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:
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.
SCA = Sudden cardiac arrest
SCD = Sudden cardiac death
|Abnormal Cardiac Rhythms|
|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|
|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|
|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|
|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|
Various criteria have been used to define SCA and SCD in the medical literature.3 Difficulties in deriving a specific definition include the following:
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:
SCA usually occurs in individuals with some form of underlying structural heart disease, most notably 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:
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:
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.
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
Fifteen to 25% of cardiac arrests are noncardiac in origin.21,41
Noncardiac disease triggers for SCA/SCD include:
"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:
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.
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:
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:
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
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.
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
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
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.
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:
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).
|Condition||Common Associated Clinical Setting64|
|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.
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:
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.
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:
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.
The optimal approach to the primary prevention of SCA varies among the following categories:
There are two approaches to reduce the risk of SCA in the general population:
Patients with HF and LV systolic dysfunction, regardless of the etiology, are at an increased risk of SCA.
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.
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.
|Class||NYHA Functional Classification||Specific Activity Scale|
|I||Patients 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).|
|II||Patients 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.|
|III||Patients 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.|
|IV||Patients 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).|
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.
|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 are subdivided into:
Ia – Quinidine, Procainamide, Disopyramide
Ib – Lidocaine, Tocainide, Mexiletine, Phenytoin
Ic – Flecainide, Propafenone, Ecainide, Moricizine
Class II agents include:
Metoprolol, Propranolol, Esmolol, Atenolol
Class III agents include:
Amiodarone, Sotalol, Azimilide, Bretylium, Cloflium, Dofetilide, Tedisamil, Ibutilide, Sematilide
Class IV agents include:
Class V agents include:
Magnesium, Digitalis (digoxin), Adenosine
Despite advances in the treatment of heart disease, the outcome of patients experiencing SCA remains poor.157-160 For example:
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
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.
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:
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
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
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.
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:
There are also several poor prognostic features in patients with SCA who survive until admission:
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:
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
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
Despite the benefits of bystander CPR, it is not always performed. Reasons for this include204:
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:
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.
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.
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.
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.
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:
The ALS rule includes the BLS criteria, as well as, two additional criteria219:
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.
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 :
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.
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.
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.
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:
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:
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:
The impact of comorbidities was more prominent with longer EMS response intervals.
The reported long-term survival of resuscitated SCD survivors is variable and may depend upon multiple factors:
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
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:
Other factors have been identified that predict a lower likelihood of survival to hospital discharge240,241:
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:
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:
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
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
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.
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.
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.
SCD is the most common cause of cardiovascular death in the developed world.
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.
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:
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:
The management of SCA includes acute treatment of the arrest, and for SCA survivors, a comprehensive evaluation and secondary prevention.
Secondary prevention of SCD, usually with an ICD, is appropriate for most SCA survivors.
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.)