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Post Graduate Medicine
January, 2003
SECTION: CME CREDIT ARTICLE; Vol. 113, No. 1; Pg. 31
LENGTH: 4696 words
HEADLINE: Discovering the cause of syncope
BYLINE: Karen E. Hauer, MD; Karen E. Hauer, MDDr Hauer is assistant clinical
professor of medicine and director of internal medicine clerkships, University
of California, San Francisco, School of Medicine. Correspondence: Karen E.
Hauer, MD, University of California, San Francisco, School of Medicine, Division
of General Internal Medicine, 400 Parnassus Ave, Box 0320, San Francisco, CA
94143. E-mail: [email protected].
HIGHLIGHT:
A guide to the focused evaluation
BODY:
PREVIEW Syncope has many causes. Although the most common ones are generally
benign and do not require extensive evaluation, cardiac syncope has high rates
of recurrence and death. In this article, Dr Hauer describes how physical
examination and electrocardiographic findings can guide further evaluation to
provide the largest diagnostic yield at the lowest cost.
Syncope is a common problem, accounting for 3% of emergency department
visits.1 (Reference) Evaluation of syncope can be challenging for many reasons.
First, syncope is not a diagnosis; rather, it is a symptom with many possible
causes. Common causes, such as the vasovagal faint, are not serious. However,
other causes are deadly and require further investigation. In addition, the
history of a syncopal event often is unclear because the patient has amnesia and
there were no witnesses to the event. As many as 45% of cases elude diagnosis
after a standard workup, and many tests commonly used in syncope evaluation are
costly and have a low diagnostic yield.2,3 (Reference) Syncope is caused by
transient loss of blood flow to the areas of the brain necessary for
consciousness, the brainstem reticular activating system and the bilateral
cerebral cortices. Cerebral perfusion can be diminished because of decreased
cardiac output, loss of vascular tone, or cerebrovascular disease. Differential
diagnostic considerations include other disorders that can cause loss of
consciousness, such as seizure, narcolepsy, and metabolic or drug-induced
encephalopathy. Drop attacks are characterized by a sudden loss of postural tone
without loss of consciousness. Sudden cardiac death is similar to syncope but
requires intervention (ie, electrical or chemical cardioversion for
tachyarrhythmias or atropine sulfate or a pacemaker for bradyarrhythmias) to
restore normal mental status and cardiac rhythm.
Causes
The chief causes of syncope and the approximate percentage of patients with each
diagnosis are shown in table 1.
Cardiac disease Historical clues that suggest a cardiac origin of syncope
include associated palpitations, sudden syncope without preceding symptoms, and
known organic heart disease. Syncope due to aortic stenosis or hypertrophic
cardiomyopathy is often preceded by exertion, when cardiac output cannot meet
increased demand. Palpitations may signal supraventricular or ventricular
tachyarrhythmias, and patients with bradyarrhythmias or conduction block may
have weakness, dizziness, or symptoms of associated tachyarrhythmias.
Physical examination may show left or right ventricular hypertrophy or
dilation, murmurs (ie, of aortic stenosis, hypertrophic subaortic stenosis, or
tricuspid regurgitation), gallops, irregular cardiac rate or rhythm, or a loud
S2 suggestive of pulmonary hypertension. Some disorders that cause cardiac
outflow obstruction also predispose patients to arrhythmogenic syncope. For
instance, genetic hypertrophic cardiomyopathy is associated with ventricular
arrhythmias and sudden cardiac death, and infiltrative cardiomyopathy due to
sarcoidosis or amyloidosis can cause conduction system disease.
Neurologic disease Although seizure is not a true cause of syncope, it is often
a differential diagnostic consideration. Historical features suggestive of
seizure include tonic-clonic movements, incontinence, postictal mental status
changes, loss of consciousness for longer than 5 minutes, and lateral tongue
biting.4 (Reference) A postictal state is the most helpful historical feature
for diagnosis of seizure. Because tonic-clonic activity and incontinence also
can be caused by cardiac syncope, these features alone do not confirm a
diagnosis of seizure. Cerebrovascular disease is an uncommon cause of syncope.
Vertebrobasilar insufficiency causing syncope generally has other associated
symptoms of posterior circulation insufficiency, such as vertigo, diplopia,
ataxia, and dysarthria. Carotid artery disease does not cause loss of
consciousness unless both carotid arteries are involved.
Reflex-mediated syncope Neurocardiogenic syncope results from an exaggerated
reflex response, usually to upright posture. Normally, decreased venous return
stimulates increased cardiac contractility and peripheral vasoconstriction to
maintain blood pressure. In some patients, this physiologic response stimulates
cardiac mechanoreceptors in the left ventricular wall, leading to a complex
cascade of sympathetic inhibition and parasympathetic stimulation (figure 1).
Vasovagal syncope, the most common type of syncope, results from this
mechanoreceptor reflex and is usually triggered by pain, strong emotion,
prolonged standing, or stress. ''Situational'' syncope is similar to vasovagal
syncope but is stimulated by micturition, defecation, cough, or deglutition.
Carotid sinus hypersensitivity can cause bradycardia, hypotension, or both.
Abnormal carotid hypersensitivity is common in older men with other
cardiovascular disease, although not all of them experience syncope.
Orthostatic hypotension is defined as a fall in systolic blood pressure of
greater than 20 mm Hg upon assuming upright posture. This condition results from
volume depletion, use of certain medications (particularly
antihypertensives, vasodilators, and negative chronotropes), primary autonomic
insufficiency, or secondary autonomic insufficiency due to diabetes mellitus,
amyloidosis, or alcohol abuse. Orthostatic intolerance is more common in the
elderly than in the young.
Psychiatric disease Psychiatric disease as a cause of syncope is always a
diagnosis of exclusion. Dizziness and syncope may be symptoms of a variety of
psychiatric diseases, such as anxiety, depression, somatization, panic disorder,
and substance abuse. Patients with unexplained syncope and psychiatric diagnoses
are more likely to have multiple somatic complaints, to report frequent syncope,
and to be younger than those without psychiatric diagnoses.5 (Reference)
Diagnostic evaluation
A diagnostic algorithm for syncope is shown in figure 2. A carefully taken
history and thorough physical examination yield a diagnosis in 45% of patients
with syncope.6 (Reference) Helpful information regarding the setting includes
any precipitant of reflex-mediated syncope, such as posture change, coughing,
swallowing, head turning, defecation, pain, strong emotion, fear, or prolonged
standing. Associated symptoms of reflex-mediated syncope include nausea, pallor,
warmth, diaphoresis, confusion, and palpitations. Patients rapidly recover clear
mental status after the event, although bradycardia may persist for minutes to
hours. The speed of recovery is helpful in distinguishing syncope from seizure,
which typically has a postictal state.
Palpitations or sudden syncope suggests underlying arrhythmia (although
nonsudden syncope does not exclude arrhythmia). A personal or family history of
cardiac disease (eg, hypertrophic cardiomyopathy), sudden cardiac death (due,
for example, to hypertrophic cardiomyopathy, long QT syndrome), or neurologic
disease (eg, seizure, cerebrovascular disease) is another clue.
Antiarrhythmic agents and tricyclic antidepressants are potentially
proarrhythmic, meaning that normally nontoxic drug levels can provoke
arrhythmias, especially in the presence of underlying congestive heart failure
(CHF). Oral hypoglycemic agents can cause hypoglycemia-induced loss of
consciousness. Beta blockers and calcium channel blockers can cause bradycardia
and hypotension, both of which can precipitate syncope.
Physical examination may demonstrate abnormalities in heart rate or blood
pressure, including orthostatic changes. Cardiovascular examination may reveal
evidence of chamber hypertrophy, pulmonary hypertension, murmurs, gallops, or
CHF. In the absence of carotid bruits, cerebrovascular disease, transient
ischemic attack, or stroke, carotid sinus massage for up to 5 seconds is useful
to elicit carotid sinus hypersensitivity. Such hypersensitivity is defined as a
3-second pause in rhythm, a 30-mm Hg symptomatic drop in systolic blood
pressure, or a 50-mm Hg asymptomatic drop.7 (Reference)
Electrocardiographic monitoring during the maneuver is essential to observe and
characterize changes in heart rate or rhythm. A thorough neurologic examination
is crucial to document any focal findings that would prompt further neurologic
testing.
The 12-lead electrocardiogram (ECG) adds only a 5% diagnostic yield to the
history and physical examination.6 (Reference) An ECG is nonetheless routinely
recommended because it can reveal clues to underlying cardiac disease, including
substrate for life-threatening ventricular arrhythmias (ie, Q waves, ventricular
hypertrophy, or long QT interval) or bradycardia (ie, baseline bradycardia or
type II second- or third-degree heart block). Premature atrial and ventricular
contractions are nonspecific and common. Abnormalities identified on history
taking, physical examination, and electrocardiography should selectively guide
further testing.
Cardiac evaluation Cardiac testing is indicated for patients in whom cardiac
disease is suspected on the basis of symptoms, medical history, physical
examination, or electrocardiographic findings.
Tests to rule out myocardial infarction generally should be limited to
patients with anginal symptoms or electrocardiographic evidence of cardiac
ischemia or infarction.8 (Reference)
Telemetry may be indicated for suspected arrhythmogenic syncope. In a
prospective study of 2,240 medical and cardiac patients admitted to a telemetry
unit,9 (Reference) the yield of telemetry was quite low, with less than 1% of
patients requiring transfer to the intensive care unit for management of an
arrhythmia. Telemetry can be helpful to rule out arrhythmogenic syncope when
symptoms occur with concurrent normal telemetry.
The diagnostic yield of echocardiography is about 5% to 10% in unselected
syncope patients.6 (Reference) Echocardiography is indicated when structural
heart disease is suspected. Evidence of myocardial infarction or CHF indicates a
possible arrhythmia focus. Echocardiography should always be performed before a
stress test if left ventricular outflow obstruction due to aortic stenosis or
hypertrophic cardiomyopathy is suspected; these conditions are
contraindications to stress testing.
Exercise stress testing is indicated in the evaluation of exertional syncope
after left ventricular outflow obstruction has been excluded by examination or
echocardiography. Stress testing can rule out cardiac ischemia or
catecholamine-mediated ventricular tachycardia. In the absence of a history of
exertional syncope, the diagnostic yield of stress testing in unselected syncope
patients is only 1%.6 (Reference)
Additional evaluation for arrhythmia can be performed with more prolonged or
invasive testing. The ambulatory Holter monitor is worn for 24 to 48 hours while
the patient performs usual daily activities. The brief duration of monitoring is
the main limitation except in patients with daily symptoms. Patients must be
able to keep an accurate diary of symptoms so changes in rhythm can be
correlated with symptoms.
The continuous-loop event recorder is a convenient and cost-effective device
that monitors cardiac arrhythmias over several weeks, overcoming the main
limitation of the Holter monitor. Diagnostic yield ranges from 6% to 31%.10
(Reference) Electrodes placed on the chest wall transmit data to a small
monitoring device worn on the belt or wrist. Data are stored and discarded
continuously. The patient must be able to activate the device before or after
symptoms occur, prompting it to save data for about 1 minute prior to and
several minutes after activation. Pacemaker-sized surgically implanted event
monitors can be helpful in evaluating syncope that occurs less than once a
month.11 (Reference)
The signal-averaged ECG filters multiple QRS complexes to uncover late
potentials arising from abnormal myocardium, in which reentry and ventricular
tachycardia may arise. A normal signal-averaged ECG predicts a low risk of
subsequent ventricular tachycardia, particularly when the ejection fraction is
normal. However, the test is less accurate than electrophysiologic studies in
predicting ventricular arrhythmias and cannot obviate the need for further
cardiac evaluation regardless of the result among patients with known coronary
artery disease or left ventricular dysfunction.
Electrophysiologic testing is the ''gold standard'' for diagnosis of
arrhythmias. It is recommended for patients with syncope and a history
suggestive of arrhythmia or with idiopathic syncope and known underlying heart
disease. The diagnostic yield is low in patients without underlying cardiac
disease.
Reflex-mediated syncope Tilt table testing demonstrates neurocardiogenic syncope
that is suspected but not confirmed by history taking and physical examination.
In the passive tilt table test, the patient lies on a board in the supine
position and then the table is tilted, usually to an angle of 60 degrees for 40
minutes.12 (Reference) A positive response, defined as a symptomatic drop in
heart rate or blood pressure, occurs after an average of 24 minutes. If the
response is negative, injection of isoproterenol hydrochloride (Isuprel) may
increase the diagnostic yield by augmenting cardiac contractility and
stimulating the neurocardiogenic cascade. Typically, isoproterenol is given at a
rate of 1 g/min while the patient is tilted to 60 degrees, and the dose is
adjusted upward until a positive response is achieved. Among patients with
idiopathic syncope, 49% have a positive response to the passive tilt test and
66% have a positive response after injection of isoproterenol. The specificity
of the passive tilt test for neurocardiogenic syncope is about 90%. Specificity
is lower with isoproterenol.12,13 (Reference)
The accuracy of tilt table testing is difficult to determine. The test is
not performed unless findings from history taking and physical examination are
ambiguous, thus leaving no ''gold standard'' with which to compare the results.
The protocol for the tilt table test (ie, angle, duration, and use of
isoproterenol) is not standardized, and the reproducibility is only 71% to 87%
owing to the many factors that influence autonomic function.
Treatment options for recurrent neurocardiogenic syncope include lifestyle
modifications, such as avoiding triggers and liberalizing salt intake to enhance
intravascular volume. Beta blockers, anticholinergics, the antiarrhythmic
disopyramide (Norpace), and the alpha agonist midodrine hydrochloride
(ProAmatine) blunt the neurocardiogenic reflex, and the corticosteroid
fludrocortisone (Florinef) acetate increases volume. Fluoxetine hydrochloride
(Prozac) also may be effective. Tilt table testing can be repeated to document
therapeutic efficacy, although as many as 30% of patients with a positive
response have a negative response to the second test regardless of therapy.
Cardiac pacing is helpful for cardioinhibitory (bradycardic) syncope. Dual
chamber pacing helps avoid vasodilation resulting from
atrioventricular dissociation.
Neurologic disease All syncope patients with focal neurologic signs or symptoms
should undergo neuroimaging. Patients without focal neurologic findings should
not routinely undergo neuroimaging. Similarly, electroencephalography has a low
diagnostic yield and is not indicated in the absence of findings suggestive of
seizure. It may be helpful in evaluating suspected seizure, although the limited
sensitivity and specificity must be recognized; normal findings in a patient
with a convincing seizure history do not rule out seizure, and abnormal findings
alone do not necessarily confirm the presence of a seizure disorder.
Psychiatric disease Because half of all psychiatric diagnoses may go
unrecognized during routine syncope evaluation,5 (Reference) physicians need a
high index of suspicion for psychiatric disease among syncope patients in whom
medical evaluation was nondiagnostic. Anxiety or panic disorder with
hyperventilation can be diagnosed by instructing the patient to hyperventilate
in the office to elicit syncope or presyncopal symptoms. Formal psychiatric and
substance abuse evaluation may be indicated when the cause of syncope has not
been determined.
Idiopathic syncope Depending on the aggressiveness of the workup, as many as 45%
of patients may be given the diagnosis of idiopathic syncope after routine
evaluation.6,14,15 (Reference) Although patients with idiopathic syncope have a
good prognosis, equivalent to that of age-matched controls, recurrent syncope
can have important lifestyle implications for driving or work. A diagnostic
approach to unexplained syncope is included in figure 2.
Hospitalization and prognosis
The decision to hospitalize a patient with syncope depends on the prognosis and
-- most important -- the physician's ability to identify patients at high risk
for lethal arrhythmias that could be treated during hospitalization. Prognosis
depends on whether the origin of syncope is cardiac or noncardiac. For example,
in a prospective study of 433 syncope patients,15 (Reference) the 1-year
mortality rate after cardiac syncope was about 25% and the 1-year risk of sudden
cardiac death 14%. In contrast, the 1-year mortality rate after noncardiac or
idiopathic syncope was 6% to 8% and the 1-year risk of sudden cardiac death only
3%. Of note, cardiac syncope carries a lower mortality rate today than in the
past because electrophysiologic testing is now more commonly used.
Physicians in the emergency department may not know whether syncope is
cardiac or noncardiac in origin. Four predictors of poor outcome among syncope
patients on initial presentation are an abnormal ECG (not nonspecific ST or T
wave changes or sinus tachycardia), prior ventricular arrhythmia (defined as at
least 10 premature ventricular contractions an hour or repetitive [>2] or
multifocal premature ventricular contractions), a history of CHF, and age
greater than 45 years.16 (Reference) The risk of arrhythmia or death at 1 year
ranges from 5% for patients with no risk factors, to 16% with one risk factor,
to more than 60% with three or four risk factors. My colleagues and I recommend
that patients with even one risk factor and a history suggestive of cardiac
syncope undergo cardiac evaluation.
The guideline for hospitalization after syncope from the American College of
Physicians (table 2) targets patients who would benefit from inpatient
diagnostic evaluation or from therapies that could improve outcome over several
days of hospitalization.
Elderly patients
Syncope from any cause in an elderly patient portends a poor prognosis. In a
study of syncope in elderly (age, >60) and young patients,14 (Reference) all
patients with cardiac syncope had 2-year mortality rates of 32% to 38%; in
patients with noncardiac syncope, elderly patients had a much higher mortality
rate (22%) than younger patients (5%). The high mortality rate among the elderly
may have been due to comorbidities and suggests that patients in this age-group
should receive close follow-up care regardless of syncope origin.
As with other geriatric syndromes, syncope in the elderly is often
multifaceted, frustrating physicians who seek a unifying diagnosis (table 3). A
reasonable management strategy for elderly syncope patients with multiple risk
factors is to correct these factors before more invasive testing is done.
Cardiac disease should be ruled out on the basis of clues provided during
history taking, physical examination, and electrocardiography or by selective
further testing. If not contraindicated by carotid bruit, cerebrovascular
disease, or a history of transient ischemic attack or stroke, carotid sinus
massage is helpful in diagnosis of carotid sinus hypersensitivity.
Indications for referral or consultation
Cardiologic referral is advised for syncope patients with a documented or
suspected cardiac origin on the basis of arrhythmia, underlying cardiac disease
or, possibly, advanced age alone. A cardiologist typically considers invasive
testing, including an electrophysiologic study. A neurologist should evaluate
syncope patients with abnormal findings on neurologic examination or documented
seizures. For patients with recurrent syncope and suspected psychiatric disease,
psychiatric consultation is helpful for both diagnostic evaluation and
psychiatric management.
Recommendations for driving
Physicians often are asked to make recommendations to their patients about
driving after a syncopal event. Laws regarding the use of private motor vehicles
are made at the state level. Although physicians are obligated to know the laws
of their own state regarding the reporting of syncopal events to the motor
vehicles department and driving by patients after syncope, physicians'
recommendations and awareness of the law are highly variable.17,18 (Reference)
The American Heart Association and the North American Society of Pacing and
Electrophysiology19 (Reference) issued a statement in 1996 pertaining to driving
after syncope, with specific recommendations based on arrhythmia type and
severity (table 4).
Conclusion
Syncope is a symptom with many possible causes, including cardiac, neurologic,
reflex-mediated, and psychiatric disorders. All patients with syncope should
provide a thorough history and undergo physical examination and
electrocardiographic testing. Information obtained during this initial
evaluation guides further testing. One-year mortality and sudden cardiac death
rates are highest after syncope caused by underlying cardiac disease. Patients
with other origins of syncope or with idiopathic syncope generally have a good
prognosis. PGM
The author thanks Nora Goldschlager, MD, for her critique of the manuscript.
The author discloses no financial interests in this article.
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;73(1):15-23
2. Calkins H, Byrne M, el-Atassi R, et al. The economic burden of unrecognized
vasodepressor syncope. Am J Med 1993;95(5):473-9
3. Junaid A, Dubinsky IL. Establishing an approach to syncope in the emergency
department. J Emerg Med 1997;15(5):593-9
4. Benbadis SR, Wolgamuth BR, Goren H, et al. Value of tongue biting in the
diagnosis of seizures. Arch Intern Med 1995;155(21):2346-9
5. Kapoor WN, Fortunato M, Hanusa BH, et al. Psychiatric illnesses in patients
with syncope. Am J Med 1995;99(5):505-12
6. Linzer M, Yang EH, Estes NA III, 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;126(12):989-96
7. Manolis AS, Linzer M, Salem D, et al. Syncope: current diagnostic evaluation
and management. Ann Intern Med 1990;112(11):850-63
8. 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;7(4):379-86
9. Estrada CA, Rosman HS, Prasad NK, et al. Role of telemetry monitoring in the
nonintensive care unit. Am J Cardiol 1995;76(12):960-5
10. Zimetbaum PJ, Josephson ME. The evolving role of ambulatory arrhythmia
monitoring in general clinical practice. Ann Intern Med 1999;130(10):848-56
11. Krahn AD, Klein GJ, Yee R, et al. Use of an extended monitoring strategy in
patients with problematic syncope. Reveal Investigators. Circulation
1999;99(3):406-10
12. Kapoor WN, Smith MA, Miller NL. Upright tilt testing in evaluating syncope:
a comprehensive literature review. Am J Med 1994;97(1):78-88
13. Benditt DG, Ferguson DW, Grubb BP, et al. Tilt table testing for assessing
syncope. American College of Cardiology. J Am Coll Cardiol 1996;28(1):263-75
14. Kapoor W, Snustad D, Peterson J, et al. Syncope in the elderly. Am J Med
1986;80(3):419-28
15. Kapoor WN. Evaluation and outcome of patients with syncope. Medicine
1990;69(3):160-75
16. Martin TP, Hanusa BH, Kapoor WN. Risk stratification of patients with
syncope. Ann Emerg Med 1997;29(4):459-66
17. Linzer M, Yang EH, Estes NA III, et al. Diagnosing syncope. Part 2:
Unexplained syncope. Clinical Efficacy Assessment Project of the American
College of Physicians. Ann Intern Med 1997;127(1):76-86
18. Lurie KG, Iskos D, Sakaguchi S, et al. Resumption of motor vehicle operation
in vasovagal fainters. Am J Cardiol 1999;83(4):604-6
19. 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;115(7):560-3
20. 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;94(5):1147-66
Table 1. Causes of syncope
Cause Prevalence
Cardiac
Arrhythmia 14%
Mechanical* 4%
Neurologic 10%
Neurally mediated
Vasovagal 18%
''Situational'' 5%
Orthostatic 8%
Psychiatric 2%
Idiopathic 34%
*Obstruction to cardiac outflow, decreased ejection fraction, and decreased
ventricular filling (ie, pulmonary embolus, pulmonary hypertension, and cardiac
tamponade).
Adapted from Linzer et al.6 (Reference)
Table 2. American College of Physicians criteria for hospitalization after
syncope
Definitely hospitalize patients who meet any of the following criteria:
-- A history of chest pain
-- A past history of coronary artery disease, congestive heart failure, or
ventricular arrhythmia
-- Physical examination findings of congestive heart failure, valvular disease,
or focal neurologic deficit
-- An electrocardiogram showing ischemia or infarction, arrhythmia, or bundle
branch block
Strongly consider hospitalizing patients who meet any of the following criteria:
-- A history of exertional syncope (in the absence of physical examination
evidence of aortic stenosis or other left ventricular outflow obstruction),
frequent syncope, or age >70 yr
-- Physical examination findings of tachycardia, orthostatic changes, or injury
-- Suspected cardiac disease
Adapted from Linzer et al.17 (Reference)
Table 3. Common risk factors for syncope in the elderly
Susceptibility to situational syncope
Polypharmacy and adverse drug effects on heart rate, intravascular volume, and
vascular tone (with use of beta blockers, calcium channel blockers,
antiarrhythmics, diuretics, antidepressants)
Serious cardiac and neurologic disease, other comorbidities, or atypical
presentation of disease
Decreased physiologic reserve
Table 4. Guidelines for driving after syncope or arrhythmia
Patient with ventricular tachycardia or fibrillation treated with medical
therapy or implantable cardiac defibrillator
-- Risk of recurrent arrhythmia is greatest in first 6 mo, up to 10% at 1 yr
-- Recommendation: Patient may resume driving after arrhythmia-free for 6 mo
Patient with bradycardia and syncope
-- Recommendation: Patient may resume driving 1 wk after successful pacemaker
insertion
Patient with neurocardiogenic syncope
Mild (presyncope, clear warning, and precipitant)
-- Recommendation: Patient may resume driving immediately
Severe (frequent with no warning or precipitant)
-- Recommendation: Patient should not resume driving until after institution of
therapy and a waiting period of unspecified duration
Adapted from Epstein et al.20 (Reference)
January, 2003
SECTION: CME CREDIT ARTICLE; Vol. 113, No. 1; Pg. 31
LENGTH: 4696 words
HEADLINE: Discovering the cause of syncope
BYLINE: Karen E. Hauer, MD; Karen E. Hauer, MDDr Hauer is assistant clinical
professor of medicine and director of internal medicine clerkships, University
of California, San Francisco, School of Medicine. Correspondence: Karen E.
Hauer, MD, University of California, San Francisco, School of Medicine, Division
of General Internal Medicine, 400 Parnassus Ave, Box 0320, San Francisco, CA
94143. E-mail: [email protected].
HIGHLIGHT:
A guide to the focused evaluation
BODY:
PREVIEW Syncope has many causes. Although the most common ones are generally
benign and do not require extensive evaluation, cardiac syncope has high rates
of recurrence and death. In this article, Dr Hauer describes how physical
examination and electrocardiographic findings can guide further evaluation to
provide the largest diagnostic yield at the lowest cost.
Syncope is a common problem, accounting for 3% of emergency department
visits.1 (Reference) Evaluation of syncope can be challenging for many reasons.
First, syncope is not a diagnosis; rather, it is a symptom with many possible
causes. Common causes, such as the vasovagal faint, are not serious. However,
other causes are deadly and require further investigation. In addition, the
history of a syncopal event often is unclear because the patient has amnesia and
there were no witnesses to the event. As many as 45% of cases elude diagnosis
after a standard workup, and many tests commonly used in syncope evaluation are
costly and have a low diagnostic yield.2,3 (Reference) Syncope is caused by
transient loss of blood flow to the areas of the brain necessary for
consciousness, the brainstem reticular activating system and the bilateral
cerebral cortices. Cerebral perfusion can be diminished because of decreased
cardiac output, loss of vascular tone, or cerebrovascular disease. Differential
diagnostic considerations include other disorders that can cause loss of
consciousness, such as seizure, narcolepsy, and metabolic or drug-induced
encephalopathy. Drop attacks are characterized by a sudden loss of postural tone
without loss of consciousness. Sudden cardiac death is similar to syncope but
requires intervention (ie, electrical or chemical cardioversion for
tachyarrhythmias or atropine sulfate or a pacemaker for bradyarrhythmias) to
restore normal mental status and cardiac rhythm.
Causes
The chief causes of syncope and the approximate percentage of patients with each
diagnosis are shown in table 1.
Cardiac disease Historical clues that suggest a cardiac origin of syncope
include associated palpitations, sudden syncope without preceding symptoms, and
known organic heart disease. Syncope due to aortic stenosis or hypertrophic
cardiomyopathy is often preceded by exertion, when cardiac output cannot meet
increased demand. Palpitations may signal supraventricular or ventricular
tachyarrhythmias, and patients with bradyarrhythmias or conduction block may
have weakness, dizziness, or symptoms of associated tachyarrhythmias.
Physical examination may show left or right ventricular hypertrophy or
dilation, murmurs (ie, of aortic stenosis, hypertrophic subaortic stenosis, or
tricuspid regurgitation), gallops, irregular cardiac rate or rhythm, or a loud
S2 suggestive of pulmonary hypertension. Some disorders that cause cardiac
outflow obstruction also predispose patients to arrhythmogenic syncope. For
instance, genetic hypertrophic cardiomyopathy is associated with ventricular
arrhythmias and sudden cardiac death, and infiltrative cardiomyopathy due to
sarcoidosis or amyloidosis can cause conduction system disease.
Neurologic disease Although seizure is not a true cause of syncope, it is often
a differential diagnostic consideration. Historical features suggestive of
seizure include tonic-clonic movements, incontinence, postictal mental status
changes, loss of consciousness for longer than 5 minutes, and lateral tongue
biting.4 (Reference) A postictal state is the most helpful historical feature
for diagnosis of seizure. Because tonic-clonic activity and incontinence also
can be caused by cardiac syncope, these features alone do not confirm a
diagnosis of seizure. Cerebrovascular disease is an uncommon cause of syncope.
Vertebrobasilar insufficiency causing syncope generally has other associated
symptoms of posterior circulation insufficiency, such as vertigo, diplopia,
ataxia, and dysarthria. Carotid artery disease does not cause loss of
consciousness unless both carotid arteries are involved.
Reflex-mediated syncope Neurocardiogenic syncope results from an exaggerated
reflex response, usually to upright posture. Normally, decreased venous return
stimulates increased cardiac contractility and peripheral vasoconstriction to
maintain blood pressure. In some patients, this physiologic response stimulates
cardiac mechanoreceptors in the left ventricular wall, leading to a complex
cascade of sympathetic inhibition and parasympathetic stimulation (figure 1).
Vasovagal syncope, the most common type of syncope, results from this
mechanoreceptor reflex and is usually triggered by pain, strong emotion,
prolonged standing, or stress. ''Situational'' syncope is similar to vasovagal
syncope but is stimulated by micturition, defecation, cough, or deglutition.
Carotid sinus hypersensitivity can cause bradycardia, hypotension, or both.
Abnormal carotid hypersensitivity is common in older men with other
cardiovascular disease, although not all of them experience syncope.
Orthostatic hypotension is defined as a fall in systolic blood pressure of
greater than 20 mm Hg upon assuming upright posture. This condition results from
volume depletion, use of certain medications (particularly
antihypertensives, vasodilators, and negative chronotropes), primary autonomic
insufficiency, or secondary autonomic insufficiency due to diabetes mellitus,
amyloidosis, or alcohol abuse. Orthostatic intolerance is more common in the
elderly than in the young.
Psychiatric disease Psychiatric disease as a cause of syncope is always a
diagnosis of exclusion. Dizziness and syncope may be symptoms of a variety of
psychiatric diseases, such as anxiety, depression, somatization, panic disorder,
and substance abuse. Patients with unexplained syncope and psychiatric diagnoses
are more likely to have multiple somatic complaints, to report frequent syncope,
and to be younger than those without psychiatric diagnoses.5 (Reference)
Diagnostic evaluation
A diagnostic algorithm for syncope is shown in figure 2. A carefully taken
history and thorough physical examination yield a diagnosis in 45% of patients
with syncope.6 (Reference) Helpful information regarding the setting includes
any precipitant of reflex-mediated syncope, such as posture change, coughing,
swallowing, head turning, defecation, pain, strong emotion, fear, or prolonged
standing. Associated symptoms of reflex-mediated syncope include nausea, pallor,
warmth, diaphoresis, confusion, and palpitations. Patients rapidly recover clear
mental status after the event, although bradycardia may persist for minutes to
hours. The speed of recovery is helpful in distinguishing syncope from seizure,
which typically has a postictal state.
Palpitations or sudden syncope suggests underlying arrhythmia (although
nonsudden syncope does not exclude arrhythmia). A personal or family history of
cardiac disease (eg, hypertrophic cardiomyopathy), sudden cardiac death (due,
for example, to hypertrophic cardiomyopathy, long QT syndrome), or neurologic
disease (eg, seizure, cerebrovascular disease) is another clue.
Antiarrhythmic agents and tricyclic antidepressants are potentially
proarrhythmic, meaning that normally nontoxic drug levels can provoke
arrhythmias, especially in the presence of underlying congestive heart failure
(CHF). Oral hypoglycemic agents can cause hypoglycemia-induced loss of
consciousness. Beta blockers and calcium channel blockers can cause bradycardia
and hypotension, both of which can precipitate syncope.
Physical examination may demonstrate abnormalities in heart rate or blood
pressure, including orthostatic changes. Cardiovascular examination may reveal
evidence of chamber hypertrophy, pulmonary hypertension, murmurs, gallops, or
CHF. In the absence of carotid bruits, cerebrovascular disease, transient
ischemic attack, or stroke, carotid sinus massage for up to 5 seconds is useful
to elicit carotid sinus hypersensitivity. Such hypersensitivity is defined as a
3-second pause in rhythm, a 30-mm Hg symptomatic drop in systolic blood
pressure, or a 50-mm Hg asymptomatic drop.7 (Reference)
Electrocardiographic monitoring during the maneuver is essential to observe and
characterize changes in heart rate or rhythm. A thorough neurologic examination
is crucial to document any focal findings that would prompt further neurologic
testing.
The 12-lead electrocardiogram (ECG) adds only a 5% diagnostic yield to the
history and physical examination.6 (Reference) An ECG is nonetheless routinely
recommended because it can reveal clues to underlying cardiac disease, including
substrate for life-threatening ventricular arrhythmias (ie, Q waves, ventricular
hypertrophy, or long QT interval) or bradycardia (ie, baseline bradycardia or
type II second- or third-degree heart block). Premature atrial and ventricular
contractions are nonspecific and common. Abnormalities identified on history
taking, physical examination, and electrocardiography should selectively guide
further testing.
Cardiac evaluation Cardiac testing is indicated for patients in whom cardiac
disease is suspected on the basis of symptoms, medical history, physical
examination, or electrocardiographic findings.
Tests to rule out myocardial infarction generally should be limited to
patients with anginal symptoms or electrocardiographic evidence of cardiac
ischemia or infarction.8 (Reference)
Telemetry may be indicated for suspected arrhythmogenic syncope. In a
prospective study of 2,240 medical and cardiac patients admitted to a telemetry
unit,9 (Reference) the yield of telemetry was quite low, with less than 1% of
patients requiring transfer to the intensive care unit for management of an
arrhythmia. Telemetry can be helpful to rule out arrhythmogenic syncope when
symptoms occur with concurrent normal telemetry.
The diagnostic yield of echocardiography is about 5% to 10% in unselected
syncope patients.6 (Reference) Echocardiography is indicated when structural
heart disease is suspected. Evidence of myocardial infarction or CHF indicates a
possible arrhythmia focus. Echocardiography should always be performed before a
stress test if left ventricular outflow obstruction due to aortic stenosis or
hypertrophic cardiomyopathy is suspected; these conditions are
contraindications to stress testing.
Exercise stress testing is indicated in the evaluation of exertional syncope
after left ventricular outflow obstruction has been excluded by examination or
echocardiography. Stress testing can rule out cardiac ischemia or
catecholamine-mediated ventricular tachycardia. In the absence of a history of
exertional syncope, the diagnostic yield of stress testing in unselected syncope
patients is only 1%.6 (Reference)
Additional evaluation for arrhythmia can be performed with more prolonged or
invasive testing. The ambulatory Holter monitor is worn for 24 to 48 hours while
the patient performs usual daily activities. The brief duration of monitoring is
the main limitation except in patients with daily symptoms. Patients must be
able to keep an accurate diary of symptoms so changes in rhythm can be
correlated with symptoms.
The continuous-loop event recorder is a convenient and cost-effective device
that monitors cardiac arrhythmias over several weeks, overcoming the main
limitation of the Holter monitor. Diagnostic yield ranges from 6% to 31%.10
(Reference) Electrodes placed on the chest wall transmit data to a small
monitoring device worn on the belt or wrist. Data are stored and discarded
continuously. The patient must be able to activate the device before or after
symptoms occur, prompting it to save data for about 1 minute prior to and
several minutes after activation. Pacemaker-sized surgically implanted event
monitors can be helpful in evaluating syncope that occurs less than once a
month.11 (Reference)
The signal-averaged ECG filters multiple QRS complexes to uncover late
potentials arising from abnormal myocardium, in which reentry and ventricular
tachycardia may arise. A normal signal-averaged ECG predicts a low risk of
subsequent ventricular tachycardia, particularly when the ejection fraction is
normal. However, the test is less accurate than electrophysiologic studies in
predicting ventricular arrhythmias and cannot obviate the need for further
cardiac evaluation regardless of the result among patients with known coronary
artery disease or left ventricular dysfunction.
Electrophysiologic testing is the ''gold standard'' for diagnosis of
arrhythmias. It is recommended for patients with syncope and a history
suggestive of arrhythmia or with idiopathic syncope and known underlying heart
disease. The diagnostic yield is low in patients without underlying cardiac
disease.
Reflex-mediated syncope Tilt table testing demonstrates neurocardiogenic syncope
that is suspected but not confirmed by history taking and physical examination.
In the passive tilt table test, the patient lies on a board in the supine
position and then the table is tilted, usually to an angle of 60 degrees for 40
minutes.12 (Reference) A positive response, defined as a symptomatic drop in
heart rate or blood pressure, occurs after an average of 24 minutes. If the
response is negative, injection of isoproterenol hydrochloride (Isuprel) may
increase the diagnostic yield by augmenting cardiac contractility and
stimulating the neurocardiogenic cascade. Typically, isoproterenol is given at a
rate of 1 g/min while the patient is tilted to 60 degrees, and the dose is
adjusted upward until a positive response is achieved. Among patients with
idiopathic syncope, 49% have a positive response to the passive tilt test and
66% have a positive response after injection of isoproterenol. The specificity
of the passive tilt test for neurocardiogenic syncope is about 90%. Specificity
is lower with isoproterenol.12,13 (Reference)
The accuracy of tilt table testing is difficult to determine. The test is
not performed unless findings from history taking and physical examination are
ambiguous, thus leaving no ''gold standard'' with which to compare the results.
The protocol for the tilt table test (ie, angle, duration, and use of
isoproterenol) is not standardized, and the reproducibility is only 71% to 87%
owing to the many factors that influence autonomic function.
Treatment options for recurrent neurocardiogenic syncope include lifestyle
modifications, such as avoiding triggers and liberalizing salt intake to enhance
intravascular volume. Beta blockers, anticholinergics, the antiarrhythmic
disopyramide (Norpace), and the alpha agonist midodrine hydrochloride
(ProAmatine) blunt the neurocardiogenic reflex, and the corticosteroid
fludrocortisone (Florinef) acetate increases volume. Fluoxetine hydrochloride
(Prozac) also may be effective. Tilt table testing can be repeated to document
therapeutic efficacy, although as many as 30% of patients with a positive
response have a negative response to the second test regardless of therapy.
Cardiac pacing is helpful for cardioinhibitory (bradycardic) syncope. Dual
chamber pacing helps avoid vasodilation resulting from
atrioventricular dissociation.
Neurologic disease All syncope patients with focal neurologic signs or symptoms
should undergo neuroimaging. Patients without focal neurologic findings should
not routinely undergo neuroimaging. Similarly, electroencephalography has a low
diagnostic yield and is not indicated in the absence of findings suggestive of
seizure. It may be helpful in evaluating suspected seizure, although the limited
sensitivity and specificity must be recognized; normal findings in a patient
with a convincing seizure history do not rule out seizure, and abnormal findings
alone do not necessarily confirm the presence of a seizure disorder.
Psychiatric disease Because half of all psychiatric diagnoses may go
unrecognized during routine syncope evaluation,5 (Reference) physicians need a
high index of suspicion for psychiatric disease among syncope patients in whom
medical evaluation was nondiagnostic. Anxiety or panic disorder with
hyperventilation can be diagnosed by instructing the patient to hyperventilate
in the office to elicit syncope or presyncopal symptoms. Formal psychiatric and
substance abuse evaluation may be indicated when the cause of syncope has not
been determined.
Idiopathic syncope Depending on the aggressiveness of the workup, as many as 45%
of patients may be given the diagnosis of idiopathic syncope after routine
evaluation.6,14,15 (Reference) Although patients with idiopathic syncope have a
good prognosis, equivalent to that of age-matched controls, recurrent syncope
can have important lifestyle implications for driving or work. A diagnostic
approach to unexplained syncope is included in figure 2.
Hospitalization and prognosis
The decision to hospitalize a patient with syncope depends on the prognosis and
-- most important -- the physician's ability to identify patients at high risk
for lethal arrhythmias that could be treated during hospitalization. Prognosis
depends on whether the origin of syncope is cardiac or noncardiac. For example,
in a prospective study of 433 syncope patients,15 (Reference) the 1-year
mortality rate after cardiac syncope was about 25% and the 1-year risk of sudden
cardiac death 14%. In contrast, the 1-year mortality rate after noncardiac or
idiopathic syncope was 6% to 8% and the 1-year risk of sudden cardiac death only
3%. Of note, cardiac syncope carries a lower mortality rate today than in the
past because electrophysiologic testing is now more commonly used.
Physicians in the emergency department may not know whether syncope is
cardiac or noncardiac in origin. Four predictors of poor outcome among syncope
patients on initial presentation are an abnormal ECG (not nonspecific ST or T
wave changes or sinus tachycardia), prior ventricular arrhythmia (defined as at
least 10 premature ventricular contractions an hour or repetitive [>2] or
multifocal premature ventricular contractions), a history of CHF, and age
greater than 45 years.16 (Reference) The risk of arrhythmia or death at 1 year
ranges from 5% for patients with no risk factors, to 16% with one risk factor,
to more than 60% with three or four risk factors. My colleagues and I recommend
that patients with even one risk factor and a history suggestive of cardiac
syncope undergo cardiac evaluation.
The guideline for hospitalization after syncope from the American College of
Physicians (table 2) targets patients who would benefit from inpatient
diagnostic evaluation or from therapies that could improve outcome over several
days of hospitalization.
Elderly patients
Syncope from any cause in an elderly patient portends a poor prognosis. In a
study of syncope in elderly (age, >60) and young patients,14 (Reference) all
patients with cardiac syncope had 2-year mortality rates of 32% to 38%; in
patients with noncardiac syncope, elderly patients had a much higher mortality
rate (22%) than younger patients (5%). The high mortality rate among the elderly
may have been due to comorbidities and suggests that patients in this age-group
should receive close follow-up care regardless of syncope origin.
As with other geriatric syndromes, syncope in the elderly is often
multifaceted, frustrating physicians who seek a unifying diagnosis (table 3). A
reasonable management strategy for elderly syncope patients with multiple risk
factors is to correct these factors before more invasive testing is done.
Cardiac disease should be ruled out on the basis of clues provided during
history taking, physical examination, and electrocardiography or by selective
further testing. If not contraindicated by carotid bruit, cerebrovascular
disease, or a history of transient ischemic attack or stroke, carotid sinus
massage is helpful in diagnosis of carotid sinus hypersensitivity.
Indications for referral or consultation
Cardiologic referral is advised for syncope patients with a documented or
suspected cardiac origin on the basis of arrhythmia, underlying cardiac disease
or, possibly, advanced age alone. A cardiologist typically considers invasive
testing, including an electrophysiologic study. A neurologist should evaluate
syncope patients with abnormal findings on neurologic examination or documented
seizures. For patients with recurrent syncope and suspected psychiatric disease,
psychiatric consultation is helpful for both diagnostic evaluation and
psychiatric management.
Recommendations for driving
Physicians often are asked to make recommendations to their patients about
driving after a syncopal event. Laws regarding the use of private motor vehicles
are made at the state level. Although physicians are obligated to know the laws
of their own state regarding the reporting of syncopal events to the motor
vehicles department and driving by patients after syncope, physicians'
recommendations and awareness of the law are highly variable.17,18 (Reference)
The American Heart Association and the North American Society of Pacing and
Electrophysiology19 (Reference) issued a statement in 1996 pertaining to driving
after syncope, with specific recommendations based on arrhythmia type and
severity (table 4).
Conclusion
Syncope is a symptom with many possible causes, including cardiac, neurologic,
reflex-mediated, and psychiatric disorders. All patients with syncope should
provide a thorough history and undergo physical examination and
electrocardiographic testing. Information obtained during this initial
evaluation guides further testing. One-year mortality and sudden cardiac death
rates are highest after syncope caused by underlying cardiac disease. Patients
with other origins of syncope or with idiopathic syncope generally have a good
prognosis. PGM
The author thanks Nora Goldschlager, MD, for her critique of the manuscript.
The author discloses no financial interests in this article.
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Table 1. Causes of syncope
Cause Prevalence
Cardiac
Arrhythmia 14%
Mechanical* 4%
Neurologic 10%
Neurally mediated
Vasovagal 18%
''Situational'' 5%
Orthostatic 8%
Psychiatric 2%
Idiopathic 34%
*Obstruction to cardiac outflow, decreased ejection fraction, and decreased
ventricular filling (ie, pulmonary embolus, pulmonary hypertension, and cardiac
tamponade).
Adapted from Linzer et al.6 (Reference)
Table 2. American College of Physicians criteria for hospitalization after
syncope
Definitely hospitalize patients who meet any of the following criteria:
-- A history of chest pain
-- A past history of coronary artery disease, congestive heart failure, or
ventricular arrhythmia
-- Physical examination findings of congestive heart failure, valvular disease,
or focal neurologic deficit
-- An electrocardiogram showing ischemia or infarction, arrhythmia, or bundle
branch block
Strongly consider hospitalizing patients who meet any of the following criteria:
-- A history of exertional syncope (in the absence of physical examination
evidence of aortic stenosis or other left ventricular outflow obstruction),
frequent syncope, or age >70 yr
-- Physical examination findings of tachycardia, orthostatic changes, or injury
-- Suspected cardiac disease
Adapted from Linzer et al.17 (Reference)
Table 3. Common risk factors for syncope in the elderly
Susceptibility to situational syncope
Polypharmacy and adverse drug effects on heart rate, intravascular volume, and
vascular tone (with use of beta blockers, calcium channel blockers,
antiarrhythmics, diuretics, antidepressants)
Serious cardiac and neurologic disease, other comorbidities, or atypical
presentation of disease
Decreased physiologic reserve
Table 4. Guidelines for driving after syncope or arrhythmia
Patient with ventricular tachycardia or fibrillation treated with medical
therapy or implantable cardiac defibrillator
-- Risk of recurrent arrhythmia is greatest in first 6 mo, up to 10% at 1 yr
-- Recommendation: Patient may resume driving after arrhythmia-free for 6 mo
Patient with bradycardia and syncope
-- Recommendation: Patient may resume driving 1 wk after successful pacemaker
insertion
Patient with neurocardiogenic syncope
Mild (presyncope, clear warning, and precipitant)
-- Recommendation: Patient may resume driving immediately
Severe (frequent with no warning or precipitant)
-- Recommendation: Patient should not resume driving until after institution of
therapy and a waiting period of unspecified duration
Adapted from Epstein et al.20 (Reference)