Continuing Education Activity

Syncope is a transient loss of consciousness and postural tone followed by spontaneous recovery. Numerous classification schemes may be used to identify and manage underlying conditions that produce syncope. However, this symptom ultimately results from decreased cerebral perfusion.

Syncopal episodes may occur suddenly and without warning or be preceded by symptoms that include dizziness, lightheadedness, diaphoresis, nausea, and visual disturbances. Patients may describe syncopal events in a wide variety of ways, some of which include fainting, blacking out, falling out, having a spell, or losing consciousness. Syncope is responsible for 1% to 3.5% of all emergency department visits and 6% of all hospital admissions in the United States. Underlying conditions that may decrease brain perfusion and lead to syncope can range from benign to life-threatening.

This activity is designed for healthcare professionals to enhance learners' competence in evaluating and managing syncope. Participants gain a broader grasp of syncope's pathophysiology, risk factors, and evidence-based diagnostic and interventional strategies. Greater proficiency prepares clinicians to collaborate effectively within an interprofessional team caring for affected patients.

Objectives:

• Differentiate benign from potentially life-threatening syncope based on clinical features.
• Create a clinically guided approach for evaluating syncope.
• Develop an evidence-based management plan for syncope.
• Collaborate with the interprofessional team to educate, treat, and monitor patients with syncope to improve patient outcomes.

Introduction

Syncope results from a decrease in cerebral blood flow, leading to a transient loss of consciousness and postural tone, followed by spontaneous recovery. Dizziness, lightheadedness, diaphoresis, nausea, and visual disturbances may precede syncope, but it can also occur suddenly without warning signs. This symptom is described as "fainting," "blacking out," "falling out," or "having a spell" and represents 1% to 3.5% of all emergency department visits and 6% of all hospital admissions in the United States.[1][2] This large number of emergency department visits and admissions reflects the varied etiologies of syncope, from benign to life-threatening, and the high degree of diagnostic uncertainty associated with this manifestation.

Etiology

Causes of Syncope

The causes of syncope may be classified as follows:

1. Cardiovascular disorders

• Cardiac arrhythmias, including both tachyarrhythmias and bradyarrhythmias
• Structural and obstructive disorders, including valvular abnormalities, hypertrophic cardiomyopathy, myocardial infarction, and pulmonary embolism

2. Cerebrovascular causes, such as vertebrobasilar insufficiency

3. Disorders of blood flow and vascular tone

• Vasovagal (neurocardiogenic) mechanisms
• Orthostatic hypotension from medications, autonomic failure, peripheral neuropathy, or decreased blood flow
• Situational causes, such as coughing, micturition, defecation, postprandial events, and deglutition
• Carotid sinus syncope

Various disorders manifest with symptoms resembling syncope. Conditions that mimic fainting spells include seizures, metabolic conditions (eg, hypoglycemia, hypoxia, and symptomatic anemia), and psychogenic disorders (eg, panic attacks).

Syncope is a symptom of an underlying disease process rather than a disease itself. This manifestation mimics a death-like experience, eliciting extreme consternation among both patients and their families. However, most syncopal events have benign causes, which include vasovagal (neurocardiogenic) mechanisms, volume depletion, and medication reactions. More ominous etiologies include dysrhythmia and valvular abnormalities, such as ventricular tachycardia, atrioventricular block, and critical aortic stenosis. A history of left ventricular dysfunction, with concomitant conduction system degeneration and an increased propensity for dysrhythmias, may be the most significant adverse cause of syncope. [3]

Vasovagal Syncope

Vasovagal syncope, also known as neurocardiogenic syncope or the common faint, accounts for nearly 50% of all syncope cases.[4] This condition can occur in response to specific situations, such as prolonged standing, crowded environments, hot conditions, severe pain, extreme fatigue, and stress, leading to vasodilation (sympathetic withdrawal) and bradycardia (parasympathetic activity).

Syncope is common even in healthy individuals and is often preceded by prodromal symptoms, including blurred vision, diaphoresis, nausea, dizziness, and weakness. These symptoms result in bradycardia and decreased blood pressure, ultimately causing loss of consciousness. Patients typically appear pale and usually regain consciousness within a few minutes, often experiencing generalized weakness. Unlike patients experiencing seizures, individuals who develop syncope retain sphincter control, rarely exhibit tonic-clonic activity, and do not experience confusion upon regaining consciousness.

Epidemiology

Syncope accounts for approximately 1% to 3.5% of emergency department visits in the United States. This symptom is more common in older adults, who often have multiple comorbidities and take various medications, than in younger individuals. Cardiac causes are more common in older patients, while noncardiac mechanisms (eg, vasovagal responses) more frequently occur in young adults. The incidence of syncope does not significantly differ between men and women.

Pathophysiology

Adequate cerebral blood flow maintains brain function by providing a constant supply of glucose. Any supply interruption, even for a few seconds, can lead to loss of consciousness or syncope. Cerebral blood flow is maintained by a complex mechanism that involves cardiac output, systemic vascular resistance, mean arterial pressure, and intravascular volume. Any defect in 1 or more of these systems can decrease cerebral blood flow. Approximately 3/4 of the blood is in the venous bed. Venous return interferences can reduce cardiac output.

Any episode lasting more than a few minutes is not syncope but is more likely to be related to an acute neurologic process, such as a seizure, which is often confused with fainting. However, when symptoms overlap too closely, electroencephalography (EEG) can differentiate a seizure from a syncope.

The terms "near syncope" and "presyncope" can be confusing, as they may carry different meanings for various practitioners. When defined as “a feeling that one is going to pass out but does not,” near syncope is related to syncope, with both conditions linked to cerebral hypoperfusion. Consequently, any disease process that decreases blood flow can lead to both syncope and near syncope.

History and Physical

Thorough history taking and physical examination are enough to arrive at a diagnosis in up to 50% of patients presenting with syncope. History taking should focus on the duration, preceding events, precipitating factors, and post-event manifestations.

The patient's position at the time of the event is essential. Syncope in a standing position may suggest vasovagal processes. In contrast, fainting in a supine position or without a prodrome may be due to neurocardiac causes. A detailed history of the patient's medical problems and medications must be included.

The physical examination of patients experiencing syncope should focus on abnormalities in vital signs, which may provide clues to underlying disease processes, such as orthostatic hypotension and cardiovascular compromise. Detailed cardiovascular and neurologic examinations should be included, looking for signs of vascular disease, congestive heart failure, or an acute cerebrovascular event masquerading as syncope.

Evaluation

Diagnostic testing rarely leads to a diagnosis, as most cases of syncope have a vasovagal origin and are, thus, benign. A thorough physical examination is the most important diagnostic tool, as it helps identify the etiology and exclude potentially life-threatening causes. The choice of diagnostic studies depends on findings from the history and physical examination.[5]

In older patients presenting to the emergency department, routine blood work, including hemoglobin and electrolytes, is indicated.[6] At a minimum, electrocardiography (ECG) and blood glucose are needed in older adults presenting with syncope. Further workup should include cardiac enzymes, continuous cardiac monitoring, and echocardiography if a cardiovascular etiology is suspected. A cardiac event monitor is recommended for discharge to outpatient patients suspected of having conduction abnormalities.[7] If a cerebrovascular etiology is suspected, the diagnostic tests should include a head computed tomography scan, carotid Doppler ultrasound, or brain magnetic resonance imaging with or without angiography. EEG is indicated if seizures are suspected. 

A tilt table test should be considered in the following situations:

• The episodes of syncope are recurrent, have an unknown etiology, and occur in the absence of cardiac disease.
• The diagnosis of vasovagal syncope is uncertain and requires ruling out potentially life-threatening causes.
• Differentiating between suspected reflex syncope and orthostatic hypotension syncope is necessary.

The ECG is the most effective diagnostic study, though it identifies the cause of syncope in only around 5% of cases. Meanwhile, routine blood tests yield a diagnosis in only about 2%. Approximately 45% of patients leave the emergency department without a clear diagnosis following a syncopal event, even after extensive testing. Recent data suggests that a targeted management approach may improve diagnostic outcomes and reduce the number of undiagnosed cases. For instance, echocardiography before discharge may reveal valvular disease in patients presenting with a murmur and syncope, and overnight telemetry or event monitoring may detect dysrhythmias in individuals with conduction abnormalities on their presenting ECG.[8][9][10]

Treatment / Management

Treatment of the underlying cause is the primary focus in managing syncope. Patients should sit or lie down quickly during an acute episode, with their legs elevated, to aid recovery from reflex postural hypotension. Keeping patients in a horizontal position after the event while preventing them from standing up too soon is recommended. Any injuries sustained during a fall from syncope require immediate attention.[11]

Vasovagal Syncope

Conservative measures for managing vasovagal syncope include avoiding situations or stimuli that trigger episodes, engaging in tilt training, and increasing salt and fluid intake. If these strategies fail, agents that may be considered for drug therapy include β-blockers, selective serotonin reuptake inhibitors, fludrocortisone, and midodrine.

Orthostatic Hypotension

Managing orthostatic hypotension involves rising slowly from a supine or sitting position to allow for a gradual change in posture. Avoiding medications such as diuretics and vasodilators, which can contribute to orthostatic hypotension, is also essential. Compression stockings may be used to improve venous return, and intravenous fluids are recommended for patients who have depleted intravascular volume. Midodrine may be considered as a treatment option in refractory cases.

Risk Stratification of Syncope

Disposition is often the most challenging task in caring for patients with syncope in the emergency department. Admission rates in patients presenting with syncope vary widely. About 80% of these patients are admitted in the United States, but admission rates can be as low as 10% in Canada and other regions. This discrepancy likely reflects differences in thresholds for identifying rare but clinically significant causes rather than variations in acuity.

Numerous pathways have been published to risk-stratify patients who experience syncope and improve these admission rates, but most are comparable to a thorough history and examination. The Boston Syncope Criteria focus on risk stratification for admission based on a history of cardiac disease (such as left ventricular dysfunction, dysrhythmias, or valvular disease), concomitant complaints like chest pain, dyspnea, or palpitations, and ECG abnormalities indicating ischemia, dysrhythmias, or conduction disease. These criteria suggest that patients without associated comorbidities and with unremarkable emergency department evaluations are generally safe for discharge.

The costs of evaluating syncope have grown exponentially in recent years. Approximately $2 billion is spent on patients hospitalized for syncope in the United States.[12][13]

Follow-Up

Patients with syncope of unknown etiology and without underlying heart disease generally have good outcomes. Meanwhile, individuals with syncope and underlying heart disease need regular follow-ups with a primary care physician and cardiologist. 

Differential Diagnosis

Important differential diagnoses for syncope include seizure disorders, hypoglycemia, and panic attacks. Seizures may be distinguished from syncope by the presence of an aura, tonic-clonic activity, prolonged unconsciousness, urinary or bowel incontinence, tongue biting, and confusion upon regaining consciousness. Hypoglycemia may also cause loss of consciousness, but it is typically associated with symptoms such as sweating, shakiness, and irritability. Panic attacks, on the other hand, are characterized by feelings of impending doom, palpitations, air hunger, and tingling sensations around the perioral region and fingertips. Recognizing these differences is crucial for accurately diagnosing and managing syncope.

Prognosis

The prognosis depends on the underlying cause, making identification highly important. The annual mortality rate can range from 0% to 12% in patients with noncardiac causes and 18% to 33% in patients with cardiac causes.[14]

Complications

Patients may sustain injuries from falls due to syncope. These injuries may have a greater impact if the patient was driving at the time of the event.

Consultations

The most common cause of syncope is a vasovagal reaction, which is self-limiting. A primary care physician or hospitalist can manage this condition. A cardiology consultation is necessary when a cardiac etiology is suspected. Neurology consultation is warranted when cerebrovascular causes are considered.

Deterrence and Patient Education

Education is vital for patients experiencing syncope due to vasovagal responses, orthostatic hypotension, and situational triggers. Patients should be advised to refrain from driving and avoid heights following a syncopal episode. Additionally, individuals with situational syncope should identify and avoid scenarios that may provoke an episode. For people with orthostatic hypotension, increasing fluid intake and avoiding dehydration are essential.

Pearls and Other Issues

The most important points to remember when evaluating and managing syncope are the following:

• Most syncopal episodes have a vasovagal cause and are benign.
• Syncope can be life-threatening if associated with a cardiac disorder, including rhythmic and valvular abnormalities. 
• ECG is the most helpful test in syncope, but its diagnostic yield is only 5%. Thus, a careful history and physical examination remain the most valuable tools for evaluating a syncopal event.
• Following a syncopal episode, patients should be instructed not to drive or operate heavy machinery until the completion of their workup or follow-up with their primary care provider.
• Mental illness and substance abuse should be considered in patients who have had syncope with an unclear etiology.[15]

Important alternative diagnoses include seizures, metabolic events, and panic attacks. A thorough clinical examination and judicious diagnostic testing can help identify the cause of syncope and guide treatment.

Enhancing Healthcare Team Outcomes

Most patients who visit the emergency department for syncope do not have a diagnosis at discharge. Even hospitalized patients often leave without determining the cause of their fainting spell. Syncope is benign in most cases; however, patients require close outpatient follow-up to ensure the etiology is identified and the event does not recur. A primary care physician or cardiologist must be involved in the ongoing care of patients who report experiencing this symptom.

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References

1.

Rivasi G, Ungar A, Moya A, Brignole M, Sutton R, Fedorowski A. Syncope: new solutions for an old problem. Kardiol Pol. 2021;79(10):1068-1078. [PubMed: 34668180]

2.

Mazzella AJ, Wood BS, Doad J, Hendrickson MJ, Rosman L, Gehi AK. Interhospital variability in hospital admissions for patients with low-risk syncope presenting to the emergency department. Heart Rhythm O2. 2024 Jul;5(7):435-442. [PMC free article: PMC11305874] [PubMed: 39119025]

3.

Albassam OT, Redelmeier RJ, Shadowitz S, Husain AM, Simel D, Etchells EE. Did This Patient Have Cardiac Syncope?: The Rational Clinical Examination Systematic Review. JAMA. 2019 Jun 25;321(24):2448-2457. [PubMed: 31237649]

4.

Shen WK, Brignole M. Hospital admission for syncope evaluation: Can we see the forest for the trees? Heart Rhythm. 2022 Oct;19(10):1723-1724. [PubMed: 35724871]

5.

Wu S, Chen Z, Gao Y, Shu S, Chen F, Wu Y, Dai Y, Zhang S, Chen K. Development and Validation of a Novel Predictive Model for the Early Differentiation of Cardiac and Non-Cardiac Syncope. Int J Gen Med. 2024;17:841-853. [PMC free article: PMC10924787] [PubMed: 38463438]

6.

Jansen S, van der Velde N. Syncope in older adults: challenges, approach and treatment. Age Ageing. 2024 Feb 01;53(2) [PubMed: 38331395]

7.

Freund O, Caspi I, Shacham Y, Frydman S, Biran R, Abu Katash H, Zornitzki L, Bornstein G. Holter ECG for Syncope Evaluation in the Internal Medicine Department-Choosing the Right Patients. J Clin Med. 2022 Aug 16;11(16) [PMC free article: PMC9409720] [PubMed: 36013018]

8.

Reed MJ. Approach to syncope in the emergency department. Emerg Med J. 2019 Feb;36(2):108-116. [PubMed: 30470687]

9.

Anderson TS, Thombley R, Dudley RA, Lin GA. Trends in Hospitalization, Readmission, and Diagnostic Testing of Patients Presenting to the Emergency Department With Syncope. Ann Emerg Med. 2018 Nov;72(5):523-532. [PubMed: 30342727]

10.

Altinsoy M, Sutton R, Kohno R, Sakaguchi S, Mears RK, Benditt DG. Ambulatory ECG monitoring for syncope and collapse in United States, Europe, and Japan: The patients' viewpoint. J Arrhythm. 2021 Aug;37(4):1023-1030. [PMC free article: PMC8339081] [PubMed: 34386128]

11.

du Fay de Lavallaz J, Badertscher P, Nestelberger T, Zimmermann T, Miró Ò, Salgado E, Christ M, Geigy N, Cullen L, Than M, Javier Martin-Sanchez F, Di Somma S, Frank Peacock W, Morawiec B, Walter J, Twerenbold R, Puelacher C, Wussler D, Boeddinghaus J, Koechlin L, Strebel I, Keller DI, Lohrmann J, Michou E, Kühne M, Reichlin T, Mueller C., BASEL IX Investigators. B-Type Natriuretic Peptides and Cardiac Troponins for Diagnosis and Risk-Stratification of Syncope. Circulation. 2019 May 21;139(21):2403-2418. [PubMed: 30798615]

12.

Ungar A, Mussi C, Nicosia F, Ceccofiglio A, Bellelli G, Bo M, Riccio D, Landi F, Martone AM, Langellotto A, Ghidoni G, Noro G, Abete P. The "syncope and dementia" study: a prospective, observational, multicenter study of elderly patients with dementia and episodes of "suspected" transient loss of consciousness. Aging Clin Exp Res. 2015 Dec;27(6):877-82. [PubMed: 25820493]

13.

Mechanic OJ, Pascheles CY, Lopez GJ, Winans AM, Shapiro NI, Tibbles C, Wolfe RE, Grossman SA. Using the Boston Syncope Observation Management Pathway to Reduce Hospital Admission and Adverse Outcomes. West J Emerg Med. 2019 Mar;20(2):250-255. [PMC free article: PMC6404692] [PubMed: 30881544]

14.

Kapoor WN. Current evaluation and management of syncope. Circulation. 2002 Sep 24;106(13):1606-9. [PubMed: 12270849]

15.

Salehi F, Hassanzadeh Taheri MM, Riasi H, Mehrpour O. Recurrent Syncope following Substance Abuse; a Case Report. Emerg (Tehran). 2017;5(1):e47. [PMC free article: PMC5325918] [PubMed: 28286854]

Disclosure: Shamai Grossman declares no relevant financial relationships with ineligible companies.

Disclosure: Madhu Badireddy declares no relevant financial relationships with ineligible companies.