Continuing Education Activity

Presyncope or near-syncope is often ill-defined and may have different meanings to different providers but denotes 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. Symptoms may be accompanied by a feeling of lightheadedness, general weakness, warmth, diaphoresis, nausea, palpitations or blurry vision. Although often perceived as more benign than syncope, data suggest that both the pathophysiology (cerebral hypoperfusion) and outcomes of near syncope mimic those of syncope. This activity outlines the etiologies, epidemiology, evaluation, and management of presyncope and highlights the role of the interprofessional team in caring for affected patients.

Objectives:

• Describe the epidemiology of presyncope.
• Explain the evaluation of presyncope.
• Describe appropriate management strategies for patients presenting with presyncope.
• Explain the importance of improving care coordination amongst the interprofessional team to enhance the delivery of care for patients with presyncope.

Introduction

Presyncope or near-syncope is often ill-defined and may have different meanings to different providers but denotes 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. Symptoms may be accompanied by a feeling of lightheadedness, general weakness, warmth, diaphoresis, nausea, palpitations or blurry vision. Although often perceived as more benign than syncope, data suggest that both 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) 20 mmHg or greater or a decrease in diastolic blood pressure (DBP) 10 mmHg or greater within three minutes of standing[4]. Vascular causes are less common but should be considered based on history, including pulmonary embolism, mesenteric steal, carotid insufficiency and aortic pathology[5][6][7].  

Cardiac causes, which are more ominous, include mechanical (e.g., cardiac tamponade or valvular disease) and dysrhythmic (e.g., paroxysmal ventricular tachycardia or conduction system disease). Dysrhythmias, which induce hemodynamic impairment that can cause 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 are greater than 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 the elderly than in younger populations.

Epidemiology

19% of the United States population will experience a syncopal event in their lifetime, with the majority occurring in either the early adult years or after age 70; almost 58% of patients with syncope are female[9][10].  3% of visits to emergency departments and up to 6% of admissions to hospitals in the United States are for syncope[11][12].  Accurately ascertaining the epidemiology of presyncope is more difficult as it is frequently omitted from or combined with syncope datasets, however it is likely that the incidence of presyncope is higher than that of syncope[13][14].  In one study focused specifically on presyncope, the average patient age was 56 years old and 61% of patients were female.  49% of patients were admitted to the hospital, compared to 69% of syncopal patients, despite having a similar risk of adverse outcome.  20% of presyncopal patients had an adverse outcome or required an intervention, with the most common adverse outcomes being sepsis, bradyarrhythmia, GI bleed, and acute renal failure[14].

History and Physical

The history, medication review, physical examination and ECG have the greatest utility in evaluating presyncope[15][16].  For example, vasovagal prodromes are often more than five seconds long and occur after a precipitating event. Orthostatic history may include recurrent lightheadedness after standing. Cardiac etiologies often have less than five seconds of prodrome.  Risk factors for vascular and cardiac causes such as prior history, diabetes, hypertension, and smoking history should also be closely evaluated. A patient’s medication list should be evaluated during the initial workup, with special attention given to antihypertensives, antidysrhythmics, QTc-prolonging drugs and other cardiac medications.

Vital signs should be obtained, but are often normal after the resolution of symptoms. Orthostatic vital signs are controversial but may be helpful if there is a concern for volume depletion, particularly in the elderly[17][18]. Physical examination should include careful auscultation of the heart and lungs, and palpation of the peripheral arteries and a neurologic examination. A stool hemoccult test should be performed if concern for gastrointestinal bleeding exists. Examination for trauma should also be completed if indicated by history.

Evaluation

The initial task in presyncope is to obtain vital signs. An EKG and finger stick glucose test should be performed on all patients, but there is no gold standard for diagnostic testing in presyncope[15][16]. Blood tests such as electrolytes, complete blood count, cardiac enzymes, lactate, blood cultures, and imaging modalities such as head CT and echocardiography should be guided by history and examination only[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 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 given if the patient appears dehydrated and antibiotics 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 thought to be vasovagal or dehydration with a normal work up, these patients may be discharged with close primary care provider follow-up[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 pre- 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 offer a proven uniform ground to choose 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

• 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 because of its broad differential diagnosis, which encompasses both relatively benign etiologies such as vasovagal presyncope and more concerning etiologies such as cardiac arrhythmias and GI bleed.  It is important to efficiently and accurately evaluate presyncopal patients, identifying, treating, and discharging those with easily correctable and less serious 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 in constant communication, coordinating their efforts in a synergistic manner[30][Level 5][31][Level 5].  For example, in the emergency department the triage nurse must accurately identify presyncopal patients at higher risk and triage them in a timely manner while communicating his/her concerns to the supervising physician.  The technician must quickly place the patient on telemetry if indicated, obtain an EKG, send off bloodwork to the lab, and take the patient to the radiologic suite if indicated.  The physician must maintain close communication with other members of the healthcare team, listening to their concerns and communicating his/her plans for further testing and management after an initial evaluation and diagnostic plan have been formulated.  Once an impression or diagnosis has been formed thru history, physical exam, EKG, laboratory testing, and potentially radiologic studies, the physician must not only decide how best to manage the patient and provide treatment, but also convey this plan to the other members of the healthcare team who will be involved in executing it.  This treatment plan should involve open communication and be a "two-way street", such that if other members of the team have concerns or suggestions, the physician takes them into account.  In addition, given the wide variety of potential diagnoses stemming 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][Level 5].  This collaborative effort is not only beneficial to the patient but also results in increased job satisfaction and job stability for healthcare providers[33][Level 5]. 

Review Questions

• Access free multiple choice questions on this topic.
• Click here for a simplified version.
• Comment on this article.

References

1.

Kapoor WN. Evaluation and management of the patient with syncope. JAMA. 1992 Nov 11;268(18):2553-60. [PubMed: 1404823]

2.

Hanlon JT, Linzer M, MacMillan JP, Lewis IK, Felder AA. Syncope and presyncope associated with probable adverse drug reactions. Arch Intern Med. 1990 Nov;150(11):2309-12. [PubMed: 2241439]

3.

Freeman R. Clinical practice. Neurogenic orthostatic hypotension. N Engl J Med. 2008 Feb 07;358(6):615-24. [PubMed: 18256396]

4.

Task Force for the Diagnosis and Management of Syncope. European Society of Cardiology (ESC). European Heart Rhythm Association (EHRA). Heart Failure Association (HFA). Heart Rhythm Society (HRS). Moya A, Sutton R, Ammirati F, Blanc JJ, Brignole M, Dahm JB, Deharo JC, Gajek J, Gjesdal K, Krahn A, Massin M, Pepi M, Pezawas T, Ruiz Granell R, Sarasin F, Ungar A, van Dijk JG, Walma EP, Wieling W. Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J. 2009 Nov;30(21):2631-71. [PMC free article: PMC3295536] [PubMed: 19713422]

5.

Kokturk N, Oguzulgen IK, Demir N, Demirel K, Ekim N. Differences in clinical presentation of pulmonary embolism in older vs younger patients. Circ J. 2005 Aug;69(8):981-6. [PubMed: 16041171]

6.

Imamura H, Sekiguchi Y, Iwashita T, Dohgomori H, Mochizuki K, Aizawa K, Aso S, Kamiyoshi Y, Ikeda U, Amano J, Okamoto K. Painless acute aortic dissection. - Diagnostic, prognostic and clinical implications.-. Circ J. 2011;75(1):59-66. [PubMed: 21099124]

7.

Akkersdijk GJ, van Bockel JH. Ruptured abdominal aortic aneurysm: initial misdiagnosis and the effect on treatment. Eur J Surg. 1998 Jan;164(1):29-34. [PubMed: 9537706]

8.

Kariman H, Harati S, Safari S, Baratloo A, Pishgahi M. Validation of EGSYS Score in Prediction of Cardiogenic Syncope. Emerg Med Int. 2015;2015:515370. [PMC free article: PMC4663288] [PubMed: 26649200]

9.

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 Dec;119(12):1088.e1-7. [PubMed: 17145254]

10.

Soteriades ES, Evans JC, Larson MG, Chen MH, Chen L, Benjamin EJ, Levy D. Incidence and prognosis of syncope. N Engl J Med. 2002 Sep 19;347(12):878-85. [PubMed: 12239256]

11.

Kapoor WN. Evaluation and outcome of patients with syncope. Medicine (Baltimore). 1990 May;69(3):160-75. [PubMed: 2189056]

12.

Sun BC, Emond JA, Camargo CA. Direct medical costs of syncope-related hospitalizations in the United States. Am J Cardiol. 2005 Mar 01;95(5):668-71. [PubMed: 15721118]

13.

Grossman SA, Babineau M, Burke L, Kancharla A, Mottley L, Nencioni A, Shapiro NI. Applying the Boston syncope criteria to near syncope. J Emerg Med. 2012 Dec;43(6):958-63. [PubMed: 22981659]

14.

Grossman SA, Babineau M, Burke L, Kancharla A, Mottley L, Nencioni A, Shapiro NI. Do outcomes of near syncope parallel syncope? Am J Emerg Med. 2012 Jan;30(1):203-6. [PubMed: 21185670]

15.

Linzer M, Yang EH, Estes NA, Wang P, Vorperian VR, Kapoor WN. Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Clinical Efficacy Assessment Project of the American College of Physicians. Ann Intern Med. 1997 Jun 15;126(12):989-96. [PubMed: 9182479]

16.

Linzer M, Yang EH, Estes NA, Wang P, Vorperian VR, Kapoor WN. Diagnosing syncope. Part 2: Unexplained syncope. Clinical Efficacy Assessment Project of the American College of Physicians. Ann Intern Med. 1997 Jul 01;127(1):76-86. [PubMed: 9214258]

17.

Atkins D, Hanusa B, Sefcik T, Kapoor W. Syncope and orthostatic hypotension. Am J Med. 1991 Aug;91(2):179-85. [PubMed: 1867243]

18.

Ooi WL, Hossain M, Lipsitz LA. The association between orthostatic hypotension and recurrent falls in nursing home residents. Am J Med. 2000 Feb;108(2):106-11. [PubMed: 11126303]

19.

Chiu DT, Shapiro NI, Sun BC, Mottley JL, Grossman SA. Are echocardiography, telemetry, ambulatory electrocardiography monitoring, and cardiac enzymes in emergency department patients presenting with syncope useful tests? A preliminary investigation. J Emerg Med. 2014 Jul;47(1):113-8. [PubMed: 24698512]

20.

Mendu ML, McAvay G, Lampert R, Stoehr J, Tinetti ME. Yield of diagnostic tests in evaluating syncopal episodes in older patients. Arch Intern Med. 2009 Jul 27;169(14):1299-305. [PMC free article: PMC3752785] [PubMed: 19636031]

21.

Grossman SA, Van Epp S, Arnold R, Moore R, Lee L, Shapiro NI, Wolfe RE, Lipsitz LA. The value of cardiac enzymes in elderly patients presenting to the emergency department with syncope. J Gerontol A Biol Sci Med Sci. 2003 Nov;58(11):1055-8. [PubMed: 14630890]

22.

Grossman SA. Testing in syncope. Intern Emerg Med. 2006;1(2):135-6. [PubMed: 17111787]

23.

Grossman SA, Fischer C, Lipsitz LA, Mottley L, Sands K, Thompson S, Zimetbaum P, Shapiro NI. Predicting adverse outcomes in syncope. J Emerg Med. 2007 Oct;33(3):233-9. [PMC free article: PMC2276584] [PubMed: 17976548]

24.

Grossman SA, Bar J, Fischer C, Lipsitz LA, Mottley L, Sands K, Zimetbaum P, Shapiro NI. Reducing admissions utilizing the Boston Syncope Criteria. J Emerg Med. 2012 Mar;42(3):345-52. [PubMed: 21421292]

25.

Costantino G, Dipaola F, Solbiati M, Bulgheroni M, Barbic F, Furlan R. Is hospital admission valuable in managing syncope? Results from the STePS study. Cardiol J. 2014;21(6):606-10. [PubMed: 25299505]

26.

Grossman SA, Fischer C, Kancharla A, Lipsitz LA, Mottley L, Zimetbaum P, Shapiro NI. Can benign etiologies predict benign outcomes in high-risk syncope patients? J Emerg Med. 2011 May;40(5):592-7. [PubMed: 19926429]

27.

Birnbaum A, Esses D, Bijur P, Wollowitz A, Gallagher EJ. Failure to validate the San Francisco Syncope Rule in an independent emergency department population. Ann Emerg Med. 2008 Aug;52(2):151-9. [PubMed: 18282636]

28.

Quinn J, McDermott D, Stiell I, Kohn M, Wells G. Prospective validation of the San Francisco Syncope Rule to predict patients with serious outcomes. Ann Emerg Med. 2006 May;47(5):448-54. [PubMed: 16631985]

29.

Quinn J, McDermott D. External validation of the San Francisco Syncope Rule. Ann Emerg Med. 2007 Dec;50(6):742-3; author reply 743-4. [PubMed: 18023761]

30.

Rosenstein AH, O'Daniel M. Disruptive behavior and clinical outcomes: perceptions of nurses and physicians. Am J Nurs. 2005 Jan;105(1):54-64; quiz 64-5. [PubMed: 15659998]

31.

Rosenstein AH, Naylor B. Incidence and impact of physician and nurse disruptive behaviors in the emergency department. J Emerg Med. 2012 Jul;43(1):139-48. [PubMed: 21421291]

32.

Manojlovich M, DeCicco B. Healthy work environments, nurse-physician communication, and patients' outcomes. Am J Crit Care. 2007 Nov;16(6):536-43. [PubMed: 17962497]

33.

Manojlovich M, Antonakos C. Satisfaction of intensive care unit nurses with nurse-physician communication. J Nurs Adm. 2008 May;38(5):237-43. [PubMed: 18469617]

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.