sex-matched controls in the general population.246

Factors Affecting In-Hospital SCA Outcome

The outcome of patients who experience SCA in the hospital is poor, with reported survival to hospital discharge rates of 6% to 15%.236-239 In the largest cohort of 64,339 patients at 435 hospitals who had in-hospital SCA and underwent standard resuscitation procedures, 49% of patients had return of spontaneous circulation, with 15% overall survival to hospital discharge.239

Several clinical factors have been identified that predict a greater likelihood of survival to hospital discharge236,239,240:

  • Pulse regained during first 10 minutes of CPR
  • VT or VF as initial rhythm
  • Witnessed arrest

Other factors have been identified that predict a lower likelihood of survival to hospital discharge240,241:

  • Longer duration of overall resuscitation efforts
  • Multiple resuscitation efforts

Delays in providing initial defibrillation have been associated with worse outcomes. In a report of 6,789 patients with in-hospital SCA due to VT or VF from 369 hospitals participating in the National Registry of Cardiopulmonary Resuscitation results showed241:

  • Delayed defibrillation (more than two minutes after SCA) occurred in 30% of patients and was associated with a significantly lower probability of surviving to hospital discharge.
  • Delayed defibrillation was more common with the black race, noncardiac admitting diagnosis, cardiac arrest at a hospital with fewer than 250 beds, an unmonitored hospital unit, and arrest during after-hours periods.

Multiple resuscitations involving CPR have also been associated with worse outcomes. Among 166,519 hospitalized patients (from the Nationwide Inpatient Sample, an all-payer U.S. hospital database) who underwent CPR while hospitalized between 2000 and 2009240:

  • 3.4% survived the initial CPR and ultimately had multiple rounds of CPR during their hospitalization.
  • Patients who had multiple rounds of CPR had a significantly lower likelihood of survival to discharge.
  • Those who survived multiple rounds of CPR had high hospitalization costs and were more likely to be discharged to hospice care.

Survival following in-hospital SCA treated with an AED has also been evaluated using data derived from the National Registry of Cardiopulmonary Resuscitation. When compared with usual resuscitative care, the use of an AED did not improve survival among patients with a shockable rhythm and was associated with a lower survival to hospital discharge among patients with a non-shockable rhythm.242

In 2013 the AHA issued consensus recommendations regarding strategies for improving outcomes following in-hospital SCA. While the consensus recommendations focused on many of the same factors as out-of-hospital cardiac arrest (i.e., early identification of SCA, provision of high-quality CPR, early defibrillation when indicated), the authors commented on a lack of evidence specifically focused on in-hospital SCA, with many of the current guideline recommendations based on extrapolations of data from out-of-hospital SCA. Further data specifically focusing on in-hospital SCA are required prior to making any additional recommendations.243

Impact Of Arterial Oxygen Level

Arterial hyperoxia early after SCA may have deleterious effects, perhaps due to oxidative injury. The 2008 International Liaison Committee on Resuscitation cited preclinical evidence of harm from hyperoxia and suggested a goal arterial oxygenation of 94% to 96% post SCA.244

A study to examine this issue was performed using a multicenter database including 6,326 patients with arterial blood gas analysis within 24 hours after ICU admission following cardiac arrest. The study included patients with in-hospital and out-of-hospital SCA (57% were hospital inpatients, and 43% were from the emergency department). Oxygenation status was categorized according to the first ICU arterial blood gas value, with hyperoxia defined as PaO2 ≥300 mmHg, hypoxia as PaO2 <60 mmHg, and the remaining as normoxia. The majority of patients had hypoxia (63%) with similar numbers having hyperoxia (18%) and normoxia (19%). The hyperoxia group had higher in-hospital mortality compared with the normoxia and the hypoxia groups (63% versus 45% and 57%). In a multivariable model, hyperoxia was an independent risk factor for death. Hypoxia was also an independent risk factor. Further data are needed to determine the impact of oxygen titration during and after resuscitation.245

Case Study

Scenario/Situation/Patient Description

Mr. John Jomes is a 42 year old married, father of four, stockbroker who was in a committee meeting at work at 0845 when he suddenly collapsed falling forward and hitting his forehead on the table in front of him. EMS was quickly called while one of his work compatriots performed compression-only CPR. He regained consciousness with some slight confusion noted.

EMS arrived 20 minutes later. EMS personnel related to ED personnel that the patient denied chest pain or SHOB. C/o slight neck pain with a frontal HA. BP remained 120-140/66-80, HR 35-66 sinus bradycardia to NSR with infrequent PVCs. Afebrile. Slight confusion persists. Soft neck brace remains on with patient remaining of a backboard.

In the emergency department, the patient denies any SHOB, CP. He continues to c/o slight posterior neck pain with a frontal HA. Past medical history negative for DM, HTN or any cardiac/pulmonary issues. Negative past surgical history. Patient denies alcohol and/or drug usage or exposure to toxins. He takes Tylenol prn for aches and pains. States his mother died suddenly when she was 43 years of age, as well as, his uncle (his mother’s brother) in his 30s.


12-lead ECG shows sinus bradycardia to NSR with rare PVCs.

IV of 0.9 NS infusing at 100 ml/hr.

Continuous cardiac monitoring with pulse oximetry.

Following lab tests ordered and drawn: Comprehensive metabolic panel, CBC, Lipid profile, CK-MB, CK and MB, Troponins I and T, CRP, Coagulation studies, Toxicology screen.

Soft neck brace remains in place. Patient remains on backboard.

PA and lateral chest x-ray ordered.

PA and lateral neck x-rays ordered.

Discussion of Outcomes

12-lead ECG shows no evidence of cardiac ischemia, but rhythm remains sinus bradycardia to NSR with rare unifocal PVCs.

All laboratory tests ordered are WNL or negative.

Chest and neck x-rays remain normal.

Cardiologist on-call to evaluate patient in the emergency department.

Strengths and Weaknesses

Cardiologist to evaluate patient for structural heart disease/arrhythmias/primary electrical diseases with appropriate diagnostic procedures ordered.

Wife and other family members not available at present to obtain further information on SCD in family history.


SCA and SCD refer to the sudden cessation of organized cardiac electrical activity with hemodynamic collapse.

  • The event is referred to as SCA (or aborted SCD) if an intervention (e.g., defibrillation, cardioversion, antiarrhythmic drug) or spontaneous reversion restores circulation.
  • The event is called SCD if the patient dies. However, the use of SCD to describe both fatal and nonfatal cardiac arrest persists by convention.

SCD is the most common cause of cardiovascular death in the developed world.

  • Although the risk of SCD is higher in patients with structural heart disease, as many as 10 to 15% of SCDs occur in individuals with apparently normal hearts.
  • Causes of SCD with no structural heart disease include:
    • Brugada syndrome
    • Commotio cordis
    • Early repolarization syndrome
    • Familial SCD of Uncertain Cause
    • Idiopathic VF (Primary Electrical Disease)
    • LQTS congenital or acquired
    • SQTS
    • Polymorphic VT with Normal QT Interval (CPVT)
    • Third Degree (Complete) AV Block
    • VF Secondary to PVCs
    • WPW Syndrome and Other Forms of SVT
  • Survivors of SCA should undergo extensive testing to exclude drug or toxin exposure or underlying structural heart disease that may have contributed to SCA. Therapy with an ICD should generally be recommended in survivors of SCA.
  • In families of victims of unexplained SCD, a general cardiology evaluation of first- and second-degree relatives can yield diagnosis of a heritable disease in up to 40% of families.

The exact mechanism of collapse in an individual is often impossible to establish since, for the vast majority of patients who die suddenly, cardiac electrical activity is not being monitored at the time of their collapse. In studies, however, of patients who were having cardiac electrical activity monitored at the time of their event, VT or VF accounted for the majority of episodes, with bradycardia or asystole accounting for nearly all of the remainder.

  • In the majority of patients with VT/VF, sustained ventricular arrhythmia is preceded by an increase in ventricular ectopy and the development of repetitive ventricular arrhythmia, particularly runs of nonsustained VT. In about one-third of cases, the tachyarrhythmia is initiated by an early R on T PVC. In the remaining two-thirds, the arrhythmia is initiated by a late cycle PVC.
  • There are many cardiac and noncardiac causes for a sustained ventricular tachyarrhythmia that can result in SCD. Among all SCD in all age groups, the majority (65% to 70%) are related to CHD, with other structural cardiac disease (approximately 10%), arrhythmias in the absence of structural heart disease (5% to 10%), and noncardiac causes (15% to 25%) responsible for the remaining deaths.

The risk factors for SCA are similar to those for CHD.

The approach to primary prevention of SCD varies according to a patient's clinical profile.

For the general population without known cardiac disease:

  • Apart from standard screening and management of risk factors for CHD (e.g., measurement of lipids, BP, and glucose, etc.), in patients without known cardiac disease no additional screening tests are recommended or treatment for the purpose of primary prevention of SCD.

A heart-healthy lifestyle, including habitual physical activity, a heart-healthy diet, and abstinence or cessation of cigarette smoking, is recommended for the primary prevention of SCD.

Patients with known cardiac disease (e.g., prior MI, cardiomyopathy, or HF) are at an increased risk of SCA. The approach to the primary prevention of SCA in such patients includes the following:

  • Standard medical therapies that lower the incidence of SCA.
  • Testing for the purpose of SCA risk stratification in selected subgroups.
  • ICD implantation in selected patients.

The management of SCA includes acute treatment of the arrest, and for SCA survivors, a comprehensive evaluation and secondary prevention.

  • The acute management of SCA involves standard cardiopulmonary resuscitation protocols.
  • Initial evaluation of the survivor of SCD includes the following:
    • History and physical examination
    • Laboratory testing (electrolytes, blood gas, toxin screen, etc.)
    • ECG
  • Identification and treatment of acute reversible causes, including:
    • Acute cardiac ischemia and myocardial infarction
    • Antiarrhythmic drugs or other medication (e.g., QT-prolonging drugs), toxins, and/or illicit drug ingestion
    • Electrolyte abnormalities, most notably hypokalemia, hyperkalemia, and hypomagnesemia
    • HF
    • Autonomic nervous system factors, especially sympathetic activation (e.g., physical and/or psychological stress)
  • Evaluation for structural heart disease which may also include:
    • Coronary angiography
    • Echocardiography
    • Cardiac magnetic resonance imaging (CMR)
  • Evaluation for primary electrical disease may also include:
    • Electrophysiology studies
    • Exercise testing
    • Ambulatory ECG monitoring
    • Pharmacologic challenges
  • Neurologic and psychologic assessment
  • In selected patients with a suspected or confirmed heritable syndrome, evaluation of family members

Secondary prevention of SCD, usually with an ICD, is appropriate for most SCA survivors.

  • Because of its high success rate in terminating VT and VF rapidly, along with the results of multiple clinical trials showing improvement in survival, ICD implantation is generally considered the first-line treatment option for the secondary prevention of SCD and for primary prevention in certain populations at high risk of SCD due to VT/VF. However, there are some situations in which ICD therapy is not recommended, including, but not limited to, patients with VT/VF from a completely reversible disorder and patients without a reasonable expectation of survival with an acceptable functional status for at least one year.
    • The ICD system is comprised of pacing/sensing electrodes, defibrillation electrodes, and a pulse generator.
    • Most current ICD systems utilize one, two, or three transvenous leads placed via the axillary, subclavian, or cephalic vein, with attachment to a pulse generator in the subcutaneous tissue in the infraclavicular anterior chest wall.
    • DFT testing is generally performed at the time of device implantation in patients receiving a subcutaneous ICD and is reasonable in patients undergoing a right pectoral ICD implantation or ICD pulse generator changes (on either right or left side). However, DFT testing is not required and can be omitted in patients undergoing a left pectoral transvenous ICD implantation with a right ventricular apical lead that is functioning appropriately.
    • Contemporary ICDs have extensive storage and monitoring capacities, the ability to deliver antitachycardia pacing (i.e., overdrive pacing) to terminate VT, the ability to deliver synchronized and unsynchronized shocks for VT/VF, and the option of bradycardia pacing.
    • There are a variety of complications associated with ICDs including:
      • At and around the time of implantation:
        • Bleeding
        • Cardiac perforation
        • Infection
        • Perioperative mortality
        • Shoulder related problems (i.e., decreased shoulder mobility, pain, reduced function, insertion tendonitis)
        • Long-term complications including:
        • Lead-related problems (i.e., increased defibrillation thresholds, infection, lead failure resulting in failure to pace, failure to shock, or inappropriate shocks, tricuspid valve damage, and venous thrombosis.
        • Pulse generator complications may include electronic circuit damage, electromagnetic interference, skin erosion due to the size and weight of the generator and infection of the pulse generator pocket, as well as, Twiddlers Syndrome.
        • Arrhythmia-related problems including appropriate shocks which can have an adverse effect on the quality of life, inappropriate shocks, usually due to the treatment of supraventricular tachycardias, as well as, "phantom" shocks.
  • Antiarrhythmic drugs can be considered as the primary therapy when an ICD is not indicated or refused by the patient.
    • Nearly all patients who have survived SCA should receive a beta blocker as part of their therapy, which may also provide additional antiarrhythmic benefits.
    • Because an ICD does not prevent arrhythmias, patients who have arrhythmias with symptoms or device discharges may require adjunctive antiarrhythmic therapy or consideration of catheter ablation.
    • The three main indications for concomitant antiarrhythmic drug therapy are:
      1. To reduce the frequency of ventricular arrhythmias in patients with frequent ICD shocks.
      2. To suppress other arrhythmias that cause symptoms or interfere with ICD function (e.g., causing "inappropriate" shocks).
      3. To reduce the ventricular rate of VT so that it is better tolerated hemodynamically and more amenable to termination by anti-tachycardia pacing or low-energy cardioversion.
    • For patients with an ICD who require adjunctive antiarrhythmic therapy due to ongoing arrhythmias, treatment with the combination of amiodarone plus a beta blocker rather than treatment with amiodarone alone or other antiarrhythmic agents is recommended. This approach is especially preferred in patients with significant left ventricular dysfunction who require adjunctive antiarrhythmic therapy since amiodarone does not exacerbate HF and is less proarrhythmic than other agents.
    • Adverse effects related to antiarrhythmic medications include increased DFTs and slowing of the tachycardia rate, which may preclude its recognition by the ICD.

Despite advances in the treatment of heart disease, the outcome of patients experiencing SCA remains poor. The reasons for the continued poor outcomes are likely multifactorial (e.g., delayed bystander CPR, delayed defibrillation, advanced age, decreased proportion presenting with VF.)

  • When SCA is due to a ventricular tachyarrhythmia, the outcome of resuscitation is better compared with those with asystole or pulseless electrical activity.
  • Among the many factors that appear to have an influence on the outcome of SCA, the elapsed time prior to effective resuscitation (i.e., establishment of an effective pulse) appears to be the most critical element. There are several ways to decrease the time to the onset of resuscitative efforts:
    • Rapid EMS response
      • Optimizing the EMS system within a community to reduce the response interval to eight minutes or less where possible.
    • Bystander CPR
      • The administration of bystander CPR is an important factor in determining patient outcome after out-of-hospital SCA, as early restoration or improvement in circulation has been shown to result in greater survival and better neurologic function among survivors.
      • Bystander CPR, however, is not always performed, primarily due to the bystander’s lack of CPR training and/or concerns about possible transmission of disease while performing rescue breathing.
    • Early defibrillation
      • The standard of care for resuscitation of SCA has been defibrillation as soon as possible when indicated.
      • Shorter defibrillation response intervals correlate with greater survival to hospital discharge.
    • Automated external defibrillators
      • The use of AEDs by early responders is another approach to more rapid resuscitation.
      • In most, but not all studies, AEDs have been found to improve survival after out-of-hospital cardiac arrest.
  • Several observational studies evaluating compression-only CPR versus standard CPR including rescue breathing reported no significant differences in survival or long-term neurologic function between the two groups, suggesting that compression-only CPR could be safely delivered (as long as the arrest is not a respiratory arrest).
    • It is recommended that, if a sole bystander is present or multiple bystanders are reluctant to perform mouth-to-mouth ventilation, the performance of CPR using chest compressions only be performed.
  • The induction of mild to moderate hypothermia (target temperature of 32 to 34ºC for 24 hours) may be beneficial in patients successfully resuscitated after a cardiac arrest. Improved neurologic outcome and reduced mortality have been demonstrated in series of patients with VF arrest in whom spontaneous circulation was restored, even when the patient remains comatose after resuscitation.


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This course is applicable for the following professions:

Advanced Registered Nurse Practitioner (ARNP), Certified Registered Nurse Anesthetist (CRNA), Clinical Nurse Specialist (CNS), Licensed Practical Nurse (LPN), Licensed Vocational Nurses (LVN), Registered Nurse (RN)


Advance Practice Nurse Pharmacology Credit, Cardiology, CPD: Practice Effectively, Critical Care / Emergency Care

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