Overview and Definitions

Sudden cardiac death (SCD) is defined as natural death due to cardiac causes in a person who may or may not have previously recognized heart disease but in whom the
time and mode of death are unexpected. In the context of time, "sudden" is defined for most clinical and epidemiologic purposes as 1 h or less between a change in clinical
status heralding the onset of the terminal clinical event and the cardiac arrest itself. An exception is unwitnessed deaths, in which pathologists may expand the definition of
time to 24 h after the victim was last seen to be alive and stable.

The overwhelming majority of natural deaths are caused by cardiac disorders. However, it is common for underlying heart diseasesoften far advancedto go unrecognized
before the fatal event. As a result, up to two-thirds of all SCDs occur as the first clinical expression of previously undiagnosed disease or in patients with known heart disease,
the extent of which suggests low risk. The magnitude of sudden cardiac death as a public health problem is highlighted by the estimate that ~50% of all cardiac deaths are
sudden and unexpected, accounting for a total SCD burden estimated to range from <200,000 to >450,000 deaths each year in the United States. SCD is a direct
consequence of cardiac arrest, which may be reversible if addressed promptly. Since resuscitation techniques and emergency rescue systems are available to respond to
victims of out-of-hospital cardiac arrest, which was uniformly fatal in the past, understanding the SCD problem has practical clinical importance.

Because of community-based interventions, victims may remain biologically alive for days or even weeks after a cardiac arrest that has resulted in irreversible central nervous
system damage. Confusion in terms can be avoided by adhering strictly to definitions of cardiovascular collapse, cardiac arrest, and death (Table 273-1). Although cardiac
arrest is often potentially reversible by appropriate and timely interventions, death is biologically, legally, and literally an absolute and irreversible event. Death may be delayed
in a survivor of cardiac arrest, but "survival after sudden death" is an irrational term. When biologic death of a cardiac arrest victim is delayed because of interventions, the
relevant pathophysiologic event remains the sudden and unexpected cardiac arrest that leads ultimately to death, even though delayed by interventions. The language used
should reflect the fact that the index event was a cardiac arrest and that death was due to its delayed consequences. Accordingly, for statistical purposes, deaths that occur
during hospitalization or within 30 days after resuscitated cardiac arrest are counted as sudden deaths.

Table 2731. Distinction between Cardiovascular Collapse, Cardiac Arrest, and Death

Clinical Definition of Forms of Cardiovascular Collapse

Cardiovascular collapse is a general term connoting loss of sufficient cerebral blood flow to maintain consciousness due to acute dysfunction of the heart and/or peripheral
vasculature. It may be caused by vasodepressor syncope (vasovagal syncope, postural hypotension with syncope, neurocardiogenic syncope; Chap. 20), a transient severe
bradycardia, or cardiac arrest. The latter is distinguished from the transient forms of cardiovascular collapse in that it usually requires an intervention to restore spontaneous
blood flow. In contrast, vasodepressor syncope and other primary bradyarrhythmic syncopal events are transient and non-life-threatening, with spontaneous return of
consciousness.

The most common electrical mechanism for cardiac arrest is ventricular fibrillation (VF), which is responsible for 5080% of cardiac arrests. Severe persistent
bradyarrhythmias, asystole, and pulseless electrical activity [PEA: organized electrical activity, unusually slow, without mechanical response, formerly called electromechanical
dissociation (EMD)] cause another 2030%. Pulseless sustained ventricular tachycardia (a rapid arrhythmia distinct from PEA) is a less common mechanism. Acute low
cardiac output states, having a precipitous onset, also may present clinically as a cardiac arrest. These hemodynamic causes include massive acute pulmonary emboli,
internal blood loss from a ruptured aortic aneurysm, intense anaphylaxis, and cardiac rupture with tamponade after myocardial infarction (MI). Sudden deaths due to these
causes are not included in the SCD category.

Etiology, Initiating Events, and Clinical Epidemiology

Clinical, epidemiologic, and pathologic studies have provided information on the underlying structural abnormalities in victims of SCD and identified subgroups at high risk for
SCD. In addition, studies of clinical physiology have begun to identify transient functional factors that may convert a long-standing underlying structural abnormality from a
stable to an unstable state, leading to the onset of cardiac arrest (Table 273-2).

Table 2732. Cardiac Arrest and Sudden Cardiac Death

Structural Associations and Causes
I. Coronary heart disease
A. Coronary artery abnormalities
1. Chronic atherosclerotic lesions
2. Acute (active) lesions (plaque fissuring, platelet aggregation, acute thrombosis)
3. Anomalous coronary artery anatomy
B. Myocardial Infarction
1. Healed
2. Acute
II. Myocardial hypertrophy
A. Secondary
B. Hypertrophic cardiomyopathy
1. Obstructive
2. Nonobstructive
III. Dilated cardiomyopathyprimary muscle disease
IV. Inflammatory and infiltrative disorders.
A. Myocarditis
B. Noninfectious inflammatory diseases
C. Infiltrative diseases
V. Valvular heart disease
VI. Electrophysiologic abnormalities, structural
A. Anomalous pathways in Wolff-Parkinson-White syndrome
B. Conducting system disease
VII. Inherited disorders associated with electrophysiological abnormalities (congenital long QT syndromes, right ventricular dysplasia, Brugada syndrome, catecholaminergic
polymorphic ventricular tachycardia, etc.)
Functional Contributing Factors
I. Alterations of coronary blood flow
A. Transient ischemia
B. Reperfusion after ischemia
II. Low cardiac output states
 A. Heart failure
1. Chronic
2. Acute decompensation
B. Shock
III. Systemic metabolic abnormalities
A. Electrolyte imbalance (e.g., hypokalemia)
B. Hypoxemia, acidosis
IV. Neurologic disturbances
A. Autonomic fluctuations: central, neural, humoral
B. Receptor function
V. Toxic responses
A. Proarrhythmic drug effects
B. Cardiac toxins (e.g., cocaine, digitalis intoxication)
C. Drug interactions

Cardiac disorders constitute the most common causes of sudden natural death. After an initial peak incidence of sudden death between birth and 6 months of age [the sudden
infant death syndrome (SIDS)], the incidence of sudden death declines sharply and remains low through childhood and adolescence. Among adolescents and young adults,
the incidence of SCD is approximately 1 per 100,000 population per year. The incidence begins to increase in adults over age 30 years, reaching a second peak in the age
range 4575 years, when it approximates 12 per 1000 per year among the unselected adult population. Increasing age within this range is associated with increasing risk for
sudden cardiac death (Fig. 273-1A). From 1 to 13 years of age, only one of five sudden natural deaths is due to cardiac causes. Between 14 and 21 years of age, the
proportion increases to 30%, and it rises to 88% in the middle-aged and elderly.

Young and middle-aged men and women have different susceptibilities to SCD, but the sex differences decrease with advancing age. The difference in risk for SCD parallels
the differences in age-related risks for other manifestations of coronary heart disease (CHD) between men and women. As the gender gap for manifestations of CHD closes in
the sixth to eighth decades of life, the excess risk of SCD in males progressively narrows. Despite the lower incidence among younger women, coronary risk factors such as
cigarette smoking, diabetes, hyperlipidemia, and hypertension are highly influential, and SCD remains an important clinical and epidemiologic problem. The incidence of SCD
among the African-American population appears to be higher than it is among the white population; the reasons remain uncertain.

Genetic factors contribute to the risk of acquiring CHD and its expression as acute coronary syndromes, including SCD. In addition, however, there are data suggesting a
familial predisposition to SCD as a specific form of expression of CHD. A parental history of SCD as an initial coronary event increases the probability of a similar expression in
the offspring. In a number of less common syndromes, such as hypertrophic cardiomyopathy, congenital long QT interval syndromes, right ventricular dysplasia, and the
syndrome of right bundle branch block and nonischemic ST-segment elevations (Brugada syndrome), there is a specific inherited risk of ventricular arrhythmias and SCD
(Chap. 233).

The structural causes of and functional factors contributing to the SCD syndrome are listed in Table 273-2. Worldwide, and especially in Western cultures, coronary
atherosclerotic heart disease is the most common structural abnormality associated with SCD in middle-aged and older adults. Up to 80% of all SCDs in the United States are
due to the consequences of coronary atherosclerosis. The nonischemic cardiomyopathies (dilated and hypertrophic, collectively; Chap. 231) account for another 1015% of
SCDs, and all the remaining diverse etiologies cause only 510% of all SCDs. The inherited arrhythmia syndromes (see above and Table 273-2) are proportionally more
common causes in adolescents and young adults. For some of these syndromes, such as hypertrophic cardiomyopathy (Chap. 238), the risk of SCD increases significantly
after the onset of puberty.

Transient ischemia in a previously scarred or hypertrophied heart, hemodynamic and fluid and electrolyte disturbances, fluctuations in autonomic nervous system activity, and
transient electrophysiologic changes caused by drugs or other chemicals (e.g., proarrhythmia) have all been implicated as mechanisms responsible for the transition from
electrophysiologic stability to instability. In addition, reperfusion of ischemic myocardium may cause transient electrophysiologic instability and arrhythmias.

Pathology

Data from postmortem examinations of SCD victims parallel the clinical observations on the prevalence of CHD as the major structural etiologic factor. More than 80% of SCD
victims have pathologic findings of CHD. The pathologic description often includes a combination of long-standing, extensive atherosclerosis of the epicardial coronary arteries
and unstable coronary artery lesions, which include various permutations of eroded, fissured, or ruptured plaques; platelet aggregates; hemorrhage; and/or thrombosis. As
many as 7075% of males who die suddenly have preexisting healed MIs, whereas only 2030% have recent acute MIs, despite the prevalence of unstable plaques and
thrombi. The latter suggests transient ischemia as the mechanism of onset. Regional or global left ventricular (LV) hypertrophy often coexists with prior MIs.

Prediction and Prevention of Cardiac Arrest and Sudden Cardiac Death

SCD accounts for approximately one-half the total number of cardiovascular deaths. As shown in Fig. 273-1B, the very high risk subgroups provide more focused populations
("percent per year") for predicting cardiac arrest or SCD, but the representation of such subgroups within the overall population burden of SCD, indicated by the absolute
number of events ("events per year"), is relatively small. The requirements for achieving a major population impact are effective prevention of underlying diseases and/or new
epidemiologic probes that will allow better resolution of specific high-risk subgroups within the large general populations.

Strategies for predicting and preventing SCD are classified as primary and secondary. Primary prevention, as defined in various implantable defibrillator trials, refers to the
attempt to identify individual patients at specific risk for SCD and institute preventive strategies. Secondary prevention refers to measures taken to prevent recurrent cardiac
arrest or death in individuals who have survived a previous cardiac arrest. A third category consists of interventions intended to abort sudden cardiac arrests, thus avoiding
their progression to death. This focuses primarily on out-of-hospital response strategies.

The primary prevention strategies currently used depend on the magnitude of risk among the various population subgroups. Because the annual incidence of SCD among the
unselected adult population is limited to 12 per 1000 population per year (Fig. 273-1) and >30% of all SCDs due to coronary artery disease occur as the first clinical
manifestation of the disease (Fig. 273-2A), the only currently practical strategies are profiling for risk of developing CHD and risk factor control (Fig. 273-2B). The most
powerful long-term risk factors include age, cigarette smoking, elevated serum cholesterol, diabetes mellitus, elevated blood pressure, LV hypertrophy, and nonspecific
electrocardiographic abnormalities. Markers of inflammation (e.g., levels of C-reactive protein) that may predict plaque destabilization have been added to risk classifications.
The presence of multiple risk factors progressively increases incidence, but not sufficiently or specifically enough to warrant therapies targeted to potentially fatal arrhythmias
(Fig. 273-1A). However, recent studies offer the hope that genetic markers for specific risk may become available. These studies suggest that a family history of SCD
associated with acute coronary syndromes predicts a higher likelihood of cardiac arrest as the initial manifestation of coronary artery disease in first-degree family members.

After coronary artery disease has been identified in a patient, additional strategies for risk profiling become available (Fig. 273-2B), but the majority of SCDs occur among the
large unselected groups rather than in the specific high-risk subgroups that become evident among populations with established disease (compare events per year with
percent per year in Fig. 273-1B). After a major cardiovascular event, such as acute coronary syndromes, recent onset of heart failure, and survival after out-of-hospital cardiac
arrest, the highest risk of death occurs during the initial 618 months after the event and then plateaus toward the baseline risk associated with the extent of underlying
disease. However, many of the early deaths are nonsudden, diluting the potential benefit of strategies targeted specifically to SCD. Thus, although post-MI beta-blocker
therapy has an identifiable benefit for both early SCD and nonsudden mortality risk, a total mortality benefit for ICD therapy early after MI has not been observed.

Among patients in the acute, convalescent, and chronic phases of myocardial infarction (Chap. 245), subgroups at high absolute risk of SCD can be identified. During the
acute phase, the potential risk of cardiac arrest from onset through the first 48 h may be as high as 15%, emphasizing the importance for patients to respond promptly to the
onset of symptoms. Those who survive acute-phase VF, however, are not at continuing risk for recurrent cardiac arrest indexed to that event. During the convalescent phase
after MI (3 days to ~6 weeks), an episode of sustained ventricular tachycardia (VT) or VF, which is usually associated with a large infarct, predicts a natural history mortality
risk of >25% at 12 months. At least one-half of the deaths are sudden. Aggressive intervention techniques may reduce this incidence.

After passage into the chronic phase of MI, the longer-term risk for total mortality and SCD mortality is predicted by a number of factors (Fig. 273-2B). The most important for
both SCD and nonsudden death is the extent of myocardial damage sustained as a result of the acute MI. This is measured by the magnitude of reduction of the ejection
fraction (EF) and/or the occurrence of heart failure. Various studies have demonstrated that ventricular arrhythmias identified by ambulatory monitoring contribute significantly
to this risk, especially in patients with an EF <40%. In addition, inducibility of VT or VF during electrophysiologic testing of patients who have ambient ventricular arrhythmias
[premature ventricular contractions (PVCs) and nonsustained VT] and an EF <35 or 40% is a strong predictor of SCD risk. Patients in this subgroup are now considered
candidates for implantable cardioverter defibrillators (ICDs) (see below). Risk falls off sharply with EFs >40% after MI and the absence of ambient arrhythmias and conversely
is high with EFs <30% even without the ambient arrhythmia markers.

The cardiomyopathies (dilated and hypertrophic, Chap. 238) are the second most common category of diseases associated with risk of SCD, after CHD (Table 273-2). Some
risk factors have been identified, largely related to extent of disease, documented ventricular arrhythmias, and symptoms of arrhythmias (e.g., syncope). The less common
causes of SCD include valvular heart disease (primarily aortic) and inflammatory and infiltrative disorders of the myocardium. The latter include viral myocarditis, sarcoidosis,
and amyloidosis.

Among adolescents and young adults, rare inherited disorders such as hypertrophic cardiomyopathy, the long QT interval syndromes, right ventricular dysplasia, and the
Brugada syndrome have received attention as important causes of SCD because of advances in genetics and the ability to identify some of those at risk before a fatal event.
The subgroup of young competitive athletes has received special attention. The incidence of SCD among athletes appears to be higher than it is for the general adolescent
and young adult population, perhaps up to 1 in 75,000. Hypertrophic cardiomyopathy (Chap. 238) is the most common cause in the United States, compared with Italy, where
more comprehensive screening programs remove potential victims from the population of athletes.

Secondary prevention strategies should be applied to surviving victims of a cardiac arrest that was not associated with an acute MI or a transient risk of SCD (e.g., drug
exposures, correctable electrolyte imbalances). Multivessel coronary artery disease and dilated cardiomyopathy, especially with markedly reduced left ventricular EF predict a
1- to 2-year risk of recurrence of an SCD or cardiac arrest of up to 30% in the absence of specific interventions (see below). The presence of life-threatening arrhythmias with
long QT syndromes or right ventricular dysplasia are also associated with increased risks.

Clinical Characteristics of Cardiac Arrest

Prodrome, Onset, Arrest, Death

SCD may be presaged by days to months of increasing angina, dyspnea, palpitations, easy fatigability, and other nonspecific complaints. However, these prodromal
symptoms are generally predictive of any major cardiac event; they are not specific for predicting SCD.

The onset of the clinical transition, leading to cardiac arrest, is defined as an acute change in cardiovascular status preceding cardiac arrest by up to 1 h. When the onset is
instantaneous or abrupt, the probability that the arrest is cardiac in origin is >95%. Continuous electrocardiographic (ECG) recordings fortuitously obtained at the onset of a
cardiac arrest commonly demonstrate changes in cardiac electrical activity during the minutes or hours before the event. There is a tendency for the heart rate to increase and
for advanced grades of PVCs to evolve. Most cardiac arrests that are caused by VF begin with a run of nonsustained or sustained VT, which then degenerates into VF.

The probability of achieving successful resuscitation from cardiac arrest is related to the interval from onset of loss of circulation to institution of resuscitative efforts, the setting
in which the event occurs, the mechanism (VF, VT, PEA, asystole), and the clinical status of the patient before the cardiac arrest. Return of circulation and survival rates as a
result of defibrillation decrease almost linearly from the first minute to 10 min. After 5 min, survival rates are no better than 2530% in out-of-hospital settings. Those settings in
which it is possible to institute prompt cardiopulmonary resuscitation (CPR) followed by prompt defibrillation provide a better chance of a successful outcome. However, the
outcome in intensive care units and other in-hospital environments is heavily influenced by the patient's preceding clinical status. The immediate outcome is good for cardiac
arrest occurring in the intensive care unit in the presence of an acute cardiac event or transient metabolic disturbance, but survival among patients with far-advanced chronic
cardiac disease or advanced noncardiac diseases (e.g., renal failure, pneumonia, sepsis, diabetes, cancer) is low and not much better in the in-hospital than in the out-of-
hospital setting. Survival from unexpected cardiac arrest in unmonitored areas in a hospital is not much better than that it is for witnessed out-of-hospital arrests. Since
implementation of community response systems, survival from out-of-hospital cardiac arrest has improved although it still remains low, under most circumstances. Survival
probabilities in public sites exceed those in the home environment.

The success rate for initial resuscitation and survival to hospital discharge after an out-of-hospital cardiac arrest depends heavily on the mechanism of the event. When the
mechanism is pulseless VT, the outcome is best; VF is the next most successful; and asystole and PEA generate dismal outcome statistics. Advanced age also adversely
influences the chances of successful resuscitation.

Progression to biologic death is a function of the mechanism of cardiac arrest and the length of the delay before interventions. VF or asystole without CPR within the first 46
min has a poor outcome even if defibrillation is successful because of superimposed brain damage; there are few survivors among patients who had no life support activities
for the first 8 min after onset. Outcome statistics are improved by lay bystander intervention (basic life supportsee below) before definitive interventions (advanced life
support) especially when followed by early successful defibrillation. In regard to the latter, evaluations of deployment of automatic external defibrillators (AEDs) in communities
(e.g., police vehicles, large buildings, airports, and stadiums) are beginning to generate encouraging data. Increased deployment is to be encouraged.

Death during the hospitalization after a successfully resuscitated cardiac arrest relates closely to the severity of central nervous system injury. Anoxic encephalopathy and
infections subsequent to prolonged respirator dependence account for 60% of the deaths. Another 30% occur as a consequence of low cardiac output states that fail to
respond to interventions. Recurrent arrhythmias are the least common cause of death, accounting for only 10% of in-hospital deaths.

In the setting of acute MI (Chap. 245), it is important to distinguish between primary and secondary cardiac arrests. Primary cardiac arrests are those which occur in the
absence of hemodynamic instability, and secondary cardiac arrests are those which occur in patients in whom abnormal hemodynamics dominate the clinical picture before
cardiac arrest. The success rate for immediate resuscitation in primary cardiac arrest during acute MI in a monitored setting should exceed 90%. In contrast, as many as 70%
of patients with secondary cardiac arrest succumb immediately or during the same hospitalization.

Treatment: Cardiac Arrest

An individual who collapses suddenly is managed in five stages: (1) initial evaluation and basic life support if arrest is confirmed, (2) public access defibrillation (when
available), (3) advanced life support, (4) postresuscitation care, and (5) long-term management. The initial response, including confirmation of loss of circulation, followed by
basic life support and public access defibrillation, can be carried out by physicians, nurses, paramedical personnel, and trained laypersons. There is a requirement for
increasingly specialized skills as the patient moves through the stages of advanced life support, postresuscitation care, and long-term management.

Initial Evaluation and Basic Life Support

Confirmation that a sudden collapse is indeed due to a cardiac arrest includes prompt observations of the state of consciousness, respiratory movements, skin color, and the
presence or absence of pulses in the carotid or femoral arteries. For lay responders, the pulse check is no longer recommended. As soon as a cardiac arrest is suspected,
confirmed, or even considered to be impending, calling an emergency rescue system (e.g., 911) is the immediate priority. With the development of AEDs that are easily used
by nonconventional emergency responders, an additional layer for response has evolved (see below).

Agonal respiratory movements may persist for a short time after the onset of cardiac arrest, but it is important to observe for severe stridor with a persistent pulse as a clue to
aspiration of a foreign body or food. If this is suspected, a Heimlich maneuver (see below) may dislodge the obstructing body. A precordial blow, or "thump," delivered firmly
with a clenched fist to the junction of the middle and lower thirds of the sternum may occasionally revert VT or VF, but there is concern about converting VT to VF. Therefore, it
is recommended to use precordial thumps as a life support technique only when monitoring and defibrillation are available. This conservative application of the technique
remains controversial.
The third action during the initial response is to clear the airway. The head is tilted back and the chin lifted so that the oropharynx can be explored to clear the airway. Dentures
or foreign bodies are removed, and the Heimlich maneuver is performed if there is reason to suspect that a foreign body is lodged in the oropharynx. If respiratory arrest
precipitating cardiac arrest is suspected, a second precordial thump is delivered after the airway is cleared.

Basic life support, more popularly known as CPR, is intended to maintain organ perfusion until definitive interventions can be instituted. The elements of CPR are the
maintenance of ventilation of the lungs and compression of the chest. Mouth-to-mouth respiration may be used if no specific rescue equipment is immediately available (e.g.,
plastic oropharyngeal airways, esophageal obturators, masked Ambu bag). Conventional ventilation techniques during single-responder CPR require that the lungs be inflated
twice in succession after every 30 chest compressions. Recent data suggest that interrupting chest compressions to perform mouth-to-mouth respiration may be less effective
than a continuous chest compression strategy.

Chest compression is based on the assumption that cardiac compression allows the heart to maintain a pump function by sequential filling and emptying of its chambers, with
competent valves maintaining forward direction of flow. The palm of one hand is placed over the lower sternum, with the heel of the other resting on the dorsum of the lower
hand. The sternum is depressed, with the arms remaining straight, at a rate of approximately 100 per minute. Sufficient force is applied to depress the sternum 45 cm, and
relaxation is abrupt.

Automated External Defibrillation (AED)

AEDs that are easily used by nonconventional responders, such as nonparamedic firefighters, police officers, ambulance drivers, trained security guards, and minimally
trained or untrained laypersons, have been developed. This advance has inserted another level of response into the cardiac arrest paradigm. A number of studies have
demonstrated that AED use by nonconventional responders in strategic response systems and public access lay responders can improve cardiac arrest survival rates. This
strategy is based on shortening the time to the first defibrillation attempt while awaiting the arrival of advanced life support.

Advanced Cardiac Life Support (ACLS)

ACLS is intended to achieve adequate ventilation, control cardiac arrhythmias, stabilize blood pressure and cardiac output, and restore organ perfusion. The activities carried
out to achieve these goals include (1) defibrillation/cardioversion and/or pacing, (2) intubation with an endotracheal tube, and (3) insertion of an intravenous line. The speed
with which defibrillation/cardioversion is achieved is an important element in successful resuscitation, both for restoration of spontaneous circulation and for protection of the
central nervous system. Immediate defibrillation should precede intubation and insertion of an intravenous line; CPR should be carried out while the defibrillator is being
charged. As soon as a diagnosis of VF or VT is established, a shock of at least 300 J should be delivered when one is using a monophasic waveform device or 120150 J with
a biphasic waveform. Additional shocks are escalated to a maximum of 360 J monophasic (200 J biphasic) if the initial shock does not successfully revert VT or VF. However,
it is now recommended that five cycles of CPR be carried out before repeated shocks, if the first shock fails to restore an organized rhythm, or 6090 s of CPR before the first
shock if 5 min has elapsed between the onset of cardiac arrest and ability to deliver a shock (see 2005 update of guidelines for cardiopulmonary resuscitation and emergency
cardiac care at http://circ.ahajournals.org/content/vol112/_suppl).

Epinephrine, 1 mg intravenously, is given after failed defibrillation, and attempts to defibrillate are repeated. The dose of epinephrine may be repeated after intervals of 35
min (Fig. 273-3A). Vasopressin (a single 40-unit dose given IV) has been suggested as an alternative to epinephrine.

Figure 273-3
If the patient is less than fully conscious upon reversion or if two or three attempts fail, prompt intubation, ventilation, and arterial blood gas analysis should be carried out.
Ventilation with O2 (room air if O2 is not immediately available) may promptly reverse hypoxemia and acidosis. A patient who is persistently acidotic after successful
defibrillation and intubation should be given 1 meq/kg NaHCO3 initially and an additional 50% of the dose repeated every 1015 min. However, it should not be used routinely.

After initial unsuccessful defibrillation attempts or with persistent/recurrent electrical instability, antiarrhythmic therapy should be instituted. Intravenous amiodarone has
emerged as the initial treatment of choice (150 mg over 10 min, followed by 1 mg/min for up to 6 h and 0.5 mg/min thereafter) (Fig. 273-3A). For cardiac arrest due to VF in
the early phase of an acute coronary syndrome, a bolus of 1 mg/kg of lidocaine may be given intravenously as an alternative, and the dose may be repeated in 2 min. It also
may be tried in patients in whom amiodarone is unsuccessful. Intravenous procainamide (loading infusion of 100 mg/5 min to a total dose of 500800 mg, followed by
continuous infusion at 25 mg/min) is now rarely used in this setting but may be tried for persisting, hemodynamically stable arrhythmias. Intravenous calcium gluconate is no
longer considered safe or necessary for routine administration. It is used only in patients in whom acute hyperkalemia is known to be the triggering event for resistant VF, in
the presence of known hypocalcemia, or in patients who have received toxic doses of calcium channel antagonists.

Cardiac arrest due to bradyarrhythmias or asystole (B/A cardiac arrest) is managed differently (Fig. 273-3B). The patient is promptly intubated, CPR is continued, and an
attempt is made to control hypoxemia and acidosis. Epinephrine and/or atropine are given intravenously or by an intracardiac route. External pacing devices are used to
attempt to establish a regular rhythm. The success rate may be good when B/A arrest is due to acute inferior wall myocardial infarction or to correctable airway obstruction or
drug-induced respiratory depression or with prompt resuscitation efforts. For acute airway obstruction, prompt removal of foreign bodies by the Heimlich maneuver or, in
hospitalized patients, by intubation and suctioning of obstructing secretions in the airway is often successful. The prognosis is generally very poor in other causes of this form
of cardiac arrest, such as end-stage cardiac or noncardiac diseases. Treatment of PEA is similar to that for bradyarrhythmias, but its outcome is also dismal.

Postresuscitation Care

This phase of management is determined by the clinical setting of the cardiac arrest. Primary VF in acute MI (not accompanied by low-output states) (Chap. 245) is generally
very responsive to life support techniques and easily controlled after the initial event. In the in-hospital setting, respirator support is usually not necessary or is needed for only
a short time, and hemodynamics stabilize promptly after defibrillation or cardioversion. In secondary VF in acute MI (those events in which hemodynamic abnormalities
predispose to the potentially fatal arrhythmia), resuscitative efforts are less often successful, and in patients who are successfully resuscitated, the recurrence rate is high. The
clinical picture and outcome are dominated by hemodynamic instability and the ability to control hemodynamic dysfunction. Bradyarrhythmias, asystole, and PEA are
commonly secondary events in hemodynamically unstable patients. The in-hospital phase of care of an out-of-hospital cardiac arrest survivor is dictated by specific clinical
circumstances. The most difficult is the presence of anoxic encephalopathy, which is a strong predictor of in-hospital death. A recent addition to the management of this
condition is induced hypothermia to reduce metabolic demands and cerebral edema.

The outcome after in-hospital cardiac arrest associated with noncardiac diseases is poor, and in the few successfully resuscitated patients, the postresuscitation course is
dominated by the nature of the underlying disease. Patients with end-stage cancer, renal failure, acute central nervous system disease, and uncontrolled infections, as a
group, have a survival rate of <10% after in-hospital cardiac arrest. Some major exceptions are patients with transient airway obstruction, electrolyte disturbances,
proarrhythmic effects of drugs, and severe metabolic abnormalities, most of whom may have a good chance of survival if they can be resuscitated promptly and stabilized
while the transient abnormalities are being corrected.

Long-Term Management after Survival of Out-of-Hospital Cardiac Arrest

Patients who survive cardiac arrest without irreversible damage to the central nervous system and who achieve hemodynamic stability should have diagnostic testing to define
appropriate therapeutic interventions for their long-term management. This aggressive approach is driven by the fact that survival after out-of-hospital cardiac arrest is
followed by a 1025% mortality rate during the first 2 years after the event, and there are data suggesting that significant survival benefits can be achieved by prescription of
an implantable cardioverter-defibrillator (ICD).

Among patients in whom an acute ST elevation MI, or transient and reversible myocardial ischemia, is identified as the specific mechanism triggering an out-of-hospital
cardiac arrest, the management is dictated in part by the transient nature of life-threatening arrhythmia risk during the acute coronary syndrome (ACS) and in part by the
extent of permanent myocardial damage that results. Cardiac arrest during the acute ischemic phase is not an ICD indication, but survivors of cardiac arrest not associated
with an ACS do benefit. In addition, patients who survive MI with an ejection fraction less than 3035% appear to benefit from ICDs.

For patients with cardiac arrest determined to be due to a treatable transient ischemic mechanism, particularly with higher EFs, catheter interventional, surgical, and/or
pharmacologic anti-ischemic therapy is generally accepted for long-term management.

Survivors of cardiac arrest due to other categories of disease, such as the hypertrophic or dilated cardiomyopathies and the various rare inherited disorders (e.g., right
ventricular dysplasia, long QT syndrome, Brugada syndrome, catecholaminergic polymorphic VT, and so-called idiopathic VF), are all considered ICD candidates.

Prevention of SCD in High-Risk Individuals Without Prior Cardiac Arrest

Post-MI patients with EFs <35% and other markers of risk such as ambient ventricular arrhythmias, inducible ventricular tachyarrhythmias in the electrophysiology laboratory,
and a history of heart failure are considered candidates for ICDs 30 days or more after the MI. Total mortality benefits in the range of a 2035% reduction over 25 years have
been observed in a series of clinical trials. One study suggested that an EF <30% was a sufficient marker of risk to indicate ICD benefit, and another demonstrated benefit for
patients with Functional Class 2 or 3 heart failure and ejection fractions 35%, regardless of etiology (ischemic or nonischemic) or the presence of ambient or induced
arrhythmias (see Chaps. 233 and 234). There appears to be a gradient of increasing ICD benefit with EFs ranging lower than the threshold indications. However, patients with
very low EFs (e.g., <20%) may receive less benefit.

Decision making for primary prevention in disorders other than coronary artery disease and dilated cardiomyopathy is generally driven by observational data and judgment
based on clinical observations. Controlled clinical trials providing evidence-based indicators for ICDs are lacking for these smaller population subgroups. In general, for the
rare disorders listed above, indicators of arrhythmic risk such as syncope, documented ventricular tachyarrhythmias, aborted cardiac arrest or a family history of premature
SCD in some conditions, and a number of other clinical or ECG markers may be used as indicators for ICDs.