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Sudden Cardiac Death Joseph P. Ornato INTRODUCTION AND EPIDEMIOLOGY This chapter focuses on the epidemiology and pathophysiology of sudden cardiac death in adults and strategies for prevention and treatment. See Chapters 18 (“Cardiac Rhythm Arrhythmias”), 22 (“Basic Cardiopulmonary Resuscitation”), 23 (“Defibrillation and Electrical Cardioversion”), and 24 (“Cardiac Resuscitation”) for detailed discussion of resuscitation pharmacotherapy. Sudden, unexpected, out-of-hospital cardiac arrest occurs in approximately 341,397 adult Americans each year. 1 Estimated national survival of EMS-treated out-of-hospital cardiac arrest cases is 10.8%, yielding an estimated overall out-of-hospital cardiac arrest survival rate of 5.4% (EMS-treated plus deceased-on-EMS-arrival cases). 1 There is substantial variability in the odds for survival across various geographic locations.2 Most episodes of sudden cardiac death occur in the home, although victims who experience cardiac arrest in a public place have a much better chance of survival. 3 The initial recorded cardiac arrest rhythm is more likely to be ventricular fibrillation when cardiac arrest occurs in a public location rather than in the home, likely because patients who experience cardiac arrest in the home are typically older and more likely to have one or more chronic diseases that limit or exclude participation in activities outside the home. 3 Sudden cardiac death is 30% to 80% higher among residents in the lowest compared with the highest socioeconomic quartile. 4 This association is likely due to lifestyle and healthcare disparity issues. There is a circadian pattern of sudden cardiac death and acute myo cardial infarction,5,6 and both are most likely to occur within the first few hours after awakening from sleep, when there is increased sympathetic stimulation. β-Blockade provides some protection from sudden cardiac death, particularly in patients with known coronary artery disease who have had myocardial infarction and have a low ejection fraction. Prevalence of sudden cardiac death in adults is greatest in the age group older than 45 to 50 years, with 60% occurring in males.4 There are multiple known factors contributing to the likelihood of sudden cardiac death (Table 11-1). Coronary artery disease (which is often undiagnosed before the event) is the major cause of sudden cardiac death in adults and is present in 80% of cases, followed by cardiomyopathy (10% to 15%) and other miscellaneous conditions (e.g., hereditary channelopathies, valvular disease, congenital anomalies), which account for most of the remaining 5% to 10% of cases. PATHOPHYSIOLOGY  CORONARY ARTERY DISEASE Coronary atherosclerosis is present on autopsy in 80% of sudden cardiac death victims.8 Coronary artery disease is also found in 70% to 80% of cardiac arrest victims who survive and undergo coronary angiography.9-12 Approximately one third have evidence of acute plaque rupture in areas of long-segment coronary stenosis. 10,11 A documented initial cardiac arrest rhythm of ventricular fibrillation (or shockable rhythm if an automated external defibrillator was applied) suggests that an acute coronary syn drome is the cause, since ventricular fibrillation is noted in the major ity of cases in which a coronary occlusion is found on angiography. 9-12 However, ventricular fibrillation is present in only 23% of all cardiac arrests.

hythm if an automated external defibrillator was applied) suggests that an acute coronary syn drome is the cause, since ventricular fibrillation is noted in the major ity of cases in which a coronary occlusion is found on angiography. 9-12 However, ventricular fibrillation is present in only 23% of all cardiac arrests.  SEVERE LEFT VENTRICULAR DYSFUNCTION Severe left ventricular dysfunction with a reduced ejection fraction is currently the best available predictor of sudden death risk. 4 Patients with an ejection fraction ≤35% are the primary candidates for an implantable cardioverter-defibrillator. However, almost half of sudden deaths occur in individuals with normal left ventricular function.  CARDIOMYOPATHY Cardiomyopathy with reduced left ventricular function, regardless of cause or presence of decompensated heart failure, is another predic tor of sudden cardiac death. Dilated ventricles promote dispersion of ventricular depolarization and/or repolarization, allowing “islands” of ventricular tissue to depolarize and repolarize at different rates. The lack of homogeneity in electrical activation and recovery fosters the development of circus movement reentry, which can initiate and sustain ven tricular tachyarrhythmias. Myocardial ischemia and/or infarction can also transiently diminish the homogeneity of left ventricular depolarization and repolarization. Left ventricular hypertrophy (often a result of hypertension and/or valvular heart disease) or conduction disturbances (left or right bundle branch block or a nonspecific intraventricular conduction disturbance) can create similar functional disturbances. In-hospital cardiac arrest patients with heart failure are more likely to have ventricular fibrillation as the initial documented cardiac arrest rhythm compared with non–heart failure patients. 14 New Y ork Heart Association functional class II (symptoms with moderate exertion) and III (symptoms with mild exertion) patients are at higher risk of sudden cardiac death than death from pump failure, whereas class IV patients (symptoms at rest) are more likely to die of pump failure than sudden cardiac death. 5,15 Hypertrophic cardiomyopathy is characterized by unexplained left ventricular hypertrophy associated with nondilated ventricular cham bers.16 The disorder can cluster in families, and the risk of sudden cardiac death increases at a rate of approximately 1% per year.16 Hypertrophic cardiomyopathy is the most common cardiovascular cause of sudden cardiac death in young athletes, accounting for one third of such events, and its presence disqualifies affected individuals from competitive sports. 16 Implantable cardioverter-defibrillator placement is recommended for individuals with prior documented cardiac arrest; ventricular fibrillation; hemodynamically significant or nonsustained ventricular tachycardia; a first-degree relative who has had sudden cardiac death; one or more recent, unexplained episodes of syncope; a maximum left ventricular wall thickness ≥30 mm; or an abnormal blood pressure response to exercise in the presence of other sudden death risk factors or modifiers; and in high-risk children with unexplained syn cope, massive left ventricular hypertrophy, or family history of sudden cardiac death. Arrhythmogenic right ventricular cardiomyopathy is a hereditary form of cardiac muscle disease that is characterized by right-sided heart failure, ventricular arrhythmias of right ventricular origin (i.e., ventricular tachycardia with a left bundle branch block morphology), syncope, and sudden cardiac death. 17,18 The ECG typically shows Resuscitation SECTION CHAPTER Tintinalli_Sec03_p0053-0142.indd 53 8/2/19 2:57 PM

is characterized by right-sided heart failure, ventricular arrhythmias of right ventricular origin (i.e., ventricular tachycardia with a left bundle branch block morphology), syncope, and sudden cardiac death. 17,18 The ECG typically shows Resuscitation SECTION CHAPTER Tintinalli_Sec03_p0053-0142.indd 53 8/2/19 2:57 PM 54 SECTION 3: Resuscitation T-wave inversion in the right precordial leads (V1-3). Severe right heart failure develops in the majority of cases. Patients suspected of having this disorder should be referred for cardiology evaluation. Implantable cardioverter-defibrillator placement is often the treatment of choice since β-blockers and other antiarrhythmics do not usually prevent symptomatic ventricular arrhythmias in these patients.  CONGENITAL HEART DISEASE Congenital heart disease occurs in approximately 0.8% of all live births.19 Because many children with congenital heart disease survive to adult hood as a result of improvements in cardiac surgery, sudden cardiac death is a frequent cause of later morbidity and mortality. Congenital heart defects commonly associated with sudden cardiac death in children and adults are listed in Table 11-2. The most frequent coronary artery anomaly associated with sud den cardiac death is anomalous origin of the left coronary artery from the pulmonary artery syndrome, which results in the left coro nary artery traversing between the aorta and main pulmonary artery. This disorder is being diagnosed more frequently in adults by cardiac CT and MRI. 20 Ischemic symptoms, ventricular arrhythmias, and sudden death can be triggered during exercise as a result of increasing venous return, which dilates the main pulmonary artery and compresses the anomalous coronary artery in the space between the aorta and main pulmonary artery. Treatment is surgical correction. The greatest risk of sudden cardiac death in children and adults with congenital heart disease exists in those with left heart obstruc tive lesions (e.g., aortic stenosis, aortic coarctation) and cyanotic defects (e.g., Ebstein’s anomaly, corrected transposition of the great vessels, tetralogy of Fallot). 19 Most sudden death events in this popula tion occur during exercise, with half of cases resulting from ventricular fibrillation. 19 Nonventricular arrhythmias (e.g., sinus node dysfunction, atrioventricular block, supraventricular tachyarrhythmias) are also common, even after surgical correction.19  VALVULAR HEART DISEASE Hemodynamically severe aortic stenosis can cause effort-induced dyspnea, myocardial ischemia, and ventricular arrhythmias, which can trigger syncope and sudden cardiac death. The most common causes of aortic stenosis are a congenitally bicuspid aortic valve that typically calcifies and narrows its orifice in mid-adulthood or sclerosis/ calcification of a tricuspid aortic valve, which can occur in individu als who are older than 70 or 80 years of age. A harsh, late-peaking systolic murmur at the upper-right sternal border with radiation to the neck is a typical finding in hemodynamically significant aortic stenosis.  CARDIAC PACEMAKER AND CONDUCTING SYSTEM DISEASE Sick sinus syndrome affects the heart’s primary pacemaker and can cause intermittent lightheadedness, syncope, or sudden cardiac death. Although it is more common with advancing age, primary elec trical failure of the heart can occur in infants and children. The cause is unknown, but pathologic studies reveal histologic degeneration of the sinoatrial node. In addition, the disorder often involves the atrioven tricular node and the conduction tissue between the sinoatrial and atrioventricular nodes. Therefore, sick sinus syndrome should be thought of as a diffuse degenerative disease of the heart’s electrical generation and conduction system.

ation of the sinoatrial node. In addition, the disorder often involves the atrioven tricular node and the conduction tissue between the sinoatrial and atrioventricular nodes. Therefore, sick sinus syndrome should be thought of as a diffuse degenerative disease of the heart’s electrical generation and conduction system. Idiopathic sclerodegeneration of the atrioventricular node and the bundle branches (Lenègre’s disease) or invasion of the conduction system by fibrosis or calcification spreading from adjacent cardiac structures (Lev’s disease) can lead to bradyasystolic heart block with or without cardiac arrest. In rare cases, a clinical presentation resembling the sick sinus syndrome can occur when the heart’s electrical system is affected by systemic disease, vascular compromise, or tumor. Symptomatic bradycardia is treated with pacemaker placement.  HEREDITARY CHANNELOPATHIES Sudden Arrhythmic Death Syndrome The sudden arrhythmic death syndrome is characterized by sudden cardiac death occur ring out of hospital in relatively young adults (mostly men), often during sleep or at rest, usually without any premonitory symptoms (including syncope) and with no anatomic abnormality identified at autopsy. 18,19 Genetic disorders are associated with sudden arrhythmic death syndrome, and many cases can be identified clinically based on their characteristic ECG patterns. Ion Channel Disease Cardiovascular and genetic examination of first-degree relatives can identify an inherited form of heart disease known as a “channelopathy” or “ion channel disease” in almost half of cases. Ion channel flux is responsible for the initiation, propagation, and repolarization of the cardiac action potential. Ion channel disease is caused by mutations in the genes that encode the proteins responsible for forming and interacting with the specialized sodium, potassium, and calcium ion channels within the heart. 21 There are many known ion channelopathies, modulated by a variety of causative gene defects that can have variable phenotype penetration in a given family. Genetic testing is used to screen family members for a known mutation. Common subtypes are listed in Table 11-1. TABLE 11-2 Congenital Heart Defects Commonly Associated with Sudden Cardiac Death19 •   Coronary artery anomalies (anomalous left coronary artery from the pulmonary artery [ALCAPA] syndrome) •   Aortic stenosis •   Aortic coarctation •   Tetralogy of Fallot •   Transposition of the great arteries •   Ebstein’s anomaly •   Single ventricle TABLE 11-1 Known Factors Contributing to the Likelihood of Sudden Cardiac Death Cardiovascular pathology •  Coronary  artery disease •  Severe  left ventricular dysfunction •  Cardiomyopathy •  Hypertrophic  cardiomyopathy •  Arrhythmogenic  right ventricular cardiomyopathy •  Congenital  heart disease, especially coronary artery anomalies •  Valvular  heart disease •  Cardiac  pacemaker and conducting system disease Hereditary channelopathies •  Brugada  syndrome •  Early  repolarization syndrome (ERS) •  Long  QT syndrome (LQTS) •  Short  QT syndrome (SQTS) •  Catecholaminergic  polymorphic ventricular tachycardia (CPVT) Risk factors and triggers •  Long-term  risk factor management •  Hypertension •  Hyperlipidemia •  Smoking •  Diabetes  mellitus •  Socioeconomic  status •  Unstable  atherosclerotic plaque •  Psychological  stress •  Physical  activity Tintinalli_Sec03_p0053-0142.indd 54 8/2/19 2:57 PM

ventricular tachycardia (CPVT) Risk factors and triggers •  Long-term  risk factor management •  Hypertension •  Hyperlipidemia •  Smoking •  Diabetes  mellitus •  Socioeconomic  status •  Unstable  atherosclerotic plaque •  Psychological  stress •  Physical  activity Tintinalli_Sec03_p0053-0142.indd 54 8/2/19 2:57 PM CHAPTER 11:  Sudden Cardiac Dea th      55 Brugada Syndrome Brugada syndrome most commonly affects men and consists of a prominent J-wave with a characteristic downsloping ST-segment elevation in ECG leads V 1–3 (Figure 11-1). This ECG pattern resembles a right bundle branch block and is asso ciated with a 40% to 60% incidence of life-threatening ventricular arrhythmias (particularly polymorphic ventricular tachycardia that degenerates into ventricular fibrillation) and sudden cardiac death. The syndrome exhibits an autosomal dominant inheritance that results in total loss of function of the sodium channel or in acceleration of recov ery from sodium channel activation. 22 Brugada syndrome is common in Southeast Asia (where it is called sudden unexplained nocturnal death syndrome), in the Philippines ( bangungut, “to rise and moan in sleep”), in Japan ( pokkuri, “sudden and unexpectedly ceased phenomena”), and in Thailand (lai tai , “death during sleep”). It is crucial for emergency physicians to identify this condition from its characteristic ECG pattern, because the risk of sudden cardiac death is high and can be prevented by internal cardioverter-defibrillator placement. Early Repolarization Syndrome Early repolarization syndrome is present in 1% to 2% of adults (mostly males) and has long been con sidered to be a benign variant of normal ventricular repolarization. 24 Its prevalence is higher (10%) in general athletes and reaches as high as 100% in top-performing, endurance-trained individuals. 25 Classic ECG diagnostic criteria are a prominent, notch-like J wave on the QRS downslope, followed by upsloping ST-segment elevation ( Figure 11-2). These changes are seen most prominently in the mid to lateral precor dium but can also occur just laterally or inferiorly. There is commonly reciprocal ST-segment depression in aVR. Rapid ventricular pacing or exercise usually normalizes these changes. There may be similarity or overlap between Brugada and early repo larization syndromes, but the clinical significance of early repolarization syndrome has not been established. 24 Both syndromes are often familial and more prominent in males, and drugs alter their characteristic ECG patterns (sodium channel blockers and β-blockers increase the STsegment elevation, whereas isoproterenol or mild exercise decreases the ST-segment elevation). 26,27 Referral for an outpatient cardiology evaluation might only be warranted in the case of a teenager or young adult with syncope of unknown origin and/or with a family history of sudden cardiac death at an early age and with an ECG pattern of early repolarization. Long QT Syndrome The long QT syndrome is characterized by prolongation of the corrected QT interval, syncope, and sudden death caused by torsades de pointes and ventricular fibrillation. 21 The corrected QT interval can be calculated using Bazett’s equation:

an early age and with an ECG pattern of early repolarization. Long QT Syndrome The long QT syndrome is characterized by prolongation of the corrected QT interval, syncope, and sudden death caused by torsades de pointes and ventricular fibrillation. 21 The corrected QT interval can be calculated using Bazett’s equation: QTc = QTm √R – R where QTc is the corrected QT interval in seconds, QTm is the measured QT interval in seconds, and R-R is the interval between any two con secutive R waves on the ECG in seconds. Because the QT interval is heart rate dependent, the formula “corrects” the measured QT interval to a heart rate of 60 beats/min (at which the R-R interval is 1 second). Because the square root of 1 = 1, the QT c equals the QTm at a heart rate of 60 beats/min (at which the normal QT interval limits are 0.35 to 0.44 second). Prolongation of the corrected QT interval represents dispersion in ventricular repolarization and can be hereditary or acquired (e.g., hypokalemia, hypomagnesemia, hypocalcemia, anorexia, ischemia, CNS pathology, levofloxacin, terfenadine-ketoconazole combina tions, or certain antipsychotic or antiarrhythmic drugs). 21,28 Hereditary long QT syndrome can have an autosomal recessive (Jervell and Lange-Nielsen syndrome with nerve deafness) or dominant (Romano- Ward syndrome without nerve deafness) mode of inheritance. 21 Management of patients with long QT syndrome involves avoidance of QT-prolonging drugs (an up-to-date list maintained by AzCERT can be found at http://www.QTdrugs.org) and high-intensity sports, as well as cardiology/electrophysiology referral. 21 A β-blocker is typically prescribed as prophylaxis against sudden cardiac death. Long QT syndrome patients who have syncope, torsades de pointes, or ventricular fibrillation despite β-blocker therapy are candidates for implantable cardioverter-defibrillator placement. III IV1 IV2 IV4 IV5 aVR aVL FIGURE 11-1. Brugada syndrome. Twelve-lead ECG typical of Brugada syndrome shows characteristic downsloping ST-segment elevation in leads V1 and V2 and QRS morphology resembling a right bundle branch block. III aVF aVL aVR V1 V4 V2 V5 V3 V6 FIGURE 11-2. Early repolarization syndrome. Note in V5 the prominent notch-like J wave on the QRS downslope and the upsloping ST segment. Tintinalli_Sec03_p0053-0142.indd 55 8/2/19 2:57 PM

T-segment elevation in leads V1 and V2 and QRS morphology resembling a right bundle branch block. III aVF aVL aVR V1 V4 V2 V5 V3 V6 FIGURE 11-2. Early repolarization syndrome. Note in V5 the prominent notch-like J wave on the QRS downslope and the upsloping ST segment. Tintinalli_Sec03_p0053-0142.indd 55 8/2/19 2:57 PM 56 SECTION 3: Resuscitation Short QT Syndrome An abnormally short corrected QT interval (i.e., <0.34 second) can be secondary to hypercalcemia, hyperkalemia, acidosis, systemic inflammatory syndrome, myocardial isch emia, or increased vagal tone or can be inherited in an autosomal dominant genetic pattern. 30 The genetic variety, dubbed the “short QT syndrome, ” is associated with atrial arrhythmia, including atrial fibrillation, syncope, polymorphic ventricular tachycardia, ventricular fibrillation, and sudden cardiac death. 30 Early repolarization, especially in the inferolateral leads, is noted in 65% of patients.31 These individuals should also be referred for cardiology/electrophysiology evaluation and are candidates for cardioverter-defibrillator placement if syncope or lifethreatening ventricular arrhythmias are documented. Catecholaminergic Polymorphic Ventricular Tachycardia Catecholaminergic polymorphic ventricular tachycardia is another genetically determined disorder involving defective myocardial cellular calcium handling. Affected individuals have exercise- and stress-related ventricular tachycardia, syncope, and sudden cardiac death, usually in childhood or early adulthood. Although there are no characteristic abnormalities in the ECG pattern, a significant number of affected individuals have sinus bradycardia that is not otherwise explainable. Almost half of these individuals carry a diagnosis of epilepsy as the cause of their recurrent syncope before the true cause (i.e., catecholaminergic polymorphic ventricular tachycardia) is identified. 32 β-Blockers are the mainstay of prophylaxis, with implantable cardioverter-defibrillator placement as the next step if syncope recurs. PREVENTION OF SUDDEN CARDIAC DEATH Unfortunately, the majority of sudden cardiac death victims cannot be identified in advance. Prodromal symptoms in the days to weeks preceding cardiac arrest are common but are usually too nonspecific to be of important predictive value. 33 The most common premoni tory symptoms reported by sudden cardiac death survivors or family members of victims are chest discomfort, dyspnea, and “not feeling w e l l .” Various tests have been used to try to “risk stratify” potential sudden cardiac death patients, but none are sensitive or specific enough to be useful. Tests include invasive and noninvasive assessment of left ven tricular ejection fraction, coronary angiography, ambulatory ECG monitoring, exercise testing, detection of ventricular late potentials by using signal averaging, programmed ventricular stimulation of the heart to test the inducibility of ventricular tachyarrhythmias, assessment of heart rate variability, and T-wave alternans (alternating T-wave amplitude from beat to beat on the ECG, which is visible only with special record ing equipment). 34 The best opportunity for prevention is to recognize signs and symptoms of the syndromes that place a patient at higher risk of sudden cardiac death and to admit or refer such patients for proper evaluation and prophylaxis.  ANTIARRHYTHMIC DRUG AND DEVICE THERAPY The Cardiac Arrhythmia Suppression Trial showed that potent class I sodium channel–blocking antiarrhythmic drugs (encainide, flecainide, and moricizine) are proarrhythmic and paradoxically increase the odds of developing sudden cardiac death, as compared with placebo, in patients at relatively low risk for death.

ERAPY The Cardiac Arrhythmia Suppression Trial showed that potent class I sodium channel–blocking antiarrhythmic drugs (encainide, flecainide, and moricizine) are proarrhythmic and paradoxically increase the odds of developing sudden cardiac death, as compared with placebo, in patients at relatively low risk for death. 35 The American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society have developed an up-to-date comprehensive guide to the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. 36 In general, the benefits of antiarrhythmic medications such as β-blockers, sotalol, and amiodarone in decreasing mortality from sudden cardiac death pale in comparison with the protective effects of the implantable car dioverter-defibrillator in high-risk patients, 37 including those who have been resuscitated from ventricular fibrillation or cardioverted out of sustained ventricular tachycardia. 38 Although these devices are expensive to insert, their effectiveness over conventional therapy results in a cost of less than $30,000 per year of life saved, which makes them relatively cost-effective for implantation in high-risk individuals. The Centers for Medicare and Medicaid Services is reevaluation whether to broaden its indications for implantable cardioverter-defibrillator insertion due to the efficacy and effectiveness of these devices for secondary and primary sudden cardiac death prevention in many patient populations, including patients ≥65 years. SUDDEN CARDIAC DEATH RESCUE The outcome of resuscitation is influenced strongly by the patient’s initial cardiac rhythm. In most cases in which the event has been captured during monitoring, the initiating event is either pulseless ventricular tachycardia that degenerates rapidly to ventricular fibrillation or “primary” ventricular fibrillation. EMS and in-hospital resuscitation systems are the most effective means currently known to rescue patients from sudden cardiac death. Survival from pulseless ventricular tachycardia or ventricular fibrillation is inversely related to the time interval between its onset and termina tion. Survival is optimal when both CPR and advanced cardiac life support, including defibrillation and drug therapy, are provided early. Community resuscitation strategies should include provision of early CPR, early activation of the EMS system, early defibrillation (including public access defibrillation), early advanced cardiac life support, and regionalized systems of postresuscitation care. 41,42 The Public Access Defibrillation randomized clinical trial showed that laypersons trained and equipped to use automated external defibrillators in public places can double survival to hospital discharge compared with layperson res cuers who can only perform CPR while awaiting EMS arrival. 43 These results have been confirmed in an analysis of 13,769 out-of-hospital cardiac arrest registry cases.  PULSELESS VENTRICULAR TACHYCARDIA/VENTRICULAR FIBRILLATION The likelihood of survival is relatively high if the initial rhythm is ventricular tachycardia or ventricular fibrillation (particularly if the ven tricular fibrillation is “coarse, ” the arrest is witnessed, and prompt CPR and defibrillation are provided). If the initial rhythm is not ventricular tachycardia or ventricular fibrillation, survival is typically <5% in most reported series. Asystolic patients whose cardiac arrest is unwitnessed rarely survive to hospital discharge neurologically intact. The only common exceptions are witnessed cardiac arrest patients whose initial asystole is a result of increased vagal tone or other relatively easily correctible factors, such as hypoxia of brief duration.

systolic patients whose cardiac arrest is unwitnessed rarely survive to hospital discharge neurologically intact. The only common exceptions are witnessed cardiac arrest patients whose initial asystole is a result of increased vagal tone or other relatively easily correctible factors, such as hypoxia of brief duration.  PULSELESS ELECTRICAL ACTIVITY Some sudden cardiac death events begin with a bradyarrhythmia or an organized rhythm without a pulse (e.g., pulseless electrical activity). Bradyasystole in adults is defined as a ventricular rate <60 beats/min or periods of absent heart rhythm (asystole). Bradyasystolic rhythms other than asystole can be accompanied by a pulse, or there can be no discernible pulse with each QRS (i.e., pulseless electrical activity). Bradyasystole with a pulse is often accompanied by a significant decrease in cardiac output, leading to hypotension and/or syncope. Bradycardia with or without a pulse occurs frequently during cardiac arrest, either as the initial rhythm, during the course of resuscitation, or after electrical defibrillation. Obviously, asystole occurs eventually in all dying patients. To ensure that ventricular fibrillation is not masquerading as asystole, rescuers can switch to another lead whenever a “flat line” is recorded on the ECG during resuscitation or use US if available. Primary bradyasystole occurs when the heart’s electrical system fails to generate and/or propagate an adequate number of ventricular depo larizations per minute to sustain consciousness and other vital func tions. Secondary bradyasystole is present when factors external to the heart’s electrical system cause it to fail (e.g., hypoxia). Common causes of bradyasystolic arrest are listed in Table 11-3. Tintinalli_Sec03_p0053-0142.indd 56 8/2/19 2:57 PM