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362 SECTION 7: Cardiovascular Disease  DIAGNOSTIC PATHWAYS FOR PATIENTS WITH POSSIBLE ACUTE CORONARY SYNDROME INPATIENT ADMISSION If observation beds are unavailable, patients with possible ACS needing additional testing beyond one or two troponin measurements are admitted to an inpatient bed. Specific destinations and care level are driven by stratification; those with a prior history of CAD, evidence of congestive heart failure on physical examination, recurrent chest pain, or new or presumed new ischemic ECG changes are at higher short-term risk and may be more appropriately managed in an intermediate-care (stepdown) unit. ED OBSERVATION AND TESTING ED observation unit management decreases hospital admissions, length of stay, and hospital cost while providing a high level of care. The tra ditional observation unit chest pain protocol was refined by Lateef and colleagues, 24 with patients observed for 9 hours with continuous 12-lead ST-segment ECG monitoring and serial creatine kinase-MB testing at 0, 3, 6, and 9 hours after presentation. Those who completed a negative 9-hour evaluation subsequently underwent echocardiography followed by graded exercise stress testing in the ED before discharge. With this approach, 82.1% of patients were released home from the cardiac evaluation unit. The approach of serial cardiac markers followed by objective cardiac testing remains the foundation of ED and other observation unit protocols. Although early observation unit protocols focused on low-risk patients, more recent investigations successfully studied patients with intermediate-risk chest pain. Some observation units adequately manage patients at intermediate risk for ACS, whereas some facilities manage these patients in the hospital. Any protocol that treats all patients with possible ACS equally should incorporate serial cardiac markers and stress testing. In addition, early stress testing after a negative ultra-short cardiac marker testing strategy, or exercise stress testing after one negative cardiac marker in patients with possible ACS, appears safe in low- and intermediate-risk patients. Finally, outpatient stress testing is an option for reliable low-risk patients in whom acute myocardial infarction has been excluded presenting to a facility where a mechanism exists to arrange this testing. Compliance with follow-up testing is better when scheduled before discharge. TREATMENT Clinical trials often do not include patients with possible ACS and instead focus on the higher-risk patients with positive cardiac markers or ST-segment changes on their ECG. Therefore, treatment recommendations for patients with possible ACS are derived from reviewing the risk-to-benefit profile suggested from clinical trial results in the higherrisk patient populations. Additional information on the mechanisms of action and data from clinical trials are discussed in Chapter 49, “ Acute Coronary Syndromes. ” Therapy for patients with possible ACS is linked to the patient’s stratification level. In general, patients at low risk of adverse events receive aspirin and anti-ischemic therapy with nitroglycerin while their evaluation is being completed. SPECIAL POPULATIONS Age, ethnic, racial, and gender differences are well described in patients presenting with ACSs. Most current knowledge of ACS-related symp toms and risk factors comes from population-based studies.

ceive aspirin and anti-ischemic therapy with nitroglycerin while their evaluation is being completed. SPECIAL POPULATIONS Age, ethnic, racial, and gender differences are well described in patients presenting with ACSs. Most current knowledge of ACS-related symp toms and risk factors comes from population-based studies. Studies have suggested that women are more likely to present without chest pain and often have a prodrome of fatigue. Similarly, the elderly less often present with a chief complaint of chest pain and, less frequently, have typical chest pain. Other studies have noted delayed presentation for ACS in black women 26 and less frequent chest pain with ACS in those of Asian descent.27 The Framingham criteria overestimate the risk of coronary disease when applied to Chinese patients, 28 and these patients are less likely to experience classic symptoms of ACS. Be aware of all these confounders as you assess the clinical likelihood of ACS. REFERENCES The complete reference list is available online at www.TintinalliEM.com. Syncope James Quinn INTRODUCTION AND EPIDEMIOLOGY Syncope or fainting is a symptom complex consisting of a brief loss of consciousness associated with an inability to maintain postural tone that spontaneously resolves without medical intervention with the person returning to their baseline neurologic condition. Syncope accounts for approximately 1% to 2% of ED visits each year and 1% to 6% of hospital admissions. 1-4 Over a lifetime, the prevalence of syncope ranges from 10.5% to 19%. 1,5 Syncope in the preceding year is the best predictor of recurrence.6 It can affect the young and the old, with the elderly having the greatest morbidity.7 Near syncope, a premonition of fainting without loss of consciousness, shares the same basic pathophysiologic process as syncope and carries the same risks. 8-11 PATHOPHYSIOLOGY The final common pathway of syncope is the same regardless of the underlying cause: about 10 seconds of complete disruption of blood flow or nutrient delivery to both cerebral cortices or to the brainstem reticular activating system, or reduction of cerebral perfusion by 35% to 50%. Most commonly, an inciting event causes a drop in cardiac output, which decreases oxygen and substrate delivery to the brain. Cerebral perfusion and consciousness are restored by the supine position, the response of autonomic autoregulatory centers, or restoration of a perfusing cardiac rhythm. The causes of syncope are numerous ( Table 52-1). The most common causes of syncope identified in the Framingham Heart Study were vasovagal (reflex mediated, 21%), cardiac (10%), orthostatic (9%), medication related (7%), neurologic (4%), and unknown (37%). 5 Even with exhaustive patient evaluation, the cause remains unknown in about 18% to 40% of individuals. 12,13 After ED investigation, the unknown proportion may be 50% to 60%. Diagnosis is important, because each diagnostic classification carries with it prognostic risk. Cardiac syncope doubles the risk of death, neurologic syncope increases the risk of death by 50%, and syncope of unknown cause increases the risk of death by 30%. 5 Individuals with neutrally mediated/reflex-mediated or vasovagal syncope have no increased risk of death, 5 but patients with recurrent syncope have an increased risk of injury.14 CLINICAL FEATURES  CARDIAC-RELATED SYNCOPE Patients with documented cardiac syncope have a 6-month mortality rate that exceeds 10%. Thus, a timely and thorough evaluation is warranted. 5,13 The causes of cardiac syncope are divided into two categories: structural disease and dysrhythmias ( Table 52-1). In both settings, the heart is unable to provide adequate cardiac output to maintain cerebral perfusion. CHAPTER Tintinalli_Sec07_p0329-0424.indd 362 8/2/19 6:42 PM

nd thorough evaluation is warranted. 5,13 The causes of cardiac syncope are divided into two categories: structural disease and dysrhythmias ( Table 52-1). In both settings, the heart is unable to provide adequate cardiac output to maintain cerebral perfusion. CHAPTER Tintinalli_Sec07_p0329-0424.indd 362 8/2/19 6:42 PM CHAPTER 52: Syncope 363 Syncope can occur if structural disease limits the heart’s ability to increase cardiac output to meet demand. Examples of structural cardiac disease associated with syncope include aortic stenosis, hypertrophic cardiomyopathy, pulmonary embolism, and myocardial infarction. Consider aortic stenosis as a structural cardiac cause of syncope in the elderly. The classic symptom constellation of aortic stenosis is chest pain, dyspnea on exertion, and syncope. Hypertrophic cardiomyopathy is characterized by a stiff noncompliant left ventricle, diastolic dysfunction, and outflow tract obstruction. Although it is the most common cause of sudden cardiac death in young adults, it may be first recognized in those >60 years old. 15 Massive acute pulmonary embolism may cause syncope due to obstruction of the pulmonary vascular bed and reduction in cardiac output. 16 Acute myocardial infarction may cause syncope if myocardial dyskinesia reduces cardiac output. Individual chapters in the “Cardiovascular Disease” section of this text provide more discussion on structural cardiopulmonary disorders that may cause syncope. Although both brady- and tachydysrhythmias may lead to transient cerebral hypoperfusion (Table 52-1), there is no absolute high or low heart rate that will predictably produce syncope. Symptoms depend on the autonomic nervous system’s ability to compensate for a decrease in cardiac output, the heart’s structural ability to compensate, and the degree of underlying cerebrovascular disease. Dysrhythmias usually occur in patients with congenital or acquired structural conditions (e.g., myocardial infarction, cardiomyopathy especially resulting in congestive heart failure) in which the conduction system is damaged or compro mised. These people are at high risk for arrhythmias and sudden death. Arrythmias may also occur in structurally normal hearts in patients with a primary electrolyte imbalance, as in hypomagnesemia (e.g., tor sades de pointes) and in the familial disorders of Brugada syndrome, long or short QT syndromes, and catecholamine-associated polymor phic ventricular tachycardia. Syncope from dysrhythmias is typically sudden without prodromal symptoms.  VASOVAGAL AND NEURALLY OR REFLEX-MEDIATED SYNCOPE Vasovagal syncope is the result of autonomic dysfunction that is reflex mediated or neurally mediated. It is associated with inappropriate vasodilatation, bradycardia, or both, as a result of inappropriate vagal or sympathetic tone. 17-19 A prodrome of lightheadedness, with or without nausea, pallor, and/or sweating, and an associated feeling of warmth may accompany vasovagal syncope. A slow, progressive onset with associated prodrome suggests vasovagal syncope. Vasovagal syncope may occur after exposure to an unexpected or unpleasant sight, sound, or smell; fear; severe pain; emotional distress; or instrumentation. It may also occur in association with prolonged standing or kneeling in a crowded or warm place. Situational syncope occurs during or immediately after coughing, micturition, defecation, or swallowing. Carotid sinus syndrome is a type of reflex-mediated syncope associated with carotid sinus hypersensitivity , characterized by bradycardia or hypotension. 20,21 The carotid body, located at the carotid bifurcation, contains pressure-sensitive receptors. The stimulation of an abnormally sensitive carotid body by external pressure may lead to two autonomic responses.

iated syncope associated with carotid sinus hypersensitivity , characterized by bradycardia or hypotension. 20,21 The carotid body, located at the carotid bifurcation, contains pressure-sensitive receptors. The stimulation of an abnormally sensitive carotid body by external pressure may lead to two autonomic responses. Most commonly, there is bradycardia and a pause (asystole) of >3 seconds. Less commonly, there is a vasodepressor response, lead ing to a decrease in blood pressure of >50 mm Hg without a significant change in heart rate. Carotid sinus hypersensitivity is more common in men, the elderly, and those with ischemic heart disease, hypertension, or head and neck malignancies. Although some patients may demonstrate a hypersensitive carotid sinus response on provocative testing, unless this response culminates in syncope or recurrence of prodromal symptoms and unless it is associated with an inciting event, such as shaving or turning of the head, it cannot be definitely diagnosed as the cause of syncope. About 25% of patients with carotid sinus hypersensitivity have true carotid sinus syndrome with spontaneous symptoms. 22 Consider carotid sinus hypersensitivity in older patients with recurrent syn cope and negative cardiac evaluations.  ORTHOSTATIC SYNCOPE Orthostatic syncope is suggested when postural hypotension (drop in systolic blood pressure of ≥20 mm Hg or diastolic blood pressure of ≥10 mm Hg) is associated with syncope or presyncope. 21,23 When a person assumes an upright posture, gravity shifts blood to the lower part of the body, and cardiac output drops. This change triggers the healthy autonomic nervous system to increase sympathetic output and decrease parasympathetic output, increasing heart rate and peripheral vascular resistance, and thus increasing cardiac output and blood pressure. 24,25 If the autonomic response is insufficient to counter the drop in car diac output upon standing, decreased cerebral perfusion and syncope may follow. Syncope with postural hypotension to dysfunction of the autonomic nervous system is termed neurogenic orthostatic hypoten sion. 21 Symptom onset is usually within the first 3 minutes after assuming the upright posture, but may be more delayed in some patients. 21 However, positive orthostatic changes have been documented in up to TABLE 52-1 Causes of Syncope Cardiac* Neural/Reflex Mediated Structural cardiopulmonary disease Valvular heart disease Aortic stenosis Tricuspid stenosis Mitral stenosis Cardiomyopathy Pulmonary hypertension Congenital heart disease Myxoma Pericardial disease Aortic dissection Pulmonary embolism Myocardial ischemia Myocardial infarction Dysrhythmias Bradydysrhythmias Short or long QT syndromes Stokes-Adams attack Sinus node disease Second- or third-degree heart block Pacemaker malfunction Tachydysrhythmias Ventricular tachycardia Torsades de pointes Supraventricular tachycardia Atrial fibrillation or flutter Vasovagal Situational Cough Micturition Defecation Swallow Neuralgia Carotid sinus syndrome Other Orthostatic hypotension (see text) Psychiatric Neurologic Transient ischemic attacks Subclavian steal Migraine Medications (Table 52-2) Breath holding (children) † *See Chapter 130, “Syncope, Dysrhythmias, and ECG Interpretation in Children.” †See Chapter 117, “Brief Resolved Unexplained Events.” TABLE 52-2 Drugs Commonly Implicated in Syncope •  Erectile  dysfunction drugs •  Antihypertensives •  β-Blockers •  Cardiac  glycosides •  Diuretics •  Antidysrhythmics •  Antipsychotics •  Antiparkinsonism  drugs •  Antidepressants •  Phenothiazines •  Nitrates •  Alcohol •  Cocaine Tintinalli_Sec07_p0329-0424.indd 363 8/2/19 6:42 PM

Commonly Implicated in Syncope •  Erectile  dysfunction drugs •  Antihypertensives •  β-Blockers •  Cardiac  glycosides •  Diuretics •  Antidysrhythmics •  Antipsychotics •  Antiparkinsonism  drugs •  Antidepressants •  Phenothiazines •  Nitrates •  Alcohol •  Cocaine Tintinalli_Sec07_p0329-0424.indd 363 8/2/19 6:42 PM 364 SECTION 7: Cardiovascular Disease 40% of asymptomatic patients >70 years old and in about a quarter of those <60 years old, so orthostasis does not always result in syncope.18,26 Causes of orthostatic syncope include intravascular volume loss and poor vascular tone caused by α-receptor disorders or medications. Many serious causes of syncope may be associated with orthostatic changes, so consider other life-threatening causes before attributing syncope to orthostasis and autonomic dysfunction, especially in the elderly.  PSYCHIATRIC DISORDERS Psychiatric disorders are associated with up to 40% of those with vaso vagal syncope and 37% to 62% of those with unexplained syncope. 27-29 The most frequent psychiatric diagnoses associated with syncope are generalized anxiety disorder and major depressive disorder. 30,31 A psychiatric cause for syncope should be one of exclusion, assigned only after organic causes have been excluded. Psychogenic pseudosyncope is a term reserved for patients with apparent loss of conscious without impaired cerebral perfusion. Eye closure during the event, long periods of apparent transient loss of consciousness, and increased heart rate and blood pressure are commonly seen in psychogenic pseudosyncope. 21,32 Hyperventilation may be associated with panic disorder or generalized anxiety disorders and can lead to hypocarbia, cerebral vasoconstriction, and syncope.  MEDICATION-INDUCED SYNCOPE Medications may contribute to syncope by a variety of means, and a careful history and consideration are required ( Table 52-2). The most common effect is worsening orthostasis. β-Blockers or calcium channel blockers may lead to a blunted heart rate response after orthostatic stress, and nitrates can cause venous pooling and vascular dilation. Diuretics may produce volume depletion. Some medications have proarrhythmic properties, especially as combi nation agents, increasing the concern for dysrhythmia as the cause of syncope.  NEUROLOGIC DISORDERS ASSOCIATED WITH LOSS OF CONSCIOUSNESS Neurologic causes of syncope are rare. To meet the definition of syncope, symptoms must be transient and with no persistent neurologic deficits. Patients with loss of consciousness with persistent neurologic deficits or altered mental status do not have true syncope; such patients have alternate medical disorders, many of them life threatening (e.g., stroke, sepsis, overdose). Transient brainstem ischemia, vertebrobasilar atherosclerotic disease, or basilar artery migraine may result in a decrease in blood flow to the reticular activating system, leading to sudden, brief episodes of loss of consciousness. Loss of consciousness due to this mechanism is not only rare but also typically preceded by other signs or symptoms, such as diplopia, vertigo, focal neurologic deficits, or nau sea. Subclavian steal syndrome is a rare cause of brainstem ischemia. It is characterized by an abnormal narrowing of the subclavian artery proximal to the origin of the vertebral artery, so that with exercise of the ipsilateral arm, blood is shunted, or “stolen, ” from the vertebrobasilar system to the subclavian artery supplying the arm muscles. Anatomi cally, narrowing is more common on the left. Physical examination may identify decreased pulse volume and diminished blood pressure in the affected arm.

that with exercise of the ipsilateral arm, blood is shunted, or “stolen, ” from the vertebrobasilar system to the subclavian artery supplying the arm muscles. Anatomi cally, narrowing is more common on the left. Physical examination may identify decreased pulse volume and diminished blood pressure in the affected arm. Spontaneous subarachnoid hemorrhage may present as a cause of syncope, but is usually accompanied by other symptoms such as focal neurologic deficits, headache, or persistent altered mental status, removing it from the true definition of syncope. In this case, the mechanism for syncope is thought to be an increase in intracranial pressure with a decrease in cerebral perfusion pressure. That being said, syncope from any cause can result in head injury with traumatic subarachnoid hemorrhage. See Chapter 166, “Spontaneous Subarachnoid and Intracere bral Hemorrhage, ” for further discussion. Seizure may be confused with syncope, because brief tonic-clonic movements are often associated with syncope. Distinguishing features of seizure over syncope include a previous history of seizure, confusion (postictal state) lasting more than several minutes, tongue biting, incontinence, or an epileptic aura. PRINCIPLES OF EVALUATION The goal of ED evaluation is to identify those at risk for immediate and future morbidity or sudden death. Patients presenting after nearsyncope should be managed the same as patients with syncope. 8-11 For patients with a specific diagnosis, the diagnosis directs the disposition plan. For patients without a specific diagnosis, risk stratification can guide disposition and care. Risk stratification is based on a careful history, thorough physical examination, ECG interpretation, and addi tional testing as needed.  HISTORY Obtain clinical history from the patient and any witnesses of the event. Begin with a detailed description of the events preceding the loss of consciousness, including patient position, environmental stimuli, strenu ous activity, or arm exercise. One should inquire about premonitory symptoms such as auras, headache, diplopia, vertigo, or focal weakness. Ask about chest pain and palpitations. Clarify the duration of loss of consciousness and symptoms occurring after regaining conscious ness. Symptoms associated with syncope that should raise concern of an immediately life-threatening diagnosis include chest pain (acute myocardial infarction, aortic dissection, pulmonary embolism, aortic stenosis), palpitations (dysrhythmia), shortness of breath (pulmonary embolism, congestive heart failure), headache (subarachnoid hemor rhage), and abdominal or back pain (leaking abdominal aortic aneurysm, ruptured ectopic pregnancy). A sudden event without warning and events associated with exertion raise suspicion for a cardiac dys rhythmia or structural cardiopulmonary lesion. 35 Ask about anteced ent illness and alcohol ingestion or substance abuse. The past medical history should include questions regarding underlying structural heart disease, including congenital heart disease, valvular heart disease, coro nary artery disease, congestive heart failure, pulmonary embolism and venous thromboembolism risk, and ventricular dysrhythmias. Docu ment any prior history of syncope because patients with more than five syncopal episodes in 1 year are more likely to have vasovagal syncope (autonomic dysfunction) or a psychiatric diagnosis than dysrhythmia as the cause. 6,29,31 Record all medications, including over-the-counter medications such as laxatives. Patients aggressively dieting to lose weight may have electrolyte disturbances or may be taking amphetamine-like medications. The family history is important in regard to history of prolonged QT syndrome, dysrhythmias, sudden cardiac death, or other cardiac risks.

cluding over-the-counter medications such as laxatives. Patients aggressively dieting to lose weight may have electrolyte disturbances or may be taking amphetamine-like medications. The family history is important in regard to history of prolonged QT syndrome, dysrhythmias, sudden cardiac death, or other cardiac risks. Pay special attention to patients presenting after falls or single-car motor vehicle crashes without apparent cause (frequently with a history of driving off the road), particularly if the patient is ≥65 years old, has a history of coronary artery disease, or has an abnormal ECG. 36 Clinicians may become preoccupied by the trauma evaluation and miss the pos sibility of a syncopal event. Seizure is the most common event mistaken as syncope. Mild, brief, tonic-clonic activity (“convulsive syncope”) may accompany syncope of any etiology. The two conditions do not share the same pathophysiologic mechanisms. A previous seizure disorder or premonitory and postevent symptoms may assist in differentiation. 37 A classic aura or postictal confusion and muscle pain indicate seizure, whereas characteristic pro dromal symptoms of nausea and diaphoresis suggest reflex-mediated (vasovagal) syncope. Witness information of the event may also be useful. Witnessed head turning or unusual posture during the event is consistent with seizure. A prolonged postictal phase is more common with seizure. Urinary incontinence is not useful in the distinction.  PHYSICAL EXAMINATION Signs of trauma without defensive injuries to the hands or knees may be due to a sudden event without warning, such as a dysrhythmia. Focus the physical examination on the cardiovascular and neurologic systems. Obtain blood pressure measurements in both arms. Consider Tintinalli_Sec07_p0329-0424.indd 364 8/2/19 6:42 PM

Signs of trauma without defensive injuries to the hands or knees may be due to a sudden event without warning, such as a dysrhythmia. Focus the physical examination on the cardiovascular and neurologic systems. Obtain blood pressure measurements in both arms. Consider Tintinalli_Sec07_p0329-0424.indd 364 8/2/19 6:42 PM CHAPTER 52: Syncope 365 aortic dissection or subclavian steal if blood pressures are unequal. Take orthostatic blood pressures after 5 minutes in the supine position. Repeat measurements after 1 and 3 minutes of standing. A symptomatic decrease of >20 mm Hg in the systolic pressure is considered abnormal, as is a decrease in pressure <90 mm Hg independent of the develop ment of symptoms. Cardiac examination may reveal the murmur of hypertrophic cardiomyopathy or aortic stenosis. The neurologic examination may uncover findings of focal neurologic disease or evidence of autonomic instability such as peripheral neuropathy. Perform rectal examination to check stool guaiac to evaluate for GI bleeding.  DIAGNOSIS The diagnosis of syncope is clinical, with careful evaluation of the presentation and selected use of diagnostic tests. History is most important, and most diagnostic tests have low diagnostic yield and should be guided by the history and physical examination. 38 The differential diagnosis is presented in Tables 52-1 and 52-2.  ECG AND ED MONITORING Obtain a 12-lead ECG and place the patient on a cardiac monitor. Even though the ECG leads to a diagnosis in only a few patients, it is a simple, noninvasive test and is important for risk stratification. 21,39,40 Assess the ECG for evidence of prior cardiopulmonary disease, acute ischemia or new ECG changes, dysrhythmia, heart block, and prolonged or short c interval. A prolonged QTc interval has a variable definition, but the literature suggests it is defined as >470 milliseconds, with >500 milliseconds associated with significant outcomes, 41-43 whereas a short QT c interval <350 milliseconds is concerning as well. 44 New or old left bundle conduction abnormalities (e.g., left bundle branch block, posterior or anterior fascicular block, QRS widening) are 3.5 times more likely to be associated with morbidity than ECGs lacking these findings. Non sinus rhythms are 2.5 times more likely to be associated with morbid ity than sinus rhythms. 45 Numerous studies have pointed out that the value of ED monitoring is additive to a single ECG done in the ED. 46-48 For further discussion, see below and Chapter 18, “Cardiac Rhythm Disturbances. ”  LABORATORY TESTING Laboratory testing is directed by results of the history and physical examination, and no test other than an ECG should be considered “routine. ” For example, a patient with orthostatic symptoms and a hemepositive stool test warrants at least a CBC. A reproductive-age female should have a urine pregnancy test. A transitory, wide anion gap aci dosis follows a generalized seizure but is not present in simple syncope. Serum electrolytes rarely determine the cause of syncope; however, an elevated blood urea nitrogen is a predictor of serious adverse outcome within 30 days after syncope. 49 B-type natriuretic peptide or pro–B-type natriuretic peptide levels appear to be predictive of those at risk for morbidity. One study suggests that a level >300 picograms/mL in the setting of syncope indicates risk, 50 but whether this adds any value over a history of congestive heart failure or structural disease is unclear. 51,52 See Chapter 53, “ Acute Heart Failure, ” for a discussion of the diagnostic use of B-type natriuretic peptide.  ANCILLARY TESTING Carotid Massage Carotid massage is used to diagnose carotid sinus hypersensitivity in the patient with a history suggestive of carotid sinus syndrome.

r structural disease is unclear. 51,52 See Chapter 53, “ Acute Heart Failure, ” for a discussion of the diagnostic use of B-type natriuretic peptide.  ANCILLARY TESTING Carotid Massage Carotid massage is used to diagnose carotid sinus hypersensitivity in the patient with a history suggestive of carotid sinus syndrome. However, given the small benefit of the maneuver and potential adverse events, most do not routinely perform carotid massage as part of the ED evaluation. Carotid massage can be done at the bedside with continuous ECG and blood pressure monitoring, after obtaining informed consent. Each carotid body is separately massaged for 5 to 10 seconds. The test is considered positive if symptoms are reproduced in the presence of asystole >3 seconds or a decrease in systolic blood pressure of >50 mm Hg. Do not perform carotid massage if the patient has known carotid stenosis, if bruits are present, if there is history of recent (<3 months) stroke or myocardial infarction, or if there is a history of ventricular tachycardia or fibrillation. Neurologic deficits resulting from carotid massage are rare, with deficits lasting more than 24 hours in approxi mately 0.1% of patients. 53 Only a small number of patients with carotid hypersensitivity will have the true carotid sinus syndrome. Hyperventilation Maneuver A hyperventilation maneuver (openmouthed, slow, deep breaths at a rate of 20 to 30 breaths per minute for 2 to 3 minutes) can be very useful in the young patient with undiagnosed syncope and suspected psychiatric illness. A recurrence of prodromal symptoms or syncope significantly correlates with psychiatric (anxietyprovoking) causes of syncope. Neurologic Testing When the history or physical examination does not reveal head trauma or neurologic findings, the clinical yield of CT scanning, 54 electroencephalogram, or lumbar puncture is very low. Consequently, in asymptomatic patients who have returned to baseline with an isolated syncopal event, CT or MRI is not warranted unless there is concern for a neurologic cause. Pulmonary Embolism The Pulmonary Embolism in Syncope Italian Trial study reported a 17% prevalence of pulmonary embolism in patients admitted to the hospital as a result of syncope. 55 However, a much larger multicenter study found the pulmonary embolism preva lence to be 0.15% to 2%. 56 For all ED patients presenting with syncope, the prevalence of pulmonary embolism ranges from 0.06% to 1.4%. 56,57 Therefore, pulmonary embolism assessment need not be routine, but should be reserved for those with venous thromboembolism risk factors or history or examination findings suggestive of pulmonary embolism. DECISION MAKING AND RISK ASSESSMENT  DIAGNOSIS ESTABLISHED If a cause of syncope can be determined by the initial history, physical examination, and ECG, the disposition is simple. Patients with cardiac or neurologic syncope should have appropriate specialty consultation and be admitted as necessary. Patients with clear vasovagal, orthostatic, and medication-related syncope have no increased risk of cardiovascular morbidity or mortality 7 and do not need admission as long as deficits or medication misadventures are corrected.  UNEXPLAINED SYNCOPE Despite best efforts, a diagnosis will not be established in about 40% of the patients with syncope. Table 52-3 summarizes several studies that have assessed risk-stratification variables to identify patients at risk of both short-term and 1-year morbidity and mortality. 2,58-65 Quinn et al2,59 assessed adverse outcomes at 7 and 30 days in their derivation and validation of the San Francisco Syncope Rule.

ith syncope. Table 52-3 summarizes several studies that have assessed risk-stratification variables to identify patients at risk of both short-term and 1-year morbidity and mortality. 2,58-65 Quinn et al2,59 assessed adverse outcomes at 7 and 30 days in their derivation and validation of the San Francisco Syncope Rule. Significant predictors of adverse events (primarily dysrhythmia) included (1) a history of congestive heart failure, (2) an abnormal ECG (a rhythm other than sinus, including those on rhythm strips or monitoring, conduction delays or new changes as minimal as first-degree atrioventricular block, or any morphologic changes to the QRS complex or ST segment that could not be proven to be old by prior tracings), (3) a hematocrit of <30%, (4) a complaint of shortness of breath, or (5) a systolic blood pressure of <90 mm Hg in the ED . The presence of any one of the five high-risk criteria listed above has an 89% sensitivity and 52% specificity for death at 1 year. 65 There have been inconsistent findings when validating the San Francisco Syncope Rule, which have been primarily related to definitions of syncope and the application of variables.60 Other studies identified age >65 years, 61,62 syncope without prodrome or lack of vasovagal etiology,61,63,64 positive troponin,64 systolic blood pressure >180 mm Hg, and concomitant trauma as high-risk features. 63 Using the risk factors identified in these studies can help clinicians determine patient risk and appropriate disposition. There is a consistent theme that patients with an abnormal ECG on presentation and/or a history of heart disease , particularly structural heart disease especially characterized by a history of congestive heart failure, are clearly at increased risk. Additional risk factors suggested by guidelines 40,66,67 include syncope while supine, syncope during exercise, syncope without prodromal symptoms, palpations preceding syncope, and the specific age cut points of >60 or >65 years. Tintinalli_Sec07_p0329-0424.indd 365 8/2/19 6:42 PM

ilure, are clearly at increased risk. Additional risk factors suggested by guidelines 40,66,67 include syncope while supine, syncope during exercise, syncope without prodromal symptoms, palpations preceding syncope, and the specific age cut points of >60 or >65 years. Tintinalli_Sec07_p0329-0424.indd 365 8/2/19 6:42 PM 366 SECTION 7: Cardiovascular Disease TREATMENT Treatment should be guided by the diagnosis. Patients with or at risk for life-threatening dysrhythmias can be treated with pacemakers or automatic implantable defibrillators as indicated. For patients with suspected medication causes, remove the offending agent. Rehydrate those with orthostasis and dehydration. Educate patients with vasovagal syncope; episodes are likely to recur, and patients should lie or sit down when they sense a prodrome. β-Blockers do not decrease episodes of vasovagal syncope. DISPOSITION AND FOLLOW-UP Guidelines recommend using known risk factors, such as those outlined in the text and Table 52-3, to separate patients into risk groups for disposition and management. 21,40,69 European Society of Cardiology guidelines identify high- and low-risk patients, 40 and the American Heart Association guidelines also identify intermediate-risk patients. 21,69 There is agreement that low-risk patients (those with clear reflex-mediated syncope, without a history of heart disease, who are currently asymptomatic and with a normal physical exam and ECG) can be discharged with nonurgent primary care follow-up. 21,40 There is less agreement as to which patients are at high or intermediate risk of adverse outcome, reflected by guideline discrepancies and regional variation. 70 However, patients thought to be high risk by the examin ing physician and those with active chest pain or dyspnea, exertional syncope, sudden-onset palpitations prior to syncope, ECG evidence of conduction abnormalities or ongoing arrhythmia, history of CHF or structural heart disease, or family history of sudden cardiac death are recommended for admission to the hospital or to a syn cope observation unit (if now asymptomatic). 21,69 Decisions on testing should be determined by the patient’s presentation and comorbidities.  INPATIENT EVALUATION With the exception of patients with acute life-threatening diagnoses (e.g., stroke, aortic dissection), the core of the inpatient evaluation is focused on identification of underlying heart disease and detection of dysrhythmias. The indications and utility of postsyncope testing are listed in Table 52-4.

ENT EVALUATION With the exception of patients with acute life-threatening diagnoses (e.g., stroke, aortic dissection), the core of the inpatient evaluation is focused on identification of underlying heart disease and detection of dysrhythmias. The indications and utility of postsyncope testing are listed in Table 52-4. Most patients, even those at higher risk, can be TABLE 52-4 Post-ED Testing for Syncope/Syncope Mimics Test Indication Utility Cardiac syncope ECG monitoring Admission Outpatient ambulatory monitoring if no significant cardiac disease suspected Cardiac syncope confirmed if recurrent symptoms occur during monitored dysrhythmia; excluded if recurrent symptoms reported during sinus rhythm Implantable loop recorder Recurrent syncope after admission evaluation Long-term use with diagnostic yield of >50% in patients with recurrent syncope Echocardiography History, examination, or ECG suggestive of structural heart disease Confirms and quantifies suspected structural heart disease Electrophysiology testing Documented dysrhythmia, preexcitation, or serious underlying heart disease Identifies inducible tachydysrhythmias and some bradydysrhythmias Stress testing Exercise-related syncope Identifies exercise-induced dysrhythmias and postexercise syncope Neurologic syncope CT/magnetic resonance angiography/carotid Doppler Neurologic signs or symptoms Identifies cerebrovascular abnormality or subclavian stenosis Electroencephalography Suspected seizure Documents underlying seizure disorder Reflex-mediated syncope Tilt-table testing Recurrent syncope, cardiac etiology excluded Positive test establishes diagnosis of neurocardiogenic syncope Psychogenic Psychiatric testing Young patient, no underlying heart disease Identifies underlying psychiatric disorder predisposing to syncope TABLE 52-3 Selected Syncope Scores Identifying Risks for Adverse Outcomes After Syncope Risk Rule Martin et al,58 Pittsburgh San Francisco Syncope Rule 2,59 OESIL Score for Syncope 61 Sarasin et al,62 Geneva STePS63 Canadian Syncope Risk Score Publication Year 1997 2004 2003 2003 2008 2016 Adverse outcomes assessed Arrhythmia or death at 1 y Adverse events at 7 and 30 d Death at 1 y Subsequent arrhythmia Death or need for major procedure at 10 d and 1 y Death or serious neurologic or cardiac adverse event at 30 d Risk factors for adverse outcomes after syncope ECG Abnormal ECG* Abnormal ECG* or monitoring Abnormal ECG* Abnormal ECG* Abnormal ECG* Abnormal ECG* Cardiac disease History of CHF History of CHF History of cardiac disease History of CHF History of cardiac disease History of cardiac disease Age criteria Age >45 y † Age >65 y Age >65 y † † Prodrome/vasovagal † † No prodrome † No prodrome Lack of vasovagal etiology Additional factors History of arrhythmia Dyspnea SBP <90 mm Hg Hematocrit <30% (<0.30) † † Concomitant trauma + Troponin SBP <90 mm Hg or >180 mm Hg Abbreviations: CHF = congestive heart failure; OESIL = Osservatorio Epidemiologico sulla Sincope nel Lazio; SBP = systolic blood pressure; STePS = Short-Term Prognosis of Syncope. *The definition of an abnormal ECG varies between studies, from any ECG findings other than completely normal, to more specific rhythm abnormalities, conduction disorders, ventricular hypertrophy, axis deviation, or ST-segment or T-wave abnormalities/changes. †Variable not included in risk score. Tintinalli_Sec07_p0329-0424.indd 366 8/2/19 6:42 PM