Approach to the adult patient with syncope

in the emergency department

Authors: Daniel McDermott, MD, James V Quinn, MD, MS
Section Editor: Robert S Hockberger, MD, FACEP
Deputy Editor: Michael Ganetsky, MD

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is
complete.

Literature review current through: May 2022. | This topic last updated: Aug 14, 2020.

INTRODUCTION

Syncope is a transient loss of consciousness associated with loss of

postural tone, followed quickly by a spontaneous return to baseline
neurologic function requiring no resuscitative efforts. Syncope may be
caused by benign or life-threatening conditions and it is a relatively
common reason for presenting to the emergency department (ED). Often,
the underlying cause of a syncopal episode cannot be clearly identified in
the ED, and the primary responsibility of the ED clinician becomes
determining which patients are at high risk for adverse outcomes.

This topic review will discuss how to evaluate and manage patients
presenting to the ED with syncope. Detailed discussions of specific types of
syncope and the evaluation of syncope in children and adults are found
separately. (See "Syncope in adults: Epidemiology, pathogenesis, and
etiologies" and "Syncope in adults: Clinical manifestations and initial
diagnostic evaluation" and "Reflex syncope in adults and adolescents:
Clinical presentation and diagnostic evaluation" and "Emergency evaluation
of syncope in children and adolescents" and "Causes of syncope in children
and adolescents".)
TERMINOLOGY AND EPIDEMIOLOGY

Syncope is a transient loss of consciousness associated with loss of

postural tone, followed by a spontaneous return to baseline neurologic
function requiring no resuscitative efforts. The underlying mechanism is
global hypoperfusion of both the cerebral cortices or focal hypoperfusion
of the reticular activating system. Syncope is not to be confused with a loss
of consciousness associated with altered mental status or stroke, or with
vague dizziness and chronic lightheadedness. Presyncope (ie, near syncope
or near loss of consciousness) and true syncope should be considered a
spectrum of the same symptom. Although presyncope is less dramatic, ED
clinicians should approach the evaluation in a similar fashion [1-4]. When
researchers have made a clear effort to distinguish true presyncope from
dizziness, ataxia, or vague lightheadedness, the outcomes of syncope and
presyncope have been found to be similar in terms of significant
underlying causes and outcomes [1]. The terminology and epidemiology of
syncope is explored in greater detail separately. (See "Syncope in adults:
Epidemiology, pathogenesis, and etiologies".)

Syncope is a common presenting symptom in the ED, accounting for 1 to 2

percent of all ED visits and hospital admissions in the United States [5-9].
Lifetime prevalence rates range from 10.5 to 19 percent [10,11]. Although
most causes are benign and self-limited, others are associated with
significant morbidity and mortality, particularly among older adults [12].
The differential diagnosis is broad, and management focuses on the
underlying cause when this is discernible. However, during the ED
evaluation, the cause of syncope often remains unclear, and management
must focus on risk stratification to differentiate between patients safe for
discharge and those who require immediate investigation and in-hospital
management. (See 'Differential diagnosis' below and 'Risk stratification'
below.)
DIFFERENTIAL DIAGNOSIS

After reviewing the history, physical examination findings, and the

electrocardiogram (ECG), physicians in the ED are able to determine a clear
underlying diagnosis only about 50 percent of the time [13,14]. Patients
often remain undiagnosed despite exhaustive diagnostic testing [7,15-17].
This is significant, as patients with an identified cardiac cause for syncope
have twice the risk of death as those without syncope, and patients with a
neurologic cause have a 50 percent increased risk [10]. Those with an
unknown cause of syncope have a 30 percent increased risk of death,
whereas patients with vasovagal (ie, vasovagal) syncope are at no increased
risk. Tables listing the most dangerous and most common etiologies of
syncope are provided (table 1 and table 2 and table 3).

Life-threatening conditions — The primary responsibility of the

emergency clinician is to assess whether a life-threatening cause of
syncope is present and to provide appropriate management and
disposition. The most important causes to consider are cardiac syncope,
blood loss, pulmonary embolism, and subarachnoid hemorrhage. Other
conditions such as seizure, stroke, and head injury do not meet the
technical definition of syncope but should be considered during the initial
assessment.

● Cardiac syncope – Cardiac causes are the most common life-

threatening conditions associated with syncope and thus the most
important to diagnose or predict. They include arrhythmia, ischemia,
structural/valvular abnormalities (eg, aortic stenosis, particularly in
older adults; idiopathic hypertrophic heart disease), cardiac
tamponade, and pacemaker malfunction. Prospective studies of short-
term and one-year outcomes following syncope have found patients
with cardiac syncope to be at significant risk for sudden death [6,18].
Patients with a history of cardiac disease, particularly heart failure,
were at greatest risk [19]. (See "Syncope in adults: Epidemiology,
 pathogenesis, and etiologies", section on 'Causes of syncope' and
"Syncope in adults: Management and prognosis", section on
'Treatment'.)

● Hemorrhage – Large blood loss, particularly acute severe hemorrhage,

can manifest as syncope. Important potential causes include trauma,
gastrointestinal bleeding, ruptured aortic aneurysm, ruptured ovarian
cyst, ruptured ectopic pregnancy, and ruptured spleen. (See "Initial
management of NON-hemorrhagic shock in adult trauma" and
"Approach to acute lower gastrointestinal bleeding in adults" and
"Evaluation and management of ruptured ovarian cyst" and "Ectopic
pregnancy: Clinical manifestations and diagnosis" and "Management
of splenic injury in the adult trauma patient" and "Management of
symptomatic (non-ruptured) and ruptured abdominal aortic
aneurysm", section on 'Introduction'.)

● Pulmonary embolism – Hemodynamically significant pulmonary

embolism is a relatively uncommon but well-documented and
important cause of syncope. (See "Clinical presentation, evaluation,
and diagnosis of the nonpregnant adult with suspected acute
pulmonary embolism", section on 'Clinical presentation'.)

● Subarachnoid hemorrhage – Patients presenting with syncope

associated with headache require evaluation for a possible
subarachnoid hemorrhage. (See "Aneurysmal subarachnoid
hemorrhage: Clinical manifestations and diagnosis".)

Common conditions

● Vasovagal syncope – Vasovagal syncope, a type of reflex syncope, is the

most common cause of syncope, accounting for 25 to 65 percent of
cases [14]. Patients diagnosed with vasovagal syncope have an
excellent prognosis with no increase in long-term mortality or
morbidity [10].
 Autonomic activation causes vasovagal syncope. Three types of
responses are seen: a cardioinhibitory response, a vasodepressor
response, and a mixed response with features of both. Significant
bradycardia and/or hypotension accompany the acute loss of
consciousness. Potential triggers are numerous, and determination of
the underlying cause is often made in the outpatient setting. (See
"Reflex syncope in adults and adolescents: Clinical presentation and
diagnostic evaluation".)

Most patients with vasovagal syncope experience a slow, progressive

prodrome that may include some combination of dizziness or
lightheadedness, a sense of warmth, pallor, nausea and vomiting,
abdominal pain, changes in vision, or diaphoresis associated with
some precipitating event. Examples include micturition or defecation
syncope, situational syncope (eg, while having blood drawn), or cough-
mediated syncope.

● Carotid sinus hypersensitivity – Carotid sinus hypersensitivity is a

reflex-mediated variant of vasovagal syncope, resulting from pressure
at the carotid sinus. External pressure to the neck can induce this reflex
response, causing bradycardia and hypotension. Common causes
include shaving, a tight collar, and turning of the head. Clinicians
should consider carotid hypersensitivity in older patients with
recurrent syncope and a prior negative cardiac workup. (See "Carotid
sinus hypersensitivity and carotid sinus syndrome".)

● Orthostasis – Orthostatic syncope comprises between 5 and 24 percent

of syncope cases and is defined by syncope associated with a drop in
systolic blood pressure of 20 mmHg or more with a positional change
(lying to sitting or sitting to standing). Orthostatic syncope is often
associated with a reflex tachycardia of more than 20 beats per minute.
Orthostasis is most often caused by a loss of intravascular volume,
which can be exacerbated by instability of the autonomic nervous
 system. Nevertheless, clinicians should remain cautious because
orthostasis can occur with cardiac syncope, acute gastrointestinal
bleeding, or autonomic insufficiency, particularly in older adults.
Syncope from orthostatic hypotension should be a diagnosis of
exclusion in the ED, reserved for low-risk patients who have symptoms
consistent with the diagnosis. (See "Mechanisms, causes, and
evaluation of orthostatic hypotension".)

Orthostatic vital signs are neither sensitive nor specific in assessing

volume status or diagnosing orthostatic syncope [20-22]. Symptomatic
orthostasis is most important. Many patients become symptomatic if
their systolic blood pressure drops below 90 mmHg with or without a
corresponding drop in blood pressure or elevated heart rate sufficient
to meet the criteria for orthostatic syncope. While a large portion of
the population meets the definition of orthostasis, they do not
necessarily have syncope. Older adults, pregnant women, and patients
taking drugs with vasodilating effects are predisposed to develop
symptomatic orthostasis.

● Medications – The effects of medications account for 5 to 15 percent of

syncopal events. The mechanism can be orthostasis or cardiotoxicity.
Medications often implicated include calcium channel blockers, beta
blockers, alpha blockers, nitrates, antiarrhythmics, diuretics (affecting
volume status and electrolyte concentrations), and medications
affecting the QTc interval (eg, antipsychotics and antiemetics) (table 2)
[23].

Other conditions

● Neurologic syncope – True syncope is defined by an immediate,

spontaneous return to baseline function following loss of
consciousness, without new focal neurologic findings. Thus, true
neurologic syncope reflecting underlying neurovascular disease is rare.
 Examples of neurologic syncope include subarachnoid hemorrhage,
transient ischemic attack, subclavian steal syndrome, and complex
migraine headache. Stroke and transient ischemic attacks generally
cause focal neurologic deficits that do not recover rapidly or
completely. Often, patients with cerebrovascular disease convey a
history of nonsyncopal episodes featuring neurologic deficits, possibly
including diplopia, vertigo, focal weakness, or numbness.

Syncope may be misconstrued as seizure because many patients with

transient loss of consciousness have brief convulsive episodes
secondary to cerebral hypoperfusion, particularly if bystanders or
objects keep them upright. Syncope can usually be differentiated from
seizure by the brevity of the convulsions; the absence of epileptic aura,
urinary or fecal incontinence, and tongue biting; and the lack a true
postictal phase (typically five minutes or longer). (See "Syncope in
adults: Epidemiology, pathogenesis, and etiologies".)

● Psychiatric syncope – Anxiety and panic disorders can cause situational

syncope. Emergency clinicians must be cautious when attributing
syncope to psychiatric causes. Patients with hypoxia, inadequate
cerebral perfusion, or other medical conditions may appear confused
or anxious. Patients with psychiatric syncope are generally young,
without cardiac disease, and complain of multiple episodes [24].

● Drug-induced loss of consciousness – Drugs of abuse and alcohol may

cause a transient loss of consciousness, but generally, these patients
manifest signs of toxicity and do not spontaneously return to normal
neurologic function immediately after regaining consciousness.
Alcohol can also cause symptomatic orthostasis by impairing
vasoconstriction [25].

● Metabolic – Metabolic causes of syncope include hypoglycemia and

hypoxia. Electrolyte abnormalities secondary to renal injury or other
conditions may precipitate syncope due to dysrhythmia.
 ● Rare causes – Rare causes of syncope include atrial myxoma, Takayasu
arteritis, systemic mastocytosis, and carcinoid. Anaphylaxis can involve
syncope and loss of consciousness, and both patients and witnesses
sometimes overlook or forget the more subtle, earlier symptoms, such
as flushing, itching, hives, cough, bronchospasm, or abdominal
cramping. In addition, these less dramatic symptoms may have
resolved by the time the patient is evaluated. (See "Anaphylaxis:
Emergency treatment".)

HISTORY

A thorough history is essential to determine accurately the underlying

cause of syncope. Several studies suggest that history and physical
examination lead to the diagnosis in approximately half of patients [13,14].
Other studies have assessed specific signs and symptoms to determine
which patients are at increased risk for serious outcomes, particularly
sudden death [18,26-29].

● Young patients are more likely to experience vasovagal syncope.

Nevertheless, the emergency clinician must consider the possibility of
dysrhythmia, particularly if other concerning factors exist (eg,
exertional syncope, family history of sudden death). Electrocardiogram
(ECG) findings consistent with dysrhythmia include a short or
prolonged QTc or short PR interval.

Older adult patients appear to be at greater risk for adverse outcomes

following syncope [30]. Falls and associated fractures can occur. Aortic
stenosis is of particular concern as patients get older and it is the most
common obstructive cardiac lesion. Older adult patients are more likely
to have autonomic dysfunction, orthostasis, and multiple medications,
increasing the risk for syncope [31]. Progression of diabetes can cause
autonomic dysfunction and orthostasis, as can some other conditions
such as Parkinson disease [32].
 However, several studies suggest that while age correlates with death
and other adverse outcomes, age itself is nonspecific, and a history of
underlying heart disease is more predictive [33]. As an example, one
prospective observational study of 45 consecutive patients 50 years
and older with syncope found no significant events at one month
among those whose ED evaluation was unremarkable [34]. The use of
a number of different age thresholds to define the "at-risk" age makes
it difficult to interpret the data. One study used 45 years as a cutoff,
another 75 years [18], while consensus opinions have used 60 or 70
years [13,35].

We believe there is little utility in using any absolute age threshold to

determine increased risk. Risk of adverse outcomes after syncope
gradually increases with age and should be considered in the context
of other risk factors, particularly those associated with heart disease.

● Associated symptoms and triggers – Concomitant symptoms can

provide important diagnostic clues. As an example, chest pain may
indicate an acute coronary syndrome or pulmonary embolism.
Palpitations suggest an arrhythmia. Dyspnea raises concern for
pulmonary embolism or heart failure. Abdominal or low back pain
associated with syncope raises the possibility of a rupturing abdominal
aortic aneurysm. Headache raises the possibility of subarachnoid
hemorrhage. Symptoms such as headache, paresthesias, or weakness
may suggest a neurologic cause.

The emergency clinician should seek a history consistent with

vasovagal syncope. If this diagnosis can be made, the patient is low
risk. A gradual prodrome generally precedes vasovagal syncope and
often includes a sense of warmth, nausea and vomiting, diaphoresis,
changes in vision, and pallor, either just prior to or shortly after the
event. Inquiring about potential vasovagal triggers is also helpful.
Triggers commonly associated with vasovagal syncope include visual
 stressors (eg, seeing blood during phlebotomy or watching a
childbirth), strong physical or emotional stress, micturition, defecation,
coughing, swallowing, and prolonged standing in a warm
environment.

● Position – Patients who lose consciousness with prolonged standing

(ie, minimum of 15 to 20 minutes) are more likely to have vasovagal
syncope [30]. Patients who lose consciousness while moving from a
lying to a standing position are more likely to have orthostasis.
Syncope while sitting or supine is suspicious for arrhythmia [30,36].

● Onset – Sudden loss of consciousness without warning or prodrome

suggests arrhythmia [30]. A prospective observational study of
patients with recurrent syncope found that 64 percent of patients
sustained an arrhythmia at the time of their sudden loss of
consciousness when studied with a loop recorder [37]. Injury from falls
associated with an abrupt loss of consciousness can occur. Patients
with prodromes are more likely to have vasovagal syncope and have
repeatedly been shown to be low risk [10].

● Duration of symptoms – The duration of a syncopal event is difficult to

quantify. Patients are generally unaware of the duration of their loss of
unconsciousness, and events are often unwitnessed or poorly
quantified if they are witnessed. As a rough guide, an "event" or loss of
consciousness persisting for more than four or five minutes should
raise concerns for seizure or other causes of altered mental status.

● Exertional syncope – Syncope with exertion raises the possibility of

arrhythmia or cardiac outflow obstruction (eg, aortic stenosis,
hypertrophic cardiomyopathy, or pericardial tamponade). These
patients warrant a thorough cardiac evaluation, including chest
radiograph, ECG, and echocardiography.
● Seizure versus syncope – Often, clinicians have difficulty determining
whether their patient suffered a seizure or syncope. Patients with
certain seizure disorders do not manifest generalized convulsions, and
patients with syncope may have brief tonic/clonic episodes.
Approximately 5 to 15 percent of patients thought to have syncope
may have a seizure disorder [38].

Factors suggestive of seizure include [38-40]:

• Prodrome (aura) different from that described for vasodepressor

syncope
• Eye deviation, usually superiorly and/or laterally
• Episode of abrupt onset associated with injury
• Presence of a tonic phase before the onset of rhythmic clonic activity
• Head deviation or unusual posturing during the episode
• Tongue biting (particularly involving the lateral aspect of the tongue)
• Loss of bladder or bowel control
• Prolonged post-event (postictal) phase during which the patient is
confused and disoriented

Despite these guidelines, the differentiation of seizures from syncope

is sometimes difficult, especially in the patient with a brief seizure
where the postictal phase is minimal or the patient with syncope who
takes more time than is typical to return to baseline. However, a
postictal phase and confusion without spontaneous return to baseline
mentation within minutes is more suggestive of seizure [41].

● Medications – A review of the patient's medications may reveal the

cause of syncope. This is particularly important with older adult
patients. Medications often implicated include calcium channel
blockers, beta blockers, alpha blockers, nitrates, antiarrhythmics,
diuretics (affecting volume status and electrolyte concentrations), and
medications affecting the QTc interval (eg, antipsychotics and
antiemetics) (table 2) [23].
 ● Prior episodes – A history of syncopal episodes may be of value. A
single episode or multiple episodes over many years suggests a benign
etiology. Several episodes over a short period of time in someone with
no history of syncope suggest a more significant cause, such as
dysrhythmia.

● Family history – A family history of unexplained sudden death,

dysrhythmia, or early cardiovascular disease (ie, in close relatives less
than 50 years old) places patients at increased risk for cardiac syncope
[42].

● Associated injury – Acute loss of consciousness may result in significant

injury or events that predispose to injury. Motor vehicle accidents, hip
fractures, and subdural hematomas can result. Emergency clinicians
should assess the patient for potential injuries. Although patients with
prodromal symptoms have less risk of death and other adverse
outcomes following syncope, there is no evidence that they have less
risk of acute injury from syncope (eg, from falls). Such patients may
ignore warning signs and may be just as likely to incur injury as
patients without a prodrome [18].

PHYSICAL EXAMINATION

The physical exam should focus on vital signs and a focused cardiac and
neurologic exam, as well as any specific complaints.

● Vital signs – Transient hypotension or bradycardia occur during most

syncopal events. Abnormal vital signs generally normalize by the time
of evaluation in the ED. Persistently abnormal vital signs are
concerning and must be investigated. Discrepancies between upper
extremities in pulse or blood pressure may reflect aortic dissection or
subclavian steal syndrome and should be investigated (see "Clinical
features and diagnosis of acute aortic dissection" and "Subclavian steal
syndrome", section on 'Physical examination' and "Overview of upper
 extremity peripheral artery disease" and "Overview of upper extremity
peripheral artery disease", section on 'Presentation'). Low oxygen
saturation or tachypnea may be a sign of heart failure or pulmonary
embolism.

Orthostatic vital signs should be obtained. The patient should be

supine for five minutes before the initial set is obtained. Vital signs are
retaken after the patient has been standing for three minutes and
compared with initial measurements. The following changes are
considered abnormal and may reflect hypovolemia or autonomic
dysfunction [20]:

• Drop in systolic blood pressure of 20 mmHg or more.

• Increase in heart rate of 20 beats per minute or more.

Many asymptomatic patients meet these criteria for orthostasis, but

a drop of blood pressure below 90 mmHg associated with symptoms
can be diagnostic in itself. Keep in mind that syncope from
orthostatic hypotension is a diagnosis of exclusion in the ED,
reserved for low-risk patients who have symptoms consistent with
the diagnosis. Orthostatic hypotension may be related to serious
conditions, including myocardial ischemia or acute blood loss (eg,
gastrointestinal bleeding, ruptured abdominal aortic aneurysm, or
ectopic pregnancy). (See 'Common conditions' above.)

There are reports of using wearable technology (eg, Fitbit, Apple

watch) to determine whether a change in heart rate correlated with
symptoms [43,44].

● Cardiac examination – Auscultation of the heart may reveal a rate that

is either abnormal or irregular (eg, atrial fibrillation). The clinician
should listen for murmurs, specifically for aortic and mitral stenosis.
Extra heart sounds, either an S3 or S4, can often be heard in patients
with heart failure. Findings on cardiac exam suggesting structural
 heart disease should be investigated. (See "Auscultation of cardiac
murmurs in adults" and "Auscultation of heart sounds".)

The presence of an implantable pacemaker should be noted as

malfunction may lead to syncope.

● Pulmonary examination – Auscultation of the lungs may reveal

abnormal sounds (eg, crackles, wheezes) consistent with heart failure
or other pathology (eg, pulmonary embolus, cardiac ischemia).

● Neurologic examination – Patients with syncope by definition return to

baseline neurologic function. A thorough exam should be done to
identify any subtle focal abnormality suggestive of stroke. (See "The
detailed neurologic examination in adults".)

● Neck examination – Clinicians should listen for a carotid bruit.

Murmurs of aortic stenosis may also radiate to the neck. Examine the
neck for elevated jugular venous pressure, a possible sign of heart
failure.

Some groups suggest that carotid massage be performed as part of

the evaluation of syncope. We feel this test lacks sufficient sensitivity
and specificity to play a meaningful diagnostic role in the ED. We
advise caution when considering whether to perform carotid massage
in patients with potential carotid artery disease. (See "Reflex syncope in
adults and adolescents: Clinical presentation and diagnostic
evaluation" and "Vagal maneuvers", section on 'Carotid sinus
massage'.)

● Rectal examination – A rectal exam with a stool guaiac test can identify
some patients with gastrointestinal hemorrhage, which may present
with syncope.

● Intraoral examination – Lacerations to the lateral aspect of the tongue

are suggestive of seizure [39]. (See 'History' above.)
 ● Injury assessment and general examination – The emergency clinician
should perform a head to toe exam (ie, secondary survey) looking for
evidence of trauma. Common injuries associated with falls following
syncope include facial fractures, hips fractures, wrist fractures, and
subdural hematomas. A general examination, guided by patient
complaints, may reveal important findings such as papilledema or a
pulsatile abdominal mass.

ANCILLARY STUDIES

Electrocardiogram — Practice guidelines suggest that all patients

presenting with syncope should receive an electrocardiogram (ECG)
[13,45,46]. Although the diagnostic yield of the ECG is low (2 to 7 percent
may reveal a significant abnormality), the test is inexpensive, easy to
perform, and included in most risk stratification decision tools. An
abnormal ECG suggests an underlying cardiac problem, and further
investigation is needed.

The clinician should assess the ECG looking for evidence of cardiac
arrhythmia or ischemia as the cause of syncope. Concerning ECG findings
include [47-49]:

● Non-sinus rhythm
● Left bundle branch block (LBBB)
● Signs of acute myocardial ischemia or infarction

A more comprehensive list of clinical and ECG features associated with

syncope from arrhythmia is found in the following table (table 4).
Significant ECG findings include prolonged intervals (QRS, QTc), severe
bradycardia, preexcitation, low voltage in the standard limb leads,
suggesting pericardial effusion, and abnormal conduction syndromes (eg,
Wolf-Parkinson-White and Brugada). A short QT interval has also been
associated with significant arrhythmias that could result in syncope [50,51].
(See "Syncope in adults: Clinical manifestations and initial diagnostic
evaluation", section on 'Electrocardiogram'.)

Of note, there is no consensus about what constitutes significant ECG

findings in the setting of syncope. The ECG criteria in some decision tools
are complex and lack validation by bedside physicians. Even when apps and
calculators are used for complex criteria, most require some interpretation
of findings that lack agreement or validation.

Multiple studies have assessed ECG criteria linked to dysrhythmia or

ischemia with variable results. In one prospective observational study,
patients with an ECG showing sinus rhythm and no new abnormal
morphologic changes compared with prior ECGs had substantially lower
risk of adverse events during the week following their syncope [18].
According to a subsequent prospective study, high-risk findings associated
with adverse cardiac outcomes include any non-sinus rhythm identified
from any source (ie, standard 12-lead ECG or cardiac monitor tracings
obtained in the ambulance or the ED) and any abnormal conduction of the
left bundle (ie, LBBB, left anterior or posterior fascicular block, prolonged
QRS duration) [47,52].

Cardiac monitoring — While in the ED, patients should be placed on a

cardiac monitor. Numerous studies suggest that cardiac monitoring, in
addition to the 12-lead ECG, is useful for identifying dysrhythmias while the
patient is in the ED [9,53-55]. In one prospective observational study of 95
consecutive syncope patients, major abnormalities identified by Holter
monitoring included significant bradycardia (heart rate <30 beats per
minute), sinus pauses (particularly those >2 seconds), Mobitz II block,
complete heart block, ventricular tachycardia, and frequent premature
ventricular contractions (PVCs) [56]. Such findings alert the clinician to an
arrhythmogenic cause of syncope. Atrial tachydysrhythmias may cause a
syncopal event but usually do not in patients with structurally normal
hearts [57].
Laboratory evaluation — Routine laboratory screening in patients with
syncope is not supported by evidence and seldom aids management
[8,58,59]. Hypoglycemia may rarely explain an acute syncopal event but
should be performed on all patients with altered mental status. Clinicians
should obtain other tests based on the clinical circumstances.

Electrolytes may be beneficial in critically ill patients or patients thought to

have electrolyte abnormalities from volume loss, diuretic use, or
comorbidities such as renal failure. In patients with active bleeding or
suspected anemia, a hematocrit should be obtained, and coagulation
studies may be useful. A hematocrit less than 30 increases the risk of
adverse short-term events in patients with syncope and predicts the need
for transfusion [18,60]. A urine pregnancy test should be performed in any
female of child-bearing age.

Elevated measurements of natriuretic peptides (ie, brain natriuretic peptide

[BNP] or pro-BNP) appear to be predictive of those at risk for adverse
outcomes following syncope [61-66]. A systematic review of 11 studies
(4246 patients) assessing the predictive value of cardiac biomarkers in
adults with syncope concluded that natriuretic peptides and high-sensitive
troponin were useful for identifying patients who developed adverse
cardiac events following a syncopal episode [67]. (See "Natriuretic peptide
measurement in heart failure" and "Troponin testing: Clinical use".)

Some decision tools have incorporated laboratory tests. The FAINT Score
includes BNP and troponin, while the Canadian Syncope Risk Score (CSRS)
includes troponin [68,69]. Natriuretic peptides and troponin are markers,
respectively, for heart failure and ischemic heart disease, both of which are
established risk factors for adverse events following syncope. Both of the
above scores include a history of heart disease, in particular heart failure
and arrhythmia, in addition to these biomarkers, which have become more
sensitive and useful for risk stratification.
Neurologic studies — Patients with a history of or physical exam
suspicious for a transient ischemic attack, stroke, or new onset seizure
need further evaluation. Patients without historical or examination features
suggestive of neurologic disease need no further neurologic imaging.
Despite the low diagnostic yield of brain imaging, clinicians continue to
overuse head computed tomography (CT) and magnetic resonance
imaging (MRI) in the evaluation of syncope patients [59,70]. An
electroencephalogram may be useful in some cases where it is clinically
difficult to distinguish syncope from seizure [71].

Echocardiography — Although not readily available in some EDs,

echocardiography is helpful for determining the presence of structural
heart disease and is being performed by more emergency physicians at the
bedside. Echocardiography can show valvular anomalies, wall motion
abnormalities, elevated pulmonary pressure (seen with pulmonary
embolism), and pericardial effusions. It is most useful in patients with a
known history of cardiac disease or abnormal ECG findings for further
investigation of these at-risk patients. However, routine bedside
echocardiography for unexplained syncope in patients without clinical risk
factors has no demonstrated benefit [72].

APPROACH TO DIAGNOSIS

The most important tasks for the emergency clinician faced with a syncope
patient are to identify and manage life-threatening problems and to
differentiate between patients safe for discharge and those who require
immediate investigation and in-hospital management [9,45]. In making
such determinations, clinicians should consider presyncope (ie, near loss of
consciousness) and true syncope a spectrum of the same disease process,
with no difference in management [1]. An algorithm outlining ED
management (algorithm 1) and tables listing dangerous causes of syncope
and high-risk features (table 1 and table 3) are provided. ED clinicians
should keep in mind that despite exhaustive testing, a clear diagnosis will
ultimately not be found for many patients with syncope. A subset of these
patients may have occult cardiac syncope.

When evaluating the syncope patient, emergency clinicians should keep in

mind three questions:

● Is this true syncope, or does some other serious condition account for
the patient's loss of consciousness (eg, stroke, seizure, head injury)?

● If this is true syncope, is there a clear life-threatening cause?

● If this is true syncope and the cause is not clear, is the patient at high
risk?

Life-threatening causes of syncope include hemorrhage (eg,

gastrointestinal, subarachnoid), pulmonary embolism, and cardiac syncope
from arrhythmia, acute coronary syndrome, or structural heart disease.

Patients with syncope from major hemorrhage usually have a low

hematocrit. This may not be the case if bleeding is severe and acute, in
which case the hematocrit can be misleading. Gastrointestinal bleeding is
the most common cause, and often the rectal exam or a stool guaiac test
will be positive for blood. The emergency clinician must consider other
sources of hemorrhage, including ruptured aortic aneurysm, ruptured
ectopic pregnancy, ruptured ovarian cyst, and ruptured spleen. Appropriate
diagnostic testing should be performed. Obtain a pregnancy test in all
women of child-bearing age. Bedside ultrasound can be invaluable in
determining the presence of abdominal aortic aneurysm, ectopic
pregnancy, and intraabdominal blood. (See "Approach to acute lower
gastrointestinal bleeding in adults" and "Approach to acute upper
gastrointestinal bleeding in adults" and "Ectopic pregnancy: Clinical
manifestations and diagnosis" and "Ultrasonography of pregnancy of
unknown location" and "Evaluation and management of ruptured ovarian
cyst".)
Pulmonary embolism (PE) is an uncommon but potentially dangerous
cause of syncope. Patients with PE often present with dyspnea and chest
pain and may be hypoxic. An electrocardiogram (ECG) with evidence of
right heart strain is suggestive. Most often, the diagnosis is made by
computed tomography (CT) scan. When suspecting PE, clinicians should
perform a work-up based on the patient's baseline risk for PE. Evaluation
and management of PE are discussed separately. Patients whose
presenting symptom of PE is syncope are not at increased risk of death
compared with patients whose syncope is not caused by PE [73,74]. (See
"Clinical presentation, evaluation, and diagnosis of the nonpregnant adult
with suspected acute pulmonary embolism" and "Overview of acute
pulmonary embolism in adults".)

Although the incidence of PE was purported to be as high as 17 percent

among patients hospitalized with syncope (n = 230) in a controversial study
published in 2016 by the PESIT investigators [75], subsequent studies have
refuted this finding [76-78]. According to a retrospective review of five
databases from four countries involving over 1.6 million adults who
presented to the ED for syncope, the prevalence of PE ranged from 0.5 to
2.1 percent among patients who were hospitalized, and from 0.06 to 0.55
percent for all patients [76].

Syncope associated with a significant headache suggests possible

subarachnoid hemorrhage, and evaluation with head CT and lumbar
puncture may be necessary. Should historical features or examination
findings suggest transient ischemic attack or stroke, clinicians should
obtain a CT with angiography or magnetic resonance imaging (MRI) and
neurologic consultation. Suspected seizure should be evaluated with
neuroimaging (head CT or MRI) and electroencephalogram (EEG), as an in-
patient or out-patient. A less extensive evaluation may be appropriate for
patients with an established seizure diagnosis and no concerning features
in their presentation. (See "Aneurysmal subarachnoid hemorrhage: Clinical
manifestations and diagnosis" and "Initial assessment and management of
acute stroke".)

Diagnosing cardiac syncope is especially important because the one-year

mortality of such patients approaches 30 percent, significantly higher than
noncardiac syncope or syncope of unknown etiology [6]. The mortality of
syncope patients with heart failure is even higher [19]. We suggest
clinicians obtain an ECG in all syncope patients. The emergency clinician
should study the ECG for evidence of ischemia, arrhythmia, and conduction
or electrolyte abnormalities. An abnormal ECG or concerning history
should prompt further workup, including echocardiography and cardiac
monitoring as indicated. (See 'Electrocardiogram' above and "Syncope in
adults: Clinical manifestations and initial diagnostic evaluation", section on
'Electrocardiogram'.)

Arrhythmia is the most common serious cause of cardiac syncope but may
not manifest during the course of an ED evaluation. Syncope patients
should be placed on a cardiac monitor while evaluated in the ED.
Myocardial infarction (MI) is a rare but important cause of syncope. Most
such patients have atypical presentations without ST segment elevations
on initial ECGs. MI occurs in about 3 percent of patients with syncope, and
the negative predictive value of a "normal" ECG is greater than 99 percent
[79].

Several historical factors raise concern for cardiac syncope, including a

strong family history (eg, close relative with sudden death or MI before 50
years old), a history of heart disease (eg, coronary artery disease, heart
failure, MI, valvular disease, arrhythmia), and symptoms consistent with
heart disease (eg, chest pain, palpitations, shortness of breath).

Examination findings suggestive of cardiac syncope include abnormal vital

signs, including orthostatic changes and discrepant pulses or blood
pressure, and abnormal heart sounds. If the history or physical
examination suggests structural heart disease, an echocardiogram should
be obtained. Review the patient's medication list for drugs that may affect
the heart rate or rhythm or blood pressure. The elderly and patients taking
multiple medications are at greater risk of syncope from medication effects
[23]. (See 'Physical examination' above and 'History' above.)

Patients diagnosed with vasovagal (vasovagal) syncope are at very low risk
of adverse outcomes. Historical factors, including a prodrome (eg, sense of
warmth, dizziness, pallor, diaphoresis, abdominal pain, changes in vision,
or nausea), may suggest the diagnosis. Clinicians may be able to identify
potential triggers, such as micturition, defecation, cough, prolonged
standing, or a stressful event (eg, blood draw). A history suggestive of
vasovagal syncope coupled with an unremarkable physical examination
and a normal ECG constitute a reassuring presentation, with little risk of
life-threatening complications.

Note that determining the cause of syncope in patients presenting to the

ED can be difficult [60]. Using a careful history, physical examination, and
an ECG, along with selective ancillary testing based on clinical findings,
clinicians can identify the cause in approximately 50 percent of patients in
the ED [13,14]. Even with intensive inpatient and outpatient testing (eg,
loop recorders, Holter monitors, long-term continuous rhythm monitors
[80], tilt table testing, and electrophysiology studies), clinicians remain
unable to determine the cause of syncope in many patients.

In addition, studies of long-term monitoring suggest that a brief period of

in-hospital cardiac monitoring is likely insufficient to diagnose patients with
arrhythmias causing syncope. Even 24 to 72 hours of assessment with a
Holter monitor, while it diagnoses more arrhythmias, misses important
arrhythmias that can only be detected with long-term monitors. Newer,
portable, longer-wear cardiac monitors are available and can easily be
applied in the ED. The results from prospective observational studies
suggest that the time needed to detect an arrhythmia is often longer than
that provided by a standard 48-hour Holter monitor and that these newer
monitors may improve diagnostic accuracy [81,82].

RISK STRATIFICATION

Emergency clinicians will be unable to determine an exact cause in a

significant number of patients who present to the ED with syncope. In such
instances, using risk stratification to guide management and disposition
represents a practical approach. A treatment algorithm is provided (
algorithm 1).

Using the risk factors identified in the studies described below can help
clinicians determine patient risk and appropriate disposition (table 3). While
individual studies may be limited by such factors as the size of the cohort,
the number of adverse events, and the definition of an event, a consistent
theme emerges: patients with an abnormal ECG on presentation or a
history of heart disease, particularly structural heart disease (eg, heart
failure), are at greater risk for adverse outcomes.

Risk stratification tools should be used to assist clinical judgment but

cannot replace it. When applying such tools, clinicians must be careful to
include only appropriate patients. Patients with significant underlying
pathology and patients who do not reflect the population in which the risk
stratification tool was studied are not appropriate subjects. As examples, a
syncope patient with associated acute coronary syndrome may not meet
any high-risk criteria but obviously requires admission, while patients with
loss of consciousness from head trauma or illicit drug use cannot be
assessed using a decision rule if such patients were excluded from the
rule's derivation and validation studies.

Over the past couple of decades, several research groups have identified
factors associated with increased risk for short-term and one-year
morbidity and mortality following a syncopal episode. According to
systematic reviews, each approach has limitations, and no one decision rule
should be used in isolation to determine patient risk or disposition [83,84].
That said, the groups have identified several common risk factors of
importance, and these should be incorporated into the clinician's
assessment [9,83-86]. The findings of major research groups are described
here and have been incorporated into guidelines as outlined below:

● One research group performed derivation and validation studies on

cohorts of consecutive ED patients with syncope to identify predictors
of arrhythmia and death at one year [27]. Significant risk factors were a
history of arrhythmia, an abnormal electrocardiogram (ECG), a history
of decompensated (ie, congestive) heart failure, and age over 45 years.

● Another research group assessed adverse outcomes at 7 and 30 days

in their derivation and validation of The San Francisco Syncope Rule
(SFSR) [18,87,88]. Significant predictors of adverse events (primarily
arrhythmia) included a history of acute decompensated (ie, congestive)
heart failure, abnormal ECG (non-sinus rhythm or new changes),
hematocrit less than 30, shortness of breath, and systolic blood
pressure of less than 90 mmHg at triage.

A systematic review of external validation studies of the SFSR found

that it is the most thoroughly investigated prediction rule for the
assessment of syncope and that validation studies have reported
inconsistent results [89]. Such inconsistencies may be due to the use of
different definitions for arrhythmia, different definitions for an
abnormal ECG, and differences in the clinicians interpreting the tracing
[89].

● The Osservatorio Epidemiologico sulla Sincope nel Lazio (OESIL) study

group developed a risk score based on predictors of death at one year,
which they found to be an abnormal ECG, a history of cardiovascular
disease (including heart failure), age over 65, and syncope without
prodrome [28].
 ● Researchers in Switzerland developed and validated a prediction score
for subsequent arrhythmia in patients with unexplained syncope
following a standard ED evaluation [29]. They found the significant
variables to be an abnormal ECG, a history of heart failure, and age
above 65 years. The prevalence of arrhythmia was nearly identical in
each cohort, though each phase of the study was performed in a
different country (Switzerland and the United States).

● The Short-Term Prognosis of Syncope (STePS) trial identified an

abnormal ECG, a history of cardiac disease, absence of a prodrome,
and concomitant trauma as indicators of high risk in the short term
(within 10 days of presentation) [90].

● The researchers who created the Canadian Syncope Risk Score (CSRS)
assessed adverse short-term outcomes (within 30 days) and identified
the following high-risk features: abnormal ECG, history of cardiac
disease, lack of vasovagal etiology, elevated troponin, and systolic
blood pressure <90 mmHg or >180 mmHg [68,91]. Using nine
variables, patients were stratified after an initial ED evaluation where
no obvious cause for syncope was identified into risk categories
ranging from very low to high. The CSRS has been validated in 3819
patients in several sites across Canada.

● The FAINT Score is intended to determine risk in older adults (≥ 60

years) with unexplained syncope [69]. The risk factors assessed are:
history of heart failure, history of cardiac arrhythmia, initial abnormal
ECG result, elevated pro B-type natriuretic peptide (BNP), and elevated
high-sensitivity troponin T. The score awaits external validation.

The American College of Emergency Physicians (ACEP) has published

evidence-based guidelines on the management and disposition of patients
with syncope, but these have not been updated since 2007. This policy
statement is based primarily on the risk stratification data presented in
earlier studies and suggests admission for patients with evidence of acute
decompensated (ie, congestive) heart failure or structural heart disease
and patients at high risk for adverse outcomes (table 3) [45]. The American
College of Physicians, European Society of Cardiology, American College of
Cardiology, and American Heart Association have also established
guidelines and algorithms for management and disposition [13,46]. A
group of international experts created guidelines for the ED management
of syncope patients that generally reinforces these guidelines and
algorithm [9]. We suggest that emergency clinicians use the ACEP
guidelines and the attached ED syncope algorithm, which are better suited
to the conditions of EM practice (algorithm 1).

In a study to assess their decision-making, emergency clinicians

demonstrated excellent judgment regarding patient risk but often did not
determine disposition based on their judgment, choosing to admit close to
30 percent of patients who they felt had a less than 2 percent chance of a
serious adverse outcome [60]. The researchers concluded that using
clinical judgment augmented by risk stratification may reduce hospital
admissions and save some of the estimated two billion dollars spent on
syncope each year in the United States.

PATIENT DISPOSITION

Patients with obvious cardiac or neurologic causes of syncope, as well as

those with concerning symptoms or signs, should be investigated
thoroughly in the ED and likely admitted for further in-hospital testing or
treatment. To some degree, clinician judgment determines which
symptoms or signs are "concerning," but such findings may include:

● Syncope accompanied by chest pain or shortness of breath

● Exertional syncope
● Abnormal vital signs
● Abnormal findings on cardiac, pulmonary, or neurologic examination
For well-appearing asymptomatic patients with an unclear cause, clinicians
should determine the risk for adverse outcome. Clinicians determine risk
on the basis of patient history, examination and electrocardiogram (ECG)
findings, and evidence-based guidelines. The presence of any of the
following features determines high risk (table 3). (See 'Risk stratification'
above.)

● Abnormal ECG
● History of structural heart disease or clinical findings suggestive of
heart failure
● Persistently low blood pressure (systolic <90 mmHg)
● Shortness of breath with event or during evaluation
● Elevated troponin or BNP (if obtained)
● Hematocrit <30 (if obtained)
● Older age and associated comorbidities
● Family history of sudden cardiac death

High-risk patients should be investigated in the ED and likely admitted for

inpatient monitoring and with a prolonged monitoring device if no
arrhythmia is found during admission [92]. A significant portion of these
patients will have arrhythmias detected within six hours of ED arrival.
Patients with significant arrhythmias should be admitted to cardiology for
pacemaker or automatic implantable defibrillators as indicated. Low-risk
asymptomatic patients may be discharged, provided out-patient follow-up
can be arranged and the clinician has no other concerns. Patients with
obvious vasovagal syncope who have returned to baseline and are
asymptomatic without injury should be discharged. Outpatient evaluation
of syncope, including the use of ambulatory monitors, tilt table testing, and
other diagnostic techniques, is discussed in detail separately. (See "Syncope
in adults: Clinical manifestations and initial diagnostic evaluation" and
"Syncope in adults: Epidemiology, pathogenesis, and etiologies" and
"Upright tilt table testing in the evaluation of syncope".)
Patients without any feature associated with high risk for an adverse event
but with some concerning clinical finding are generally deemed to be at
intermediate risk. The disposition of intermediate-risk patients will vary
depending upon local health care practice and resources, including the
availability of consultants, in-hospital or observation unit beds, and timely
outpatient follow-up, including the ability to initiate ambulatory monitoring
from the ED. The clinician and patient should discuss the clinical findings
and possible approaches, and the patient’s goals and preferences should
be incorporated into the determination of disposition for those deemed to
be at intermediate risk. Of note, most arrhythmias can be detected with
prolonged ambulatory monitoring of up to 15 days with the incidence
being greatest during the first 24 to 48 hours after the event [81,92-95].
There are many potential long ambulatory monitoring devices with various
features, and their use to diagnose arrhythmia in syncope is recommended
in the new American Heart Association (AHA) guidelines. The evaluation of
intermediate risk patients is reviewed in greater detail separately. (See
"Syncope in adults: Risk assessment and additional diagnostic evaluation",
section on 'Assessment based on the initial evaluation'.)

In some EDs, patients identified as intermediate risk are managed in a

syncope observation unit [96-98]. In one observational study, 103
consecutive patients presenting to an ED with syncope were randomly
assigned to standard care or care in a syncope observation unit [99].
Patients in the observation unit required fewer admissions, and no
significant differences in mortality or recurrent syncope were detected [97].
Further studies are needed to determine if such units provide a cost benefit
without missing significant outcomes. There continues to be tremendous
variability in admission patterns for patients with syncope and controversy
surrounding who benefits from admission. As more sophisticated
ambulatory monitoring is developed, the need for admission of
intermediate-risk patients will continue to evolve [9,100-103].
PREVENTION

One prospective randomized multicenter study found that instructing

patients diagnosed with vasovagal syncope in the use of physical
counterpressure maneuvers (PCM) decreased the incidence of recurrent
episodes of syncope from 51 percent to 32 percent compared with
conventional therapy [104]. Conventional therapy consisted of explaining
the mechanism underlying fainting and providing advice about lifestyle
modifications (eg, avoiding known triggers, increasing fluid and salt intake,
lying down when symptoms occur). PCM consisted of one or more of the
following: (1) leg crossing combined with tensing of the muscles of the
legs, abdomen, and buttocks; (2) arm tensing by grasping one hand with
the other and forcibly abducting the arms; or (3) squeezing an object
clasped in the dominant hand.

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected

countries and regions around the world are provided separately. (See
"Society guideline links: Syncope".)

SUMMARY AND RECOMMENDATIONS

● When evaluating the patient with syncope, the primary responsibility
of the emergency clinician is to assess whether a life-threatening cause
is present and to provide appropriate management and disposition.
The most important causes to consider are cardiac syncope, blood loss,
pulmonary embolism, and subarachnoid hemorrhage. Other
conditions such as seizure, stroke, and head injury do not meet the
technical definition of syncope but should be considered during the
initial assessment. An algorithm outlining emergency department (ED)
management (algorithm 1) and a table listing dangerous causes of
 syncope (table 1) are provided. (See 'Differential diagnosis' above and
'Approach to diagnosis' above.)

● Common but less dangerous causes of syncope include vasovagal,

carotid sinus sensitivity, orthostasis, and medication-related (table 2).
(See 'Common conditions' above.)

● Historical features that reflect increased risk of a dangerous cause of

syncope include concomitant symptoms (eg, shortness of breath,
headache, chest pain), sudden loss of consciousness without
prodrome, exertional syncope, older age, and family history of sudden
death. The clinician should carefully review the patient's medications.
Medication reactions account for a significant percentage of syncopal
episodes. (See 'History' above.)

● Syncope and seizure can be difficult to differentiate. Characteristics to

help clinicians make this distinction are described in the text. (See
'History' above.)

● Perform a careful physical examination focusing on vital signs and the

neurologic and cardiac examination. Patients with syncope often fall
and sustain secondary injuries, which may include the head (eg,
subdural hemorrhage), wrist, or hip. Perform a symptom-guided
examination looking for injuries. (See 'Physical examination' above.)

● Obtain an electrocardiogram (ECG) on all syncope patients. Significant

findings include: prolonged intervals (QRS, QTc), severe bradycardia,
preexcitation, and evidence of myocardial infarction (table 4). Other
notable findings include low voltage in the standard limb leads,
suggesting pericardial effusion; and abnormal conduction syndromes
(eg, Wolf-Parkinson-White, Brugada, and short QT syndromes). (See
'Electrocardiogram' above.)

● Emergency clinicians rely on information garnered from the history,

examination, and ECG to assess the patient with syncope. While
 performing their assessment, they should keep in mind three
questions (algorithm 1):

• Is this true syncope, or does some other serious condition account

for the patient's loss of consciousness (eg, stroke, seizure, head
injury)?

• If this is true syncope, is there a clear life-threatening cause?

• If this is true syncope and the cause is not clear, is the patient at
high risk? (See 'Approach to diagnosis' above.)

● Patients with obvious cardiac or neurologic causes of syncope, as well

as those with concerning symptoms or signs, should be investigated
thoroughly in the ED and likely admitted to inpatient or observation
units. Patients with obvious vasovagal syncope who have returned to
baseline and are asymptomatic without injury can be discharged. (See
'Patient disposition' above.)

● For well-appearing asymptomatic patients with an unclear cause,

clinicians should determine the risk for adverse outcome. Clinicians
determine risk on the basis of patient history, physical examination,
ECG findings, laboratory studies if indicated (eg, BNP, troponin), and
evidence-based guidelines. We suggest augmenting clinical judgment
with validated decision tools. A composite table of high-risk features
based on findings from several studies is provided (table 3). High-risk
patients should be investigated in the ED and likely admitted. Low-risk
asymptomatic patients may be discharged, with appropriate
outpatient follow-up. The disposition of intermediate-risk patients will
vary depending upon local healthcare practice and resources, including
the availability of consultants and timely outpatient follow-up, the
ability to initiate ambulatory monitoring from the ED, and risk
tolerance. Patient goals and preferences should be incorporated into
the determination of disposition for those deemed to be at
 intermediate risk. (See 'Risk stratification' above and 'Patient
disposition' above.)
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