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GUIDELINE FOR THE MANAGEMENT OF SYNCOPE IN
THE EMERGENCY DEPARTMENT (ED)
Simon Clarke
Emergency Department
Frimley Park NHS Foundation Trust
Emergency Department Syncope Guideline
Page 1
1. INTRODUCTION
Syncope is defined as a transient loss of consciousness with loss of postural tone, due to
global cerebral ischaemia, usually associated with spontaneous, rapid and complete
recovery. It is a relatively common symptom and has been estimated as being the primary
complaint in 1.7% of presentations to UK Emergency Departments (ED) [1]. There are >1600
presentations to Frimley for syncope.
Syncope is a symptom not a disorder in itself; it may be caused by a large number of
diseases (see Box 1) which range from benign to potentially life-threatening conditions.
Syncope may present diagnostic difficulties and it has been estimated that initial ED history,
examination and ECG will only suggest a diagnosis in 22-60% of cases [1-4]. This diagnostic
uncertainty is reflected in the variation in rates of specific diagnoses and the wide range of
published admission rates for syncope (25-83%) [1, 2, 3, 5-13] (see Appendix 2). Even after
extensive investigations no cause will be found in up to 3-24% of cases [5, 14-16].
Concern about missing the serious underlying causes of syncope has been shown to lead to
low-risk patients being admitted for cardiac monitoring and further tests which have both
resource and clinical risk implications. 1 year mortality ranges from 5.6%-15%, but there is
little published data on short-term mortality rates: Silverstein [2] noted a 3% in-hospital rate
while Quinn [17] reported a 1 month death rate of 1.4%.
A literature search was undertaken to find if there is any evidence for identifying patients
who can be safely discharged from the ED. In particular, the following evidence was
scrutinised:
1. studies that have identified individual factors (from the history, examination, or
investigations that are available in the ED) that suggest a specific cause.
2. studies that have developed risk stratification scores for patients with syncope, with
special reference to those that were undertaken in EDs
3. published guidelines by accredited professional bodies
Medline and Embase were searched using the terms: [syncope OR collapse]. References
were reviewed
Appendix 2 contains a summary of the individual studies scrutinised.
Emergency Department Syncope Guideline
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Box 1. Causes of Syncope [22, 27, 29, 30, 31]
NEURALLY (REFLEX)-MEDIATED

Vasovagal – emotional distress, orthostatic stress

Carotid sinus syncope

Situational – cough, sneeze, micturition, swallowing, defecation, visceral pain, laughing, post-prandial,
post-exercise

Atypical
ORTHOSTATIC

Autonomic failure - age-related, diabetic neuropathy, Parkinson’s disease, amyloid neuropathy, multiple
system atrophy, spinal cord injuries, uraemia

Drug-induced – hypotensives, negative inotropes, CNS depressants, anticholinergics

Volume depletion – dehydration, blood loss, Addison’s
CARDIOVASCULAR

Arrhythmias – sinus node dysfunction, AV conduction disease, PPM malfunction, SVT, VT, drug-induced
arrhythmias (esp QT prolongers)

Structural heart disease – outflow obstruction (valvular stenosis, HOCM), atrial myxoma, pericardial
disease/ effusion

Myocardial ischaemia

Pulmonary vascular – PE, pulmonary hypertension

Aortic dissection
NEUROLOGICAL

Subclavian steal syndrome
PSYCHIATRIC

Chronic anxiety

Major depression
Emergency Department Syncope Guideline
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2. CLINICAL FEATURES WITH PROGNOSTIC VALUE
Syncope itself does not predict future morbidity and mortality [18] but there are a number
of studies that have shown that cardiac syncope does have prognostic value [2, 3, 7, 15, 1921]. One cohort study indicated that patients with syncope of unknown cause also had a
slightly increased risk of all cause mortality compared with matched patients without
syncope [21]; but the authors referenced some recent electrophysiological studies have
revealed that 45-80% of cases of unknown syncope have a cardiac origin. Orthostatic
syncope has also been shown to be associated with a two-fold increased risk of mortality,
primarily due to associated co-morbidities [22].
A number of risk scores have been developed (Table 1) which used multivariate analysis to
identify clusters of features that predict different outcomes.
Table 1. Risk Stratification Scores
Score
Martin, 1997 [23]
Oh, 1999 [20]
Sarasin, 2003 [24]
OESIL Score, 2003 [25]
San Francisco Syncope Risk Score,
2004 [8]
EGSYS Score [16]
Risk Factors
 abnormal ECG
 age >45 years
 history
of
ventricular
arrhythmias
 history of congestive cardiac
failure
1. abnormal ECG
2. absence of nausea or vomiting
in the prodrome
3. underlying cardiac disease
 abnormal ECG
 age >65 years
 history of congestive cardiac
failure
 abnormal ECG
 age >65 years
 history of cardiac disease
 absence of prodrome
 abnormal ECG
 dyspnoea
 history of congestive cardiac
failure
 haematocrit <30%
 Palpitations before syncope
 Heart disease or abnormal
ECG or both
 Syncope during effort
 Syncope while supine
 Precipitating or predisposing
factors or both (warm,
crowded place/ prolonged
orthostasis/ fear, pain,
emotion)
 Nausea/ vomiting in prodrome
Outcome
CVS deaths & arrhythmias at 1
year.
1 & 2 predictive of arrhythmias at
1 year.
3. predict mortality at 1 year.
Arrhythmias (unspecified follow
up) in patients whose initial ED
assessment could not identify any
cause.
All cause mortality at 1 year.
Serious outcome (death, MI,
arrhythmia, PE, CVA, significant
haemorrhage, return to ED for
related condition) within 1 week.
2 year mortality
Unfortunately, there are potential limitations in each system. Martin’s, Sarasin’s, the OESIL
and EGSYS risk scores used long-term outcomes which are not relevant when considering
Emergency Department Syncope Guideline
Page 4
whether a patient should be admitted from an ED; conversely, the San Francisco Syncope
Risk Score was developed to predict serious outcomes within 1 week of the index visit. Also,
none of the systems has been successfully validated: no attempt has been made with
Martin’s, Sarasin’s or the EGSYS systems. Reed [13] showed that the OESIL score was safe if
a score of 0 was taken as the cut-off but this was at the expense of a 55% in admissions,
while Ammirati [4] applied the score to his population of patients yet found that 24.6% of
those who were eventually diagnosed with cardiac syncope were discharged from the ED.
The validity of the San Francisco system has also been questioned with sensitivities as low as
68% [11, 12] being reported.
However, the similarity between the systems is striking and all of them identified cardiac
disease, particularly congestive heart failure, as predicting adverse outcomes. Table 2 shows
the ECG criteria defined by each system.
Table 2. ECG Criteria used by Risk Scores
Martin, 1997
Oh, 1999








Sarasin, 2003
OESIL, 2003
San Francisco, 2004
EGSYS, 2008






















Conduction disorders – CHB, Mobitz II block, pacemaker malfunction
Rhythm abnormalities – VT (≥3 beats), sinus pauses ≥2s, symptomatic SVT, slow AF
(RR intervals >3s)
Symptomatic sinus bradycardia
Old MI
LVH/RVH
Other
Conduction disorders – LAD, BBB, IV conduction delay, any AV block, short PR
interval
Rhythm abnormalities – AF, atrial flutter, multifocal atrial tachycardia, junctional
rhythm, paced rhythm
Repetitive/frequent premature ventricular beats
Old MI
LVH/RVH
Conduction disorders – BBB, Mobitz I, bifascicular block, sinus pause ≥2s - <3s
Rhythm abnormalities – AF, sinus bradycardia 36-45/min.
Multiple premature ventricular beats
Old MI
LVH/RVH
Conduction disorders – CHB, 2nd degree AV block, BBB or IV conduction delay
Rhythm abnormalities – AF, atrial flutter, SVT, multifocal atrial tachycardia,
frequent or repetitive premature supraventricular or ventricular complexes, VT
(sustained or non-sustained), paced rhythm
Old MI
LVH/RVH
LAD
ST/T wave changes consistent with ischaemia
Not sinus rhythm
New change compared with old ECG
Conduction disorders – 2nd or 3rd degree AV block, BBB
Rhythm abnormalities – SVT, VT, pre-excited ventricular beats
Sinus bradycardia
Acute or old MI
LVH/RVH,
Long QT, Brugada
Emergency Department Syncope Guideline
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3. CLINICAL FEATURES THAT SUGGEST A DIAGNOSIS
Since cardiac and orthostatic syncope are associated with an increased risk of mortality, it
would be informative to identify the features that can be used to diagnose these types of
syncope. In particular, the search concentrated on the following key aspects of the history:
precipitants, prodrome, and recovery.
3.1. Neurally-Mediated Syncope
Precipitants:

Typical precipitant eg fear/anxiety, hot/crowded place, pain, instrumentation [6, 14,
27, 33]

Prolonged standing [27].

During/after meal [27].

After exertion (in the absence of structural heart disease with a fixed cardiac output
eg AS) [27]

Head movement, wearing a tight collar, shaving suggests carotid sinus sensitivity [14,
33].
Prodrome:

Vasovagal syncope tends to have a longer prodrome than cardiac syncope but there
is considerable overlap [6, 33].

Abdominal discomfort during the prodrome [28]
Recovery:

Nausea/sweating during the recovery [28]
Other Features:

Absence of cardiac disease [27].

Long history (up to 4 years) of recurrent episodes [28]
3.2. Orthostatic Syncope
Precipitants:

After standing up (especially after exertion) [27].

Prolonged standing especially in hot, crowded place [27]
Emergency Department Syncope Guideline
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
Soon after changes to medication particularly drugs with hypotensive effects [27, 33]
or those that interact with them.
Other Features:

History of autonomic neuropathy (eg DM, Parkinson’s disease) [27, 29, 30, 31, 33]
3.3. Cardiac Syncope
Precipitants:

While sitting or lying [6, 14, 28, 33]

During exertion [28]

After exertion, when other features of a structural heart disease with a fixed cardiac
output (eg aortic stenosis) are identified [14, 33].

Fast palpitations occurring prior to syncope [14, 28]
Prodrome:

Absent or brief (<5 sec) prodrome [6, 33] although there is considerable overlap with
vasovagal syncope.

Nausea and vomiting during the prodrome are very unusual features of arrhythmic
syncope [20].
Recovery:

Immediate recovery with an absence of fatigue [32]
Other Features:

Symptoms/risk factors suggesting acute coronary syndrome, PE etc [33].

A past history of cardiovascular disease [33]

Drug history: eg QT prolongers, diuretics [33]

A positive family history of sudden cardiac death, Brugada syndrome, HOCM, long
QT syndrome [27, 33].

Examination features of structural heart disease with outflow obstruction, or cardiac
failure [33].

ECG abnormalities [33].
3.4. Features Distinguishing Seizures from Syncope

Although brief seizure activity may occur during syncope, tongue-biting, cyanosis,
and frothing at the mouth are suggestive of a convulsion rather than syncope [34].
Emergency Department Syncope Guideline
Page 7

Recovery of orientation <30 seconds suggests syncope [33] whereas disorientation
during the recovery phase suggests a seizure [34].
Box 2. American College of Physicians, 1997 [29, 30]. Criteria for Admission
ADMISSION INDICATED:


History of:
o
IHD, CCF, ventricular arrhythmia
o
Accompanying chest pain
Physical signs of:
o

Significant valvular disease, CCF, CVA, focal neurology
ECG findings:
o
Ischaemia, arrhythmia (serious bradycardia of tachycardia), increased QT, BBB
ADMISSION OFTEN INDICATED:

Sudden loss of consciousness with injury, rapid heart action, or exertional syncope

Frequent spells, suspicion of IHD or arrhythmia (eg use of drugs associated with
torsades de pointes)

Moderate-severe orthostatic hypotension

Age> 70 years
4. PUBLISHED GUIDELINES
4.1. The American College of Physicians
These guidelines were published in 1997 [29, 30]; they included recommended criteria for
admission (see Box 2) but some of these indications were rather vague (eg no definition was
given for ‘significant’ valvular disease or ‘moderate-severe’ orthostatic hypotension).
Crane [1] undertook a retrospective cohort study of the ACP guidelines (see Appendix 2).
This showed that there was a significant difference in 1 year mortality between those in
whom admission was indicated, often indicated and not indicated. However, there was no
significant difference in 1 week and 1 month mortality which are arguably more relevant
outcomes when deciding who needs emergency admission. Indeed, following the guideline
would have lead to one patient being discharged who died within 1 week and admission
Emergency Department Syncope Guideline
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rates would have been increased (only 68% of those who fulfilled the criteria for admission
were actually admitted).
Box 3. American College of Emergency Physicians, 2004 [9]. Criteria for Admission.
Patients for Whom an Underlying Cause of Syncope is not Immediately Apparent from the Initial
assessment
Level A Evidence. None.
Level B Evidence.
1. Evidence of heart failure or structural heart disease.
2. In the presence of factors that suggest a high risk (from the San Francisco Risk Factor score):

Abnormal ECG (acute ischaemia, dysrrhythmias, significant conduction abnormalities)

Haematocrit <30%

History or examination findings of heart failure, ischaemic or structural heart disease
Level C Evidence. None
It would seem that the ACP guidelines have limited application for Emergency Department
use.
4.2. American College of Emergency Physicians
The American College of Emergency Physicians (ACEP) developed guidelines in 2001 [33]
which they updated in 2007 [26]. The 2001 version studied the evidence for stratifying risk
in patients presenting with syncope and, in particular, looked at features of the initial ED
assessment that predicted cardiac syncope. ACEP devised criteria for admission and
categorised them according to the level of evidence that underpinned them; these included
level B and C evidence based criteria.
A subsequent retrospective cohort study [9] indicated that using only the level B criteria had
100% sensitivity and 81% specificity for identifying cardiac syncope (ie all patients who were
finally diagnosed with cardiac syncope were identified as high risk in the ED). However,
using both level B and C criteria would have increased the admission rate by 13.5% without
increasing sensitivity. Therefore, the 2007 revision of the guidelines removed the level C
criteria (see Box 3).
Unfortunately, the guideline incorporates the San Francisco Syncope Risk Score which has
subsequently had its external validity questioned [11, 12] (see section 2), so again, it may
not be suitable for use in our population of patients.
4.3. European Society of Cardiology
Emergency Department Syncope Guideline
Page 9
The ESC guidelines were first developed in 2004 [27] but were significantly rewritten in 2009
[22]. In particular, syncope was defined more precisely, with transient loss of consciousness
not caused by global cerebral ischaemia (eg CVA, seizures & migraine) being separated from
the list of causes.
The aspects of the guidelines that are most relevant to ED practice recommend an initial
assessment which involves a history, examination (including lying and standing BP
measurements) and a 12-lead ECG. The information from this clinical evaluation is used to
Box 4. European Society of Cardiologists, 2009 [22]. Criteria for Admission
1. Severe structural or ischaemic heart disease

Heart failure

LV ejection failure

Previous MI
2. Clinical/ECG findings suggesting arrhythmic syncope

Syncope during exertion or supine

Palpitations at time of syncope

FH of sudden cardiac death

Non-sustained VT

Bifascicular block or other IV conduction delay (QRS ≥120ms)

Sinus bradycardia <50/min. or sinoatrial block in absence of –ve inotropes or physical
training

Pre-excited QRS

Long or short QT

Brugada
Arrhythmogenic right ventricular cardiomyopathy
answerthree
key questions:
co-morbidities
1. Is3.itImportant
syncope?

Severe anaemia

Electrolyte abnormalities
2. If it is syncope, can the underlying aetiology be diagnosed?
3. If the aetiology cannot be determined, is there any evidence to suggest an increased risk
of cardiovascular events or death?
Box 4 shows the clinical factors that have been deemed to indicate a high risk and they were
derived from international guidelines for cardiac pacing and risk stratification/ prevention of
Emergency Department Syncope Guideline
Page 10
sudden cardiac death. These are outcomes that are relevant when trying to decide whether
patients need to be admitted from the ED.
5. DISCUSSION
The clinical approach published by the European Society of Cardiologists (22) contains the
most up to date evidence, including the EGSYS score. It would seem sensible to adopt the
overall strategy developed by the ESC and their criteria for admission:
1. Patients who are diagnosed with a condition that requires admission (eg MI, PE etc).
2. Those in whom a diagnosis is not immediately apparent but who have the risk
factors listed in Box 4.
The criteria used for admission are derived from other guidelines that do not directly
address syncope and do not contain all of the ECG criteria identified by the risk scores (Table
2). The factors noted in all of the other risk scores (Table 1) but not listed by the ESC warrant
further investigation but have little evidence to suggest a short-term risk. Therefore, they
could be categorised as criteria when discharge can be considered with early out-patient
review in a cardiology clinic.
Additionally, it should not be forgotten that there may be other reasons for admission such
as elderly patients who live alone and have no social support, who would be at risk if they
collapsed at home and were unable to summons help.
Patients who do not fit any of these criteria can be considered safe for discharge for follow
up in primary care, possibly with referral for tilt-table testing in the elderly.
The suggested guideline is in Appendix 1 (below).
Emergency Department Syncope Guideline
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6. REFERENCES
1. Crane SD. Risk stratification of patients with syncope in an accident and emergency
department. Emerg Med J. 2002; 19; 23-27.
2. Silverstein MD, Singer DE, Mulley AG, et al. Patients with syncope admitted to
medical intensive care units. JAMA. 1982; 248; 1185-1189.
3. Kapoor WN. Evaluation and outcomes of patients with syncope. Medicine. 1990; 69;
160-174.
4. Ammirati F, Colivicchi F and Santini M. Diagnosing syncope in clinical practice. 2000;
21; 935-940.
5. Blanc JJ, L’Her C, Touiza A, et al. Prospective evaluation and outcome of patients
admitted for syncope over a 1 year period. Eur Heart J. 2002; 23; 815-820.
6. Martin GJ, Adams SL, Martin HG, et al. Prospective evaluation of syncope. Ann Emerg
Med. 1984; 13; 499-504.
7. Eagle KA, Black HR, Cook EF, et al. Evaluation of prognostic classifications for patients
with syncope. Am J Med. 1985; 79; 455-460.
Emergency Department Syncope Guideline
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8. Quinn JV, Stiell IG, McDermott DA, et al. Derivation of the San Francisco Syncope
Rule to predict patients with short-term serious outcomes. Ann Emerg Med. 2004;
43; 224-232.
9. Elseber AA, Decker WW, Smars PA et al. Impact of the application of the American
College of Emergency Physicians recommendations for the admission of patients
with syncope on a retrospectively studied population presenting to the emergency
department. Am Heart J. 2005; 826-831.
10. Quinn J, McDermott D, Stiell I, et al. Prospective validation of the San Francisco
Syncope Rule to predict patients with serious outcomes. Ann Emerg Med. 2006; 47;
448-454.
11. Sun BC, Mangione CM, Merchant G et al. External validation of the San Francisco
Syncope Rule. Ann Emerg Med. 2007; 49; 420-427.
12. Birnbaum A, Esses D, Bijur P, et al. Failure to validate the San Francisco Syncope Rule
in an independent emergency department population. Ann Emerg Med. 2008; 52;
151-159.
13. Reed MJ, Newby DE, Coull AJ, et al. The Risk stratification Of Syncope in the
Emergency department (ROSE) pilot study: a comparison of existing syncope
guidelines. Emerg Med J. 2007; 24; 270-275.
14. Wayne HH. Syncope. Physiological considerations and an analysis of the clinical
characteristics in 510 patients. Am J Med. 1961; 30; 418-438.
15. Day SC, Cook EF, Funkenstein H, et al. Evaluation and outcome of emergency room
patients with transient loss of consciousness. Am J Med. 1982; 73; 15-23.
16. Del Rosso A, Ungar A, Maggi R, et al. Clinical predictors of cardiac syncope at initial
evaluation in patients referred urgently to a general hospital: the EGSYS score. Heart,
2008; 94; 1620-1626.
Emergency Department Syncope Guideline
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17. Quinn J, McDermott D, Kramer N, et al. Death after emergency department visits for
syncope: how common and can it be predicted. Ann Emerg Med. 2008; 51; 585-590.
18. Kapoor WN and Hanusa BH. Is syncope a risk factor for poor outcomes? Comparison
of patients with and without syncope. Am J Med. 1996; 100; 646-655.
19. Kapoor WN, Karpf M, Wieand S, et al. A prospective evaluation and follow-up of
patients with syncope. New Engl J Med. 1983; 309; 197-204.
20. Oh JH, Hanusa BH and Kapoor WN. Do symptoms predict cardiac arrhythmias and
mortality in patients with syncope? Arch Intern Med. 1999; 159; 375-380.
21. Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. New
Engl J Med. 2002; 347; 878-885.
22. The task force for the diagnosis and management of syncope of the European
Society of Cardiology. Guidelines for the diagnosis and management of syncope
(version 2009). Eur Heart J. 2009; 30; 2631-2671.
23. Martin TP, Hanusa BH and Kapoor WN. Risk stratification of patients with syncope.
Ann Emerg Med. 1997; 29; 459-466.
24. Sarasin FP, Hanusa BH, Perneger T, et al. A risk score to predict arrhythmias in
patients with unexplained syncope. Acad Emerg Med. 2003; 10; 1312-1317.
25. Colivicchi F, Ammirati, Melina D, et al. Development and prospective validation of a
risk stratification system for patients with syncope in the emergency department:
the OESIL risk score. Eur Heart J, 2003; 24; 811-819.
26. Huff JS, Decker WW, Quinn JV, et al. Clinical policy: critical issues in the evaluation
and management of adult patients presenting to the emergency department with
syncope. Ann Emerg Med. 2007; 49; 431-444.
Emergency Department Syncope Guideline
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27. Brignole M, Alboni P, Benditt DG, et al. Guidelines on management (diagnosis and
treatment) of syncope – update 2004. Eur Heart J. 2004; 25; 2054-2072.
28. Alboni P, Brignole M, Menozzi C, et al. Diagnostic value of history in patients with
syncope with or without heart disease. J Am Coll Cardiol. 2001; 37; 1921-1928.
29. Linzer M, Yang EH, Estes M, et al. Diagnosing syncope part 1: value of history,
physical examination, and electrocardiography. Ann Intern Med. 1997; 126; 989-996.
30. Linzer M, Yang EH, Estes M, et al. Diagnosing syncope part 2: unexplained syncope.
Ann Intern Med. 1997; 127; 76-86.
31. Kapoor WN. Evaluation and management of the patient with syncope. JAMA. 1992;
268; 2553-2560.
32. Calkins H, Shyr Y, Frumin H, et al. The value of the clinical history in the
differentiation of syncope due to ventricular tachycardia, atrioventricular block, and
neurocardiogenic syncope. Am J Med. 1995; 98; 365-373.
33. American College of Emergency Physicians. Clinical policy: critical issues in the
evaluation and management of patients presenting with syncope. Ann Emerg Med.
2001; 37; 771-776.
34. Hoefnagels WAJ, Padberg GW, Overweg J, et al. Transient loss of consciousness: the
value of the history for distinguishing seizure from syncope. J Neurol. 1991; 238; 3943.
35. Kapoor WN, Karpf M, Maher Y et al. Syncope of unknown origin. The need for a
more cost-effective approach to its diagnostic evaluation. JAMA. 1982; 247; 26872691.
Emergency Department Syncope Guideline
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7. APPENDICES
7.1. APPENDIX 2. EMERGENCY DEPARTMENT SYNCOPE GUIDELINE
Syncope is defined as a transient loss of consciousness with loss of postural tone, due to global cerebral
ischaemia, usually associated with spontaneous, rapid and complete recovery. See Box 1 for the list of causes.
Initial assessment includes:

full history

examination (including measurement of lying/standing BP – see Box 2)

12-lead ECG

Seizure? See Box 3

Trauma  Head injury  manage accordingly

No LOC?
IS IT SYNCOPE?
All of the following:
1.
Was LOC complete?
2.
Was LOC transient with rapid onset &
short duration?
3.
Was postural tone lost?
4.
Was recovery spontaneous, complete &
without sequelae?
NO

Fall  Fall’s pathway
o
Altered mental status  manage accordingly
Persistent LOC?
o
Coma?  manage accordingly
o 4 Intoxication?  manage accordingly
CARDIAC? See Box
ADMIT
YES
CAN THE AETIOLOGY BE
DETERMINED?
o
YES
Emergency Department Syncope Guideline
ORTHOSTATIC? See Box 5
ASSESS MOBILITY ON
CLINICAL DECISION UNIT CONSIDER DISCHARGE IF
SAFE SOCIAL
CIRCUMSTANCES
Page 16
NO
NEURALLY-MEDIATED? See Box 6
IS THERE EVIDENCE SUGGESTING A
HIGH RISK OF CVS EVENTS OR
DEATH?
YES
HIGH RISK. See Box 7
DISCHARGE
ADMIT
NO
MODERATE RISK. See Box 8
CONSIDER DISCHARGE IF SAFE SOCIAL
CIRCUMSTANCES WITH EARLY OUTPATIENT REVEIW
LOW RISK.
DISCHARGE
BOX 1. CAUSES OF SYNCOPE
No high or moderate risk factors
NEURALLY (REFLEX)-MEDIATED

Vasovagal – emotional distress, orthostatic stress

Carotid sinus syncope

Situational – cough, sneeze, micturition, swallowing, defecation, visceral pain, laughing, postprandial, post-exercise

Atypical
ORTHOSTATIC

Autonomic failure - age-related, diabetic neuropathy, Parkinson’s disease, amyloid
neuropathy, multiple system atrophy, spinal cord injuries, uraemia

Drug-induced – hypotensives, negative inotropes, CNS depressants, anticholinergics

Volume depletion – dehydration, blood loss, Addison’s
CARDIOVASCULAR

Arrhythmias – sinus node dysfunction, AV conduction disease, PPM malfunction, SVT, VT,
drug-induced arrhythmias (esp QT prolongers)

Structural heart disease – outflow obstruction (valvular stenosis, HOCM), atrial myxoma,
pericardial disease/ effusion

Myocardial ischaemia

Pulmonary vascular – PE, pulmonary hypertension

Aortic dissection
BOX 2. ORTHOSTATIC HYPOTENSION
NEUROLOGICAL
1.

Measure BP after patient has been supine for 5 minutes
Subclavian steal syndrome
2. Stand patient for 3 minutes – take BP measurements intermittently & record the lowest
PSYCHIATRIC
reading

Chronic anxiety
Orthostatic
hypotension:
Emergency
Department
Syncope Guideline


Major depression
Fall in SBP ≥20mmHg

Fall in DBP ≥10mmHg
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BOX 3. FEATURES THAT DISTINGUISH SEIZURES FROM SYNCOPE
Although brief seizure activity may occur during syncope, tongue-biting, cyanosis, and frothing at the
mouth are suggestive of a convulsion rather than syncope.
Recovery of orientation <30 seconds suggests syncope whereas disorientation during the recovery
phase suggests a seizure.
BOX 4. FEATURES SUGGESTING CARDIAC SYNCOPE
Precipitants:

While sitting or lying.

During exertion.

After exertion, with other features of a structural heart disease with a fixed cardiac output
(eg aortic stenosis).

Fast palpitations occurring prior to syncope.
Prodrome:

Absent or brief (<5 sec) although considerable overlap with vasovagal syncope.

Nausea and vomiting during the prodrome are very unusual features of arrhythmic syncope.
Other Features:

Symptoms/risk factors suggesting acute coronary syndrome, PE etc.

A past history of cardiovascular disease.

Drug history: eg QT prolongers, diuretic.

A positive family history of sudden cardiac death, Brugada syndrome, HOCM, long QT
syndrome.

Examination features of structural heart disease with outflow obstruction, or cardiac.
ECG abnormalities:

Sinus bradycardia < 40/min. in awake, repetitive sinoatrial block, sinus pauses >3 secs.

Mobitz II 2nd degree AV block or complete heart block

Alternating LBBB & RBBB

VT or rapid SVT

Non-sustained polymorphic VT, long or short QT

PPM/ICD malfunction with cardiac pauses

Acute ischaemia +/- MI
Emergency Department Syncope Guideline
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BOX 5. FEATURES SUGGESTING ORTHOSTATIC SYNCOPE
Precipitants:

After standing up (especially after exertion).

Prolonged standing especially in hot, crowded place.

Soon after changes to medication especially drugs with hypotensive effects or those that
interact with them.
Other Features:

History of autonomic neuropathy (eg DM, Parkinson’s disease).
BOX 6. FEATURES SUGGESTING NEURALLY-MEDIATED SYNCOPE
Precipitants:

Typical precipitant eg fear/anxiety, hot/crowded place, pain, instrumentation

Prolonged standing.

During/after meal.

After exertion (in the absence of structural heart disease with a fixed cardiac output eg AS).

Head movement, wearing a tight collar, shaving suggests carotid sinus sensitivity.
Prodrome:

Vasovagal syncope tends to have a longer prodrome than cardiac syncope but there is considerable
overlap.

Abdominal discomfort during the prodrome
Recovery:

Nausea/sweating during the recovery.
Other Features:

Absence of cardiac disease.
Long history (up to 4 years) of recurrent episodes.
BOX 7. REQUIRES ADMISSION - HIGH RISK OF SHORT-TERM ADVERSE OUTCOMES
1. Severe structural or ischaemic heart disease

Heart failure

LV ejection failure

Previous MI
2. Clinical/ECG findings suggesting arrhythmic syncope

Syncope during exertion or supine

Palpitations at time of syncope

FH of sudden cardiac death
Emergency Department Syncope Guideline
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BOX 8. MODERATE RISK – ECG CRITERIA FROM PUBLISHED RISK SCORES

RBBB

Mobitz I 2nd degree AV block

1st degree AV block

AF or atrial flutter
Emergency Department Syncope Guideline
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Emergency Department Syncope Guideline
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