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EMERGENCY MEDICINE PRACTICE . EMPRACTICE NET A N E V I D E N C E - B A S E D A P P ROAC H T O E M E RG E N C Y M E D I C I N E

January 2004

Syncope: An ED Approach To Risk Stratification

Volume 6, Number 1 Authors

It’s Sunday morning. You’ve just discharged the last Saturday night warrior from the ED when you get a call that the local EMS crew is bringing in a woman who has had a syncopal episode at church. When the crew arrives, you get a typical story from the paramedic. “She’s a 44-year-old woman who was sitting during a 20-minute sermon. When the congregation stood, she stood and then fell to the ground. She awoke seconds after falling, no serious injuries noted. She takes a heart pill of some kind, and a water pill. She says she has high blood pressure. Heart rate on our monitor was 60 and normal sinus. BP in the left arm was 110/64. Sats 99% on two liters. No other complaints. Her husband is on the way.” You introduce yourself to the patient, who tells you that her heart doctor recently increased the dose of her heart pill. The patient thinks this might be the problem. She denies any serious symptoms now or before the event. You’re thinking, “Too much betablocker—case solved.” Just then, the patient’s anxious husband arrives. He corroborates the EMS story. Then he adds, “I sure hope this isn’t that bleed on her brain like the last time she passed out in church. Her heart doctor also said we should watch out for the main blood vessel in her chest. It was big on the last scan they took.” So much for the slam-dunk case.

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YNCOPE is a common and challenging symptom that brings patients to the ED. It is estimated that 12%-40% of adults younger than 40 years will experience at least one episode of syncope, with up to 20% experiencing syncope before the end of adolescence.1-3 Patients older than 75 years have a reported 6% annual incidence of syncope.2 Syncope accounts for 3% of all ED visits and up to 6% of all hospital admissions.1,4-6 The overall cost per hospital admission was estimated to be about $5300 in 1996.2 According to data from the year 2000 collected by the Healthcare Cost and Utilization Project, syncope ranked 58 in a list of the top 100 diagnoses for U.S. hospital stays. Syncope accounted for 229,867 hospital discharges and an aggregate charge of $2,122,072,519.7 Syncope has many causes, which range from benign, self-limited problems to immediately life-threatening events. The etiology of syncope can be difficult to diagnose. Syncope is a transient event, and not a specific disease entity; furthermore, the patient often is completely asymptomatic at the time of the Guest Editor Keith A. Marill, MD, Emergency Medicine Attending, Massachusetts General Hospital; Faculty, Harvard Medical School, Boston, MA.

Associate Editor Andy Jagoda, MD, FACEP, ViceChair of Academic Affairs, Department of Emergency Medicine; Residency Program Director; Director, International Studies Program, Mount Sinai School of Medicine, New York, NY.

Editorial Board Judith C. Brillman, MD, Associate Professor, Department of Emergency Medicine, The University of New Mexico Health

Sciences Center School of Medicine, Albuquerque, NM. W. Richard Bukata, MD, Clinical Professor, Emergency Medicine, Los Angeles County/USC Medical Center, Los Angeles, CA; Medical Director, Emergency Department, San Gabriel Valley Medical Center, San Gabriel, CA. Francis M. Fesmire, MD, FACEP, Director, Heart-Stroke Center, Erlanger Medical Center; Assistant Professor of Medicine, UT College of Medicine, Chattanooga, TN. Valerio Gai, MD, Professor and Chair, Department of Emergency Medicine, University of Turin, Italy. Michael J. Gerardi, MD, FAAP, FACEP, Clinical Assistant Professor, Medicine, University of Medicine and Dentistry of New Jersey; Director, Pediatric Emergency

Medicine, Children’s Medical Center, Atlantic Health System; Department of Emergency Medicine, Morristown Memorial Hospital. Michael A. Gibbs, MD, FACEP, Chief, Department of Emergency Medicine, Maine Medical Center, Portland, ME. Gregory L. Henry, MD, FACEP, CEO, Medical Practice Risk Assessment, Inc., Ann Arbor, MI; Clinical Professor, Department of Emergency Medicine, University of Michigan Medical School, Ann Arbor, MI; Past President, ACEP. Jerome R. Hoffman, MA, MD, FACEP, Professor of Medicine/Emergency Medicine, UCLA School of Medicine; Attending Physician, UCLA Emergency Medicine Center; Co-Director, The Doctoring Program, UCLA School of Medicine,

Donald J. Kosiak, Jr., MD Emergency Medicine Chief Resident, Department of Emergency Medicine, Mayo Clinic and Mayo Graduate School of Medicine, Rochester, MN. Wyatt W. Decker, MD, FACEP Chair, Department of Emergency Medicine, Mayo Clinic and Mayo Medical School, Rochester, MN. Peer Reviewers David C. Pigott, MD, FACEP Assistant Professor of Emergency Medicine, Department of Emergency Medicine, The University of Alabama at Birmingham, Birmingham, AL. Sid M. Shah, MD Assistant Clinical Professor, Michigan State University, Sparrow/MSU Emergency Medicine Residency Program, Lansing, MI. CME Objectives Upon completing this article, you should be able to: 1. describe cardiac, central nervous system, vasovagal, and metabolic/drug-related causes of syncope; 2. describe ways that the history and physical examination can be used to identify potentially lethal causes of syncope; 3. discuss factors that indicate the need for diagnostic tests such as the ECG; and 4. describe an evidence-based process for the ED encounter that can risk stratify patients to determine who should be admitted vs. who can safely be discharged.

Date of original release: January 1, 2004. Date of most recent review: December 5, 2003. See “Physician CME Information” on back page. Los Angeles, CA. Francis P. Kohrs, MD, MSPH, Lifelong Medical Care, Berkeley, CA. Michael S. Radeos, MD, MPH, Attending Physician, Department of Emergency Medicine, Lincoln Medical and Mental Health Center, Bronx, NY; Assistant Professor in Emergency Medicine, Weill College of Medicine, Cornell University, New York, NY. Steven G. Rothrock, MD, FACEP, FAAP, Associate Professor of Emergency Medicine, University of Florida; Orlando Regional Medical Center; Medical Director of Orange County Emergency Medical Service, Orlando, FL. Alfred Sacchetti, MD, FACEP, Research Director, Our Lady of Lourdes Medical Center, Camden, NJ; Assistant Clinical Professor

of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA. Corey M. Slovis, MD, FACP, FACEP, Professor of Emergency Medicine and Chairman, Department of Emergency Medicine, Vanderbilt University Medical Center; Medical Director, Metro Nashville EMS, Nashville, TN. Mark Smith, MD, Chairman, Department of Emergency Medicine, Washington Hospital Center and Georgetown University School of Medicine, Washington, DC. Charles Stewart, MD, FACEP, Colorado Springs, CO. Thomas E. Terndrup, MD, Professor and Chair, Department of Emergency Medicine, University of Alabama at Birmingham, Birmingham, AL.

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prolonged confusion. When defined broadly, syncope may be due to any condition that temporarily decreases the availability of critical nutrients such as oxygen or glucose to the brain, or that disrupts or poisons brain function. The brain requires an adequate supply of glucose and oxygen to work properly. When the minimum threshold is not met, syncope will occur within 10 seconds.9 Syncope can also be defined more narrowly as being due to any condition that causes a sudden decrease in, or brief cessation of, cerebral blood flow to the brainstem and, specifically, the reticular activating system. Thus, any condition that decreases cerebral blood flow below a critical level would be a potential etiologic agent. It has been suggested that the cause of syncope can be broken into five broad categories: 1) cardiac; 2) central nervous system; 3) vasovagal/psychogenic; 4) metabolic and drug-related; and 5) unknown.1,2,16,18-20 Because of the mortality associated with cardiac-related syncope, many elect to view the fundamental branch on the decisionmaking pathway as that separating the cardiogenic causes of syncope from the non-cardiogenic causes.5,16,20 Cardiogenic causes can be further separated into primarily obstructive or dysrhythmia-related. Table 1 summarizes the causes of syncope.

evaluation. Also, the cause can be multifactorial, which makes a final diagnosis complicated. In as many as 50% of ED patients, no readily apparent diagnosis is available on ED discharge.1,4-6,8 The principal task of the ED practitioner is to identify those patients at risk for an adverse outcome. However, even with extensive and costly testing such as echocardiograms and electrophysiology studies, it is often difficult to be sure that the exact cause of syncope has been determined, or that potentially lethal causes have been ruled out. This issue of Emergency Medicine Practice is designed to help clinicians maximize the ED work-up of syncope as well as differentiate those patients who are at high risk for an adverse outcome from those who can safely be discharged home.

Critical Appraisal Of The Literature Syncope has been studied throughout the history of medicine.9,10 However, the literature that discusses syncope mainly consists of small, retrospective evaluations, cohort studies, and many case reports. Clinical guidelines regarding the evaluation and diagnosis of syncope have been published by organizations such as the American College of Emergency Physicians (ACEP), the American College of Physicians (ACP), and the European Society of Cardiology.11-14 A few prospective trials have been done, but most are small in scale. More recently, a larger emphasis has been placed in this area, and several large, quality studies have been completed or are currently under investigation.15-17

Cardiogenic Syncope There are many cardiac-related causes of syncope, but they can all generally be placed into one of two categories. The cause of syncope can be due to a primary dysrhythmia or related to obstruction of blood flow. The obstruction-to-flow category can be further subdivided into obstructive and vascular causes. (Review Table 1 for a list of common causes under each category.) Inadequate cardiac output is the underlying premise in all of these patients with cardiogenic syncope.

Pathophysiology Syncope is defined as a sudden and transient loss of consciousness associated with a loss of postural tone, with a spontaneous and full recovery. There is also an absence of

Table 1. Etiology Of Syncope. Cardiac Causes Obstruction to flow • Subaortic stenosis • Aortic valve stenosis • Mitral valve stenosis • Atrial myxoma (rare) • Pulmonic valve stenosis • Hypertrophic cardiomyopathy • Dilated cardiomyopathy • Restrictive cardiomyopathy • Pericardial tamponade • Severe congestive heart failure Vascular disease • Pulmonary emboli • Pulmonary hypertension • Acute myocardial infarction • Air embolism • Aortic dissection/leaking

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Noncardiac Causes

aortic aneurysm • Subclavian steal syndrome

• Subarachnoid hemorrhage • Subdural/epidural hemorrhage

Vasodepressor (vasovagal, neurocardiogenic) • Situational • Micturition • Post-tussive • Swallow • Defecation • Valsalva (weightlifters) • Carotid sinus sensitivity

Dysrhythmias Tachydysrhythmias • Supraventricular tachycardia • Ventricular tachycardia • Ventricular fibrillation • Atrial fibrillation with fast conduction • Wolff-Parkinson-White syndrome • Prolonged QT syndrome • Brugada syndrome

Orthostatic • Anemia/GI bleed • Dehydration Central nervous system / neurologic • Seizure (excluded by most syncope studies) • Neuralgias (trigeminal, glossopharyngeal) • Neurologic (TIA, strokes, migraines [rare])

Bradydysrhythmias • Atrioventricular block • Atrial fibrillation with slow conduction • Sick sinus syndrome • Pacemaker malfunction

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Metabolic / toxic • Hypoglycemia • Hypoxia • Drug-induced • Carbon monoxide poisoning • Chemical / toxic gas exposure • Carotid sinus sensitivity • Infectious agent Psychogenic • Somatization disorder • Anxiety disorder • Conversion disorder • Panic disorder • Hyperventilation • Breath-holding spells

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Congenital long QT syndrome refers to a collection of heritable defects of the myocardial Na+ and K+ channel proteins that cause prolongation of the QT interval on the resting ECG and predispose the patient to a specific malignant ventricular dysrhythmia—torsades de pointes. The condition may be either autosomal recessive (Jervell and Lang-Nielson syndromes) or autosomal dominant (Romano-Ward syndrome).28 Torsades de pointes is defined as polymorphic ventricular tachycardia that occurs in the setting of a prolonged QT interval. The ECG is of critical importance in the evaluation of these patients. The QT interval is measured from the onset of the Q wave to the end of the T wave. The QT interval normally varies with heart rate, so several formulas, such as Bazzet’s, are available to derive the heart rate-corrected (QTc) interval. The QTc is considered abnormally long when it is greater than 0.45 in men, 0.46 in children, and 0.47 in women in units of seconds.29 The ECG may also demonstrate a notched or bifid T wave in leads V2 to V4. Syncope in patients with long QT syndrome is usually due to self-limited episodes of torsades de pointes. Torsades de pointes may also be persistent and deteriorate into ventricular fibrillation and resultant sudden cardiac death. The risk of sudden death increases in proportion to the duration of the QTc.29,30 A prolonged QT interval and the associated risk of torsades de pointes can also be acquired. Medicines that prolong the QT interval by blocking the K+ repolarization channels or via other mechanisms, or exacerbate the problem by altering drug metabolism, are potential causes. Drugs associated with acquired long QT syndrome include type IA antidysrhythmics such as procainamide and quinidine as well as type III antidysrhythmics such as sotalol, phenothiazines, haloperidol, tricyclic antidepressants, erythromycin, pentamidine, and the nonsedating antihistamines astemizole (Hismanal) and terfenadine (Seldane). Drugs implicated in prolonging the hepatic metabolism of these agents include erythromycin, ketoconazole, cimetidine, and cisapride. Other etiologies of an acquired prolonged QT interval include electrolyte disturbances such as hypokalemia and hypomagnesemia, a low protein diet, severe bradycardia, and an acute cerebrovascular accident.31,32 Brugada syndrome is another autosomal dominant cardiac dysrhythmia disease.33,34 Brugada syndrome is recognized throughout the world, and it has been estimated that this syndrome may be responsible for 4%-12% of all cases of unexplained sudden cardiac death.35 It is characterized by syncopal episodes in patients with structurally normal hearts who demonstrate characteristic ECG patterns that define the syndrome. The disease is caused by a defect in the Na+ myocardial membrane channel protein, which leads to abnormalities of depolarization. The ECG manifestations include a pseudo-right bundle branch block and persistent downsloping ST segment elevation in leads V1 to V3.33-37 The presence of these ECG findings is not always constant and can confuse the diagnosis. As with prolonged QT syndrome, patients with Brugada syndrome are predisposed to ventricular dysrhythmias that can deteriorate into ventricular fibrillation and sudden cardiac death.

Dysrhythmias are responsible for many episodes of syncope. In fact, cardiac dysrhythmias are the most common cause of syncope in patients with underlying heart disease, including coronary artery disease, congestive heart failure, and structural heart disease.19,21,22 Dysrhythmias can be due to the heart beating too fast, too slow, or in an abnormal manner.

Tachycardic Dysrhythmias Tachycardic dysrhythmias cause decreased cardiac output by not allowing sufficient time for the heart to properly and completely fill during diastole. Examples include ventricular tachycardia and supraventricular tachycardias such as atrioventricular reentrant and atrioventricular nodal reentrant tachycardia as well as atrial fibrillation or atrial flutter. The atrial tachydysrhythmias may occur in the setting of Wolff-Parkinson-White syndrome, where there is an unconcealed bypass tract between the atrial and ventricular myocardial tissue. Ventricular fibrillation can also be considered a tachydysrhythmia, but in this case loss of cardiac output may be primarily due to unsynchronized and ineffective myocardial contraction. Patients with tachydysrhythmias have a spectrum of presentations from completely asymptomatic to full cardiac arrest.23

Bradycardic Dysrhythmias Bradycardic dysrhythmias can also cause syncope. Bradycardia may have an intrinsic cardiologic etiology, such as dysfunction of the specialized cardiac conduction system at the level of the sinoatrial or atrioventricular nodes, or within the His-Purkinje bundle branch fibers. It may also be due to extrinsic factors, such as excessive cholinergic stimulation or negative chronotropic poisoning, such as from excessive beta- or calcium-channel-blocking agents. Sick sinus syndrome is commonly seen in our aging population.24,25 This is a dysrhythmia that presents with periods of normal cardiac rhythm, mixed with sinus bradycardia, asystolic pauses, and/or sinoatrial block. It can be a sign of other underlying heart disease. A pacemaker is generally warranted for treatment of this condition.25 Other bradycardic rhythms that can cause syncope are the heart blocks. Specifically, second-degree type II heart block and third degree or complete heart block are common causes of syncope. If the ventricular escape rhythm is unable to maintain cerebral perfusion, a syncopal event known as a Stokes-Adams attack will occur.19,26 Pacemaker malfunction may cause syncope. Possible etiologies include device malfunction or battery exhaustion, failure to sense, failure to capture, or disruption of communication such as damage to the leads.27 Careful interrogation of pacemaker function should be performed by the cardiologist for all patients who present with syncope who have a pacemaker.

The Rare But Deadly Dysrhythmias Two dysrhythmia syndromes deserve special attention. They are long QT syndrome and Brugada syndrome. They occur infrequently in the general population, but to miss a case could be deadly to the patient.

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Dysrhythmic Causes Of Cardiac Syncope

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Obstructive Causes Of Cardiac Syncope

Generalized seizures include atonic seizures, where there is a sudden transient loss of postural tone, and absence seizures, where there is a brief loss of consciousness without loss of postural tone. Cerebrovascular accidents and transient ischemic attacks are common neurologic events that are sometimes confused with syncope.39 (See also the October 2003 issue of Emergency Medicine Practice, “Transient Ischemic Attacks: Transient Trouble Or Action-Warranted Attacks?”) Mechanistically, it would seem that only a cerebrovascular event involving the vertebrobasilar system or both cerebral hemispheres should lead to depressed consciousness and syncope. Since occlusion of both carotid arteries simultaneously would be unlikely, compromise of both cerebral hemispheres would likely only occur due to a large hemorrhagic stroke and mass effect. Associated specific neurologic symptoms and signs often distinguish stroke syndromes from syncope. Disease involving both hemispheres would be expected to demonstrate widespread deficits, and patients with vertebrobasilar disease often demonstrate diplopia, ataxia, vertigo, and dysarthria.9

Like the other cardiac causes of syncope, this is also a large group. (Table 1 lists the causes of syncope due to obstruction.) These diseases of the heart valves, musculature, and pericardial lining can cause obstruction to forward flow of blood through the heart, and acute and chronic compromise in cardiac output. It is important to remember, however, that obstruction itself is sometimes not the acute cause of syncope and sudden death in affected patients. Many of these conditions are associated with primary disease of the myocardial tissue, such as with hypertrophic cardiomyopathy, or secondary myocardial abnormalities, such as left ventricular hypertrophy. The abnormal myocardial tissue or hypertrophy predisposes patients to ventricular dysrhythmias, which may often be the primary etiology of syncope and sudden death.38 Additional factors that may be causative or contribute to acute symptoms include myocardial ischemia exacerbated by hypertrophy, abnormal peripheral vascular and ventricular baroreflexes, and acute conduction block.

Non-Cardiogenic Syncope Vasodepressor Syncope

Metabolic Syncope

Vasodepressor syncope (also termed neurocardiogenic, neurogenic, or vasovagal syncope) is the most common cause of syncope. The exact mechanism of vasodepressor syncope is poorly understood. In vasodepressor syncope, there is a failure in, or possibly an interruption of, the sympathetic excitation to the heart and peripheral vascular system.9,20 This is followed by excess parasympathetic excitation, which leads to severe vasodilation and bradycardia. This is termed the Bezold-Jarisch reflex. These autonomic alterations and the ensuing transient hypotension may cause the patient to experience dizziness, weakness, pallor, sweating, lightheadedness, and, ultimately, possible syncope.9 These episodes are often associated with an increase in emotional lability, such as in a patient under stress, in a crowded environment, or during prolonged standing. Situational syncope is related to vasodepressor syncope, except it is usually associated with a specific activity such as coughing, micturition, or defecation. The mechanism of situational syncope is thought to be similar to that of vasodepressor syncope, and it’s generally considered a variant. Orthostatic hypotension is also related to vasodepressor syncope. This condition has a variety of etiologies, including volume depletion, medications, advanced age, and certain illnesses. (Orthostatic hypotension will be discussed in more detail later in this review.)

The critical substrates for brain metabolism include glucose and oxygen. Compromised delivery or utilization of either of these substances can lead to syncope or prolonged loss of consciousness. Many of the mechanisms described thus far address compromised blood flow to the brain. There may also be an inadequate blood concentration of these substrates. Hypoglycemia is a common cause of altered consciousness and syncope-like events in diabetic patients.40 The most common etiology is an imbalance between insulin or oral hypoglycemic administration and food intake. Other uncommon causes such as insulinomas have also been described in these patients.41 Hypoxemia can occur due to inadequate or ineffective ventilation, and loss or malfunction of red blood cell hemoglobin. Finally, the brain may be provided with an adequate supply of oxygen, but the cells may be unable to utilize it. There are a variety of drugs and poisons that can acutely affect each step of the oxygen delivery process. Hemorrhage and red cell lysis can contribute to syncope, but loss of blood volume and flow is often more important than loss of oxygen-carrying capacity with hemorrhage. Finally, other metabolic derangements can impair systems critical for brain function. Perhaps most importantly, hypo- or hyperkalemia can lead to cardiac dysfunction, dysrhythmias, and syncope.

Neurologic Syncope

Drugs and poisons can cause or exacerbate all of the mechanisms responsible for syncope. Syncope may occur due to toxic effects of appropriate therapeutic dosing or intentional or inadvertent overdosage. Accidental exposure at home or work is possible. Intentional environmental exposure to a wide variety of toxic and lethal agents must also be considered today. Terrorists have successfully disseminated sarin vapor, a cholinergic agent, in the Tokyo subway, and the Russian military has demonstrated the

Drug-Related Syncope And Poisoning

Neurologic conditions rarely cause, but often mimic, syncope. The most common neurologic condition that is confused with syncope is seizure. By definition, complex seizures are associated with an impairment in consciousness. These seizures may be partial and localized to one area of the brain, or generalized throughout both hemispheres. There may or may not be obvious associated automated or tonic-clonic activities suggesting epileptoform activity.

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Differential Diagnosis Clearly, the differential diagnosis of syncope is wide. As always, the emergency clinician should consider the most lethal diagnoses first. Cardiovascular disease is associated with the highest long-term mortality, and patients are often at high risk for recurrent unstable events in the ED as well.

Cardiogenic Syncope Beyond the usual benefits of a firm diagnosis, there are two important reasons to correctly identify cardiogenic syncope. First, syncope from cardiogenic causes has a one-year mortality rate ranging between 18% and 33%, compared to 0%-12% for non-cardiogenic causes and 6% for unexplained causes.1,4,5,14,44,45 Second, the treatment of many of the conditions responsible for cardiogenic syncope has advanced dramatically in the past decade. Many of the conditions can be successfully treated with medications and potentially cured with invasive procedures. One study conducted by Martin et al developed and validated a clinical prediction rule for risk stratification of patients with syncope. The authors first derived the prediction rule by reviewing the charts of 252 patients presenting to the ED with syncope. The study was validated using 374 patients. The study found four factors that were useful for risk stratification: 1) age greater than 45 years; 2) history of ventricular dysrhythmias; 3) history of congestive heart failure; and 4) an abnormal ECG. In the validation cohort, one-year mortality ranged from 1.1% with no risk factors to 27.3% with three or more risk factors.46 Another study done by Alboni et al found that the presence of suspected or certain heart disease on examination was an independent predictor of a cardiac cause of syncope, with a sensitivity of 95% and a specificity of 45%. The same study found that the absence of heart disease on history and physical examination ruled out a cardiac cause of syncope in 97% of subjects.47 Cardiac syncope can occur without exertion or while in a sitting or supine position. In fact, a complaint of syncope while sitting is highly suggestive of a cardiac origin.

Obstructive Causes Of Cardiac Syncope Table 1 lists some of the causes of syncope due to obstructive cardiologic disease. Valvular disease, particularly of the left side of the heart, is associated with syncope. In fact, syncope, along with angina and congestive heart failure, is one of the three most common presenting complaints of patients with aortic stenosis.50 This disease, along with conditions such as hypertrophic cardiomyopathy and other causes of structural heart disease, is usually associated with exertional syncope. Hypertrophic cardiomyopathy is a complex cardiac disease with a large spectrum of clinical variance.51 Its diagnosis is generally based on a combination of physical examination findings and diagnostic testing such as echocardiography. Classic physical findings include a loud S-4 heart sound and a harsh and crescendo-decrescendo systolic murmur. The murmur is best heard between the apex and the left sternal border.52 During strain, such as a Valsalva maneuver, the murmur will increase in volume secondary to an increase in gradient. Squatting or an isometric handgrip can decrease the murmur’s intensity. Murmurs on examination are usually characteristic for each specific valvular disorder. For example, aortic stenosis has a characteristic diamond-shaped, midsystolic murmur most often radiating to the neck. It can also be associated with an S-4 heart sound.52 (Further discussion about evaluation of murmurs can be found under the cardiac examination section of this review.) One special group of valvular patients is the group that has undergone artificial valve replacement. The combination of mechanical heart valves and syncope is an ominous sign that could suggest a number of complications, includ-

Dysrhythmic Causes Of Cardiac Syncope Sustained ventricular tachycardia is most commonly due to a reentrant electrical wavefront involving a scar from a prior myocardial infarction. The diagnosis must be entertained in any patient with a history of prior myocardial infarction. The patient may feel palpitations, chest discomfort, or lightheadedness prior to syncope. Ventricular tachycardia may also occur in patients with dilated or hypertrophic cardiomyopathies, valvular diseases, and other uncommon conditions such as right ventricular dysplasia. Supraventricular tachycardias and atrial fibrillation and atrial flutter are more common than ventricular tachycardia, but are less commonly associated with syncope. Syncope, however, is more likely to occur if the rate is very rapid or if there is an abnormal vasomotor response.48 Patients with Wolff-Parkinson-White syndrome have a bypass tract

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between the atria and ventricles, allowing rapid conduction with a relatively short refractory period. These patients are at particular risk for atrial fibrillation and atrial flutter with rapid, aberrant conduction to the ventricles via the bypass tract as well as cardiovascular instability. Symptomatic sinus bradycardia should be suspected particularly in elderly patients with evidence of a slow or varying sinus heart rate in the ED. The emergency physician should check for current use of oral or ophthalmologic beta-blocking agents, calcium-channel blockers, and other agents or conditions that may increase vagal tone. Evidence of second degree type II or type III heart block or a paced rhythm on the ECG should raise the suspicion for a symptomatic bradycardic dysrhythmia. In one prospective cohort, patients with atrioventricular block had minimal prodromal symptoms (mean duration of warning, < 2 seconds) and a shorter duration of residual/ recovery symptoms as compared to patients with ventricular tachycardia.49 Evidence of a long QT interval and/or abnormal notched T wave on the ECG suggests possible congenital or acquired long QT syndrome. A family history of sudden death or the use of medicines associated with this syndrome should raise suspicion further. Brugada syndrome appears to be most common in males from Southeast Asia and is suggested by characteristic ECG findings.

effectiveness of an aerosolized fentanyl derivative to transiently incapacitate and inadvertently kill both terrorists and hostages in a Moscow auditorium.42,43

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syncope. Medical conditions may cause occult gastrointestinal or vaginal bleeding, or internal hemorrhage from a vascular catastrophe such as a ruptured abdominal aortic aneurysm. The vasodepressor syncopal syndromes are common but generally suggest low morbidity and mortality. The key may be to keep a healthy suspicion for other, more serious conditions while making this diagnosis in patients with a suggestive history who appear well. Features of the history that suggested vasodepressor as opposed to dysrhythmic syncope in one study included palpitations, blurred vision, nausea, warmth, diaphoresis, or lightheadedness prior to syncope, and the presence of nausea, warmth, diaphoresis, or fatigue following syncope. Vasodepressor syncope was associated with more than five seconds of warning symptoms and more prolonged recovery symptoms.49 The emergency physician should also be wary for significant trauma that may have occurred during the syncopal event. Carotid sinus sensitivity can also cause syncope. A bradycardic response can be elicited when the carotid sinus is stimulated. This is more common in the elderly population. This can be seen in patients who are wearing neck ties or who have tight collars, or even during simple activities such as shaving. Carotid sinus massage is a useful test in patients with suspected carotid sinus sensitivity.61 A positive test is defined as one that causes at least a three-second pause during massage of the carotid sinus. This test can be difficult to master and should be reserved for those who have been trained in its proper use. It should be avoided in patients with known or suspected carotid artery disease.

ing valvular thrombosis, structural failure, paravalvular regurgitation, or ventricular dysrhythmia. Careful evaluation must be undertaken, and hospital admission of these patients is recommended.53,54 There are other, less obvious types of obstructive cardiologic conditions. Cardiac tamponade can present as syncope. This can be difficult to diagnose in the ED. The classic findings of Beck’s triad (distant/muffled heart sounds, pulsus paradoxus, and hypotension) are only present in about one-third of the patients who present with cardiac tamponade. If signs and symptoms are suggestive, a bedside echocardiogram may rapidly clarify the diagnosis. The treatment remains needle decompression of the pericardial fluid, either in the cardiac catheterization lab or the ED, if emergent. Congestive heart failure is another cause of obstruction to flow. Although newer modalities such as the use of B-type natriuretic peptide have been investigated to aid in the diagnosis of congestive heart failure, it remains largely a clinical diagnosis.

Vascular Causes Of Cardiac Syncope Other types of heart disease that can present as syncope include those that primarily affect the vascular system. They include aortic dissection, a large pulmonary embolus, pulmonary hypertension, and myocardial infarction.55-60 Enough case reports exist regarding the vascular causes of syncope to make even the most seasoned emergency practitioner sweat. For instance, syncope has been observed in 13% of patients with pulmonary embolism, and up to 20% of patients with a massive pulmonary embolism will complain of syncope.55-58 Each of these conditions is associated with its own classic signs and symptoms and will not be reviewed in detail in this article.

Neurologic Syncope One of the most difficult mimickers of syncope is seizure, as it can be difficult to be sure whether a “spell” was syncope or a seizure. (See also the October 2000 issue of Emergency Medicine Practice, ”Seizures: Accurate Diagnosis And

Vascular Syncope External or internal hemorrhage due to medical conditions or trauma may serve as an obvious or occult cause of

Cost- And Time-Effective Strategies For Patients With Syncope be 100% sensitive and 46% specific for cardiac problems. Following this rule led to an 18% reduction in the admission rate.15 It appears that using a simple, systematic approach to the evaluation of patients who present with syncope can be very beneficial.

1. Limit testing. Let the history and physical examination dictate the need for diagnostic tests. Obtaining routine tests like CBCs, electrolyte studies, CT scans, and echocardiograms has not been proven beneficial in the literature. While no formal cost-benefit analyses of limited evaluation of syncope in the ED exist, it stands to reason that routine tests that do not impact management will add unnecessary costs.

3. Use observation units. It’s not surprising that most patients admitted to the hospital for further evaluation for a potential cardiac cause of their syncope turn out not to have a cardiac cause. Even if no further diagnostic studies are performed during the hospital stay, this still adds considerable cost to the patient and the healthcare system. In the subset of patients who are at higher risk for morbidity or mortality from their syncopal episode— but who do not clearly need to be admitted to the hospital—it is possible that an observation unit stay can risk stratify patients with greater accuracy than a much shorter ED visit. Several prospective studies using observation protocols are under way. One article detailed a possible algorithm for the use of an observation unit in the ED setting.108 ▲

2. Limit admissions. Syncope leads over 225,000 hospital admissions per year in the United States. Elesber et al studied the application of the ACEP level A and B recommendations for admission in 201 patients presenting with syncope.16 These recommendations proved to be 100% sensitive for finding cardiac-related causes of syncope. They also cut down the admission rate by 29%.16 Quinn et al derived a rule for admitting patients that included: 1) age greater than 75; 2) an abnormal ECG; 3) shortness of breath on presentation; 4) a respiratory rate greater than 24; or 5) a history of congestive heart failure.15 They found this rule to

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from peripheral vertigo generally do not have a feeling of faintness or alteration in their level of consciousness. Central vertigo may be due to a tumor such as an acoustic neuroma, multiple sclerosis, or neurovascular disease such as vertebrobasilar insufficiency. Patients with the latter condition may experience syncope as well as vertigo. Features that distinguish vertigo syndromes from syncope include associated auditory complaints, evidence of nystagmus on ocular examination, or inducible nystagmus with the Hall-Pike maneuver.66,67 The Hall-Pike maneuver may only reproduce vertigo and nystagmus from cupulolithiasis, but not other peripheral causes of vertigo such as neuronitis. A subarachnoid, subdural, or epidural bleed can also present as a syncopal episode, and obtaining a careful history is key. A history of a severe headache with acute “thunderclap” onset may help point to a subarachnoid bleed, while a recent or distant history of head trauma may help to diagnose a subdural or epidural hematoma as the cause of syncope. Drop attacks are also sometimes included as a neurologic cause of syncope. However, they are most often not associated with a loss of consciousness. They are generally believed to be caused by a transient ischemic attack involving the posterior circulation to the brain. (See also the October 2003 issue of Emergency Medicine Practice, “Transient Ischemic Attacks: Transient Trouble Or Action-Warranted Attacks?”) Therefore, most authors consider drop attacks a mimic of syncope. Another neurologic cause sometimes considered in the differential diagnosis is narcolepsy. Migraine headaches can cause bizarre symptoms, including transient neurologic deficits and syncope. Keep this option in the differential diagnosis, especially in patients with a history of atypical migraines.

Table 2. Diagnostic Questions To Determine Whether Loss Of Consciousness Is Due To Seizure Or Syncope. Question

Points (if yes)

At times do you wake with a cut tongue after your spells? At times do you have a sense of déjà vu or jamais vu before your spells? At times is emotional stress associated with losing consciousness? Has anyone ever noted your head turning during a spell? Has anyone ever noted that you are unresponsive, have unusual posturing or jerking limbs during your spells, or have no memory of your spells afterwards? (score as yes for any positive response) Has anyone ever noted that you are confused after a spell? Have you ever had lightheaded spells? At times do you sweat before your spells? Is prolonged sitting or standing associated with your spells?

2

Metabolic Syncope Hypoglycemia should be considered in any known diabetic patient presenting with a syncope-like syndrome. Many case reports exist in the literature associating syncope and hypoglycemia.40,41 However, it is difficult to imagine that hypoglycemia can correct itself without intervention in order to fit with the standard definition of syncope that includes spontaneous and full resolution. Hypoxia can also lead to syncope. Any condition that leads to a decrease in oxygenation or ventilation can lead to hypoxia, and ultimately a syncopal episode. This includes a wide variety of pulmonary and other acute and chronic disease processes. Keep this diagnosis in mind, particularly in young children who may play a high-risk game of inducing syncope by breath-holding, choking each other, or placing bags over their head until syncope occurs.68

1 1 1 1

1 -2 -2 -2

Syncope Due To Toxins And Poisons There are a variety of agents, including narcotics, benzodiazepines, and barbiturates, that can cause both central nervous system and respiratory depression. Exposure to variants with a rapid onset and short half-life may simulate syncope. Decreased oxygen delivery to the central nervous system can also be caused by alterations in hemoglobin function. Carbon monoxide poisoning and methemoglobin-

The patient has seizures if the point score is ≥ 1, and syncope if the point score is