Cardiovascular Collapse, Cardiac Arrest, and Sudden
Overview and Definitions
vast majority of naturally occurring sudden deaths are caused by cardiac
disorders. The magnitude of sudden cardiac death (SCD) as a public health
problem is highlighted by estimates that more than 300,000 deaths occur each
year in the
SCD must be defined carefully. In the context of time, "sudden" is defined, for most clinical and epidemiologic purposes, as 1 h or less between the onset of the terminal clinical event, or an abrupt change in clinical status, and death. 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.
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 death, cardiac arrest, and cardiovascular collapse (Table 39-1). 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. Currently, the accepted definition of SCD is natural death due to cardiac causes, heralded by abrupt loss of consciousness within 1 h of the onset of acute symptoms, in an individual who may have known preexisting heart disease but in whom the time and mode of death are unexpected. When biologic death of the 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 artificial methods. The language used should reflect the fact that the index event was a cardiac arrest and that death was due to its delayed consequences.
Etiology, Initiating Events, and Clinical Epidemiology
Clinical and epidemiologic studies have identified populations at high risk for SCD. In addition, a large body of pathologic data provides information on the underlying structural abnormalities in victims of SCD, and studies of clinical physiology have begun to identify a group of transient functional factors that may convert a long-standing underlying structural abnormality from a stable to an unstable state (Table 39-2). This information is developing into an understanding of the causes and mechanisms of SCD.
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), 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 the age of 30 years, reaching a second peak in the age range of 45 to 75 years, when the incidence approximates 1 to 2 per 1000 per year among the unselected adult population. Increasing age within this range is a powerful risk factor for sudden cardiac death, and the proportion of cardiac causes among all sudden natural deaths increases dramatically with advancing years. From 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 then to 88% in the middle-aged and elderly.
Young and middle-aged men and women have very different susceptibilities to SCD, but the gender differences decrease with advancing age. In the 45- to 64-year-old age group, the male SCD excess is nearly 7:1. It falls to 2:1 or less in the 65- to 74-year-old age group. The difference in risk for SCD parallels the risks for other manifestations of coronary heart disease in men and women. As the gender gap for manifestations of coronary heart disease closes in the seventh and eighth decades of life, the excess risk of SCD in males also 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.
Hereditary factors contribute to the risk of SCD, but largely in a nonspecific manner; they represent expressions of the hereditary predisposition to coronary heart disease. A few specific syndromes, such as congenital long QT interval syndromes (Chap. 230), right ventricular dysplasia, and the syndrome of right bundle branch block and non-ischemic ST-segment elevations (Brugada syndrome), are characterized by specific hereditary risk of SCD. There are also recent data suggesting a familial predispositon to SCD as a specific pattern of coronary heart disease expression.
The major categories of structural causes of, and functional factors contributing to, the SCD syndrome are listed in Table 39-2. Worldwide, and especially in western cultures, coronary atherosclerotic heart disease is the most common structural abnormality associated with SCD. Up to 80% of all SCDs in the United States are due to the consequences of coronary atherosclerosis. The cardiomyopathies (dilated and hypertrophic, collectively; Chap. 239) account for another 10 to 15% of SCDs, and all the remaining diverse etiologies cause only 5 to 10% of these events. Transient ischemia in the 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 transition from electrophysiologic stability to instability. In addition, reperfusion of ischemic myocardium may cause transient electrophysiologic instability and arrhythmias.
Data from postmortem examinations of SCD victims parallel the clinical observations on the prevalence of coronary heart disease as the major structural etiologic factor. More than 80% of SCD victims have pathologic findings of coronary heart disease. The pathologic description often includes a combination of long-standing, extensive atherosclerosis of the epicardial coronary arteries and acute active coronary lesions, which include a combination of fissured or ruptured plaques, platelet aggregates, hemorrhage, and thombosis. In one study, chronic coronary atherosclerosis involving two or more major vessels with 75% stenosis was observed in 75% of the victims. In another study, atherosclerotic plaque fissuring, platelet aggregates, and/or acute thrombosis were observed in 95 of 100 individuals who had pathologic studies after SCD.
As many as 70 to 75% of males who die suddenly have prior myocardial infarctions (MIs), but only 20 to 30% have recent acute MIs. A high incidence of left ventricular (LV) hypertrophy coexists with prior MIs.
Clinical Definition of Forms of Cardiovascular Collapse (Table 39-1)
Cardiovascular collapse is a general term connoting loss of effective blood flow due to acute dysfunction of the heart and/or peripheral vasculature. Cardiovascular collapse may be caused by vasodepressor syncope (vasovagal syncope, postural hypotension with syncope, neurocardiogenic syncope-Chap. 21), 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 achieve resuscitation. In contrast, vasodepressor syncope and many primary bradyarrhythmic syncopal events are transient and non-life-threatening, with spontaneous return of consciousness.
The most common electrical mechanism for true cardiac arrest is ventricular fibrillation (VF), which is responsible for 65 to 80% of cardiac arrests. Severe persistent bradyarrhythmias, asystole, and pulseless electrical activity (an organized electrical activity without mechanical response, formerly called electomechanical dissociation) cause another 20 to 30%. Sustained ventricular tachycardia (VT) with hypotension is a less common cause. Acute low cardiac output states, having precipitous onset, also may present clinically as a cardiac arrest. The causes include massive acute pulmonary emboli, internal blood loss from ruptured aortic aneurysm, intense anaphylaxis, cardiac rupture after myocardial infarction, and unexpected fatal arrhythmia due to electrolyte disturbances.
Clinical Characteristics of Cardiac Arrest
Prodrome, Onset, Arrest, Death
SCD may be presaged by days, weeks, or months of increasing angina, dyspnea, palpitations, easy fatigability, and other nonspecific complaints. However, these prodromal complaints are generally predictive of any major cardiac event; they are not specific for predicting SCD.
The onset of the terminal event, 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 ECG recordings, fortuitously obtained at the onset of a cardiac arrest, commonly demonstrate changes in cardiac electrical activity in the minutes or hours before the event. There is a tendency for the heart rate to increase and for advanced grades of premature ventricular contractions (PVCs) to evolve. Most cardiac arrests that are caused by VF begin with a run of sustained or nonsustained VT, which then degenerates into VF.
Sudden unexpected loss of effective circulation may be separated into "arrhythmic events" and "circulatory failure." Arrhythmic events are characterized by a high likelihood of patients being awake and active immediately prior to the event, are dominated by VF as the electrical mechanism, and have a short duration of terminal illness (<1 h). In contrast, circulatory failure deaths occur in patients who are inactive or comatose, have a higher incidence of asystole than VF, have a tendency to a longer duration of terminal illness, and are dominated by noncardiac events preceding the terminal illness.
The onset of cardiac arrest may be characterized by typical symptoms of an acute cardiac event, such as prolonged angina or the pain of onset of MI, acute dyspnea or orthopnea, or the sudden onset of palpitations, sustained tachycardia, or light-headedness. However, in many patients, the onset is precipitous, with minimal forewarning.
Cardiac arrest is, by definition, abrupt. Mentation may be impaired in patients with sustained VT during the onset of the terminal event. However, complete loss of consciousness is a sine qua non in cardiac arrest. Although rare spontaneous reversions occur, it is usual that cardiac arrest progresses to death within minutes (i.e., SCD has occurred) if active interventions are not undertaken promptly.
The probability of achieving successful resuscitation from cardiac arrest is related to the interval from onset to institution of resuscitative efforts, the setting in which the event occurs, the mechanism (VF, VT, pulseless electrical activity, asystole), and the clinical status of the patient prior to the cardiac arrest. Those settings in which it is possible to institute prompt cardiopulmonary resuscitation (CPR) 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 the outcome for patients with far-advanced chronic cardiac disease or advanced noncardiac diseases (e.g., renal failure, pneumonia, sepsis, diabetes, cancer) is not much more successful in hospital than in the out-of-hospital setting.
The success rate for initial resuscitation and survival to hospital discharge after an out-of-hospital cardiac arrest depends in part on the mechanism of the event. When the mechanism is VT, the outcome is best; VF is the next most successful; and asystole and pulseless electrical activity generate dismal outcome statistics (Fig. 39-1). Advanced age also influences adversely 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 4 to 6 min has a poor outcome, and 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 support-see below) prior to definitive interventions (advanced life support-defibrillation) and even more by early defibrillation. In regard to the latter, the notion that deployment of automatic external defibrillators in communities (e.g., police vehicles, large buildings, stadiums, etc.) will result in improved survival is currently being evaluated.
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, it is important to distinguish between primary and secondary cardiac arrests. Primary cardiac arrests refer to those that occur in the absence of hemodynamic instability, and secondary cardiac arrests are those that 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 approach 100%. In contrast, as many as 70% of patients with secondary cardiac arrest succumb immediately or during the same hospitalization.
Identification of Patients at Risk for Sudden Cardiac Death
Primary prevention of cardiac arrest depends on
the ability to identify individual patients at high risk. One must view the
problem in the context of the total number of events and the population pools
from which they are derived. The annual incidence of SCD among an unselected
adult population is 1 to 2 per 1000 population (Fig. 39-2A), largely
reflecting the prevalence of those coronary heart disease patients among whom
SCD is the first clinically recognized manifestation (20 to 25% of first
coronary events are SCD). The incidence (percent per year) increases
progressively with the addition of identified coronary risk factors to
populations free of prior coronary events. The most powerful factors are age,
elevated blood pressure, LV hypertrophy, cigarette smoking, elevated serum
cholesterol level, obesity, and nonspecific electrocardiographic abnormalities.
These coronary risk factors are not specific for SCD but rather represent
increasing risk for all coronary deaths. The proportion of coronary deaths that
are sudden remains at approximately 50% in all risk categories. Despite the
marked relative increased risk of SCD with addition of multiple risk
factors (from 1 to 2 per 1000 population per year in an unselected population
to as much as 50 to 60 per 1000 in subgroups having multiple risk factors for
coronary artery disease), the absolute incidence remains relatively low
when viewed as the relationship between the number of individuals who have a
preventive intervention and the number of events that can be prevented.
Specifically, a 50% reduction in annual SCD risk would be a huge relative
decrease but would require an intervention in up to 200 unselected individuals
to prevent one sudden death. These figures highlight the importance of primary
prevention of coronary heart disease. Control of coronary risk factors may be
the only practical method to prevent SCD in major segments of the population,
because of the paradox that the majority of events occur in the large
unselected subgroups rather than in the specific high-risk subgroups (compare
"Events/Year" with "Percent/Year" in Fig. 39-2A).
Under most conditions of higher level of risk, particularly those indexed to a
recent major cardiovascular event (e.g., MI, recent onset of heart failure,
survival after out-of-hospital cardiac arrest), the highest risk of sudden
death occurs within the initial 6 to 18 months and then decreases toward
baseline risk of the underlying disease (Fig. 39-2B). Accordingly,
preventive interventions are most likely to be effective when initiated early.
For patients with acute or prior clinical manifestations of coronary heart disease, high-risk subgroups having a much higher ratio of SCD risk to population base can be identified. The acute, convalescent, and chronic phases of MI provide large population subsets with more highly focused risk (Chap. 243). The potential risk of cardiac arrest from the onset through the first 72 h after acute MI (the acute phase) may be as high as 15 to 20%. The highest risk of SCD in relation to MI is found in the subgroup that has experienced sustained VT or VF during the convalescent phase (3 days to 8 weeks) after MI. A greater than 50% mortality in 6 to 12 months has been observed among these patients, when managed with conservative medical therapy, and at least 50% of the deaths are sudden. Aggressive intervention techniques may reduce this incidence.
After the acute phase of MI, long-term risk for total mortality and SCD are predicted by a number of factors. The most important for both SCD and non-SCD is the extent of myocardial damage sustained during the acute event. This is measured by the degree of reduction in the ejection fraction (EF), functional capacity, and/or the occurrence of heart failure. Increasing frequency of postinfarction PVCs, with a plateau above the range of 10 to 30 PVCs per hour on 24-h ambulatory monitor recordings, also indicates increased risk, but advanced forms (salvos, nonsustained VT) may be more powerful predictors. PVCs interact strongly with decreased left ventricular EF. The combination of frequent PVCs, salvos or nonsustained VT, and an EF 35% identifies patients who have an annual risk of greater than 20%. The risk falls off sharply with decreasing PVC frequency and the absence of advanced forms, as well as with higher EF. Despite the risk implications of postinfarction PVCs, improved outcome as a result of PVC suppression has not been demonstrated (Chap. 230).
The extent of underlying disease due to any cause and/or prior clinical expression of risk of SCD (i.e., survival after out-of-hospital cardiac arrest not associated with acute MI) identify patients at very high risk for subsequent (recurrent) cardiac arrest. Survival after out-of-hospital cardiac arrest predicts up to a 30% 1-year recurrent cardiac arrest rate in the absence of specific interventions (see below).
A general rule is that the risk of SCD is approximately one-half the total cardiovascular mortality rate. As shown in Fig. 39-2A, the very high risk subgroups provide more focused population fractions ("Percent/Year") for predicting cardiac arrest or SCD; but the impact on the overall population, indicated by the absolute number of preventable events ("Events/Year"), is considerably smaller. The requirements for achieving a major population impact are effective prevention of the underlying diseases and/or new epidemiologic probes that will allow better resolution of subgroups within large general populations.
The individual who collapses suddenly is managed in four stages: (1) the initial response and basic life support; (2) advanced life support; (3) postresuscitation care; and (4) long-term management. The initial response and basic life support can be carried out by physicians, nurses, paramedical personnel, and trained lay persons. 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 Response and Basic Life Support
The initial response will confirm whether a sudden collapse is indeed due to a cardiac arrest. Observations for respiratory movements, skin color, and the presence or absence of pulses in the carotid or femoral arteries will promptly determine whether a life-threatening cardiac arrest has occurred. As soon as a cardiac arrest is suspected or confirmed, contacting an emergency rescue system (e.g., 911) should be the immediate priority.
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 by the clenched fist to the junction of the middle and lower third of the sternum may occasionally revert VT or VF, but there is concern about converting VT to VF. Therefore, it has been recommended to use precordial thumps as an advanced life support technique 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 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 CPR require the lungs to be inflated 10 to 12 times per minute, i.e., once every fifth chest compression when two persons are performing the resuscitation and twice in succession every 15 chest compressions when one person is carrying out both ventilation and chest wall compression.
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 80 to 100 per minute. Sufficient force is applied to depress the sternum 3 to 5 cm, and relaxation is abrupt.
Advanced Life Support
Advanced life support 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) intubation with an endotracheal tube, (2) defibrillation/cardioversion and/or pacing, and (3) insertion of an intravenous line. Ventilation with O2 (room air if O2 is not immediately available) may promptly reverse hypoxemia and acidosis. The speed with which defibrillation/cardioversion is carried out is an important element for successful resuscitation. When possible, 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 VT or VF is obtained, a 200-J shock should be delivered. Additional shocks at higher energies, up to a maximum of 360 J, are tried if the initial shock does not successfully abolish VT or VF. 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 3 to 5 min (see Fig. 39-3A).
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. Intravenous NaHCO3, which was formerly used in large quantities, is no longer considered routinely necessary and may be dangerous in larger quantities. However, the 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 10 to 15 min.
After initial unsuccessful defibrillation attempts, or with persistent electrical instability, a bolus of 1 mg/kg lidocaine is given intravenously (Chap. 243), and the dose is repeated in 2 min in those patients who have persistent ventricular arrhythmias or remain in VF. This is followed by a continuous infusion at a rate of 1 to 4 mg/min. If lidocaine fails to provide control, other antiarrhythmic therapies should be tried. For persistent, hemodynamically unstable ventricular arrhythmias, intravenous amiodarone has emerged as the 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. 39-3A). Intravenous procainamide (loading infusion of 100 mg/5 min to a total dose of 500 to 800 mg, followed by continuous infusion at 2 to 5 mg/min) may be tried for persisting, hemodynamically stable arrhythmias; or bretylium tosylate (loading dose 5 to 10 mg/kg in 5 min; maintenance dose 0.5 to 2 mg/min) may be tried as an alternative for unstable 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 secondary to bradyarrhythmias or asystole is managed differently (Fig. 39-3B). 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 now available to attempt to establish a regular rhythm, but the prognosis is generally very poor in this form of cardiac arrest, even with successful electrical pacing. Pulseless electrical activity (PEA) is treated similarly to bradyarrhythmias, but its outcome is also dismal. The one exception is bradyarrhythmic/asystolic cardiac arrest secondary to airway obstruction. This form of cardiac arrest may respond promptly to removal of foreign bodies by the Heimlich maneuver or, in hospitalized patients, by intubation and suctioning of obstructing secretions in the airway.
This phase of management is determined by the clinical setting of the cardiac arrest. Primary VF in acute MI (Chap. 243) is generally very responsive to life-support techniques and easily controlled after the initial event. Patients are maintained on a lidocaine infusion at the rate of 2 to 4 mg/min for 24 to 72 h after the 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 those 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 pulseless electrical activity are commonly secondary events in hemodynamically unstable patients.
The outcome after in-hospital cardiac arrest associated with non-cardiac diseases is poor, and in the few successfully resuscitated patients, the postresuscitation course is dominated by the nature of the underlying disease. Patients with cancer, renal failure, acute central nervous system disease, and uncontrolled infections, as a group, have a survival rate of less than 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 an excellent chance of survival if they can be resuscitated promptly and maintained while the transient abnormalities are being corrected.
Long-Term Management after Survival of Out-of-Hospital Cardiac Arrest
Patients who do not suffer irreversible injury of the central nervous system and who achieve hemodynamic stability should have extensive diagnostic and therapeutic testing to guide long-term management. This aggressive approach is driven by the fact that statistics from the 1970s indicated survival after out-of-hospital cardiac arrest was followed by a 30% recurrent cardiac arrest rate at 1 year, 45% at 2 years, and a total mortality rate of almost 60% at 2 years. Historical comparisons suggest that these dismal statistics may be significantly improved by newer interventions, but the magnitude of the improvement is unknown because of the lack of concurrently controlled intervention studies.
Among those patients in whom an acute transmural MI is the cause of out-of-hospital cardiac arrest, the management is the same as in any other patient who suffers cardiac arrest during the acute phase of a documented MI (Chap. 243). For almost all other categories of patients, however, extensive diagnostic studies are carried out to determine etiology, functional impairment, and electrophysiologic instability as guides to future management. In general, patients who have out-of-hospital cardiac arrest due to chronic ischemic heart disease, without an acute MI, are evaluated to determine whether transient ischemia or chronic electrophysiologic instability was the more likely cause of the event. If there is reason to suspect an ischemic mechanism, coronary revascularization by angioplasty or bypass surgery, plus drugs (most commonly beta blockers), are used to reduce ischemic burden.
Electrophysiologic instability has been identified by the use of programmed electrical stimulation to determine whether sustained VT or VF can be induced (Chap. 230). If so, this information can be used as a baseline against which to evaluate drug efficacy for prevention of inducibility. The rationale for this approach is the assumption that suppression of inducibility predicts long-term benefit by the drug that achieves such suppression. For patients for whom successful drug therapy could not be identified by this technique, insertion of an implantable cardioverter-defibrillator (ICD), antiarrhythmic surgery (e.g., coronary bypass surgery, aneurysmectomy, cryoablation), or empiric amiodarone therapy have been recommended (Chap. 230). Primary surgical success, defined as surviving the procedure and reverting to a noninducible status without drug therapy, is better than 90% when patients are selected for ability to be mapped in the operating room. However, only a small fraction of patients meet the criteria. In addition, VT/VF cannot be induced in a number of survivors of cardiac arrest (30 to 50%), and inducible arrhythmias can be suppressed by drugs in no more than 20 to 30% of those whose arrhythmias can be induced. Because of these limitations of drug therapy and surgical approaches, ICD therapy has evolved into the most commonly used strategy for cardiac arrest survivors. ICDs have long been recognized to have very good success rates for sensing and reverting life-threatening arrhythmias, but improvement in long-term total survival outcomes remained lacking until a number of studies solidified the benefit of ICD therapy for specific subgroups. After empiric amiodarone therapy had been suggested to be as good as, or better than, conventional antiarrhythmic drug therapy for survivors of cardiac arrest, ICDs were demonstrated to be superior to amiodarone. Moreover, ICDs were also found to be superior for high risk patients with VT after myocardial infarction.