Introduction

Presyncope, or near-syncope, is often poorly defined and may have different meanings to different healthcare providers, but it denotes a state of near-fainting or a prodrome of syncope. The most uniform definition is “feeling like one was going to pass out but without actual loss of consciousness.” Near syncope can last for seconds to minutes. A feeling of lightheadedness, general weakness, warmth, diaphoresis, nausea, palpitations, or blurry vision may accompany symptoms. Although often perceived as less severe than syncope, data suggest that the pathophysiology (cerebral hypoperfusion) and outcomes of near syncope mimic those of syncope.

Etiology

The etiologies of presyncope are diverse, ranging from the benign to the life-threatening. Presyncope causes are the same as for syncope and include cardiac and noncardiac etiologies. Cardiac presyncope may be associated with palpitations and may occur while in a sitting or supine position, or during effort or exercise.

Most common are noncardiac etiologies that include vasovagal or neurocardiogenic, and causes related to volume shifts, such as orthostatic hypotension, medication-induced, vascular, and sepsis. Vasovagal presyncope is common and is often characterized by a prodrome, including nausea, flushing, diaphoresis, blurred vision, and lightheadedness. High-risk medications include antihypertensives, cardiovascular agents, and antipsychotics.[1][2] Orthostatic hypotension can be caused by medications, primary and secondary autonomic disorders such as neurodegenerative diseases, and bed rest in the elderly[3]. Guidelines define orthostatic hypotension as a decrease in systolic blood pressure (SBP) of 20 mm Hg or greater, or a decrease in diastolic blood pressure (DBP) of 10 mmHg or greater, within 3 minutes of standing.[4] Vascular causes are less common but should be considered based on the history, including pulmonary embolism, mesenteric steal syndrome, carotid insufficiency, and aortic pathology.[5][6][7] 

Cardiac causes, which are more ominous, include mechanical (eg, cardiac tamponade or valvular disease) and dysrhythmic (eg, paroxysmal ventricular tachycardia or conduction system disease). Dysrhythmias, which induce hemodynamic impairment that can lead to a critical decrease in cardiac output and cerebral blood flow, are the most common cardiac cause [8][4]. Bradycardias are the most common dysrhythmias, but tachy-dysrhythmias that compromise stroke volume can also cause presyncope and syncope. Structural cardiovascular disease causes presyncope when circulatory demands exceed the heart’s ability to increase output. The most frequent structural causes are aortic stenosis and hypertrophic cardiomyopathy. Atypical cardiovascular causes of presyncope should be considered more closely in older people than in younger populations.

Epidemiology

Approximately 19% of the U.S. population will experience a syncopal episode during their lifetime, most commonly in early adulthood or later in life, after the age of 70. Nearly 58% of individuals presenting with syncope are female.[9][10].  Approximately 3% of visits to emergency departments and up to 6% of hospital admissions in the United States are for syncope.[11][12] Accurately determining the epidemiology of presyncope is challenging, as it is often underreported or grouped with syncope in datasets. However, its incidence is likely higher than that of syncope.[13][14]  In one study specifically focused on presyncope, the average patient age was 56 years, and 61% were female. Hospital admission occurred in 49% of presyncopal patients, compared to 69% of those with syncope, despite a similar risk of adverse outcomes. Notably, 20% of presyncopal patients experienced an adverse event or required an intervention, with the most common outcomes including sepsis, bradyarrhythmia, gastrointestinal bleeding, and acute renal failure.[14]

History and Physical

The history, medication review, physical examination, and ECG have the most excellent utility in evaluating presyncope.[1][15] For example, vasovagal prodromes typically last more than 5 seconds and follow a recognizable precipitating event. A history of orthostatic intolerance may include recurrent lightheadedness upon standing. In contrast, cardiac causes often present with prodromes lasting less than five seconds. Risk factors for vascular and cardiac etiologies, such as prior cardiac history, diabetes, hypertension, and smoking, should be carefully assessed. Medication review is essential during the initial evaluation, with particular attention to antihypertensives, antiarrhythmics, QTc-prolonging agents, and other cardiac medications.

Vital signs should be obtained, although they are often normal once symptoms have resolved. While the utility of orthostatic vital signs remains controversial, they may be helpful in evaluating suspected volume depletion, especially in older adults.[16][17] A physical examination should include careful auscultation of the heart and lungs, as well as palpation of the peripheral arteries, and a neurological examination. A stool hemoccult test should be performed if there is concern for gastrointestinal bleeding. Trauma evaluation should be conducted when indicated by the clinical history.

Evaluation

The initial task in presyncope is to obtain vital signs. An EKG and fingerstick glucose test should be performed on all patients; however, there is no gold standard for diagnostic testing in presyncope.[18][15] Blood tests, such as electrolytes, complete blood count, cardiac enzymes, lactate, and blood cultures, as well as imaging modalities like head CT and echocardiography, should be guided by the history and examination alone.[19][20][21] Routine blood tests typically only confirm clinical suspicion. Head CT should be limited to patients with signs of trauma, neurologic deficits, or neurologic complaints[22]. An echo is often recommended only if a new murmur is heard. A tilt table test can be considered as an outpatient test to help identify postural hypotension.

Common predictors that may indicate a need for further workup include a cardiac or valvular disease history (ventricular dysrhythmia, congestive heart failure), a newly abnormal ECG, anemia or severe volume depletion (from a gastrointestinal bleed), syncope while supine or with effort, report of palpitations or chest pain, persistent abnormal vital signs, or family history of sudden death.

Treatment / Management

As noted, patients with near syncope are as likely as those with syncope to experience critical interventions or adverse outcomes; however, presyncope patients are less likely to be admitted.[14] Treatment and management depend on the apparent etiology of the patient’s presyncope. Fluids should be administered if the patient appears dehydrated, and antibiotics should be considered if there is a concern for sepsis. Hospital admission should be based on the potential for adverse outcomes if further evaluation or treatment is delayed.

Most near syncope diagnoses are presumptive, cannot be confirmed by standard criteria, and may not be able to exclude cardiac conduction causes that have potentially life-threatening consequences. The need for prompt risk stratification and concern for cardiac etiology may be a factor influencing emergency department physicians to pursue extensive evaluations for many patients who present to the emergency department with presyncope.

The Boston Syncope Criteria has accurately screened patients with presyncope for risk of adverse outcomes at 30 days.[23][13] The Boston criteria recommend admitting patients with high-risk factors, including symptoms of acute coronary syndrome, a cardiac or valvular disease history, family history of sudden death, signs of conduction disease, persistently abnormal vital signs, or profound volume depletion, such as with gastrointestinal bleeding.[23][24] If the etiology of presyncope is determined to be vasovagal or dehydration, and the workup is normal, these patients may be discharged with close follow-up by their primary care provider.[25][26][13] There have been multiple other scoring systems developed to guide the rationale for inpatient versus outpatient management of syncope, but most have excluded presyncope or near-syncope from their studies due to the lack of uniformity in defining this population.[27][28][29] Thus, the value and success of such evaluations do not provide a proven uniform basis for choosing between inpatient versus outpatient evaluation of patients with presyncope.

Finally, a patient’s social situation, coping capacity, and ability to return home safely must be considered for any patient who presents to the emergency department with presyncope. If a patient is discharged from the emergency department, regardless of etiology, they should have close follow-up with their primary care physician or cardiologist, ideally scheduled before discharge.

Differential Diagnosis

Differential diagnoses include the following:

• Cardiac myxoma
• Cough syncope
• Defecation syncope
• Dysrhythmias
• Micturition syncope
• Postprandial syncope 
• Sick sinus syndrome
• Sinoatrial block
• Sinus pause 
• Swallow syncope

Enhancing Healthcare Team Outcomes

Presyncope can be challenging to evaluate in a healthcare setting due to its broad differential diagnosis, which encompasses both relatively benign etiologies, such as vasovagal presyncope, and more concerning etiologies, including cardiac arrhythmias and gastrointestinal bleeding. It is essential to efficiently and accurately evaluate presyncopal patients, identifying, treating, and discharging those with easily correctable and less severe diagnoses, whilst stabilizing and providing a higher level of care to patients with more serious causes of presyncope who have the potential to decompensate and incur significant morbidity and potentially mortality.  This requires an interprofessional team approach in the healthcare setting, with all members maintaining constant communication and synergistically coordinating their efforts.[30][31] 

In the emergency department, the triage nurse plays a critical role in promptly identifying patients at higher risk for presyncopal episodes and communicating concerns to the supervising physician. Technicians are responsible for placing patients on telemetry when indicated, obtaining ECGs, sending laboratory samples, and facilitating transport to radiology when necessary. The physician must maintain open communication with all team members, addressing their observations and clearly outlining the diagnostic and management plan after the initial evaluation. Once a diagnosis or clinical impression is established through history, physical examination, ECG, lab work, and possibly imaging, the physician should not only determine the appropriate treatment but also ensure the plan is communicated effectively to the team. This process should remain collaborative, allowing team members to share input or concerns that may enhance patient care

Additionally, given the wide range of potential diagnoses arising from a presyncopal presentation, consultants from multiple specialties may be involved, including cardiology, neurology, and gastroenterology.  Open and cordial communication between providers that relies on closed-loop communication is crucial in these instances.[32] This collaborative effort is not only beneficial to the patient but also results in increased job satisfaction and job stability for healthcare providers.[33]

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Disclosure: James Whitledge declares no relevant financial relationships with ineligible companies.

Disclosure: Nissa Ali declares no relevant financial relationships with ineligible companies.

Disclosure: Hajira Basit declares no relevant financial relationships with ineligible companies.

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