Emp Syncope

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
Its Sunday morning. Youve 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. Shes 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. Youre thinking, Too much betablockercase solved. Just then, the patients anxious husband arrives. He corroborates
the EMS story. Then he adds, I sure hope this isnt 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.
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, Childrens Medical

Center, Atlantic Health System;
Medicine, Morristown
Memorial Hospital.
Michael A. Gibbs, MD, FACEP, Chief,
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
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
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,
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.
COPYRIGHTED MATERIALDO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC
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
Emergency Medicine Practice
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
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
www.empractice.net January 2004
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 dysrhythmiatorsades 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 Bazzets, 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.
January 2004 www.empractice.net
Dysrhythmic Causes Of Cardiac Syncope
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 its 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.
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 murmurs 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
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
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 Becks 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.

Its 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 hospitalit
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
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 dj 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?
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 <1.
Source: Sheldon R, Rose S, Ritchie D, et al. Historical criteria that
distinguish syncope from seizures. J Am Coll Cardiol 2002 Jul
3;40(1):142-148.
Effective Treatment.) Another study examined just the

presence of tongue biting. That study found that tongue
biting was found only in the seizure patients, but its absence
did not exclude the possibility of a seizure.63 While a lateral
tongue laceration appeared specific in this study, it has been
observed in patients with psychogenic seizures. Finally, a
recent study of patients with syncope or seizures found a
simple set of questions (outlined in Table 2) useful in
distinguishing a syncopal episode from a seizure.64 (This
diagnostic approach has yet to be validated independently.)
In general, unconsciousness lasting more than five
minutes, a slow return to full alertness, and disorientation
or an aura prior to the event are suggestive of a seizure.8,62,64,65 Sweating and nausea prior to the episode, a brief
loss of consciousness, a quick return to baseline mental
status, and a lack of tongue biting are more indicative of a
primary syncopal event.8,62,64,65
Vertigo is a symptom that refers to an abnormal
sensation of movement or rotation of the patient or his or
her environment. (See also the March 2001 issue of Emergency Medicine Practice, The Dizzy Patient: An EvidenceBased Diagnosis And Treatment Strategy.) Vertigo can
cause diaphoresis, pallor, nausea, vomiting, and difficulty
with ambulationsimilar to syncope. This disequilibrium
can range from a simple spinning sensation to full veering,
staggering, and/or imbalance. Vertigo can be divided into
centrally or peripherally mediated causes. Peripheral
vertigo is much more common, and patients who suffer
emia can present with acute loss of consciousness. Methemoglobinemia is caused by a variety of agents, including
nitrates, local anesthetics, and sulfonamides. Pulse oximetry
is unreliable in the setting of both of these poisonings, and
the diagnosis should be made by direct measurement of a
blood sample with a multiple wave-length co-oximeter. In
the setting of smoke inhalation from a residential or
industrial fire and mental status changes, the diagnosis of
cyanide toxicity must also be entertained. In the petroleum,
rubber, and mining industries, exposure to hydrogen sulfide
can cause altered mental status and syncope. Both cyanide
and hydrogen sulfide arrest cellular respiration by interfering with mitochondrial cytochrome function. Cholinergic
and anticholinergic toxidromes may include syncope among
a variety of characteristic symptoms. Toxic exposures
should be in the differential diagnosis of syncope when
several members of the same family or from the same
location present to the ED simultaneously for evaluation.
Emergency Department Evaluation
Infection-Related Syncope
Just as the list of the potential causes of syncope is quite
Infection can be the primary cause of a syncopal episode or

a secondary cause by leading to dehydration, sepsis, and
hypotension.26 The history and physical examination will
often identify the primary site of infection and the mechanism leading to syncope.
Table 3. Important Historical Facts.
Patients presenting to the ED with syncope should be

treated as a possible emergency; avoid prolonged wait
times. Whenever possible, they should be taken immediately to an area in the ED that provides for close cardiac
monitoring, intravenous access, oxygen therapy, and
invasive procedures if they become necessary. The initial
evaluation in the ED begins as all encounters should, with
stabilization of the patient (i.e., ABCs, IV, O2, monitor).
History
The cause of syncope is revealed by a careful history and
physical examination in approximately 40%-50% of
patients.1,2,4-6,47,71 A detailed account of the syncopal episode
from any bystanders or family members can be very helpful
in the diagnosis. Table 3 is a list of important historical
features that should be asked of syncopal patients.14
Is It Really Syncope?
Questions about just prior to the event

Activity (exertional vs. rest, during or after, changing position)
Precipitating events (warm room, stress, fear, intense pain)
Other factors (crowded area, prolonged standing, postprandial)
Psychiatric Syncope
Psychiatric conditions can mimic syncope. They can range
from fully conscious actions for secondary gain purposes to
dissociative states where the patient has no conscious
control over the activity. While psychiatric conditions that
mimic syncope exist, they must remain a diagnosis of
exclusion. A study by Kapoor et al of syncope patients
found that up to 20% of the population studied met
diagnostic criteria for at least one major psychiatric disorder
or substance abuse problem. Up to one-half of these patients
with a psychiatric disorder did not have their disorder
identified by the attending physician. This study found that
patients who have suffered a syncopal event and carry a
psychiatric diagnosis were more likely to report frequent
episodes of syncope (four or more within one year), to be
younger than control groups who did not have a psychiatric
diagnosis, and to have multiple somatic complaints
associated with the event.69
Questions about the onset of the attack

Associated symptoms (headache, nausea, vomiting,
abdominal pain, sweating, visual aura, blurred vision, pain in
back, neck, or shoulder)
Timing of symptoms / attack (prolonged vs. immediate)
Questions about the attack (obtain information

from bystanders)
Fall (sudden vs. gradual, slumping vs. fall without protection)
Duration of loss of consciousness (seconds vs. minutes)
Movements (jerking, tonic and/or clonic activity, none;
duration)
Other associated findings (other injuries caused by fall)
Questions about the period following the attack

Duration of confusion / postictal state
Associated symptoms (headache, nausea, vomiting,
abdominal pain, sweating, visual aura, blurred vision, pain in
back, neck, or shoulder)
Other associated findings (other injuries caused by fall,
tongue biting, incontinence, mental status)
Prehospital Care
Prehospital care of patients with syncope and altered mental
status should include a fundamental diagnostic and
therapeutic protocol. Assessment for and/or treatment of
hypoglycemia and hypoxia should be completed. Naloxone
should be administered for depressed consciousness and
possible opiate intoxication. Occult head trauma must be
considered, and the neck should be immobilized if there is a
suspicion of trauma or the patient suffered an injury to the
head or neck from syncope. An IV catheter should be placed
if the patient is hypotensive or tachycardic. Recall that in the
setting of trauma, hypotension in the field is an independent
predictor of morbidity and mortality, even if the patient is
normotensive upon ED arrival.70
Questions about past medical history / family history

Family history of sudden death, fainting, congenital heart
problems
Significant metabolic problems (thyroid, diabetes)
Previous cardiac history
Medications (prescribed, over-the-counter, herbal,
recreational)
Previous history of fainting (time since last event, associated
symptoms, similar feelings, previous diagnosis)
Source: Brignole M, Alboni P, Benditt D, et al; Task Force on Syncope,
European Society of Cardiology. Guidelines on management (diagnosis
and treatment) of syncope. Eur Heart J 2001 Aug;22(15):1256-1306.
significantly less common in black than white high school

blood donors.72 On the other hand, syncope due to vascular
diseases may be more common in older blacks due to the
higher prevalence of uncontrolled hypertension.
The past medical, social, and family histories are all
relevant to the evaluation. A past history of cardiovascular
disease increases the likelihood of cardiac syncope and
portends a higher 12-month mortality rate.72 A history of
illicit substance use or the possibility of surreptitious
poisoning should be assessed. The emergency physician
should always inquire about a history of sudden death in
the family. Sudden death in young adults suggests the
possibility of long QT syndrome, familial cardiomyopathy,
or other genetic illnesses.
The Drug Did It!

A review of the patients medications should not be
overlooked. Medication use has been implicated as the
cause of syncope in 3%-13% of patients.73-75 A careful review
of medications the patient is taking, including over-thecounter preparations, should be performed. The patient
should be asked which medications are new and/or if any
recent changes have been made to the dosage or dosing
interval. Some common drugs that are associated with druginduced syncope include beta-blockers, calcium-channel
blockers, insulin, drugs of abuse (opiates, cocaine, etc.),
diuretics, antidysrhythmics, digoxin, nitrates, sildenafil,
ACE inhibitors, antidepressants, phenothiazines, alcohols,
and central-acting antihypertensives. Finally, check for
possible adverse drug interactions. One study of patients
with syncope who take medicines found that 51% of
patients were positive for a potential drug-drug interaction
that may have explained their syncopal event.75
The Event
Finding out exactly what happened is the goal of the initial
evaluation. Taking the time to obtain a step-by-step history
of the acute event may be the most important factor in
ultimately making an accurate diagnosis. Interview the
patient and, ideally, a witness to the event. Although the
patient can be very helpful in discussing what may have
happened just before the event, any past history of similar
episodes, and current status, he or she may not recall the
actual event. A witness (family member, friend, neighbor,
EMS provider, or other bystander) can relate such information as duration of unconsciousness, evidence of movements suggesting a seizure, events just prior to the spell,
duration of confusion following the spell, and/or other
important details. A witness may also be able to predict
other potential associated injuries.
Certain clusters of historical information can help
indicate the right direction when trying to determine the
cause of the syncopal episode. For instance, a history of a
stressful event or other obvious precipitating circumstances
may suggest a vasodepressor cause of syncope. A syncopal
episode that occurs only after standing may point to
orthostasis or hypovolemia. A complaint of cough and
dyspnea in association with syncope suggests possible
pulmonary embolism or other obstructive cardiopulmonary
disease. Any associated focal neurologic deficits suggest an
underlying neurologic event. Rapid onset and offset with no
warning before, or confusion after, the event suggests a
transient dysrhythmia or other cardiac cause.4,46,49,71 One
study found that most patients with otherwise typical
vasovagal syncope had warning symptoms for minutes
prior to the syncopal event. In fact, the study stated that in
the absence of any warning signs or symptoms, the practitioner should be leery about making the diagnosis of
vasovagal syncope.4
The Physical Examination

Vital Signs
As with any physical examination, the emergency physician
should begin with the vital signs. Abnormalities in one or
more may point to a specific cause of syncope. For instance,
tachycardia and hypotension may represent hypovolemia as
a cause of the syncopal episode. Taking the blood pressure
in both arms and looking for concordance is helpful. A
difference greater than 20 mmHg in blood pressure between
both arms suggests thoracic aortic dissection. Tachypnea
may point to pulmonary embolism or congestive heart
failure as a cause of syncope.
Orthostatic Changes In Syncope

Many debates have centered on the significance of orthostatic hypotension. Orthostatic hypotension is usually
defined as a decline of 20 mmHg or greater in systolic blood
pressure on standing.76-78 Measurements are usually taken
after lying supine for five minutes. The blood pressure is
then repeated after standing for 1-3 minutes. A study done
by Atkins et al found that most patients who have orthostatic changes would be discovered in the first few minutes
of standing.76 However, the presence of orthostatic changes
does not necessarily mean that they caused a particular
episode of syncope. In this same study, 29% of those with a
Demographics And Past History

The patients demographic information is also important.
Studies have consistently demonstrated that advancing age
and male gender are associated with cardiovascular and
neurologic causes of syncope.17,39,49 Vasovagal reactions were
Continued on page 11
long, there are many symptoms that can be confused with

syncope. The emergency physician must first determine if
the patients complaint is truly syncope. Vertigo, dizziness,
faintness, lightheadedness, seizure, hypoglycemia, presyncope, and drop attacks can all be mistaken for syncope.
It is important to determine whether there was a loss of
consciousness and postural tone. Syncope is associated with
a brief, transient loss of consciousness accompanied by a
generalized weakness and loss of muscular tone. Drop
attacks are defined as a loss of postural tone while remaining conscious. Lightheadedness usually refers to a feeling of
faintness. It can be a precursor to syncope (pre-syncope).
Dizziness, vertigo, and pre-syncopal episodes are generally
not associated with a loss of consciousness.
The distinction between these symptoms can be
important. All can be associated with syncope, but they
may have a different underlying mechanism, treatment,
and prognosis.52
NO
Patient with syncope?
YES
Consider seizure, drop attack, vertigo, or psychiatric

disorder (Class III)
Assess ABCs (Class II)

History, physical examination, and ECG (Class II)
Findings of
life threat?
NO
Elderly
Congestive heart
failure
Abnormal ECG
Acute coronary
syndrome /
coronary artery
disease
Over 45; otherwise

healthy
No significant ECG
findings
No clear inciting
event
Young
Normal ECG
Prodrome
suggesting
vasodepressor or
orthostatic
etiology
High risk
Intermediate risk
Low risk
Work up and treat

(Class III)
Stable syncope patient
YES
Consider:
Pulmonary
embolism
Subarachnoid
hemorrhage
Aortic dissection/
aneurysm
Myocardial
infarction
Gastrointestinal
bleed
Ventricular
dysrhythmia
Heart block
Carbon monoxide
poisoning
Clinical Pathway: Risk Stratification In Patients With Syncope
Admit to monitored hospital bed

(Class II)
Consider
admission
(Class II)
Possible ED
observation
unit stay
(Class III)
Outpatient
workup if
available
promptly
and patient
is reliable
(Class III)
Discharge to home
with primary care
follow-up (Class II)
The evidence for recommendations is graded using the following scale. For complete definitions, see back page. Class I: Definitely
recommended. Definitive, excellent evidence provides support. Class II: Acceptable and useful. Good evidence provides support. Class III:
May be acceptable, possibly useful. Fair-to-good evidence provides support. Indeterminate: Continuing area of research.
This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending
upon a patients individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright 2004 EB Practice, LLC. 1-800-249-5770. No part of this publication may be reproduced in any format
without written consent of EB Practice, LLC.
10
younger than 60 years of age have orthostatic blood

pressure drops.2,76,77 What is most important is not the actual
measurement of the change when standing, but the ability
to reproduce the patients symptoms on standing.76
proven cardiac cause of syncope would have been missed if

the work-up ended at just orthostatic pressures.76 Another
study found that orthostatic changes were the cause of
syncope in 24% of the patients who presented to the ED for
the evaluation of syncope.77 In this same study, orthostatic
changes were also found in patients with other diagnosed
causes of syncope. Also complicating the picture is the fact
that orthostatic hypotension is present in about 40% of
patients over 70 years old and that up to 23% of patients
Physical Findings
Due to time constraints, ambient noise, and numerous
distractions, it can be a challenge to perform a quality
cardiac and neurologic examination in the ED. Several key
features are important. For example, the presence of a new
murmur may suggest a cardiac etiology of syncope.
Ten Pitfalls To Avoid

1. Failure to obtain a detailed history of the acute event.
Remember that the most important step in obtaining an
accurate diagnosis is the history of present illness. Invest the
time to tease out the facts from the patient, family, and
bystanders. This investment will yield returns in a more
efficient ED diagnostic workup, a more accurate diagnosis, and
a higher quality of emergency care.
Patients who suffer from syncopespecifically those at the

extremes of ageshould follow up with their primary care
provider after discharge from the ED. If you do not explicitly
instruct or arrange this for your patients, they will assume it is
not important. They may also assume that if syncope happens
again, they dont need to see a practitioner because it was
nothing the last time. Take time to explain why follow-up is
important. Make sure they understand the importance of it,
and document that the conversation took place.
2. Failure to consider and diagnose life-threatening causes

of syncope.
Syncope is generally a benign process. However, one must
be proactive in trying to identify life-threatening causes,
most of which are cardiac-related. Generally, other
physical examination findings may help, but if you dont
keep your differential large, you will miss the rare lifethreatening conditions.
7. Failure to inform patients about the potential for recurrent

syncope and the dangers associated with it.
Again, if you dont take the time to inform your patients about
the possible dangers of syncope, they will assume that its
benign. Patients should be warned about possible triggers of
syncope, associated signs and symptoms, and the risk of a
sudden attack. Particularly in the elderly, instructions should
be provided for procedures to decrease the risk of falls, such as
using a cane or walker, taking extra time to equilibrate when
changing position, and paying attention to symptoms and
feelings that may precede the syncopal attack.
3. Failure to treat life-threatening causes of syncope.

Its one thing to recognize the potential high-risk patient in
front of you; its another to begin aggressive treatment in a
patient who now appears stable. Dont fall into this trap. If you
identify a potentially life-threatening cause, you must act
quickly to prevent possible disaster.
8. Failure to inform patients about the risk of returning

to activities such as driving, sports, and operating
heavy machinery.
Some municipalities now have laws requiring physicians to
report patients who have syncope.103,104 People with
occupations that are at high risk for disastrous outcomes
include truck drivers, bus drivers, airplane pilots, and heavy
equipment operators, to name a few. The emergency physician
could be held liable for a bad outcome if he or she did not
provide and document counseling about the risks of driving
after syncope.
4. Failure to admit patients who are clearly at high risk for

morbidity and mortality.
While some patients may not appear acutely ill in the ED, they
are still at higher risk for morbidity and mortality. Factors
associated with higher risk include male gender, advanced
age, syncope without warning, and cardiovascular risk factors
or a history of cardiac disease. Patients with these and other
characteristics described in this article may require admission
for observation and further evaluation. It may sometimes be
difficult to convince consultants of this. Recall that in most
situations, you are the only physician who has seen and
examined the patient, and you are now their physician. Dont
settle for outpatient follow-up when the right thing to do is to
admit the patient. Your patient is counting on you to be their
advocate. Insist on the admission.
9. Failure to assess for a prolonged QTc.

Remember to assess for both a long QTc (0.45 seconds in men,
0.46 in children, and 0.47 in women) and an abnormal notched
T wave. If abnormalities are present, consider congenital or
acquired prolonged QT syndrome. Also, when checking the
patients medication list, be alert for medicines known to
cause acquired prolonged QT syndrome.
5. Failure to consider multiple causes of syncope.

In many cases, there are multiple causes of a syncopal episode.
Your job is to think of the causes that make a patient too high
a risk to send home for outpatient management. Just because
a patient had an obvious stressor prior to the syncopal
episode, or you find orthostatic hypotension, this does not
mean that cardiac causes have been ruled out.
10. Failure to obtain continuous ECG monitoring while in the

ED in addition to the static ECG.
Continuous ECG monitoring increases the sensitivity for acute
ischemia and increases the likelihood of capturing an
intermittent dysrhythmia. The automated alarm may help to
alert the ED staff to patients with recurrent syncope in the ED.
All patients with a possible cardiac cause of syncope should be
placed on continuous ECG monitoring in the ED.
6. Failure to arrange outpatient follow-up for patients

with syncope.
11
Continued from page 9
altered mental status suggests a metabolic or pharmacologic

etiology, and poor cognitive function increases the possibility of a qualitative or quantitative medication error.
Findings consistent with congestive heart failure are

indicators of high risk of early mortality, including sudden
death.11 These and other key features can be used to help
risk stratify syncope patients. Although they may not
identify the exact cause, important physical findings can
help to determine if the patient can be discharged home or
should be admitted for further evaluation.
Other Examination Findings

Consider the possibility of trauma due to a fall in all
syncope patients. The greatest concern is for occult trauma
to the head and neck. The neck should be immobilized until
the extent of trauma, if any, can be fully evaluated. The scalp
and neck should be inspected and palpated for hematomas
and tenderness.
A careful abdominal examination should be undertaken to feel for tenderness, masses, or distention. An
abdominal aortic aneurysm can present as syncope associated with abdominal or back pain. Other abdominal
findings such as those of an acute abdomen should be
searched for and treated if found. A rectal examination
with stool guaiac to examine for an occult gastrointestinal
bleed should be considered in all adult patients presenting
with syncope.
The Cardiac Examination

The cardiovascular examination should not only focus on
the auscultation of the chest, but also the non-auscultory
findings as well. Subtle abnormalities and changes can help
sort out difficult cases in a loud ED.
Neck veins provide information regarding the patients
volume status and can give an idea of right heart function.
Neck vein distention can suggest right-sided heart failure,
constrictive pericarditis, tricuspid stenosis, superior vena
cava obstruction, and a variety of other cardiopulmonary
diseases. Venous distention measured as greater than 4 cm
above the sternal angle, most commonly with the head of
the bed at a 45 angle, is considered elevated.52
Characteristics of the carotid pulse waveforms can also
be helpful. Large, bounding pulses may indicate volume
excess or high stroke volume conditions such as obstructive
causes or a complete heart block. Small, weak pulses may
indicate such conditions as hypovolemia, congestive heart
failure, or severe aortic stenosis.59,79,80
When auscultating the heart, it can be very difficult to
determine a benign murmur from a life-threatening one.
Some characteristics to listen for are diastolic vs. systolic
timing, the response of the murmur to changes in position,
and whether there is any response to a Valsalva maneuver.
Also, abnormalities in the heart sounds themselves can be
helpful. For instance, an S-3 heart sound can be indicative of
congestive heart failure. A midsystolic click suggests mitral
valve prolapse.
As mentioned, the peripheral vascular examination
should include monitoring the blood pressure in both arms.
Check for capillary refill, edema, or cyanosis. Pulses should
be palpated at several locations and compared for strength
and character. Auscultation of the central pulses should be
undertaken looking for the presence of bruits.
Diagnostic Testing
Electrocardiography
An ECG should be performed on most patients with
syncope. Although the chance of finding the cause of
syncope is 2%-12% with the ECG alone,4,12 the cardiac causes
can be extremely dangerous and potentially lethal. An ECG
is easy to obtain, is relatively inexpensive, and can lead to
immediate treatment of life-threatening problems. The ECG
yields information beyond the rate and rhythm. Examples
include ischemic changes, a short PR interval and delta
wave suggestive of Wolff-Parkinson-White syndrome, a
prolonged QT interval, evidence of right heart strain, and/
or evidence of Brugada syndrome.
A completely normal ECG can also be used to risk
stratify patients. Georgeson et al searched for evidence of
acute cardiac ischemia in patients who presented with
syncope without chest pain and found that 18 of 251
patients were ultimately diagnosed with acute cardiac
ischemia, all of whom had ischemic abnormalities on their
presenting ECGs.81 Thus, a patient with no chest pain or
cardiac risk factors and a normal ECG is unlikely to have an
ischemic cause for syncope.
A normal ECG also lowers the likelihood of a primary
dysrhythmic cause for syncope. The ECG can be supplemented with continuous ECG monitoring in the ED, and
outpatient ambulatory cardiac event recording. Continuous
ECG monitoring in the ED with periodic physician inspection of the 12-lead tracing increases the diagnostic yield for
ongoing ischemia.82 Cardiac event recorders with continuous automatic dysrhythmia detection increase the sensitivity for relevant dysrhythmia detection when worn for 2-4
days after a syncopal event.83 The latest innovation in this
field is the subcutaneously implantable loop recorder.
Recording can be activated automatically or manually, and
the device can be implanted for one year or more.84,85
The Neurologic Examination

Neurologic examination findings can help point to certain
etiologies such as central nervous system thrombotic or
hemorrhagic disorders as the cause of syncope. At a
minimum, the examination should include an assessment of
cranial nerve function, motor and sensory function in the
extremities, reflexes, and orientation. Nystagmus, diplopia,
and dysarthria may all suggest disease of the
vertebrobasilar system, including thrombosis or dissection.
Vertebrobasilar disease can also affect the long motor and
sensory tracts traveling through the brainstem, resulting in
focal weakness or numbness in the extremities. Cerebellar
involvement may be suggested by ataxia or veering to one
side with ambulation. Assess for physical findings, as they
may relate to neurovascular causes of syncope. For example,
evidence of atrial fibrillation or a carotid bruit would
suggest an embolic source of disease. Isolated ongoing
Chest X-Ray
The chest x-ray is a commonly ordered test in patients
presenting with syncope. Its value is less well-established
12
history and physical examination, routine blood work is not

recommended. The following is a look at each test individually, and a summary of what the literature tells us.
Complete Blood Count

In one prospective study, 134 complete blood counts (CBCs)
were performed, and no cases of occult bleeding were
found.4 Four cases of suspected gastrointestinal bleeding
were confirmed by low hemoglobin. These results are
similar to those found in several retrospective reviews.1,4,12,18
One study stated that the CBC did confirm the need for
admission of the patient, but it did not help in the diagnosis
of the cause of syncope. This study stated that two patients
out of 33 had elevations of the white blood cell count that
led to their admission.18 From this information, we can
conclude that the routine use of a CBC does not add to the
work-up of syncope if it is not already clinically indicated.
This conclusion is supported by ACEP, ACP, and European
Society of Cardiology guidelines.11,12,14
Head Computed Tomography

Obtaining a routine head CT on all patients with syncope is
also not supported by the current literature. Day et al found
that a head CT demonstrated important new abnormalities
in seven of 20 patients who had either a focal seizure or a
focal deficit on physical examination, but in zero of 17
patients who did not have focal findings.1 In a pooled case
series presented by Linzer et al of 195 patients who were
studied with head imaging, the average yield of CT was 4%.
All patients who had positive scans had a focal abnormality
on neurologic examination or a witnessed seizure.12 In
general, the routine use of a head CT for the diagnosis of the
cause of syncope is not supported by current literature.
Electrolytes/Glucose
Electrolytes are defined as sodium, potassium, chloride,
bicarbonate, blood urea nitrogen, and creatinine. In one
prospective study, only one non-suspected abnormality was
detected in 134 electrolyte and/or glucose panels. This was
a case of a serum sodium level of 101 mEq/L in a patient
with diuretic-induced orthostasis.4 In a retrospective review,
five of 130 tests drawn proved helpful, although only one
was an unexpected metabolic abnormality.1 Another
retrospective study found that by dividing the electrolyte
panel into individual components, two abnormalities that
proved helpful were identified in 33 patients.18 In the same
study, the blood urea nitrogen and creatinine values
contributed to the decision to admit one of 33 cases by
confirming the clinical impression of dehydration.18 In
general, drawing routine electrolyte panels on patients
with syncope is not supported by the literature; it should
be guided by the medical history and medications of
the patient.
Electroencephalography
As with obtaining a head CT, an electroencephalogram
(EEG) is only indicated if there is a suggestive finding in the
history and physical examination. Several studies have been
performed regarding the use of EEG as a diagnostic tool.12,86
Little evidence exists of its benefit in a syncope patient with
no history of seizure activity. This test is unlikely to uncover
the cause of syncope if it was not already suggested by the
history and physical examination. Therefore, the routine use
of an EEG is not recommended.
Echocardiography
The literature regarding the use of echocardiography as a
screening tool for syncope is mixed. Some case reports have
shown a benefit to the use of echocardiography, but larger
studies have found this not to be the case. Unsuspected
causes of syncope found on echocardiography are reported
in 5%-10% of patients.13,71,85,87,88 The European Task Force
Guidelines on the management of syncope gives echocardiography a Class I recommendation for use in patients
with syncope when cardiac disease is suspected.14 The
problem is that echocardiography is not readily available in
most EDs. Although the diagnostic benefit may be similar to
that of the ECG, the fact that a formal study is up to seven
times the cost and that it is not readily available makes it
difficult to recommend this test for routine use in the ED.13
Echocardiography should be performed when cardiac
disease is suspected, but in patients with no underlying
cardiac history, no cardiac symptoms, and a normal physical
examination, echocardiography is likely to add little to the
diagnostic evaluation.
Cardiac Laboratory Tests

Cardiac serum markers are of little value unless indicated
by the history and physical examination. In one study of
patients with syncope and no chest pain, 18 of 251 patients
(7%) were diagnosed with cardiac ischemia as the cause of
their syncope. However, all 18 patients had ischemic
abnormalities (ST-segment elevation or depression, pathologic Q waves, or T wave abnormalities) identified on their
initial ECG.81 In syncope patients who deny chest pain or
discomfort on examination, have no cardiac history, and
have a normal ECG, the chance of cardiac ischemia being
the cause of syncope is highly unlikely. Routine use of
cardiac markers to search for the cause of syncope is
unnecessary.89 The evaluation of cardiac ischemia should be
reserved for patients who have suggestive history or
physical examination findings.
Serum/Urine Pregnancy Test
Laboratory Testing
Although there is no prospective study that shows an

absolute benefit of obtaining a pregnancy test in women of
childbearing age, common sense guides us to do this. This is
In general, unless one has a specific reason to suspect an

abnormality in the laboratory evaluation based on the
13
than that of the ECG. The chest x-ray can be helpful in a

select number of causes of syncope. For instance, one might
find a widened mediastinum in case of aortic dissection, or
an enlarged heart or other evidence of congestive heart
failure. Another possible finding is the classic x-ray findings
of pulmonary embolism, including Hamptons hump or
Westermarks sign. However, the absence of these x-ray
findings does not rule out these etiologies as the cause of
syncope. Again, unless guided by the history and physical
examination findings, it is unlikely that a routine chest x-ray
will uncover the cause of syncope.
2) syncope during exercise; 3) syncope while supine; 4) a

family history of sudden death in a person less than 30
years old; and 5) syncope with an odd history.3 The first
warning bell in the list could suggest one of the variants of
the long QT syndrome.
Pediatric patients should have a careful cardiac
examination. Other physical features associated with
cardiac disease (e.g., deafness, ataxia, abnormal facies,
congenital syndromes, and Marfan habitus) or neurologic
disease (e.g., ash-leaf spots, caf-au-lait spots, and cleft
palate) should be sought.94
Based on the preceding data and case reports of sudden
death,96 the following recommendations about children
presenting with syncope can be made. First, obtain a
detailed family history for all patients who seek medical
attention for syncope. Ask specifically about a family history
of cardiac dysrhythmias or sudden, unexplained death.
Second, all children should undergo a thorough physical
examination to assess for cardiac pathology. This includes
an ECG and, possibly, cardiac monitoring while in the ED.
a relatively inexpensive test that can be performed in a

noninvasive way. Pregnancy is associated with a risk of
internal hemorrhage from ectopic implantation as well as
external vaginal hemorrhage. Furthermore, the propensity
for supraventricular tachydysrhythmias in patients with
and without preexcitation, and for premature ventricular
contractions, seems higher during pregnancy.90,91
Other Studies
No studies currently support the routine ED use of liver
enzymes, arterial blood gasses, toxicology screens, coagulation studies, or urine dipsticks for screening purposes.
Abnormalities have been found in all of these test groups;
however, random screening is not justified unless clinically
indicated by the history and physical examination.
Management
The wide range of causes of syncope results in an even
wider range of possible treatment strategies. The goal in the
ED is to identify life threats and treat them accordingly.
When no immediate life threat is identified, the goal shifts to
risk stratifying the patient for likelihood of an adverse
outcome. However, in about one-third to one-half of cases, it
may also be possible to identify the cause of syncope. Table
4 lists the common causes of syncope and the potential
treatments for each cause. At this time, there are no largescale, randomized, controlled trials studying the advantages
and disadvantages of inpatient vs. outpatient management
of patients with syncope. (See the disposition section later in
this article.)
Table 4. Medical Care Of Syncope.

I. Vasodepressor syncope / Metabolic / Psychiatric
Patients with specific triggers (stress, drawing blood) need
no specific treatment
Specific treatments
Nonpharmacologic measures
Hypovolemia: Fluid resuscitation
Vasodepressor: Avoidance of triggering situations
Orthostatic hypotension: Dangling the legs over the
side of the bed prior to standing; Slowly changing
positions; Support stockings
Pharmacologic measures
Discontinuation of potential pharmacological causes
that are not necessary
Orthostatic hypotension: Midodrine, phenylephrine;
Caffeine, theophylline; Fludrocortisone
Vasodepressor: Beta-blockers; Selective serotonin
reuptake inhibitors; Scopolamine
Permanent pacemakers: Useful in patients with
carotid sinus hypersensitivity
Special Circumstances
Pediatric Syncope
Syncope in children is generally a benign event. As stated
earlier, up to 20% of patients experience syncope before the
end of adolescence.2,3,92 There are a few serious, but rare,
causes of syncope in children.
Little research is done in this population. The only
population-based study of syncope in children to date was
done by Driscoll et al.93 The study examined 151 patients
between the ages of 1 and 22 years presenting between 1987
and 1991 with symptoms consistent with syncope. The
authors estimated that the incidence of syncopal episodes in
children coming to medical attention per 100,000 population
was 125.8. For both male and female patients, the rate of
syncopal episodes peaked in the 15- to 19-year-old age
groups, but the peak for female patients was much greater
than that in males. Only one patient was ultimately found to
have a long QT syndrome. The majority of children were
thought by the evaluating physician to have had vasodepressor syncope. Recurrence of syncopal episodes occurred
in 9% of the 151 patients. No deaths related to syncope were
reported in this group of children at follow-up.93
Just as in their adult counterparts, a detailed history
and physical examination may be sufficient to define the
cause of syncope in many cases.3,93-95 In a recent review
by McLeod, several anecdotal but useful warning bells
in the history are defined. They include: 1) syncope in
response to loud noise, fright, or extreme emotional stress;
II. Structural heart disease

Treatment is directed at the underlying problem; admission
is often warranted
III. Dysrhythmias
Bradycardia
Discontinue / decrease medications if can be done safely
A permanent pacemaker is generally indicated for
symptomatic bradycardia and high-grade AV block
Tachycardia
Ventricular tachycardiaACLS guidelines for immediate
treatment, electrophysiologic testing may be warranted;
possible automatic implantable cardioverter/defibrillator
placement, antidysrhythmic therapy, or radio frequency
catheter ablation as needed
Supraventricular tachycardiaACLS guidelines for
immediate treatment, ED studies with radiofrequency
catheter ablation may be warranted
14
Elderly Patients
Disposition
Syncope is a common presenting complaint of the elderly. It

has an annual incidence of 6% and a recurrence rate of
about 30%.97 As most emergency physicians have found in
practice, syncope in the elderly can often lead to a timeconsuming and challenging evaluation.
Syncope from any cause in the elderly patient population is usually associated with a poor prognosis. First, from
a primary event standpoint, syncope is responsible for 2%15% of falls in geriatric subjects.98 Data have shown that
injury is the sixth-leading cause of death in patients older
than 65 years.97-100 Falls are directly or indirectly the cause of
death in as many as 12% of people in the geriatric population.98,101 Second, the underlying cause of syncope in the
elderly population is more likely to be of a cardiac nature.
As stated earlier, syncope of cardiac etiology has a much
worse prognosis. There are a number of specific cardiac
etiologies that are much more common in the elderly
population. These include dysrhythmias (such as bradycardia or sick sinus syndrome), atrioventricular blocks (such as
second-degree Mobitz II and third-degree block), and
ventricular ectopy (such as ventricular tachycardia).
Congestive heart failure is more prominent in the elderly.
These patients may present with reverse postural
Disposition of syncope patients can fit into three main

categories: 1) patients who clearly need to be admitted; 2)
those who are safe to discharge home with follow-up; and 3)
patients who have some higher-risk features but are not
clearly at risk for morbidity and mortality from this event.
Who Needs To Be Admitted?

A patient should be admitted to the hospital for rapid workup and diagnostic procedures if the initial evaluation reveals
concerns about the risk of sudden death. The ACEP clinical
guidelines on syncope state criteria for patients that
absolutely need to be admitted to the hospital for further
evaluation and treatment.11 These criteria include all
patients with: 1) a history of congestive heart failure or
ventricular dysrhythmias; 2) associated chest pain or other
symptoms compatible with acute coronary syndrome; 3)
evidence of significant congestive heart failure or valvular
heart disease on physical examination; and 4) ECG findings
of ischemia, dysrhythmia, prolonged QT interval, or bundle
branch block.
The European Task Force Guidelines on the management of syncope also have recommendations as to which
15
syncope, which would occur with recumbency.97 The

prevalence of valvular disorders also increases with age.
Syncope is a common presenting complaint in patients with
aortic stenosis. This is significant because once symptoms
such as syncope begin in these patients, they are at high risk
for mortality. In fact, left untreated, the life expectancy is
three years or less.
Finally, syncope in the elderly for all reasons is much
more dangerous. In a study of syncope in patients 60 years
or older, mortality rates were compared between the elderly
and a younger control group of patients. The mortality rate
from non-cardiac syncope was 22% and 5% in the two
groups, respectively.102 This difference is likely due to the
general decrease in reserve of older patients and the fact that
they are more likely to have multiple comorbidities.
Neurologic causes are much more common in the
elderly population. A cerebrovascular event such as a
stroke can often present with a syncopal-type episode.
Another often-overlooked cause in the elderly is carotid
sinus syndrome.
Syncope related to orthostatic hypotension, gastrointestinal bleeding, and medications are more common in this
age group. Orthostatic hypotension can be present in up to
40% of patients over the age of 70. Reproduction of the
patients symptoms upon standing is just as helpful as a
numerical change in the heart rate or blood pressure.2,76
Keep in mind that syncope can be multifactorial,
especially in the elderly. A recent study found that up to
18% of all cases of syncope had multiple potential causes.80
This study also found that the presence of multiple potential
causes of syncope was an independent predictor of increased mortality. Because of the higher risk of mortality
from all causes of syncope in the elderly, maintain a very
low threshold for admission of these patients either to the
hospital ward or a dedicated observation unit.
Third, special attention should be directed toward children

who have a history or complaint of exercise-induced or
exertional syncope. Extra time should be given to these
children, and a cardiac cause must be aggressively ruled
out. Fourth, just as in adults, the use of adjunctive diagnostic laboratory tests should be guided by the history and
physical examination. While one review advocated for
serum glucose, basic electrolytes, and a CBC in all children,94
this recommendation has not been independently validated.
Finally, children who have negative findings in the personal
and family history, a normal physical examination, and nonexertional syncope are unlikely to have a cardiac cause of
syncope, and are at low risk for sudden death. These
patients usually can be discharged home with
outpatient follow-up.
All children who have had a syncopal episode should
be reexamined by a primary care physician and referred for
more advanced studies as appropriate.3,94,95
Management of syncope in children is dependent on
the underlying cause. As with all conditions in emergency
medicine, start with the ABCs. If the primary cause is
suspected to be neurally mediated syncope, the mainstay of
therapy is reassurance.3 Advice to maximize fluid intake
may be appropriate, and a warning to avoid precipitating
events is warranted. For frequent, recurrent syncope, close
primary care follow-up is recommended. If this cannot be
arranged, then admitting the child for further testing and
possible pharmacologic management with drugs such as
fludrocortisone and/or a beta-blocker may be warranted.3
If the ED evaluation suggests a cardiac or neurologic
cause, admission for further diagnostic testing and monitoring is required. If an underlying dysrhythmic cause is
identified, the child should be admitted to a service with
cardiac monitoring and advanced life support availability.
strategies on page 6.
Also, be sure to consider the social situation of the
patient, the ability to get a follow-up appointment in a
particular institution or community, and the patients
wishes. All of these factors may alter management.
patients need to be hospitalized after a syncopal episode.

Table 5 is a summary based on these recommendations.
Other published guidelines on syncope support the criteria
above.12,13,71 Patients with worrisome pulmonary findings
such as a pulmonary embolism as well as patients with any
signs of instability (such as severe orthostatic hypotension),
functional bleeding (such as a gastrointestinal bleed), or
sustained tachycardia or bradycardia without a clear cause
should also be admitted for further evaluation and possible
treatment.
Discharge Instructions
Driving Recommendations
Should people who suffer from syncope be limited from
driving? Driving an automobile is not a guaranteed right
it is a privilege that may be restricted when it poses a threat
to other people. The occurrence of a syncopal episode
during driving could have serious consequences to the
patient, his or her passengers, and others on the roads. Laws
exist in many municipalities regarding what is required
when a patient has a syncopal episode.103,104 Physicians
should be aware of the laws in the state in which they
practice. In 1996, the American Heart Association and the
North American Society of Pacing and Electrophysiology
issued statements regarding driving after syncope.107,108
A study by Akiyama et al found that 2% of syncopal
patients reported losing consciousness while driving.105
Only a small number of patients reported having an
accident while driving. They concluded that although it was
common for their patients to have symptoms of possible
dysrhythmia while driving, accidents were found to be
uncommon; they actually occurred at a lower frequency
than the annual accident rate of the general population.105
Another study by Maas et al examined patient compliance
with no driving advice given by their doctor.106 They
found that three of 104 patients instructed not to drive
reported a syncopal episode while driving within the next
year. This resulted in one car crash with minor injury. Nine
patients had stopped driving prior to the initial evaluation
by the investigative team. On follow-up, all 95 patients who
had been driving prior to being told to stop had continued
to drive irrespective of any recommendations.106
Who Can Safely Be Discharged?

Most patients in whom the suspicion for a cardiac cause of
syncope is low can be safely evaluated in the ED and
discharged for outpatient follow-up. In general, patients
younger than 40 years with an isolated syncopal event who
also have a normal physical examination, a normal ECG,
and no evidence of structural or ischemic heart disease can
safely be sent home from the ED. Patients may be advised to
minimize driving, playing sports, or operating heavy
machinery pending follow-up evaluation. Patients should
generally follow up with their primary care physician
within the next week or return to the ED sooner if they have
additional syncopal events.
Everyone Else
Finally, another group represents the gray area. The ACEP
guidelines define this group of patients as having: 1) age
greater than 60; 2) a history of congenital heart disease; 3) a
history of coronary artery disease in the absence of chest
pain or ischemia during the examination; 4) a family history
of unexpected sudden death; or 5) exertional syncope in
younger patients without an obvious benign etiology.11 This
includes a large number of patients who present with
syncope, and some clinical judgment is required. These
patients may be good candidates for an observation unit.
This is discussed in detail in the section on cost-effective
Summary
Table 5. When To Hospitalize A Patient With

Syncope: A Summary Of The European Task
Force On Syncope Recommendations.
For diagnosis
Suspected or known heart
disease
ECG patterns known to
cause syncope
Syncope occurring during
exertion
Syncope causing severe
injury
Family history of sudden
death
For treatment
Cardiac dysrhythmias
causing syncope
Syncope due to acute
coronary syndrome
Syncope due to structural
cardiac disease
Stroke or focal neurologic
In patients with syncope, the primary goal of the emergency

medicine practitioner is to be able to identify those who are
at high risk for morbidity and mortality. Identifying lowerrisk patients who can be safely discharged from the ED with
outpatient evaluation can result in significant savings.
The inability of the emergency physician to establish
the cause of each syncopal episode does not mean that the
patient has not been appropriately treated. Indeed, up to
50% of the cases will never have a cause identified after a
detailed evaluation.1,4-6,8 Even so, analyzing the information
obtained through a thorough history, physical examination,
baseline ECG, and other indicated studies allows emergency
physicians to safely risk stratify patients and make appropriate disposition decisions.
disorders
Patients with repeat
vasodepressor syncope for
which pacemaker
implantation is planned
Other categories that

occasionally may need to
be admitted
Patients without heart
problems, but sudden
onset of palpitations
Patients with syncope in
supine position
Patients with frequent
recurrent syncope
Patients with minimal or
mild heart disease when
there is high suspicion for
cardiac-related syncope
References
Evidence-based medicine requires a critical appraisal of the
literature based upon study methodology and number of
subjects. Not all references are equally robust. The findings
of a large, prospective, randomized, and blinded trial
16
1.*
Day SC, Cook EF, Funkenstein H, et al. Evaluation and outcome of

emergency room patients with transient loss of consciousness. Am J
Med 1982 Jul;73(1):15-23. (Retrospective; 198 patients)
2.
Decker W. Down for the count! The evaluation of syncope. 2002.
(Lecture practice guidelines)
3.
McLeod KA. Syncope in childhood. Arch Dis Child 2003 Apr;88(4):350353. (Review)
4.* Martin GJ, Adams SL, Martin HG, et al. Prospective evaluation of
syncope. Ann Emerg Med 1984 Jul;13(7):499-504. (Prospective; 170
patients)
5.
Kapoor WN. Evaluation and outcome of patients with syncope.
Medicine (Baltimore) 1990 May;69(3):160-175. (Retrospective; 433
patients)
6.* Kapoor WN. Evaluation and management of the patient with syncope.
JAMA 1992 Nov 11;268(18):2553-2560. (Review)
7.
HCUPnet, Healthcare Cost and Utilization Project. Agency for Healthcare
Research and Quality, Rockville, MD. http://www.ahrq.gov/data/
hcup/hcupnet.htm. (National database)
8.
Kapoor WN. Syncope. N Engl J Med 2000 Dec 21;343(25):1856-1862.
(Review)
9.
Abboud FM. Neurocardiogenic syncope. N Engl J Med 1993 Apr
15;328(15):1117-1120. (Editorial)
10. Lewis T. A lecture on vasovagal syncope. BMJ 1932;1:873-876.
(Historical reference)
11.* American College of Emergency Physicians. Clinical policy: critical
issues in the evaluation and management of patients presenting with
syncope. Ann Emerg Med 2001 Jun;37(6):771-776. (Practice guideline)
12. Linzer M, Yang EH, Estes NA 3rd, et al. Diagnosing syncope. Part 1:
Value of history, physical examination, and electrocardiography.
Clinical Efficacy Assessment Project of the American College of
Physicians. Ann Intern Med 1997 Jun 15;126(12):989-996. (Practice
guideline)
13. Linzer M, Yang EH, Estes NA 3rd, et al. Diagnosing syncope. Part 2:
Unexplained syncope. Clinical Efficacy Assessment Project of the
American College of Physicians. Ann Intern Med 1997 Jul 1;127(1):7686. (Practice guideline)
14.* Brignole M, Alboni P, Benditt D, et al; Task Force on Syncope,
European Society of Cardiology. Guidelines on management
(diagnosis and treatment) of syncope. Eur Heart J 2001
Aug;22(15):1256-1306. (Practice guideline)
15. Quinn J, McDermott D, Stiell I, et al. Physician judgment in evaluating
patients with syncope. Acad Emerg Med 2002;9:452-453. (Abstract,
retrospective; 559 patients)
16. Elesber A, Decker W, Smars P, et al. Evaluation of the safety and costeffectiveness of the ACEP clinical policy in regards to admission of the
syncopal patient. Acad Emerg Med 2002;9:370-371. (Abstract,
retrospective; 201 patients)
17. Colivicchi F, Ammirati F, Melina D, et al; OESIL (Osservatorio
Epidemiologico sulla Sincope nel Lazio) Study Investigators.
Development and prospective validation of a risk stratification system
for patients with syncope in the emergency department: the OESIL risk
score. Eur Heart J 2003 May;24(9):811-819. (Prospective cohort; 270
patients)
18. Junaid A, Dubinsky IL. Establishing an approach to syncope in the
emergency department. J Emerg Med 1997 Sep-Oct;15(5):593-599.
(Retrospective chart review; 33 patients)
19. Turnbull C, Bono M. Evaluating syncope in the acute setting.
Emergency Medicine 2002;11:14-20. (Review)
20. Chen L, Jahangir A, Decker W, et al. Predictors for bradycardia and
tachycardia in patients with syncope. A clinical score index for
diagnosis. Circulation 2001;104 (17 Suppl II):346. (Abstract)
21. Hayes OW. Evaluation of syncope in the emergency department.
Emerg Med Clin North Am 1998 Aug;16(3):601-615, viii. (Review)
22. Benditt DG, Lurie KG, Fabian WH. Clinical approach to diagnosis of
syncope. An overview. Cardiol Clin 1997 May;15(2):165-176. (Review)
23. Olshansky B, Hahn EA, Hartz VL, et al. Clinical significance of
17
syncope in the electrophysiologic study versus electrocardiographic

monitoring (ESVEM) trial. The ESVEM Investigators. Am Heart J 1999
May;137(5):878-886. (Multicenter, randomized, controlled trial; 486
patients)
24. Brignole M. Sick sinus syndrome. Clin Geriatr Med 2002 May;18(2):211227. (Review)
25. Gold MR. Permanent pacing: new indications. Heart 2001
Sep;86(3):355-360. (Review)
26. Rosenfeld ME, Beckerman B, Ward MF, et al. Lyme carditis: complete
AV dissociation with episodic asystole presenting as syncope in the
emergency department. J Emerg Med 1999 Jul-Aug;17(4):661-664. (Case
report)
27. Leung FW, Oill PA. Ticket for admission: unexplained syncopal attacks
in patients with cardiac pacemaker. Ann Emerg Med 1980 Oct;9(10):527528. (Case report)
28. Moss AJ. Long QT Syndrome. JAMA 2003 Apr 23-30;289(16):2041-2044.
(Review)
29. Moss AJ. Measurement of the QT interval and the risk associated with
QTc interval prolongation: a review. Am J Cardiol 1993 Aug
26;72(6):23B-25B. (Review)
30. Nemec J, Hejlik JB, Shen WK, et al. Catecholamine-induced T-wave
lability in congenital long QT syndrome: a novel phenomenon
associated with syncope and cardiac arrest. Mayo Clin Proc 2003
Jan;78(1):40-50. (Prospective; 42 patients)
31. Viskin S. Long QT syndromes and torsades de pointes. Lancet 1999
Nov 6;354(9190):1625-1633. (Review)
32. Al-Khatib SM, LaPointe NM, Kramer JM, et al. What clinicians should
know about the QT interval. JAMA 2003 Apr 23-30;289(16):2120-2127.
(Review)
33. Brugada J, Brugada R, Brugada P. Right bundle-branch block and STsegment elevation in leads V1 through V3: a marker for sudden death
in patients without demonstrable structural heart disease. Circulation
1998 Feb 10;97(5):457-460. (Cohort; 63 patients)
34. Wilde AA, Antzelevitch C, Borggrefe M, et al; Study Group on the
Molecular Basis of Arrhythmias of the European Society of Cardiology.
Proposed diagnostic criteria for the Brugada syndrome. Eur Heart J
2002 Nov;23(21):1648-1654. (Consensus development conference,
review)
35. Antzelevitch C, Brugada P, Brugada J, et al. Brugada syndrome: a
decade of progress. Circ Res 2002 Dec 13;91(12):1114-1118. (Review)
36. Jones R, Gage A. Brugada syndrome as the cause of syncope in a 49year-old man. Ann Emerg Med 2000 Aug;36(2):156-159. (Case report)
37. Vanpee D, Blommaert D, Gillet JB, et al. A young man with recurrent
syncopes, right bundle branch block and ST segment elevation. Am J
Emerg Med 1999 Oct;17(6):601-603. (Case report)
38. Sorgato A, Faggiano P, Aurigemma GP, et al. Ventricular arrhythmias
in adult aortic stenosis: prevalence, mechanisms, and clinical
relevance. Chest 1998 Feb;113(2):482-491. (Review)
39. Davidson E, Rotenbeg Z, Fuchs J, et al. Transient ischemic attackrelated syncope. Clin Cardiol 1991 Feb;14(2):141-144. (Retrospective
cohort; 37 patients)
40. Pavlovic SU, Kocovic D, Djordjevic M, et al. The etiology of syncope in
pacemaker patients. Pacing Clin Electrophysiol 1991 Dec;14(12):20862091. (Retrospective review; 46 patients)
41. Tavintharan S, Mukherjee JJ. A rare cause of syncope in a patient with
diabetes mellitusa case report. Ann Acad Med Singapore 2001
Jul;30(4):436-439. (Case report)
42. Lee EC. Clinical manifestations of sarin nerve gas exposure. JAMA
2003 Aug 6;290(5):659-662. (Review)
43. Wax PM, Becker CE, Curry SC. Unexpected gas casualties in
Moscow: a medical toxicology perspective. Ann Emerg Med 2003
May;41(5):700-705. (Review)
44.* Kapoor WN, Hanusa BH. Is syncope a risk factor for poor outcomes?
Comparison of patients with and without syncope. Am J Med 1996
Jun;100(6):646-655. (Prospective; 470 patients)
45. Oh JH, Hanusa BH, Kapoor WN. Do symptoms predict cardiac
arrhythmias and mortality in patients with syncope? Arch Intern Med
1999 Feb 22;159(4):375-380. (Prospective cohort; 497 patients)
46.* Martin TP, Hanusa BH, Kapoor WN. Risk stratification of patients with
syncope. Ann Emerg Med 1997 Apr;29(4):459-466. (Prospective cohort;
252 patients in first and 375 patients in second)
47. Alboni P, Brignole M, Menozzi C, et al. Diagnostic value of history in
patients with syncope with or without heart disease. J Am Coll Cardiol
2001 Jun 1;37(7):1921-1928. (Prospective; 341 patients)
48. Doi A, Miyamoto K, Uno K, et al. Studies on hemodynamic instability
in paroxysmal supraventricular tachycardia: noninvasive evaluations
by head-up tilt testing and power spectrum analysis on electrocardiographic RR variation. Pacing Clin Electrophysiol 2000 Nov;23(11 Pt
should carry more weight than a case report.

To help the reader judge the strength of each reference,
pertinent information about the study, such as the type of
study and the number of patients in the study, will be
included in bold type following the reference, where
available. In addition, the most informative references cited
in the paper, as determined by the authors, will be noted by
an asterisk (*) next to the number of the reference.
associated with probable adverse drug reactions. Arch Intern Med 1990
Nov;150(11):2309-2312. (Retrospective; 70 patients)
75. Gaeta TJ, Fiorini M, Ender K, et al. Potential drug-drug interactions in
elderly patients presenting with syncope. J Emerg Med 2002
Feb;22(2):159-162. (Retrospective; 263 patients)
76. Atkins D, Hanusa B, Sefcik T, et al. Syncope and orthostatic hypotension. Am J Med 1991 Aug;91(2):179-185. (Prospective; 223 patients)
77. Sarasin FP, Louis-Simonet M, Carballo D, et al. Prevalence of
orthostatic hypotension among patients presenting with syncope in
the ED. Am J Emerg Med 2002 Oct;20(6):497-501. (Prospective; 650
patients)
78. Goldschlager N, Epstein AE, Grubb BP, et al; Practice Guidelines
Subcommittee, North American Society of Pacing and Electrophysiology. Etiologic considerations in the patient with syncope and an
apparently normal heart. Arch Intern Med 2003 Jan 27;163(2):151-162.
(Review)
79. Meyer MD, Handler J. Evaluation of the patient with syncope: an
evidence based approach. Emerg Med Clin North Am 1999
Feb;17(1):189-201, ix. (Review)
80. Chen LY, Gersh BJ, Hodge DO, et al. Prevalence and clinical outcomes
of patients with multiple potential causes of syncope. Mayo Clin Proc
2003 Apr;78(4):414-420. (Retrospective cohort; 987 patients)
81. Georgeson S, Linzer M, Griffith JL, et al. Acute cardiac ischemia in
patients with syncope: importance of the initial electrocardiogram. J
Gen Intern Med 1992 Jul-Aug;7(4):379-386. (Prospective, multicenter;
251 patients)
82. Fesmire FM, Percy RF, Bardoner JB, et al. Usefulness of automated
serial 12-lead ECG monitoring during the initial emergency
department evaluation of patients with chest pain. Ann Emerg Med
1998 Jan;31(1):3-11. (Prospective, observational; 1000 patients)
83. Balmelli N, Naegeli B, Bertel O. Diagnostic yield of automatic and
patient-triggered ambulatory cardiac event recording in the evaluation
of patients with palpitations, dizziness, or syncope. Clin Cardiol 2003
Apr;26(4):173-176. (Prospective cohort; 101 patients)
84. Seidl K, Rameken M, Breunung S, et al; Reveal-Investigators.
Diagnostic assessment of recurrent unexplained syncope with a new
subcutaneously implantable loop recorder. Europace 2000 Jul;2(3):256262. (Prospective cohort; 133 patients)
85. Arthur W, Kaye GC. Current investigations used to assess syncope.
Postgrad Med J 2001 Jan;77(903):20-23. (Review)
86. Davis TL, Freemon FR. Electroencephalography should not be routine
in the evaluation of syncope in adults. Arch Intern Med 1990
Oct;150(10):2027-2029. (Retrospective; 73 patients)
87. Recchia D, Barzilai B. Echocardiography in the evaluation of patients
with syncope. J Gen Intern Med 1995 Dec;10(12):649-655. (Retrospective; 128 patients)
88. Sarasin FP, Junod AF, Carballo D, et al. Role of echocardiography in the
evaluation of syncope: a prospective study. Heart 2002 Oct;88(4):363367. (Prospective cohort; 650 patients)
89. Morag R, Brenner B. Syncope. http://www.emedicine.com/. Accessed
September 27, 2002. (Review)
90. Widerhorn J, Widerhorn AL, Rahimtoola SH, et al. WPW syndrome
during pregnancy: increased incidence of supraventricular
arrhythmias. Am Heart J 1992 Mar;123(3):796-798. (Case series; 3
patients)
91. Shotan A, Ostrzega E, Mehra A, et al. Incidence of arrhythmias in
normal pregnancy and relation to palpitations, dizziness, and syncope.
Am J Cardiol 1997 Apr 15;79(8):1061-1064. (Comparative; 162 patients)
92. Lewis DA, Dhala A. Syncope in the pediatric patient. The
cardiologists perspective. Pediatr Clin North Am 1999 Apr;46(2):205219. (Review)
93.* Driscoll DJ, Jacobsen SJ, Porter CJ, et al. Syncope in children and
adolescents. J Am Coll Cardiol 1997 Apr;29(5):1039-1045. (Retrospective;
151 patients)
94. Prodinger RJ, Reisdorff EJ. Syncope in children. Emerg Med Clin North
Am 1998 Aug;16(3):617-626, ix. (Review)
95. Johnsrude CL. Current approach to pediatric syncope. Pediatr Cardiol
2000 Nov-Dec;21(6):522-531. (Review)
96. Driscoll DJ, Edwards WD. Sudden unexpected death in children and
adolescents. J Am Coll Cardiol 1985 Jun;5(6 Suppl):118B-121B.
(Retrospective; 515 patients)
97. Olsky M, Murray J. Dizziness and fainting in the elderly. Emerg Med
Clin North Am 1990 May;8(2):295-307. (Review)
98. Baraff LJ, Della Penna R, Williams N, et al. Practice guideline for the
ED management of falls in community-dwelling elderly persons.
Kaiser Permanente Medical Group. Ann Emerg Med 1997 Oct;30(4):480492. (Practice guideline, review)
99. Sorock GS. Falls among the elderly: epidemiology and prevention. Am
1):1623-1631. (Prospective; 36 patients)

Calkins H, Shyr Y, Frumin H, et al. The value of the clinical history in
the differentiation of syncope due to ventricular tachycardia,
atrioventricular block, and neurocardiogenic syncope. Am J Med 1995
Apr;98(4):365-373. (Prospective cohort; 80 patients)
50. Gilman JK. Syncope in the emergency department. A cardiologists
perspective. Emerg Med Clin North Am 1995 Nov;13(4):955-971.
(Review)
51. Kofflard MJ, Ten Cate FJ, van der Lee C, et al. Hypertrophic
cardiomyopathy in a large community-based population: clinical
outcome and identification of risk factors for sudden cardiac death and
clinical deterioration. J Am Coll Cardiol 2003 Mar 19;41(6):987-993.
(Comparative; 225 patients)
52. Braunwald E. Valvular heart disease. In: Heart Disease: A Textbook of
Cardiovascular Medicine. 6th ed. St. Louis, MO: W.B. Saunders
Company; 2001:1643-1722. (Textbook chapter)
53. Harrison EC, Rashtian MY, Allen DT, et al. An emergency physicians
guide to prosthetic heart valves: valve-related complications. Ann
Emerg Med 1988 Jul;17(7):704-710. (Review)
54. Vongpatanasin W, Hillis LD, Lange RA. Prosthetic heart valves. N Engl
J Med 1996 Aug 8;335(6):407-416. (Review)
55. Varon J, Fromm RE Jr. Syncope: the forgotten sign of pulmonary
embolism. J Emerg Med 1998 Jan-Feb;16(1):117-118. (Editorial)
56. Wolfe TR, Allen TL. Syncope as an emergency department presentation of pulmonary embolism. J Emerg Med 1998 Jan-Feb;16(1):27-31.
(Case report)
57. Bell WR, Simon TL, DeMets DL. The clinical features of submassive
and massive pulmonary emboli. Am J Med 1977 Mar;62(3):355-360.
(Cohort; 327 patients)
58. Stein PD, Willis PW 3rd, DeMets DL. History and physical examination in acute pulmonary embolism in patients without preexisting
cardiac or pulmonary disease. Am J Cardiol 1981 Feb;47(2):218-223.
(Prospective cohort; 215 patients)
59. Kuhlmann TP, Powers RD. Painless aortic dissection: an unusual cause
of syncope. Ann Emerg Med 1984 Jul;13(7):549-551. (Case report)
60. Young J, Herd AM. Painless acute aortic dissection and rupture
presenting as syncope. J Emerg Med 2002 Feb;22(2):171-174. (Case
report)
61. Schweitzer P, Teichholz LE. Carotid sinus massage. Its diagnostic and
therapeutic value in arrhythmias. Am J Med 1985 Apr;78(4):645-654.
(Review)
62. Hoefnagels WA, Padberg GW, Overweg J, et al. Syncope or seizure?
The diagnostic value of the EEG and hyperventilation test in transient
loss of consciousness. J Neurol Neurosurg Psychiatry 1991
Nov;54(11):953-956. (Prospective; 119 patients)
63. Benbadis SR, Wolgamuth BR, Goren H, et al. Value of tongue biting in
the diagnosis of seizures. Arch Intern Med 1995 Nov 27;155(21):23462349. (Prospective; 106 patients)
64.* Sheldon R, Rose S, Ritchie D, et al. Historical criteria that distinguish
syncope from seizures. J Am Coll Cardiol 2002 Jul 3;40(1):142-148.
65. Bergfeldt L. Differential diagnosis of cardiogenic syncope and seizure
disorders. Heart 2003 Mar;89(3):353-358. (Review)
66. Lanska DJ, Remler B. Benign paroxysmal positioning vertigo: classic
descriptions, origins of the provocative positioning technique, and
conceptual developments. Neurology 1997 May;48(5):1167-1177.
(Review)
67. Froehling DA, Silverstein MD, Mohr DN, et al. The rational clinical
examination. Does this dizzy patient have a serious form of vertigo?
JAMA 1994 Feb 2;271(5):385-388. (Review)
68. Shlamovitz GZ, Assia A, Ben-Sira L, et al. Suffocation roulette: a case
of recurrent syncope in an adolescent boy. Ann Emerg Med 2003
Feb;41(2):223-226. (Case report)
69. Kapoor WN, Fortunato M, Hanusa BH, et al. Psychiatric illnesses in
patients with syncope. Am J Med 1995 Nov;99(5):505-512. (Prospective
cohort; 414 patients)
70. Shapiro NI, Kociszewski C, Harrison T, et al. Isolated prehospital
hypotension after traumatic injuries: a predictor of mortality? J Emerg
Med 2003 Aug;25(2):175-179. (Retrospective cohort; 490 patients)
71. Pancioli A, McNeil P. The clinical challenge of syncope: a costconscious and outcome-driven approach to patient evaluation and
disposition. Emerg Med Rep 1998 Sep 14;19. (Review)
72. Newman BH. Vasovagal reactions in high school students: findings
relative to race, risk factor synergism, female sex, and non-high school
participants. Transfusion 2002 Dec;42(12):1557-1560. (Retrospective
cohort; 1302 subjects)
73. Kapoor WN. Current evaluation and management of syncope.
Circulation 2002 Sep 24;106(13):1606-1609. (Review).
74. Hanlon JT, Linzer M, MacMillan JP, et al. Syncope and presyncope
49.
18
Physician CME Questions

1.
2.
3.
4.
5.
Which of the following does not suggest a high-risk

cause of syncope?
a. Age greater than 45 years
b. Prodrome suggesting vasodepressor or orthostatic
etiology
c. History of ventricular dysrhythmias or CHF
d. An abnormal ECG
7.
The highest mortality rates are generally associated

with which of the following categories of syncope?
a. Cardiac
b. Central nervous system
c. Vasovagal/psychogenic
d. Metabolic/drug-related
8.
A complaint of syncope while sitting most likely

suggests which of the following causes?
a. Cardiac
b. Central nervous system
c. Vasovagal/psychogenic
d. Metabolic/drug-related
9.
ECG findings of a pseudo-right bundle branch block

and persistent downsloping ST segment elevation in
leads V1 to V3 characterize:
a. torsades de pointes.
b. Wolff-Parkinson-White syndrome.
c. Brugada syndrome.
d. sick sinus syndrome.
10. Which of the following suggests a seizure rather

than syncope?
a. Waking with a cut tongue after the episode
b. Lightheadedness
c. Sweating before the episode
d. An episode associated with prolonged sitting
or standing
All of the following regarding syncope in the ED are

true except:
a. Its cost to the healthcare system in the United
States exceeds $2 billion per year.
b. The ED practitioner must reach a specific diagnosis
before discharging a patient with syncope.
c. Syncope is common in young and elderly patients.
d. ECGs can help risk stratify patients with syncope.
11. Questioning witnesses is a high-yield way to reveal

duration of unconsciousness, events just prior to the
spell, and duration of confusion following the spell.
a. True
b. False
A brief, transient loss of consciousness plus generalized weakness and loss of muscular tone characterize:
a. seizures.
b. syncope.
c. vertigo.
d. drop attacks.
12. A finding of orthostatic hypotension:

a. is generally defined as a decline of 20 mmHg or
greater in systolic blood pressure on standing.
b. rules out life-threatening causes of syncope.
c. is present in less than 5% of patients over 70 years.
d. all of the above.
Unconsciousness lasting more than five minutes, a

slow return to full alertness, and disorientation or an
aura prior to the event suggest syncope, not seizure.
a. True
b. False
13. A chest x-ray should be ordered in all patients with

syncope in order to rule out potentially lethal causes
such as aortic dissection and pulmonary embolism.
a. True
b. False
Which of the following can cause syncope?

a. Bradycardic dysrhythmias
b. Tachycardic dysrhythmias
c. Long QT syndrome
d. Brugada syndrome
e. All of the above
14. Which of the following is/are red flag(s) in the

history of pediatric patients with syncope?
a. Syncope in response to loud noise or stress
b. Syncope during exercise
c. Syncope while supine
d. A history of sudden death in a family member less
than 30 years old
e. Any of the above
Which of the following is the most common?

a. Vasodepressor syncope
b. Cardiogenic syncope
c. Neurologic syncope
d. Metabolic/drug-related syncope
6.
19
J Prev Med 1988 Sep-Oct;4(5):282-288. (Review)

100. Sattin RW, Lambert Huber DA, DeVito CA, et al. The incidence of fall
injury events among the elderly in a defined population. Am J
Epidemiol 1990 Jun;131(6):1028-1037. (Population-based surveillance
data)
101. Nelson RC, Amin MA. Falls in the elderly. Emerg Med Clin North Am
1990 May;8(2):309-324. (Review)
102.* Kapoor W, Snustad D, Peterson J, et al. Syncope in the elderly. Am J
Med 1986 Mar;80(3):419-428. (Prospective; 400 patients)
103. Simpson CS, Klein GJ, Brennan FJ, et al. Impact of a mandatory
physician reporting system for cardiac patients potentially unfit to
drive. Can J Cardiol 2000 Oct;16(10):1257-1263. (Retrospective,
epidemiologic; 994 patients)
104. Strickberger SA, Cantillon CO, Friedman PL. When should patients
with lethal ventricular arrhythmia resume driving? An analysis of state
regulations and physician practices. Ann Intern Med 1991 Oct
1;115(7):560-563. (Survey)
105. Akiyama T, Powell JL, Mitchell LB, et al; Antiarrhythmics versus
Implantable Defibrillators Investigators. Resumption of driving after
life-threatening ventricular tachyarrhythmia. N Engl J Med 2001 Aug
9;345(6):391-397. (Prospective, randomized, controlled trial; 909
patients)
106. Maas R, Ventura R, Kretzschmar C, et al. Syncope, driving recommendations, and clinical reality: survey of patients. BMJ 2003 Jan
4;326(7379):21. (Prospective; 104 patients)
107. Epstein AE, Miles WM, Benditt DG, et al. Personal and public safety
issues related to arrhythmias that may affect consciousness:
implications for regulation and physician recommendations. A
medical/scientific statement from the American Heart Association and
the North American Society of Pacing and Electrophysiology.
Circulation 1996 Sep 1;94(5):1147-1166. (Consensus statement)
108. Hauer KE. Discovering the cause of syncope. A guide to the focused
evaluation. Postgrad Med 2003 Jan;113(1):31-38, 95; quiz 2. (Review)
Physician CME Information
15. An ECG:
a. can identify extremely dangerous and potentially
lethal causes of syncope.
b. is easy, inexpensive, and can facilitate rapid
treatment of life-threatening problems.
c. can be used to risk stratify patients with syncope.
d. all of the above.
This CME enduring material is sponsored by Mount Sinai School of Medicine and
has been planned and implemented in accordance with the Essentials and
Standards of the Accreditation Council for Continuing Medical Education. Credit
may be obtained by reading each issue and completing the printed post-tests
administered in December and June or online single-issue post-tests
administered at www.empractice.net.
Target Audience: This enduring material is designed for emergency medicine
physicians.
16. Which of the following patients may be safely

discharged from the ED for outpatient follow-up?
a. A patient with a history of congestive heart failure
or ventricular dysrhythmias
b. A patient with chest pain or other symptoms
compatible with acute coronary syndrome
c. A patient younger than 40 with an isolated
syncopal event and normal physical findings, a
normal ECG, and no evidence of heart disease
d. A patient with ECG findings of dysrhythmia,
prolonged QT interval, or bundle branch block
Needs Assessment: The need for this educational activity was determined by a
survey of medical staff, including the editorial board of this publication; review
of morbidity and mortality data from the CDC, AHA, NCHS, and ACEP; and
evaluation of prior activities for emergency physicians.
Date of Original Release: This issue of Emergency Medicine Practice was published
January 1, 2004. This activity is eligible for CME credit through January 1,
2007. The latest review of this material was December 5, 2003.
Discussion of Investigational Information: As part of the newsletter, faculty may
be presenting investigational information about pharmaceutical products that
is outside Food and Drug Administration approved labeling. Information
presented as part of this activity is intended solely as continuing medical
education and is not intended to promote off-label use of any pharmaceutical
product. Disclosure of Off-Label Usage: This issue of Emergency Medicine Practice
discusses no off-label use of any pharmaceutical product.
Faculty Disclosure: In compliance with all ACCME Essentials, Standards, and
Guidelines, all faculty for this CME activity were asked to complete a full
disclosure statement. The information received is as follows: Dr. Marill, Dr. Kosiak,
Dr. Decker, Dr. Pigott, and Dr. Shah report no significant financial interest or
other relationship with the manufacturer(s) of any commercial product(s)
discussed in this educational presentation.
Class Of Evidence Definitions

Each action in the clinical pathways section of Emergency Medicine Practice
receives an alpha-numerical score based on the following definitions.
Class I
Always acceptable, safe
Definitely useful
Proven in both efficacy and
effectiveness
Level of Evidence:
One or more large prospective
studies are present (with
rare exceptions)
High-quality meta-analyses
Study results consistently
positive and compelling
Class II
Safe, acceptable
Probably useful
Level of Evidence:
Generally higher levels
of evidence
Non-randomized or retrospective studies: historic, cohort, or
case-control studies
Less robust RCTs
Results consistently positive
Class III
May be acceptable
Possibly useful
Considered optional or
alternative treatments
Level of Evidence:
Generally lower or intermediate
levels of evidence
Case series, animal studies,

consensus panels
Occasionally positive results
Accreditation: Mount Sinai School of Medicine is accredited by the Accreditation

Council for Continuing Medical Education to sponsor continuing medical
education for physicians.
Indeterminate
Continuing area of research
No recommendations until
further research
Credit Designation: Mount Sinai School of Medicine designates this educational

activity for up to 4 hours of Category 1 credit toward the AMA Physicians
Recognition Award. Each physician should claim only those hours of credit
actually spent in the educational activity. Emergency Medicine Practice is approved
by the American College of Emergency Physicians for 48 hours of ACEP Category
1 credit (per annual subscription). Emergency Medicine Practice has been reviewed
and is acceptable for up to 48 Prescribed credit hours by the American Academy
of Family Physicians. Emergency Medicine Practice has been approved for 48
Category 2-B credit hours by the American Osteopathic Association.
Level of Evidence:
Evidence not available
Higher studies in progress
Results inconsistent,
contradictory
Results not compelling
Earning Credit: Two Convenient Methods
Significantly modified from: The

Emergency Cardiovascular Care
Committees of the American Heart
Association and representatives
from the resuscitation councils of
ILCOR: How to Develop EvidenceBased Guidelines for Emergency
Cardiac Care: Quality of Evidence
and Classes of Recommendations;
also: Anonymous. Guidelines for
cardiopulmonary resuscitation and
emergency cardiac care. Emergency
Cardiac Care Committee and
Subcommittees, American Heart
Association. Part IX. Ensuring
effectiveness of community-wide
emergency cardiac care. JAMA
1992;268(16):2289-2295.
Print Subscription Semester Program: Paid subscribers with current and

valid licenses in the United States who read all CME articles during each
Emergency Medicine Practice six-month testing period, complete the posttest and the CME Evaluation Form distributed with the December and June
issues, and return it according to the published instructions are eligible for
up to 4 hours of Category 1 credit toward the AMA Physicians Recognition
Award (PRA) for each issue. You must complete both the post-test and CME
Evaluation Form to receive credit. Results will be kept confidential. CME
certificates will be delivered to each participant scoring higher than 70%.
Online Single-Issue Program: Paid subscribers with current and valid
licenses in the United States who read this Emergency Medicine Practice CME
article and complete the online post-test and CME Evaluation Form at
www.empractice.net are eligible for up to 4 hours of Category 1 credit
toward the AMA Physicians Recognition Award (PRA). You must complete
both the post-test and CME Evaluation Form to receive credit. Results will
be kept confidential. CME certificates may be printed directly from the Web
site to each participant scoring higher than 70%.
Emergency Medicine Practice is not affiliated with any pharmaceutical firm or medical device manufacturer.
President and CEO: Robert Williford. Publisher: Heidi Frost. Research Editors: Ben Abella, MD, University of Chicago; Richard Kwun, MD, Mount Sinai School of Medicine.
Direct all editorial or subscription-related questions to EB Practice, LLC: 1-800-249-5770 Fax: 1-770-500-1316 Non-U.S. subscribers, call: 1-678-366-7933
EB Practice, LLC 305 Windlake Court Alpharetta, GA 30022
E-mail: emp@empractice.net Web Site: http://www.empractice.net
Emergency Medicine Practice (ISSN 1524-1971) is published monthly (12 times per year) by EB Practice, LLC, 305 Windlake Court, Alpharetta, GA 30022. Opinions expressed are not necessarily
those of this publication. Mention of products or services does not constitute endorsement. This publication is intended as a general guide and is intended to supplement, rather than
substitute, professional judgment. It covers a highly technical and complex subject and should not be used for making specific medical decisions. The materials contained herein are not
intended to establish policy, procedure, or standard of care. Emergency Medicine Practice is a trademark of EB Practice, LLC. Copyright 2004 EB Practice, LLC. All rights reserved. No part of this
publication may be reproduced in any format without written consent of EB Practice, LLC. Subscription price: $299, U.S. funds. (Call for international shipping prices.)
20

Emp Syncope

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Emp Syncope

Uploaded by

Copyright:

Available Formats

EMERGENCY MEDICINE

YNCOPE is a common and challenging symptom that brings patients to

Sciences Center School of

Medicine, Childrens Medical

Donald J. Kosiak, Jr., MD

Date of original release: January 1, 2004.

prolonged confusion. When defined broadly, syncope may

evaluation. Also, the cause can be multifactorial, which

Critical Appraisal Of The Literature

Table 1. Etiology Of Syncope.

Emergency Medicine Practice

www.empractice.net January 2004

Congenital long QT syndrome refers to a collection of

Dysrhythmias are responsible for many episodes of

The Rare But Deadly Dysrhythmias

January 2004 www.empractice.net

Emergency Medicine Practice

Dysrhythmic Causes Of Cardiac Syncope

Obstructive Causes Of Cardiac Syncope

Generalized seizures include atonic seizures, where there is

Like the other cardiac causes of syncope, this is also a large

Vasodepressor syncope (also termed neurocardiogenic,

The critical substrates for brain metabolism include glucose

Drugs and poisons can cause or exacerbate all of the

Drug-Related Syncope And Poisoning

Neurologic conditions rarely cause, but often mimic,

Emergency Medicine Practice

www.empractice.net January 2004

Obstructive Causes Of Cardiac Syncope

Dysrhythmic Causes Of Cardiac Syncope

January 2004 www.empractice.net

Emergency Medicine Practice

between the atria and ventricles, allowing rapid conduction

effectiveness of an aerosolized fentanyl derivative to

syncope. Medical conditions may cause occult

ing valvular thrombosis, structural failure, paravalvular

Vascular Causes Of Cardiac Syncope

Cost- And Time-Effective Strategies For Patients With Syncope

3. Use observation units.

Emergency Medicine Practice

www.empractice.net January 2004

from peripheral vertigo generally do not have a feeling of

Table 2. Diagnostic Questions To Determine

Points (if yes)

At times do you wake with a cut tongue

Syncope Due To Toxins And Poisons

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

January 2004 www.empractice.net

Emergency Medicine Practice

Effective Treatment.) Another study examined just the

Emergency Department Evaluation

Just as the list of the potential causes of syncope is quite

Infection can be the primary cause of a syncopal episode or

Table 3. Important Historical Facts.

Patients presenting to the ED with syncope should be

Questions about just prior to the event

Questions about the onset of the attack

Questions about the attack (obtain information

Questions about the period following the attack

Emergency Medicine Practice

Questions about past medical history / family history

www.empractice.net January 2004

significantly less common in black than white high school

The Drug Did It!