Syncope:​Evaluation and

Differential Diagnosis
Max Bayard, MD;​Fereshteh Gerayli, MD;​and James Holt, MD
East Tennessee State University, Johnson City, Tennessee

Syncope is an abrupt, transient, and complete loss of consciousness associated with an inability to maintain postural tone;​
recovery is rapid and spontaneous. The condition is common, resulting in about 1.7 million emergency department visits in
2019. The immediate cause of syncope is cerebral hypoperfusion, which may occur due to systemic vasodilation, decreased
cardiac output, or both. The primary classifications of syncope are cardiac, reflex (neurogenic), and orthostatic. Evaluation
focuses on history, physical examination (including orthostatic blood pressure measurements), and electrocardiographic
results. If the findings are inconclusive and indicate possible adverse outcomes, additional testing may be considered.
However, testing has limited utility, except in patients with cardiac syncope. Prolonged electrocardiographic monitoring,
stress testing, and echocardiography may be beneficial in patients at higher risk of adverse outcomes from cardiac syncope.
Neuroimaging should be ordered only when findings suggest a neurologic event or a head injury is suspected. Laboratory
tests may be ordered based on history and physical examination findings (e.g., hemoglobin measurement if gastrointestinal
bleeding is suspected). Patients are designated as having lower or higher risk of adverse outcomes according to history,
physical examination, and electrocardiographic results, which can inform decisions regarding hospital admission. Risk
stratification tools, such as the Canadian Syncope Risk Score, may be beneficial in this decision;​some tools include cardiac
biomarkers as a component. The prognosis of patients with reflex and orthostatic syncope is good;​cardiac syncope is more
likely to be associated with adverse outcomes. (Am Fam Physician. 2023;​108(5):454-463. Copyright © 2023 American Acad-
emy of Family Physicians.)

Syncope is an abrupt, transient, and complete evaluated for syncope in emergency departments
loss of consciousness associated with an inability were admitted, and 10% were given observa-
to maintain postural tone;​recovery is rapid and tion status.4
spontaneous. The definition of syncope does not
include loss of consciousness caused by other con- Pathophysiology
ditions, such as seizures or head trauma. Presyn- The immediate cause of loss of consciousness in a
cope refers to the symptoms that occur before an syncopal episode is cerebral hypoperfusion. The
episode of syncope, such as graying out or tunnel two primary mechanisms of this hypoperfusion
vision;​these symptoms may progress to syncope are systemic vasodilation and decreased car-
or resolve without total loss of consciousness.1 diac output. Either, or both, can lead to syncope.
Syncope is a common symptom that results Systemic vasodilation may be due to autonomic
in substantial use of health care resources and nervous system dysfunction, excessive response
expenses. The lifetime incidence of syncope is to various stimuli (e.g., emotion, position, other
reported to range between 19% and 41%, and it triggers), and medication. Decreased cardiac out-
is more prevalent with advanced age and female put may be caused by intrinsic heart disease (e.g.,
sex.1,2 Syncope was the cause of 1.7 million U.S. coronary artery disease, heart failure, valvular
emergency department visits in 2019, or 1.1% of disease), or it may be secondary to hypovolemia,
all such visits.3 As of 2014, 25% of individuals orthostatic hypotension, or neurally mediated
bradycardia (as in vasovagal syncope).
CME This clinical content conforms to AAFP cri-
Differential Diagnosis
teria for CME. See CME Quiz on page 447.
Author disclosure:​ No relevant financial
Syncope must be distinguished from other
relationships. nontraumatic conditions that lead to transient
loss of consciousness. These include seizures,

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 SYNCOPE
SORT:​KEY RECOMMENDATIONS FOR PRACTICE

Evidence
Clinical recommendation rating Comments
History, physical examination (including orthostatic blood C Consensus guidelines
pressure), and electrocardiographic results should be obtained
in individuals presenting with syncope.1,5

Neurologic imaging, including carotid ultrasonography and B Expert opinion and systematic review of
computed tomography or magnetic resonance imaging of the observational studies showing lack of patient
head, should not be ordered as part of the evaluation for syn- benefit
cope in the absence of neurologic signs or symptoms.1,27

Individuals who experience syncope during exertion should C Consensus guidelines

have an exercise stress test.1,5,12

Patients with low-risk features suggestive of reflex or orthostatic C Consensus guidelines

syncope should be managed without hospital admission.1,5

Patients with high-risk features suggestive of cardiac syncope C Consensus guidelines

should be admitted to the hospital or observation unit.1,5

Risk stratification scores may be used in the management of B Systematic reviews and validation studies
patients with syncope, but they have not been shown to be assessing adverse patient outcomes, but
superior to physician judgment.5,36-39 tools did not perform better than physician
judgment

A = consistent, good-quality patient-oriented evidence;​ B = inconsistent or limited-quality patient-oriented evidence;​ C = consensus, disease-
oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to [Link] ww.
[Link]/afpsort.

psychogenic causes, and rare condi-

tions such as vertebrobasilar transient BEST PRACTICES IN NEUROLOGY
ischemic attacks, subclavian steal syn-
drome, cataplexy, hypoglycemia, and Recommendations From Choosing Wisely
drop attacks.5,6 Jerking movements are Recommendation Sponsoring organization
not unique to seizures and may also
occur in syncope. Features of these Avoid computed tomography of the head in asymp- American College of
tomatic adult patients in the emergency department Emergency Physicians
movements that suggest syncope as with syncope, insignificant trauma, and a normal
the etiology include an onset follow- neurologic evaluation.
ing loss of consciousness, asymmetry,
loss of muscle tone, and being fewer in In the evaluation of simple syncope and a normal American College of
neurologic examination, do not obtain brain imaging Physicians
number, such as fewer than 10 move- studies (i.e., computed tomography or magnetic
ments, per episode. Loss of conscious- resonance imaging).
ness for less than 30 seconds suggests
syncope;​a duration longer than 60 Do not perform imaging of the carotid arteries for American Academy of
simple syncope without other neurologic symptoms. Neurology
seconds suggests seizures. Confusion
after the event suggests that seizures Do not routinely order electroencephalography as American Epilepsy
are the cause.5,7 part of the initial syncope workup. Society
Syncope is categorized as cardiac, Source:​For supporting citations and to search Choosing Wisely recommendations relevant
ref lex (neurogenic), or orthostatic to primary care, see [Link] [Link]/pubs/afp/collections/[Link].
(Table 1).1,5,8-11 More than one of these
mechanisms may be involved in
any given episode. Cardiac syncope is caused by cerebral provoking factor, such as fear, pain, or emotional dis-
hypoperfusion due to decreased cardiac output. It is the type tress, is the source of the syncopal episode.
of syncope most often associated with sudden cardiac death Orthostatic syncope occurs with positional changes,
and increased mortality.5 such as movement from a supine to standing position, when
Reflex syncope is the most common type of syncope return of blood to the heart is temporarily diminished. This
in all age groups. It may result from decreased cardiac can be exacerbated by dehydration, blood loss, or medica-
output, systemic vasodilation, or both. Typically, a tion use. In patients with autonomic dysfunction, failure of

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 SYNCOPE
TABLE 1

Classification of Syncope
Type of syncope Scenario Clinical features

Reflex (neurogenic;​35% to 48% of cases*)

Carotid sinus Associated with pressure on the neck, Stimulation of the carotid sinus can cause ventricular
hypersensitivity such as shaving, wearing a tight collar, and pause or a drop in systolic blood pressure, which is
turning the head;​consider in patients with reproducible with carotid sinus massage
unexplained falls

Situational Occurs during or after defecation, urina- Absence of heart disease;​patient has likely had previous
tion, or coughing, or after eating or exercise similar experiences

Vasovagal Inappropriate (nonphysiologic) vasodila- May have prodromal features, such as nausea, warmth,
tion and bradycardia;​caused by fear, pain, or diaphoresis
noxious stimuli, heat, or stress

Cardiac (5% to 21% of cases*)

Arrhythmia Palpitations may precede syncope;​some- Abnormal electrocardiographic findings (e.g., bradyar-
times lacks prodrome;​may be unprompted rhythmias, tachyarrhythmias, pacemaker dysfunction);​
family history of sudden death;​personal history of heart
disease;​abrupt onset of palpitations or symptoms while
supine or prone

Structural Cardiac tamponade Hypotension, tachycardia, increased jugular venous

pressure, pulsus paradoxus

Hypertrophic cardiomyopathy Family history of sudden cardiac death, systolic murmur

that intensifies during Valsalva maneuver

Infiltrative diseases (e.g., amyloidosis, Arrhythmias, heart block, heart failure

sarcoidosis, hemochromatosis)

Valvular Aortic, mitral, or pulmonic stenosis Symptoms depend on severity;​may cause heart
failure, exertional angina;​murmur may be heard on
examination

Vascular (may be Acute myocardial infarction or ischemia Chest pain, diaphoresis, shortness of breath, onset with
associated with exertion
electrocardio-
graphic changes) Aortic dissection Hypotension or shock, severe sharp chest pain that
possibly radiates to the back

Pulmonary embolism Shortness of breath;​fatigue;​may be asymptomatic

Orthostatic (4% to 24% of cases*)

Autonomic failure Neurogenic-mediated orthostasis;​failure of May be seen in patients with Parkinson disease, Lewy
autonomic nervous system to compensate body dementia, multiple sclerosis, diabetes mellitus,
for positional changes connective tissue disorders, advanced age, or spinal
cord injury

Drug-induced Numerous medications may cause vasodi- Recent initiation or increased dose of medications
lation or decreased cardiac output (consider anticholinergics, diuretics, antihypertensives,
dopaminergics, opiates, antipsychotics, sedatives, and
tricyclic antidepressants)

Postural ortho- Common in young adults;​more common Severe orthostasis with marked tachycardia
static tachycardia in females
syndrome

Volume depletion Caused by poor oral intake, gastrointestinal History of blood or fluid loss;​low blood pressure;​ele-
losses, acute blood loss, and diuretics vated heart rate

*—Frequency of emergency department visits attributed to each classification of syncope.

Information from references 1, 5, and 8-11.

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 SYNCOPE

compensatory vasoconstriction also

TABLE 2 decreases cerebral perfusion.

Significance of History and Physical Examination Findings Initial Evaluation

in Patients With Syncope The evaluation of a syncopal event
History findings Significance focuses on whether the underlying
cause is likely to lead to an adverse
Description of episode
outcome. The history, physical exam-
After exercise or with triggers May indicate reflex syncope
ination (including orthostatic mea-
such as cough, micturition,
and defecation surements), and electrocardiographic
(ECG) results are the primary tools to
During exertion or while May indicate cardiac etiology determine the etiology of the synco-
supine;​associated with chest pal event.1,5 In one prospective study
pain, palpitations, shortness
of breath, or lack of prodrome
of patients presenting with syncope,
the etiology in 64% of patients was
During positional changes or May indicate orthostatic hypotension diagnosed with certainty (24%) or
prolonged standing high likelihood (40%) based only on
With a prodrome of anxiety, May indicate reflex syncope history, physical examination, and
emotional distress, fear, or ECG results.10 Table 2 discusses find-
pain;​or a feeling of warmth ings from the history and physical
examination for syncope and their
With nausea afterward May indicate reflex syncope
relevance.1,11-15
Medical history Information from the history and
Current medical conditions, Presence of ischemic or structural heart physical examination can help classify
especially cardiac disease or history of arrhythmia increases like- the patient as being at lower or higher
lihood of cardiac syncope
risk of adverse outcomes. Corroborat-
Family history May suggest Brugada syndrome, hypertrophic ing information from someone who
cardiomyopathy, or rare conditions observed the episode is also beneficial.
Important history information includes
How long patient has been More than 4 years of syncopal episodes may
having syncope indicate low risk of cardiac etiology
symptoms and activities before the syn-
copal episode, previous similar epi-
Medications May cause or exacerbate syncope sodes, history of heart disease, recent
Physical examination findings
illness, and the patient’s current med-
ications. The cardiac examination may
Arrhythmias Tachycardia, bradycardia, and irregular rhythm
may indicate cardiac syncope identify an arrhythmia or murmur, and
the neurologic examination may find a
Cranial nerve, motor, or Neurologic conditions rarely cause syncope, focal deficit, mental status change, or
speech deficits but they can occur due to head trauma fol-
postictal state. Findings that indicate
lowing a syncopal episode
higher risk include associated chest
Murmurs May suggest valvular disease pain or shortness of breath, occurrence
with exertion or while supine, sudden
Orthostatic blood pressure A drop in systolic blood pressure of ≥ 20 mm
Hg or diastolic blood pressure of ≥ 10 mm Hg
onset of palpitations or lack of pro-
is diagnostic for orthostatic hypotension drome, family history of sudden cardiac
death, personal history of cardiac dis-
Vital signs Systolic blood pressure < 90 mm Hg or > 180 ease, systolic blood pressure less than
mm Hg indicates higher risk
90 mm Hg, gastrointestinal bleeding,
Patients with reflex syncope may have higher
persistent bradycardia, and previously
baseline heart rate but less variation in heart
rate with maneuvers (e.g., orthostatic) undiagnosed murmur (Table 3).1,5,11-13
Orthostatic blood pressure and
Information from references 1 and 11-15. heart rate should be measured after
the patient has been supine for five

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 TABLE 3 TABLE 4

Syncopal Findings Associated With Lower Higher-Risk ECG Findings in Patients With
and Higher Risk Syncope
Lower risk Higher risk ECG findings Significance

Episode history Changes consistent with Suggests high risk of

After prolonged standing Associated with chest pain, acute ischemia adverse events, such as
shortness of breath, abdom- Mobitz type II or third- cardiac arrest or death
During or after a meal
inal pain, headache degree atrioventricular block
Caused by head rotation
or pressure on carotid Associated with sudden- Persistent bradycardia
sinus onset palpitations Sinus pauses
Caused by positional Family history of sudden Ventricular or supraventricu-
change from supine or cardiac death at young age lar tachyarrhythmias
sitting to standing Lack of prodrome
Complete left bundle branch Increased risk of adverse
With a prodrome typical In a male patient
block events within 30 days
for reflex syncope Occurs during exertion
First-degree atrioventricular
With a trigger such as Occurs while sitting or block
cough, defecation, or supine
micturition Multiple premature ventricu-
In an older patient lar contractions
In a younger patient
Nonsinus rhythm
Medical history Other abnormalities consis-
Absence of known heart History of heart disease tent with acute or chronic
disease ischemia
History of recurrent Short PR interval
episodes with simi-
lar low-risk features, Short PR interval and delta Consider Wolff-Parkin-
particularly in a patient wave son-White syndrome
younger than 40 years
Elevated ST segment in V1 Consider Brugada
Physical examination and/or V2 with inverted T syndrome
Normal physical exam- Persistent bradycardia < 40 waves in these leads
ination findings beats per minute in the
Prolonged QT interval QTc longer than 470 ms
absence of physical training
for men or 480 ms for
Suggestion of gastrointesti- women indicates long
nal bleeding QT syndrome;​can be
Previously undiagnosed congenital or acquired
systolic murmur (e.g., from medications,
Unexplained systolic blood electrolyte imbalance)
pressure < 90 mm Hg
ECG = electrocardiographic.
Information from references 1, 5, and 11-13. Information from references 1, 5, and 17.

minutes. The patient stands, and the blood pressure and high-grade heart blocks, and ventricular and supraventricu-
pulse are checked within one minute and again at three lar tachyarrhythmias may be identified. Certain congenital
minutes. There is no consensus regarding additional inter- and acquired conditions that can cause syncope have recog-
vals at which to check blood pressure and heart rate. A nizable ECG abnormalities (Table 4).1,5,17
drop in systolic blood pressure of 20 mm Hg or more or a
drop in diastolic blood pressure of 10 mm Hg or more upon Further Evaluation
standing is diagnostic of orthostatic hypotension. Increased If the history, physical examination, and ECG findings do
heart rate is not necessary for diagnosis because this may not clearly identify the patient’s risk level for adverse out-
not occur in patients with autonomic dysfunction.5 Patients comes, further evaluation may be indicated. Although
with early-onset orthostatic hypotension, which occurs various additional tests are commonly ordered, many are
within 15 to 60 seconds of standing, may be at higher risk of performed without evidence of benefit in the evaluation of
adverse outcomes.16 syncope (Table 5).1,5,6,12,18-23
ECG findings may suggest a cardiogenic cause of syncope Overuse of testing and resources is common when eval-
and the need for further workup. Bradycardia, sinus pauses, uating patients with possible syncope. This was the focus of

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 SYNCOPE
TABLE 5

Further Testing for Patients With Syncope

Test Indication Comments
Carotid sinus For patients older than 40 years with syn- Carotid sinus syndrome confirmed if the test causes bradycar-
massage cope of unknown etiology compatible dia or hypotension that reproduces symptoms
with a reflex mechanism

Carotid ultra- Neurologic findings;​otherwise, carotid Loss of consciousness not usually a symptom of transient
sonography imaging should not be performed ischemic attack associated with carotid stenosis;​focal neuro-
logic signs and symptoms would be expected with transient
ischemic attack

Chest CT For patients with findings suggestive of Per systematic review, the prevalence of pulmonary embolism
angiography pulmonary embolism in patients with syncope is 0.8%;​not certain whether pulmo-
nary embolism caused the syncope

Echocardiog- For patients with suspected structural Individuals at least 60 years of age with abnormal ECG results
raphy heart disease based on initial assessment or elevated B-type natriuretic peptide levels may benefit from
(can identify aortic stenosis, hypertrophic transthoracic echocardiography, which the American College
cardiomyopathy, pericardial tamponade, of Radiology recommends if clinical suspicion of cardiac eti-
aortic dissection, acute right ventricular ology based on history, physical examination, or ECG results
strain as seen in pulmonary embolism,
and other structural conditions)

Electroen- Suspected seizure Should not be ordered as part of the basic workup of syncope
cephalography but appropriate if seizure is suspected

Electrophysi- Asymptomatic sinus bradycardia (< 50 Should not be obtained in patients with syncope who have
ologic study beats per minute), bifascicular bundle normal ECG results and normal heart structure unless
branch block, and tachycardia;​otherwise arrhythmic etiology is otherwise suspected
has only limited usefulness in the workup
of syncope

Head CT Only if intracranial disease is highly sus- CT and magnetic resonance imaging of the head have other-
pected as contributing to the syncope or wise not been shown to be of benefit in evaluation of syncope
there is suspicion of head trauma due to
syncope

Laboratory Based on clinical findings Hemoglobin if gastrointestinal bleeding is suspected

testing Human chorionic gonadotropin in women of childbearing age
d-dimer assay if pulmonary embolism is suspected
B-type natriuretic peptide and troponin if cardiac etiology
suspected
Basic metabolic panel if dehydration and electrolyte abnor-
malities suspected

Prolonged Demonstrated utility in diagnosing Currently a lack of sufficient evidence as to whether long-
ECG arrhythmias that may be the cause of term monitoring with implantable loop recorders decreases
monitoring syncope;​duration of monitoring is mortality
partially dependent on the frequency of
syncopal episodes

Stress testing For patients who experience syncope Syncope during exercise is likely cardiac, whereas syncope
during or after exertion after exercise could be cardiac or reflex

Tilt table Should be considered in individuals when Tilt table testing may help differentiate syncope with abnor-
testing the initial evaluation does not provide mal movements from seizures;​also may be beneficial to help
clear diagnosis of reflex syncope, ortho- patients recognize symptoms and learn physical maneuvers
static syncope, positional orthostatic
tachycardia syndrome, or psychogenic
pseudosyncope

CT = computed tomography;​ECG = electrocardiographic.

Information from references 1, 5, 6, 12, and 18-23.

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 SYNCOPE

a study in which 1,020 hospitalists were given a scenario of more than 12 hours had a higher sensitivity for identifying
textbook orthostatic hypotension:​hydrochlorothiazide had arrhythmias than did shorter intervals. Following discharge, if
recently been added to a 59-year-old man’s blood pressure the cause of syncope remains unknown, and a cardiac cause is
regimen. He had a syncopal episode after standing and recov- still suspected, prolonged ECG monitoring is recommended.1
ered fully within two minutes. In the emergency department, Monitoring for 15 days showed greater sensitivity for identify-
orthostatic testing resulted in a drop in systolic blood pres- ing causative arrhythmias than did shorter intervals.26 Table 6
sure of 25 mm Hg, and ECG results were normal. Although shows ECG monitoring options for syncope.5,12,22,23
medication change and discharge would be appropriate, 83%
of respondents thought that further workup with additional IMAGING STUDIES
testing (admission, echocardiography, stress testing, or tilt Imaging studies are often ordered in the evaluation of syn-
table testing) would be performed at their institutions.24 cope but are seldom beneficial. Regarding computed tomog-
raphy of the head, numerous studies have demonstrated that
LABORATORY TESTING in the absence of head trauma or neurologic abnormalities,
Laboratory testing may be ordered based on the patient’s his- it provides almost no benefit, and despite the lack of benefit,
tory and physical examination findings. Examples include about 50% of patients presenting with syncope have com-
hemoglobin measurement due to a suspected hemorrhage, puted tomography or magnetic resonance imaging of the
d-dimer assay if pulmonary embolism is considered, and head.27 A systematic review found that less than 0.1% of those
pregnancy test when warranted. B-type natriuretic peptide who had computed tomography of the head had findings that
and troponin levels should be considered if cardiac syncope explained the syncopal episode.28 In the absence of physical
is suspected;​elevated results are associated with a higher risk examination findings consistent with symptomatic carotid
of adverse outcomes.5,25 stenosis, carotid ultrasonography is not recommended.1,18,29

PROLONGED ECG MONITORING ECHOCARDIOGRAPHY AND STRESS TESTING

Prolonged ECG monitoring may detect arrhythmias that Echocardiography is recommended if history, physical
could be the source of syncope, but the effect on mortality is examination, or ECG findings suggest structural cardiac
not known. Among individuals with risk factors for cardiac abnormalities.1,12 Stress testing is recommended if syncope
syncope, inpatient or emergency department monitoring for is associated with exertion.5,18

CAROTID SINUS MASSAGE

TABLE 6 Carotid sinus massage may be diagnostic in indi-
viduals with syncope associated with carotid
Prolonged Electrocardiographic Monitoring sinus hypersensitivity. 5 History findings sug-
Options for Syncope gestive of carotid sinus hypersensitivity include
Type of monitor How it is used Patient selection onset of symptoms with head turning, shaving,
or wearing tight collars and in those with a his-
Event monitor Activated automat- For individuals with weekly
ically or by patient to monthly symptoms;​can
tory of neck surgery or radiation. Carotid sinus
be used for 30 to 60 days syndrome is diagnosed if the carotid sinus mas-
sage reproduces symptoms and produces bra-
Holter monitor Continuous mon- For individuals with daily dycardia or hypotension. This is performed in a
itoring with leads episodes;​records all data
on chest for 24 to 48 hours
setting in which continuous ECG monitoring and
beat-to-beat blood pressure monitoring are avail-
Implantable Requires a minor For individuals with infre- able.5 Carotid sinus massage is a safe procedure
loop recorder surgical procedure;​ quent, recurrent, or severe in patients without critical carotid stenosis who
activated automat- symptoms;​can be used
ically or by patient for 2 to 3 years
have not had a recent transient ischemic attack
or stroke. Neurologic complications are rare, and
Patch monitor Continuous mon- For individuals with weekly when they do occur, most are transient.30,31
itoring for 3 to 14 symptoms;​can be used
days via a patch on for up to 14 days
TILT TABLE TESTING
the upper chest
There is considerable debate about the utility of tilt
Information from references 5, 12, 22, and 23. table testing.32,33 If the diagnosis of reflex syncope
is highly likely based on the history and physical

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 SYNCOPE

department with syncope

FIGURE 1 are admitted to the hospital,
mortality is 1.4% at 30 days
Transient loss of consciousness and 7% after one year.34,35
Patients with a clear diag-
Is syncope diagnosed? nosis of reflex or orthostatic
syncope who are low risk
can be discharged.1,5 Indi-
No Yes viduals who are not clearly
Treat as indicated History and physical examination; ortho-
at low risk should be admit-
static measurements; electrocardiography* ted or observed (i.e., in the
emergency department or
syncope unit, if available).1,5
Risk stratification†; consider risk
calculators and laboratory testing
Most commonly, these are
patients who may have car-
diac syncope or an underly-
ing condition that warrants
Low risk: outpatient management Higher risk: admit patient, perform expe- treatment (e.g., gastroin-
dited evaluation, or refer for consultation testinal bleeding, pulmo-
nary embolism).5
Risk stratification scores
Orthostatic syncope Reflex syncope
have not been shown to be
Cardiac syncope Other suspected
suspected cause (e.g., pulmonary superior to physician judg-
Treatment options If diagnosis is unclear, embolism, gastroin- ment, but they can be used
testinal bleeding)
include: consider tilt table testing to help determine a patient’s
and carotid sinus massage Testing as indicated;
Hydration
if diagnostic, treat
risk.5,36 A recent systematic
Education
condition Treat as indicated review concluded that the
Lifestyle changes
Treatment options include: Consider prolonged Canadian Syncope Risk
Medication reduction
Medication reduction electrocardiographic Score was the most accurate
Pharmacotherapy monitoring if testing
Education
is not diagnostic
scoring tool for classifying
Trigger avoidance individuals as being at low
Pharmacotherapy or high risk of adverse out-
Pacemaker if symptoms
are severe and recurrent
comes within 30 days.37 In a
validation study of the tool,
*—See Tables 1 and 2 for more information regarding diagnosis.
no patients (n = 3,819) clas-
†—See Tables 3, 4, 5, and 7 for more information regarding risk stratification and further testing.
sified as low or very low risk
Evaluation of syncope. had ventricular arrhythmia
Information from references 1, 5, 8, and 12.
or died within 30 days. 38
Components of the assess-
ment include ECG findings,
examination, tilt table testing is not needed, although it physician diagnosis, predisposition to vasovagal symptoms,
may be beneficial if this diagnosis is in doubt. Additionally, history of heart disease, systolic blood pressure, and tropo-
it may help to diagnose delayed orthostatic hypotension, nin level (Table 7).39
postural orthostatic tachycardia syndrome, or psychogenic
pseudosyncope.1,5,19 Treatment
CARDIAC SYNCOPE
Risk Stratification and Disposition The treatment of cardiac syncope is directed at the underly-
The decision to admit a patient with syncope is based on ing etiology. A structural etiology may require procedural
whether the initial assessment clearly identifies a low- intervention. Arrhythmic etiology may be treated with med-
risk condition or a higher-risk condition (Figure 1).1,5,8,12 ication, cardiac pacing, catheter ablation, or an implantable
Although 30% to 50% of people presenting to the emergency cardioverter-defibrillator.5

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 SYNCOPE
TABLE 7

Canadian Syncope Risk Score

Category Comments Points
REFLEX SYNCOPE
Predisposition to vasovagal Triggered by being in warm/ −1
Education and reassurance are the symptoms crowded place, prolonged stand-
primary interventions for reflex syn- ing, fear, emotion, or pain
cope. The patient should avoid triggers
History of heart disease Coronary artery disease, atrial 1
of situational syncope, and onset of fibrillation or flutter, heart failure,
the prodrome should prompt changes valvular disease, nonsinus rhythm
in position or environment. Physical
Systolic blood pressure < 90 mm On any reading 2
countermeasures, such as isometric Hg or > 180 mm Hg
muscle contractions, may avert an epi-
sode, particularly in patients who are Elevated troponin levels > 99th percentile of normal 2
population
younger than 60 years and have a pro-
longed prodrome.5 Abnormal QRS axis < 30 or > 100 degrees 1
Medication changes and cardiac pac- QRS duration > 130 ms — 1
ing may be considered in individuals
Corrected QT interval > 480 ms — 2
who have recurrent syncopal episodes
despite lifestyle changes. Stopping or Emergency department Vasovagal syncope −2
reducing the dosage of blood pres- diagnosis Cardiac syncope 2
sure medications, alpha blockers, and Neither 0
vasodilators may reduce syncopal
Total score Risk of arrhythmia or death Risk category
episodes. 5,40 Fludrocortisone, which
increases plasma volume, may reduce −2 to 0 0.2% to 0.9% Very low
syncopal episodes in younger individ- 1 1.9% Low
uals with baseline low blood pressure. 2 to 3 3.8% to 7.5% Medium
Midodrine, an alpha blocker, has some 4 to 5 14.3% to 25.4% High
evidence of effectiveness but should be 6 to 8 41.1% to 74.5% Very high
avoided in those with hypertension,
Note:​Link to risk score:​[Link] [Link]/calc/3951/canadian-syncope-risk-score.
heart failure, or urinary retention.1,41
Adapted with permission from Thiruganasambandamoorthy V, Stiell IG, Sivilotti MLA, et al.
Only weak evidence indicates that the Predicting short-term risk of arrhythmia among patients with syncope:​The Canadian Syn-
antidepressants fluoxetine and paroxe- cope Arrhythmia Risk Score. Acad Emerg Med. 2017;​24(11):​1321.
tine may decrease syncopal episodes.1,42
Patients who have frequent, severe epi-
sodes of reflex syncope with documented asystole may bene- Numerous other queries were completed in PubMed, limited to
fit from placement of a dual chamber pacemaker.5,43 reviews, systematic reviews, guidelines, clinical trials, and ran-
domized controlled trials;​key terms included orthostasis, elec-
trocardiogram/syncope, carotid sinus massage, tilt table testing,
ORTHOSTATIC SYNCOPE syncope risk scoring, and implantable loop recorder. In addition
First-line treatment of orthostatic syncope is education and to the research of articles from the past five years, multiple lon-
reassurance. The patient should avoid triggers such as a rapid ger and less-restrictive searches were completed. Search dates:​
movement from supine to standing. Adequate hydration and September through November 2022.
salt intake are recommended, and stopping offending medica-
tions should be considered. Physical countermeasures, support The Authors
stockings, abdominal binders, and elevating the head of the MAX BAYARD, MD, is a professor in the Department of Family
patient’s bed more than 10 degrees may help. If symptoms persist, Medicine at East Tennessee State University, Johnson City.
midodrine and fludrocortisone may help.1,5 FERESHTEH GERAYLI, MD, is a professor in the Department
of Family Medicine at East Tennessee State University.
This article updates previous articles on this topic by Runser, et
al.9;​ Gauer 44;​and Miller, et al.45 JAMES HOLT, MD, is a professor in the Department of Family
Medicine at East Tennessee State University.
Data Sources:​Key sources were Essential Evidence Plus,
PubMed, the Cochrane database, Turning Research into Practice Address correspondence to Max Bayard, MD, East Tennessee
database, DynaMed, and the Agency for Healthcare Research State University College of Medicine, 917 W. Walnut St., John-
and Quality. An initial PubMed search, limited to random- son City, TN 37604 (bayard@​[Link]). Reprints are not avail-
ized controlled trials, systematic reviews, and guidelines from able from the authors.
the past five years, was completed using the term syncope.

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 SYNCOPE

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personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2024. Elsevier Inc. Todos los derechos reservados.