Syncope and Syncope Mimics

Authors: Jamie Zink, MD (EM Resident Physician, Virginia Tech Carilion EM Residency) and Andrew Moore, MD (Assistant Professor of Emergency Medicine, Virginia Tech Carilion School of Medicine) // Reviewed by: Andrew Grock, MD; Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Case #1

A 73-year-old male with a past medical history of congestive heart failure (EF 20-25%) and hypertension presents following an episode of loss of consciousness (LOC) while walking 2 hours prior to arrival. He thinks he may be dehydrated and denies the following: a podrome, head trauma, other traumatic injury, chest pain, shortness of breath, or abdominal pain. The LOC lasted about 10 seconds and the patient quickly returned to baseline. He is currently asymptomatic and asking to be discharged.

Vitals: HR 83, RR 18, BP 145/93, Temp 97.9°F, SpO2 94%

Case #2

A 20-year-old female who is 33 weeks pregnant (G1P0) with no known PMHx presents after LOC for approximately 2 minutes. Prior to the episode she reports feeling in her usual state of good health. During her LOC, her eyes reportedly deviated to the left and she had urinary incontinence. The patient took about 15 minutes to return to baseline. Currently endorsing fatigue and blurry vision bilaterally, otherwise denies any symptoms. She denies prodromal symptoms, fevers, chills, nausea, vomiting, shortness of breath, chest pain, or abdominal pain.

Vitals: HR 91, RR 18, BP 173/111, Temp 99.2°F, SpO2 98%


Syncope, or brief LOC, is a fairly common presentation, accounting for 1-2% of ED visits annually in the United States.2,3 Nonetheless, it can be a frustrating chief complaint for emergency medicine (EM) physicians. By the time the patient sees you, most have normal and stable vital signs, and are back to baseline without symptoms. Furthermore, the list of potential etiologies is near endless, as syncope can be caused by an arrhythmia, a benign etiology (e.g., vagal), or near any dangerous diagnosis in the EM textbook. Studies do show the prevalence of syncope etiologies (in descending order of prevalence) are: vasovagal/reflex-mediated (21%), cardiogenic (10%), and syncope caused by orthostatic hypotension (9%).2–4 Other, less common causes are medication related (7%) and neurologic (4%).3 Of the many causes of syncope, most are benign, with only about 10% being critical.1,3 Of those critical diagnoses, cardiac etiologies are associated with the worst outcomes, carrying a >10% 6-month mortality rate.3 In the end, over one third of ED syncope patients never discover the etiology.4 That said, each cause shares the same common pathway – a brief interruption of blood flow/nutrients to the brain or decrease in cerebral perfusion by >35%, most commonly by a drop in cardiac output.5Of note, near syncope (fainting without LOC) shares the same basic pathophysiology and risks as syncope.6,7

Additionally, syncope can present similarly to several other conditions, further obfuscating the picture. Fortunately, the emergency department’s (ED) job is not necessarily to diagnose the exact cause of syncope (assuming it truly was syncope), but to rule out life threatening conditions and risk stratify for admission versus discharge with outpatient management. As such, having a systematic approach to risk stratifying and working up syncope while considering mimics is absolutely essential.

Of course, some patients will require immediate action, resuscitation, and a targeted history and physical. As with every patient, start with the basics when warranted:

Assess ABCDEs and vital signs. Place the patient on the monitor, obtain an ECG and obtain 2 large bore IV’s. If the patient is hypotensive, consider performing a RUSH exam.1

Syncope Mimics

Syncope mimics achieve LOC via different physiologic mechanisms and must be identified as management is completely different.4


One study showed that 40 out of 822 patients presenting with syncope ultimately were diagnosed with seizure.3 While syncope causes LOC through global cerebral hypoperfusion, some seizures cause LOC by decreasing or disorganizing activity in the reticular activating system (RAS).8 Seizures are certainly variable in presentation and can sometimes be obvious based on history, however, nonconvulsive seizures can be difficult to clinically distinguish from syncope.4Conversely, syncopal episodes may present with reports of “shaking” and are presumed to be seizures, but are actually myoclonic jerks related to cerebral hypoperfusion.4

Unfortunately, there are no diagnostic tests in the ED for differentiating syncope from seizure after they have occurred. That said, some clinical signs such as a prolonged return to baseline as well as the presence of tongue lacerations or incontinence can suggest seizure activity.9 The most important aspect is complete return to neurologic baseline following the transient loss of consciousness.

Temporal lobe epilepsy, in particular, is associated with ictal asystole and can present with sudden collapse or unexplained falls in some cases.10 During these episodes, patients may remain unresponsive for 2 to 3 minutes with their eyes closed. Without an EEG during the episode, this is indistinguishable from syncope.10 That said, EEG monitoring is rarely warranted in the ED if the patient has returned to baseline, and seizure can usually be worked up outpatient.4

Metabolic Disorders

Many different metabolic disorders cause LOC and can mimic syncope, including hypoglycemia, hypoxemia, heat stroke, carbon monoxide poisoning, hyperventilation, and toxic ingestions.4 Importantly, patients with LOC from metabolic disorders typically remain altered or symptomatic until their underlying metabolic derangement is corrected.4

Hypoglycemia is usually associated with autonomic symptoms and should always be considered in patients with diabetes, especially if on insulin or oral hypoglycemics.4

Hypoxemia can additionally cause LOC and should be considered in patients with underlying lung pathology, particularly if on home oxygen or if hypoxia is noted in the ED.

Exertional heat stroke (history of strenuous activity in a hot environment for a prolonged time) should be fairly obvious based on history. Non-exertional heat stroke may be less obvious, in which the patient, typically elderly or disabled, inherently lacks the ability to cool themselves.11,12 Risk factors include lack of air conditioning and social isolation. Non-exertional heat stroke should also be considered in patients with congenital absence of sweat glands or with history of severe burns, progressive systemic scleroderma, hyperthyroidism, and pheochromocytoma.11,12

Recent exposure to structural fires as well as vehicle exhaust or space heaters in an enclosed environment should raise concern for carbon monoxide toxicity.13 Symptoms range from headaches, nausea, and flu like illness to LOC and death.13 Consider this especially if multiple patients present from the same area with similar symptoms. Check a co-oximetry on suspected CO toxic patients and treat with exogenous oxygen. If airway/breathing is intact, place on high flow oxygen via nonrebreather and evaluate for possible hyperbaric therapy. If airway/breathing not intact, intubate, place on 100% FiO2, and transfer to a facility with hyperbaric capabilities. LOC secondary to CO poisoning is an indication for hyperbaric oxygen.13

Hyperventilation can cause transient LOC secondary to hypocapnia causing cerebral vasoconstriction, and thus, cerebral hypoperfusion.14 However, because hyperventilation is not always accompanied by a decrease in pCO2, it stands to reason that there may be another mechanism responsible.4 If hyperventilation is present, consider infection, salicylate overdose, primary lung etiology, pregnancy, pain, and severe anxiety.4

Other toxic ingestions that can present with LOC include salicylates, narcotics, insulin and hypoglycemics, cholinesterase inhibitors, antidepressants, antihypertensives, and vasodilators.4


Several stroke presentations can mimic syncope. Acute ischemia of the vertebrobasilar system can cause LOC.4 If secondary to a TIA, these symptoms by definition would be transient. One study showed that 38 of 772 (4.9%) patients with stroke or TIA had syncope or presyncope on initial presentation.15 Another study of 483 patients in the ED with syncope found that 37 (7.7%) had TIA-related syncope, which was highly concomitant with hypertension and ischemic heart disease.16

Consider TIA in all patients with multiple episodes of unexplained LOC, particularly if they have stroke risk factors, and direct the history and physical exam to thoroughly evaluating for any unidentified resolved or persistent neurologic deficits.4

Intracranial Hypertension

Case reports of LOC from increased ICP secondary to mass lesions, subdural hematomas, and cerebral venous sinus thrombosis have been described in the literature.17,18 Although rare, consider increased ICP if there is a history of recent head trauma, recurrent unexplained headaches, or focal neurologic symptoms.

Psychogenic Pseudosyncope

The appearance of LOC without true loss of consciousness, termed psychogenic pseudosyncope, is a form of conversion disorder and is clinically similar to psychogenic nonepileptic seizures, but without the characteristic bodily movements.4One study found 14% of 939 patients referred to an outpatient center with undiagnosed syncope had psychogenic pseudosyncope.19 It is diagnosed by precipitating an episode during EEG monitoring, which will reveal normal alpha waves without EEG abnormalities.20 True syncope will have background suppression or delta wave slowing.20

Patients tend to be young, female, have other psychiatric comorbidities, and display an increased number of “syncopal” events leading up to their presentation.21 Characteristics include prolonged duration, high frequency of episodes, little or no post-ictal state, no injuries sustained from episodes, and unusual triggers, such as exercise or lying supine without typical predisposing factors such as noxious stimuli.20,21


Cataplexy, a pathognomonic symptom of narcolepsy, involves sudden onset, transient loss of skeletal muscle tone without loss of consciousness, and may be confused with syncope.4 Unlike syncope, patients typically remember the episode as they do not have LOC. Patients will often feel the onset of muscle weakness and can sometimes sit or lie down to avoid injury before reaching maximal intensity.4,22 Triggers are often easily identified as this is preceded by strong emotions, either positive (more common) or negative.22


Obtain a history from the patient AND witnesses.

Ask about triggering events and prodromal symptoms. What was the patient doing right before their LOC? Exertion preceding syncope in the absence of a prodrome or trigger is highly concerning for a cardiac etiology.1,3,23

Ask about past medical history (especially cardiac hx and VTE risk factors) to help with risk stratification. Any family history of sudden, unexplained death?

Has the patient syncopized before and if so, was this different?

How long did it take for the patient to return to baseline? A prolonged recovery may be indicative of seizure activity.

Ask about any symptoms that may be associated with syncope. This can be tremendously helpful in elucidating the etiology (see Syncope Plus).

Perform a thorough medication reconciliation.

Syncope Plus

Other symptoms, when present with syncope, can provide important clues to the etiology. Use the following word associations as a guide for considering critical diagnoses. These are of course not absolutes.

Syncope + headache = SAH, elevated ICP, RCVS, cervical vessel dissection

Syncope + chest pain = MI, PE, aortic dissection, aortic stenosis, tamponade

Syncope + shortness of breath = PE, dysrhythmia (when associated with CHF), MI, hypoxia, aortic stenosis, tamponade

Syncope + palpitations = dysrhythmia

Syncope + vomiting = MI, GI bleed

Syncope + abdominal or back pain = AAA, dissection, GI bleed, ectopic pregnancy

Syncope + vaginal bleeding = ectopic pregnancy

Physical Exam

The physical exam should focus primarily on cardiovascular and neuro systems. Commonly, the following are performed: bilateral upper extremity blood pressures, cardiac auscultation for murmurs, a complete neuro exam to evaluate for any focal deficits, mental status assessment as a sustained alteration may suggest a post-ictal state or metabolic encephalopathy.1 Evaluate for tongue lacerations as well as abdominal tenderness and/or a pulsatile mass. Lastly, consider a rectal exam if the history suggests GI bleed. Occult blood testing is poorly evidence based; however, the presence of gross blood is important to note.

Of course, don’t forget to rule out traumatic injuries during the exam that may have been sustained during the syncopal episode.


An ECG is required on every suspected syncope case. Admit any patient with ischemia, conduction abnormalities, prolonged QT or QTc, dangerous syncope syndrome (Wolf-Parkinson-White, Brugada, hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia), or other concerning dysrhythmias.24 Consider echocardiography in patients with significant cardiac history or with ECG abnormalities.4

Blood glucose should be checked if you suspect hypoglycemia, particularly if the patient is diabetic. A pregnancy test is commonly performed in women of childbearing age, and absolutely must be done if there is any abdominal, flank, or pelvic pain or vaginal bleeding to rule out ectopic pregnancy.

More advanced labs and imaging should be ordered as clinically indicated but are often nondiagnostic.1


In cases of actual syncope, once other life-threatening etiologies have been ruled out, the patient’s arrythmia risk determines disposition. Limited data for clinical decision rules exist as most of them failed external validation. One option is the Canadian Syncope Risk tool which has been externally validated. Generallypatients that are low risk (no cardiovascular risk factors) with a normal ECG, normal vitals, and a clear vasovagal mechanism may be discharged without labs or imaging.1 Patients that are low risk but without clear cause may be observed with or without labs prior to discharge and do not necessarily require outpatient follow up. Intermediate-risk patients (elderly with a likely vasovagal mechanism or young patients with some cardiovascular risks and no clear cause) with a normal ECG may be observed with or without labs and may be considered for a short admission to a monitored bed vs outpatient follow up with ambulatory monitoring.1

Admit all patients that are high risk for an arrythmia as well as those found to have an underlying etiology requiring specific treatment (PE, ACS, AAA rupture, etc.).1

Case Wrap Up and Conclusion

Case #1 is very concerning for cardiogenic syncope, especially given the patient’s history of heart failure, exertion preceding syncope, and the reported lack of prodrome. The patient’s ECG met voltage criteria for LVH and additionally revealed nonspecific repolarization abnormalities.  A chest X-ray was performed revealing cardiomegaly. A troponin, CBC and CMP were unremarkable. Pro-BNP was moderately elevated but unchanged from baseline. The patient had two runs of non-sustained ventricular tachycardia while on telemetry and was ultimately admitted for AICD placement. This patient should not be sent home, despite being asymptomatic!

Case #2 is consistent with eclampsia. Pay attention to the history of pregnancy, the story concerning for seizure (eye deviation, urinary incontinence, and prolonged return to baseline), and the hypertension on arrival. The patient’s ECG was normal sinus without abnormality.  A CBC, CMP, and UA were performed. The CBC and CMP were unremarkable, however the UA revealed heavy proteinuria. The patient was given 6 grams of magnesium through intravenous bolus and admitted to OB.

Syncope can be a difficult chief complaint as it can be challenging to differentiate from mimics. That said, take a good history and perform a thorough physical exam to appropriately risk stratify patients and tailor therapy. Everyone gets an ECG. Further testing may be warranted based on H&P.

Take Home Points

– Every syncope patient deserves an ECG and telemetry monitoring while in the ED. Additional targeted testing may be warranted based on elements from the history and physical exam. There is no role for broadly ordering screening labs on every syncope patient.

– Up to one-third of patients with syncope will be undiagnosed after their ED evaluation.

– The job of an EM physician is not to diagnose the exact etiology of syncope, but to risk stratify patients, rule out critical diagnoses, and treat as needed. Determine who can go home and who needs to stay.

– Rule out traumatic injuries that may have been sustained during the syncopal episode.

– Consider syncope mimics, especially emergencies such as seizures, metabolic disorders, stroke/TIA, and intracranial hypertension.


  1. Quinn J, D’Souza P. Syncope. EM:RAP CorePendium. Accessed November 30, 2021.
  2. Chen LY, Shen WK, Mahoney DW, Jacobsen SJ, Rodeheffer RJ. Prevalence of syncope in a population aged more than 45 years. Am J Med. 2006;119(12):1088.e1-7. doi:10.1016/j.amjmed.2006.01.029
  3. Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med. 2002;347(12):878-885. doi:10.1056/NEJMoa012407
  4. Coleman DK, Long B, Koyfman A. Clinical Mimics: An Emergency Medicine–Focused Review of Syncope Mimics. J Emerg Med. 2018;54(1):81-89. doi:10.1016/j.jemermed.2017.09.012
  5. Thiruganasambandamoorthy V, Quinn J. Syncope. In: Tintinalli JE, Ma OJ, Yealy DM, et al., eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 9th ed. McGraw-Hill Education; 2020. Accessed November 30, 2021.
  6. Grossman SA, Babineau M, Burke L, et al. Do outcomes of near syncope parallel syncope? Am J Emerg Med. 2012;30(1):203-206. doi:10.1016/j.ajem.2010.11.001
  7. Bastani A, Su E, Adler DH, et al. Comparison of 30-Day Serious Adverse Clinical Events for Elderly Patients Presenting to the Emergency Department With Near-Syncope Versus Syncope. Ann Emerg Med. 2019;73(3):274-280. doi:10.1016/j.annemergmed.2018.10.032
  8. Yu L, Blumenfeld H. Theories of impaired consciousness in epilepsy. Ann N Y Acad Sci. 2009;1157:48-60. doi:10.1111/j.1749-6632.2009.04472.x
  9. Sheldon R, Rose S, Ritchie D, et al. Historical criteria that distinguish syncope from seizures. J Am Coll Cardiol. 2002;40(1):142-148. doi:10.1016/s0735-1097(02)01940-x
  10. Fincham RW, Shivapour ET, Leis AA, Martins JB. Ictal bradycardia with syncope: a case report. Neurology. 1992;42(11):2222-2223. doi:10.1212/wnl.42.11.2222
  11. Atha WF. Heat-related illness. Emerg Med Clin North Am. 2013;31(4):1097-1108. doi:10.1016/j.emc.2013.07.012
  12. Hifumi T, Kondo Y, Shimizu K, Miyake Y. Heat stroke. J Intensive Care. 2018;6:30. doi:10.1186/s40560-018-0298-4
  13. Rose JJ, Wang L, Xu Q, et al. Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy. Am J Respir Crit Care Med. 2017;195(5):596-606. doi:10.1164/rccm.201606-1275CI
  14. Cipolla MJ. Control of Cerebral Blood Flow. Morgan & Claypool Life Sciences; 2009. Accessed November 30, 2021.
  15. Ryan DJ, Kenny RA, Christensen S, Meaney JFM, Fagan AJ, Harbison J. Ischaemic stroke or TIA in older subjects associated with impaired dynamic blood pressure control in the absence of severe large artery stenosis. Age Ageing. 2015;44(4):655-661. doi:10.1093/ageing/afv011
  16. Davidson E, Rotenbeg Z, Fuchs J, Weinberger I, Agmon J. Transient ischemic attack-related syncope. Clin Cardiol. 1991;14(2):141-144. doi:10.1002/clc.4960140210
  17. Bruner DI, Jamros C, Cogar W. Subdural Hematoma Presenting as Recurrent Syncope. J Emerg Med. 2015;49(3):e65-68. doi:10.1016/j.jemermed.2015.01.037
  18. Larimer P, McDermott MW, Scott BJ, Shih TT, Poisson SN. Recurrent syncope due to refractory cerebral venous sinus thrombosis and transient elevations of intracranial pressure. The Neurohospitalist. 2014;4(1):18-21. doi:10.1177/1941874413493183
  19. Iglesias JF, Graf D, Forclaz A, Schlaepfer J, Fromer M, Pruvot E. Stepwise evaluation of unexplained syncope in a large ambulatory population. Pacing Clin Electrophysiol PACE. 2009;32 Suppl 1:S202-206. doi:10.1111/j.1540-8159.2008.02291.x
  20. Raj V, Rowe AA, Fleisch SB, Paranjape SY, Arain AM, Nicolson SE. Psychogenic pseudosyncope: diagnosis and management. Auton Neurosci Basic Clin. 2014;184:66-72. doi:10.1016/j.autneu.2014.05.003
  21. Benbadis SR, Chichkova R. Psychogenic pseudosyncope: an underestimated and provable diagnosis. Epilepsy Behav EB. 2006;9(1):106-110. doi:10.1016/j.yebeh.2006.02.011
  22. Dauvilliers Y, Siegel JM, Lopez R, Torontali ZA, Peever JH. Cataplexy–clinical aspects, pathophysiology and management strategy. Nat Rev Neurol. 2014;10(7):386-395. doi:10.1038/nrneurol.2014.97
  23. Writing Committee Members, Shen WK, Sheldon RS, et al. 2017 ACC/AHA/HRS guideline for the evaluation and management of patients with syncope: A report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Heart Rhythm. 2017;14(8):e155-e217. doi:10.1016/j.hrthm.2017.03.004
  24. Sud S, Klein GJ, Skanes AC, Gula LJ, Yee R, Krahn AD. Predicting the cause of syncope from clinical history in patients undergoing prolonged monitoring. Heart Rhythm. 2009;6(2):238-243. doi:10.1016/j.hrthm

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