California RN and LPN Nursing CEUs
Meet Your California RN or LVN Continuing Education Requirements Quickly & Affordably.

Authors: Pamela Downey (MSN, ARNP)

Outcomes

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, and factors that influence the outcome of such an event.

Objectives

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

  1. Differentiate between 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 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 structural heart disease and primary electrical disease evaluation 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.

Introduction

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. 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.

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 due to 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
Acronym Meaning Acronym Meaning
AF Atrial fibrillation PVC Premature ventricular contraction
AV Atrioventricular block SQTS Short QT syndrome
CPVT Catechaminergic polymorphic ventricular tachycardia SVT Supraventricular tachycardia
LQTS Long QT syndrome VF Ventricular fibrillation
NSVT Nonsustained ventricular tachycardia VT Ventricular tachycardia
PEA Pulseless electrical activity WPW Wolff-Parkinson-White
Cardiac/Noncardiac Diagnoses
ACS Acute coronary syndrome MI Myocardial infartion
ARVC Arrhythmogenic right ventricular STEMI ST elevation MI
CHD Coronary heart disease NSTEMI Non-ST elevation MI
CHF Congestive hear failure PTSD Posttraumatic stress disorder
CVD Cardiovascular disease SIDS Sudden infant death syndrome
HCM Hypertrophic cardiomyopathy SUDEP Sudden unexplained death in epilepsy
HF Heart failure SUNDS Sudden unexplained nocturnal death syndrome
Cardiac Interventions/Management
ACE Angiotensin-converting enzyme EMI Electromagnetic interference
AED Automated external difibrillator EP Electrophysiologic
CABG Coronary artery bypass graft ESU Electrosurgery unit
CCB Calcium channel blocker ETT Exercise tolerance testing
CMR Cardiac magnetic resonance imaging ICD Implantable cardioverter-defibrillator
CRP C-reactive protein LVEF Left ventricular carioverter-defibrillator
CRT Cardiac resynchronization therapy MRI Magnetic resonance imaging
CRT-D Cardiac resynchronization therapy defibrillator PCI Percutaneous coronary intervention
DFT Defibrillation threshold testing S-ICD Subcutaneous coronary intervention
ECT Electrocardiogram WCD Wearable cardioverter-defibrillator
Others
EMS Emergency medical services AHA American Heart Association
BLS Basic life support HRS Heart Rhythm Society
ALS Advanced life support LV Left ventricular
CARES Cardiac Arrest Registry to Enhance Survival PA Posteroanterior
ACC American College of Cardiology IV Intravenous

Definitions

Various criteria have been used to define SCA and SCD in the medical literature. 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 before 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 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.

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 signify a reversed event, usually by CPR, defibrillation, cardioversion, or cardiac pacing. Sudden cardiac death should not describe events that are not fatal.

Epidemiology

The following observations illustrate SCA:

  • 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.
  • SCD is the mechanism of death in over 60% of patients with known CHD.
  • SCA is the initial clinical manifestation of CHD in approximately 15% of patients.

Etiology

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

Coronary Heart Disease (CHD)

Although not specifically mentioned in most of these studies, heart failure (HF) is a relatively common cause of SCD. Although the risk of arrhythmic and non-arrhythmic 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:

  • Acute pericardial tamponade
  • Acute myocardial rupture
  • Aortic dissection
  • Congenital coronary artery anomalies
  • HF and cardiomyopathy, 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

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

Noncardiac Disease

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

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 many individuals. Still, 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.

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

Several clinical characteristics and other factors are associated with an increased risk of SCA among individuals without prior clinically recognized heart disease. Most risk factors for CHD are also risk factors for SCA. These include:

  • 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.

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 and a multitude of other complications.

Exercise

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

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

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. 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 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, interactions of mutations or polymorphisms in specific genes and environmental factors likely influence this risk.

Serum C-Reactive Protein (CRP)

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

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. In comparison, heavy alcohol consumption (six or more drinks per day) or binge drinking increases the risk for SCD.

Psychosocial Factors

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

Caffeine

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

Fatty Acids

After myocardial infarction, elevated plasma nonesterified fatty acid (free fatty acid) concentrations were associated with ventricular arrhythmias and SCD. However, nonesterified fatty acids were not associated with SCD in the Cardiovascular Health Study, a population-based cohort of older adults. 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. 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.

Management

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
Condition Common Associated Clinical Setting
Acidosis Diabetes, diarrhea, drug overdose, renal dysfunction, sepsis, shock
Anemia Gastrointestinal bleeding, nutritional deficiencies, recent trauma
Cardiac Tamponade Post-cardiac surgery, malignancy, post-myocardial infarction, pericarditis, trauma
Hyperkalemia Drug 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
Hypothermia Alcohol intoxication, significant burns, drowning, drug overdose, elderly patient, endocrine disease, environmental exposure, spinal cord disease, trauma
Hypovolemia Significant burns, diabetes, gastrointestinal losses, hemorrhage, malignancy, sepsis, trauma
Hypoxia Upper airway obstruction, hypoventilation (CNS** dysfunction, neuromuscular disease), pulmonary disease
Myocardial Infarction Cardiac arrest
Poisoning History of alcohol or drug abuse, altered mental status, classic toxidrome (e.g., sympathomimetic), occupational exposure, psychiatric disease
Pulmonary Embolism Immobilized patient, recent surgical procedure (e.g., orthopedic), peripartum, risk factors for thromboembolic disease, recent trauma, presentation consistent with acute pulmonary embolism
Tension Pneumothorax Central 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.

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.

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

Coronary angiography and echocardiography may be part of an urgent initial evaluation in the appropriate clinical setting.

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

Evaluation for Primary Electrical Diseases

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 determining prognosis.

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 are 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:

  • Screening and risk stratification 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 various tests can identify subgroups that benefit from specific therapies, such as an ICD.
    • However, 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 in the general population without known CVD.
    • 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 SCA risk stratification is not recommended.
  • Interventions may be expected to reduce SCA risk in any individual (e.g., smoking cessation or other lifestyle modifications). Such interventions generally target the underlying disorders that predispose to SCA.
    • Many traditional risk factors associated with CHD development are also associated with SCA.
    • Management of these risk factors may reduce SCA incidence 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. 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.
        • 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 to prevent 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.
        • 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 time.
        • Patients with known heart disease should be encouraged to exercise in a supervised setting such as a cardiac rehabilitation program regularly.
      • Smoking cessation
      • Moderation of alcohol consumption
        • Excess alcohol intake increases SCA risk, while light-to-moderate alcohol consumption (i.e., ≤2 drinks per day) is associated with a lower risk of CAD and cardiovascular mortality.
        • It is reasonable to expect that moderate alcohol intake will also reduce SCA.
      • Effective treatment of diabetes
    • There is no definitive evidence that risk factor reduction in the general population lowers the SCA rate. However, several studies have demonstrated that interventions to treat risk factors can lower total cardiovascular and coronary mortality. Since most CHD mortality is due to SCD, these results suggest that reducing risk factors will also reduce SCD rates.
      • 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. Compared to the control group, the intervention group had significant CHD and coronary mortality reductions.

Post Myocardial Infarction

Patients who have had an MI are at an increased risk of SCA. However, this risk varies significantly among post-MI patients according to several factors.

The approach to the prevention of SCA in post-MI patients includes the following:

  • Standard Medical Therapies
    • Both beta-blockers and ACE inhibitors (or angiotensin II receptor blockers):
      • Reduce overall mortality after an MI and are routinely administered.
      • Lower the incidence of SCD.
      • The benefit, however, may be limited to three years post MI.
    • Beta-blockers post-MI is useful for a longer time in patients with post-MI HF.
  • Risk stratification to identify those patients at the highest risk of SCA.
  • ICD implantation in selected patients.

Heart Failure and Cardiomyopathy

Regardless of the etiology, patients with HF and LV systolic dysfunction 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 or eplerenone) may lower the risk of SCA.

Counseling Patients and Families

Given the mounting evidence related to the primary prevention of SCA, it is now 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 with frequent arrhythmia recurrences and device discharges may benefit from adjunctive therapies, such as antiarrhythmic drugs or catheter ablation.

Antiarrhythmic Drugs

Antiarrhythmic drugs are less effective than an ICD for secondary prevention of SCD. Consequently, their use in the setting of SCD is limited to an adjunctive role as described above, or in patients who do not want or are not candidates for an ICD (e.g., due to marked comorbidities or end-stage HF that make death likely).

Prognosis And Outcomes Following Sudden Cardiac Arrest

Despite advances in the treatment of heart disease, the outcome of patients experiencing SCA remains poor (Wong et al., 2014).

  • 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) (Wong et al., 2014).
  • 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 (Smith et al., 2015).

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

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. These results should be considered hypothesis-generating for larger-scale studies (Patterson et al., 2017).

Neurologic Prognosis Following SCA

Survivors of SCA have variable susceptibility to hypoxic-ischemic brain injury, depending on the duration of circulatory arrest, the 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.

Asystole

When the initially 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. 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 include:

  • 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 with SCA due to PEA (also called electrical-mechanical dissociation) have a poor outcome.

Ventricular Tachyarrhythmia

The outcome is much better when the initial rhythm is sustained ventricular tachyarrhythmia. Acute MI or myocardial ischemia is the underlying cause of VF for many of the patients who survive hospital discharge.

Survival is approximately 65% to 70% in patients with hemodynamically unstable VT. 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.

SCA due to Noncardiac Causes

As many as one-third of cases of SCA are due to noncardiac causes. Trauma, nontraumatic bleeding, intoxication, near drowning, and pulmonary embolism are the most common noncardiac etiologies.

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 (Chan et al., 2014).

The cause of death in-hospital is most often noncardiac, usually anoxic encephalopathy, or respiratory complications from long-term ventilator dependence.

In addition to later initiation of CPR and the presence of asystole or PEA (electromechanical dissociation), several other factors are associated with a decreased likelihood of survival with neurologic function intact following out-of-hospital SCA:

  • 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 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. 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. After more than 12 minutes without CPR, the survival rate is only 2% to 5%.

Time to Resuscitation

These observations constitute the rationale for providing 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.

However, the response times of both BLS and ALS services have increased, possibly due to population growth and urbanization. Thus, bystander CPR and even defibrillation have been recommended and implemented in some settings. Such interventions permit more rapid responses than those provided by BLS or ALS personnel, with better survival as a result.

Bystander CPR

The administration of CPR by a layperson bystander (bystander CPR or bystander-initiated CPR) is important 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.

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 importance of bystander CPR and support for compression-only bystander CPR comes from a combination of retrospective and prospective studies.

These observations were subsequently confirmed in larger studies (Nakahara et al., 2015).

  • 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%). Recipients of bystander CPR had a significantly greater chance of neurologically intact survival (8.4% versus 4.1% without bystander CPR) (Nakahara et al., 2015). Bystanders' early defibrillation was also associated with significantly greater survival odds 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%).

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

  • The bystander's lack of CPR training.
  • The bystander's concerned about the possible transmission of disease while performing rescue breathing.
  • Neighborhood demographics (racial composition and income level) also appear to be a factor in the performance rates of bystander CPR.

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 CPR.

Chest Compression-Only CPR

Bystander CPR with only chest compressions improves survival to hospital discharge, compared with chest compressions with interruptions for rescue breathing, with an absolute improvement in mortality of 2.4% (Zhan et al., 2017).

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.

In a nationwide study of Japanese out-of-hospital cardiac arrest victims between 2005 and 2012, chest compression-only CPR improved the number of SCA victims receiving bystander CPR and the number of patients surviving with favorable neurological outcomes (Iwami et al., 2015). 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.

Timing of Defibrillation

VF's standard of care for resuscitation has been defibrillation as soon as possible. In the Seattle series of over 12,000 EMS-treated patients, 4,546 had witnessed VF. The defibrillation response interval was significantly correlated with survival to hospital discharge (odds ratio 0.88 for every one-minute increase in response time). Subsequent studies have shown similar benefits, with earlier defibrillation associated with improved survival (Nakahara et al., 2015).

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. 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. Survival to hospital discharge was significantly increased with routine CPR before defibrillation, primarily in patients whose initial response interval was four minutes or longer.

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

Early defibrillation and CPR should be performed as recommended in the 2010 ACLS guidelines for SCA and ventricular tachyarrhythmia patients.

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 improved survival after out-of-hospital cardiac arrest.

Predictive Value of BLS and ALS Rules

The OPALS study group has proposed two terminations of resuscitation rules for use by EMS personnel. The rule for BLS providers equipped with AEDs includes the following three criteria:

  1. Event not witnessed by EMS personnel

  2. No AED was used, or manual shock was applied in the out-of-hospital setting

  3. No return of spontaneous circulation in the out-of-hospital setting

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

  1. Arrest not witnessed by a 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.

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 various 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.

The effect of CPR quality has been evaluated in several studies (Brouwer et al., 2015):

  • 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).
  • In a study of 3,098 patients with out-of-hospital cardiac arrest, the return of spontaneous circulation was highest at a rate of 125 compressions per minute. 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. They may provide prognostic information, suggesting that the cardiac output maintained during CPR determines the 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 an unfavorable neurologic recovery risk.

On the other hand, the induction of mild to moderate hypothermia (target temperature 32 to 34ºC for 24 hours) may benefit 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 survival rate for out-of-hospital cardiac arrest was observed with the addition of an ACLS program.
  • 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.

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 arrests.

Effect of Gender

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

  • 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 higher one-month survival than women following SCA due to the higher likelihood of VF/VT as their presenting rhythm.
  • Women have a greater survival with favorable neurologic outcomes when considering only patients with VF/VT as the initial rhythm.

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. 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.

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%. Several clinical factors have been identified that predict a greater likelihood of survival to hospital discharge:

  • Pulse regained during the 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 discharge:

  • Longer duration of overall resuscitation efforts
  • Multiple resuscitation efforts

Delays in providing initial defibrillation have been associated with worse outcomes. Delayed defibrillation (more than two minutes after SCA) occurred in 30% of patients and was associated with a significantly lower probability of hospital discharge survival.

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

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 before making additional recommendations.

Impact Of Arterial Oxygen Level

Arterial hyperoxia early after SCA may have deleterious effects, perhaps due to oxidative injury. In a multivariable model, hyperoxia was an independent risk factor for death. Hypoxia was also an independent risk factor.

Case Study

Scenario/Situation/Patient Description

Mr. John Jomes is a 42-year-old married father of four, a 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 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. A soft neck brace remains on, with the patient remaining on 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. The patient denies alcohol 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 and his uncle (his mother’s brother) in his 30s.

Interventions/Strategies

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 a 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 the 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 a patient in the emergency department.

Strengths and Weaknesses

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

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

Summary

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 diagnose 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 with cardiac electrical activity monitored at the time of their event, VT or VF accounted for most episodes, with bradycardia or asystole accounting for nearly all of the remainder.

  • In most 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 sustained ventricular tachyarrhythmia resulting in SCD. Among all SCD in all age groups, the majority (65% to 70%) are related to CHD, with other structural cardiac diseases (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 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 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, or illicit drug ingestion
    • Electrolyte abnormalities, most notably hypokalemia, hyperkalemia, and hypomagnesemia
    • HF
    • Autonomic nervous system factors, especially sympathetic activation (e.g., physical or psychological stress)
  • Evaluation for structural heart disease which may also include:
    • Coronary angiography
    • Echocardiography
    • Cardiac magnetic resonance imaging (CMR)
  • Evaluation for a 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 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 during device implantation in patients receiving a subcutaneous ICD. It is reasonable in patients undergoing a right pectoral ICD implantation or ICD pulse generator changes (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 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 include:
        • 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, infection of the pulse generator pocket, and Twiddlers Syndrome.
        • Arrhythmia-related problems include appropriate shocks that can harm the quality of life, inappropriate shocks, usually due to the treatment of supraventricular tachycardias, and "phantom" shocks.
  • Antiarrhythmic drugs can be considered 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 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:
      • To reduce the frequency of ventricular arrhythmias in patients with frequent ICD shocks.
      • To suppress other arrhythmias that cause symptoms or interfere with ICD function (e.g., causing "inappropriate" shocks).
      • 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 of 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 influence the outcome of SCA, the elapsed time before effective resuscitation (i.e., the 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 resulted 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 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 improved 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, CPR performance using chest compressions should 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 a series of patients with VF arrest in whom spontaneous circulation was restored, even when the patient remains comatose after resuscitation.

References

  • Arnson Y, Suleiman M, Glikson M, et al. Role of defibrillation threshold testing during implantable cardioverter-defibrillator placement: data from the Israeli ICD Registry. Heart Rhythm 2014; 11:814.
  • Phan K, Kabunga P, Kilborn MJ, Sy RW. Defibrillator Threshold Testing at Generator Replacement: Is it Time to Abandon the Practice? Pacing Clin Electrophysiol 2015; 38:777.
  • Phan K, Ha H, Kabunga P, et al. Systematic Review of Defibrillation Threshold Testing at De Novo Implantation. Circ Arrhythm Electrophysiol 2016; 9:e003357.
  • Russo AM, Stainback RF, Bailey SR, et al. ACCF/HRS/AHA/ASE/HFSA/SCAI/SCCT/SCMR 2013 appropriate use criteria for implantable cardioverter-defibrillators and cardiac resynchronization therapy: a report of the American College of Cardiology Foundation appropriate use criteria task force, Heart Rhythm Society, American Heart Association, American Society of Echocardiography, Heart Failure Society of America, Society for Cardiovascular Angiography and Interventions, Society of Cardiovascular Computed Tomography, and Society for Cardiovascular Magnetic Resonance. J Am Coll Cardiol 2013; 61:1318.
  • Wilkoff BL, Fauchier L, Stiles MK, et al. 2015 HRS/EHRA/APHRS/SOLAECE expert consensus statement on optimal implantable cardioverter-defibrillator programming and testing. Heart Rhythm 2016; 13:e50.
  • Yannopoulos D, Bartos JA, Raveendran G, et al. Coronary Artery Disease in Patients With Out-of-Hospital Refractory Ventricular Fibrillation Cardiac Arrest. J Am Coll Cardiol 2017; 70:1109.
  • Wei D, Tao L, Huang M. Genetic variations involved in sudden cardiac death and their associations and interactions. Heart Fail Rev 2016; 21:401.

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?
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