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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vendhan Ramanujam M.B.B.S [2] Antara Chatterjee, M.D[3]

Synonyms and keywords: Faintness; generalized weakness; lightheadedness; near blackout; near fainting; near syncope


Presyncope is the sensation of feeling faint, lightheadedness[1] and muscular weakness without actually losing consciousness. The presyncope stage may occur for only a few seconds as a prodrome before losing consciousness. Presyncope is most often due to cardiovascular etiology.


Presyncope may be classified into following subtypes based on the inciting mechanism leading to the final event of transient global hypoperfusion. Presyncope suggests global cerebral hypoperfusion or a toxic/metabolic derangement. Hypoperfusion usually results from a drop in blood pressure (BP).

Cardiac Non-Cardiac
Dysrythmia Neurally-mediated (reflex)
Structural disease Orthostatic hypotension mediated


It is thought that presyncope is the result of the interaction between the circulatory system and the autonomic nervous system. The autonomic nervous system is vital for the maintenance of internal homeostasis including regulation of blood pressure, heart rate, fluid and electrolyte balance, and body temperature. Syncope or presyncope occurs as a result of brain hypoxia, which is usually secondary to a reduction of cerebral perfusion pressure. However, not every reduction in blood pressure leads to brain hypoxia. This is because the cerebral circulation is autoregulated so that brain perfusion is maintained in the face of significant changes in mean blood pressure. This homeostatic mechanism allows regional cerebral blood flow to remain constant over a range of cerebral perfusion pressure (CPP) of 50 to 150 mm Hg or mean arterial pressure (MAP) of 60 to 160 mm Hg. So, as MAP or CPP increases, resistance in small cerebral arteries increases via vasoconstriction and vice versa.[2] Blood pressure below the lower level result in syncope secondary to brain hypoxia.

When standing, initially the force of gravity pools 500 to 800 mL of blood in the distensible veins below heart level.[3] This increases capillary pressure and plasma is lost to interstitial fluid. Pooling of blood in the veins decreases venous return to the heart with subsequent reduction of cardiac output, which in turn, triggers compensatory mechanisms to prevent the reduction of arterial pressure. Compensatory mechanisms include: sympathetic outflow upregulation by the central autonomic network (CAN); and the venoarterial reflex, leg pumping of skeletal muscles, the cerebral autoregulatory mechanism, and to a lesser extent, the renin angiotensin aldosterone system (RAAS).

The autonomic supply to the cardiovascular system is coordinated at the CAN located in the brain stem. The sympathetic nervous system acts as the main effector in the hemodynamic response to postural stressors. Upon standing, there is an initial reduction of cardiac filling and thus, of stroke volume. Pressure receptors in the heart, carotids, and aortic arch sense the perturbation and send impulses to the CAN. This initiates sympathetic vasomotor outflow and norepinephrine is released to vascular beds in the skeletal muscles and cutaneous vasculature; causing vasoconstriction, venoconstriction, as well as increased heart rate and contractility. Venoconstriction causes a correction of orthostasis by increasing cardiac filling for a given amount of gravitational pooling of blood. At the same time, leg pumping of skeletal muscles enhances venous return to the heart and the venoarterial reflex augments arterial vasoconstriction in response to venous distention.

Postural stress in the atrium is sensed by mechanoreceptors as a decreased in atrial stretch. This causes increase of arginine vasopressin (AVP) and decrease in A-type atrial natriuretic peptide (ANP) secretion. This results in “anti-natriuresis” that leads to an increase of ECF volume and cardiac filling.

The pathophysiology of syncope is summarized as a reduction in systemic blood pressure that causes a decrease in the global cerebral blood flow, which results in loss of consciousness. A sudden cessation of cerebral blood flow for 6 to 8 seconds has been shown to cause loss of consciousness.[4]


Presyncope may be caused by

  • a temporary drop in blood pressure
  • dehydration
  • prolonged standing
  • intense nausea or pain
  • hypoglycemia, or low blood sugar, which may or may not be due to diabetes
  • neurally mediated hypotension, which causes blood pressure to drop when a person stands up from a sitting or lying position
  • Vagal presyncope
  • side effect of some medications
  • Cardiac arrhythmia

Differentiating Presyncope from other Diseases

The differentiation between syncope and non-syncopal conditions with real or apparent LOC can be achieved in most cases with a detailed clinical history,[5] [6] [7] but sometimes can be extremely difficult.

Epidemiology and Demographics

Patients of all age groups may develop presyncope. The prevalence of the causes of syncope is different depending on the clinical settings in which the patient is evaluated and the age of the patients. Furthermore, other differences depend on diagnostic definitions, geographical factors, and local care pathways, making a comparison between different studies difficult.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.[8] [9]  3% of visits to emergency departments and up to 6% of admissions to hospitals in the United States are for syncope.[10] [11] Reflex syncope is the most frequent cause of syncope in any setting. Syncope secondary to cardiovascular disease is the second most common cause. The number of patients with a cardiovascular cause varies widely between studies; higher frequencies are observed in emergency settings mainly in older subjects, and in settings oriented toward cardiology. In patients <40 years OH is a rare cause of syncope; OH is frequent in very old patients. Non-syncopal conditions, misdiagnosed as syncope at initial evaluation, are more frequent in emergency referrals and reflect the multifactorial complexity of these patients. The high unexplained syncope rate in all settings justifies new strategies for evaluation and diagnosis. In the elderly multiple causes are often present and the medical history may be less reliable than in the young.[12] [13] [14] .

Risk Factors

There are no established risk factors for [disease name].


The most potent risk factor in the development of [disease name] is [risk factor 1]. Other risk factors include [risk factor 2], [risk factor 3], and [risk factor 4].


Common risk factors in the development of [disease name] include [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].


Common risk factors in the development of [disease name] may be occupational, environmental, genetic, and viral.


There is insufficient evidence to recommend routine screening for presyncope.

Natural History, Complications, and Prognosis

If left untreated, patients with presyncope may progress to develop syncope which leads to actual loss of consciousness.

Common complications of presyncope include major trauma due to falls, sudden cardiac death, seizure, recurrent hospitalization.

Prognosis of presyncope depends on the underlying cause. Patients with presyncope with structural heart disease and primary electrical disease are at high risk of overall mortality and sudden cardiac death. Young patients with reflex presyncope have an excellent prognosis.[4]Morbidity in patients with presyncope is associated with recurrence of episodes and physical injury. Young patients with psychiatric disease have high rates of recurrence of pseudosyncope.[4]

In patients with presyncope presenting to the emergency department, 29.1% have minor trauma, 4.7% have major trauma, and in older patients with carotid disease, 43% have major trauma. Morbidity is particularly high in the elderly, and is associated with loss of confidence, fear of falling, depression, fractures, and institutionalization.[4]


The diagnosis of presyncope is made based on complete medical history of the patient including preexisting conditions such as diabetes and heart disease, and medications the patient takes. Physical exam will help guide further diagnostic testing, which may include:

  • complete blood count and basic metabolic panel
  • urinalysis
  • thyroid function tests
  • glucose test
  • electrocardiogram
  • Holter monitoring
  • tilt table test
  • echocardiogram

History and Symptoms

The majority of patients with presyncope report:

  • lightheadedness, general weakness
  • dizziness
  • confusion
  • tunnel vision, blurry vision
  • slurred speech
  • trouble hearing
  • sweating
  • nausea or vomiting
  • headache
  • heart palpitations

These symptoms can last from just a few seconds to several minutes before they pass.

Physical Examination

Patients with complains of presyncope usually appear normal. A careful and comprehensive physical examination is essential in a patient presenting with presyncope. Blood pressure should to be checked in both arms, and in the supine and standing positions. Signs to look for in the physical exam are dehydration, flushing, carotid bruits, cardiac murmurs, abdominal masses, varicose veins, and signs of endocrine disorders in skin, eyes and thyroid.

Carotid sinus massage

Carotid sinus massage (CSM) is indicated in patients older than 40 years with presyncope of unknown etiology after initial evaluation.


An ECG may be helpful in the diagnosis of cause of presyncope. ECG monitoring is indicated in patients who have clinical or ECG findings suggestive of arrhythmic presyncope and is diagnostic when a correlation between pesyncope and an arrhythmia is detected. Several ECG ambulatory monitoring methods are available: conventional ambulatory Holter monitoring, in-hospital monitoring, event recorders, external or implantable loop recorders (ILRs), and remote (at home) telemetry.[15]

Echocardiography or Ultrasound

Echocardiography/ultrasound may be helpful in the diagnosis of presyncope due to structural heart disease such as severe aortic stenosis, obstructive cardiac tumor or thrombi, pericardial tamponade, aortic dissection, and congenital anomalies of coronary artery. It is a class IIa recommendation from the American College of Cardiology/American Heart Association if there is clinical suspicion of structural heart disease and it is of no benefit unless cardiac etiology is suspected.[3]

Orthostatic challenge

The tilt table test is a simple test that moves a patient from a supine to an upright position using a tilt table. It is used to examine autonomic neural regulation of cardiovascular orthostatic responses.[16]

Other Diagnostic Studies

Assessment of global autonomic function may be helpful in the diagnosis of etiology of presyncope. This entails a number of maneuvers, pressor testing, Valsalva maneuver, phenylephrine test, amyl nitrite inhalation. These are performed while heart rate variability and blood pressure are monitored.


The mainstay of treatment for presyncope are 2 main treatment strategies: conservative/nonpharmacologic therapy and medical treatment. The treatment varies based on the cause of presyncope.

  • Pharmacologic medical therapy is recommended among patients with recurrent episodes despite adequate conservative therapy. This list includes beta blockers, fludrohydrocortisone, midodrine, calcium channel blockers, anticholinergic agents, and serotonin transporter inhibitors.

  • Conservative therapy includes lifestyle modifications like avoidance of provocative triggers such as heat, prolonged standing, decongestants, excess caffeine, large meals, and alcohol; increased salt and fluid intake; reduction or withdrawal of antihypertensive medications, and physical counterpressure maneuvers.[3] Physical counter maneuvers and simple postural maneuvers like leg crossing, leg raising, genuflexion, toe-raising to contract calf/gastrocnemius muscle, squatting, and isotonic contraction of the thighs/quadriceps muscle are easy to teach to patients and may be useful in mild orthostatic symptoms. Compression support stockings are also effective in patients with postural hypotension and those with accentuated postural venous pooling. An abdominal binder and small frequent meals are advised in patients with post-prandial hypotension. In patients with supine hypertension and postural hypotension, elevation of the head-of-bed by 6 to 8 inches may also be helpful.

Secondary Prevention

Effective measures for the secondary prevention of presyncope include patient education and treatment. Patients need to be aware of triggers that may predispose to or precipitate syncopal spells and orthostatic intolerance.

Causes by Organ System

Cardiovascular Acute coronary syndrome, acute myocardial infarction, acute myocarditis, Adams-Stokes syndrome, anomalous origins of coronary arteries, aortic aneurysm, aortic dissection, aortic stenosis, arrhythmogenic right ventricular dysplasia, atrial myxoma, atrioventricular block, AV nodal reentrant tachycardia, bifascicular block, bradyarrhythmia, brugada syndrome, cardiac tamponade, catecholaminergic polymorphic ventricular tachycardia, channelopathy, complete atrioventricular block, dehydration, dilated cardiomyopathy, epsilon wave, hemorrhage, hypertrophic cardiomyopathy, hypotension, Jervell and Lange-Nielsen syndrome, long QT syndrome, mitral stenosis, orthostatic hypotension, paroxysmal ventricular tachycardia, persistent atrial flutter, preexcitation syndrome, prolonged corrected QT interval, pulmonic stenosis, retroperitoneal hemorrhage, ruptured abdominal aortic aneurysm, saddle embolus, second degree AV block, short corrected QT interval, short QT syndrome, sick sinus syndrome, significant sinus pause, subclavian steal syndrome, supraventricular tachyarrhythmia, third degree heart block, ventricular arrhythmia, ventricular tachycardia, Wolff-Parkinson-White syndrome
Chemical/Poisoning Carbon monoxide, cocaine, ethanol
Dental No underlying causes
Dermatologic No underlying causes
Drug Side Effect ACE inhibitor, alpha blockers, amitriptyline, antiarrhythmics, antidepressants, antiemetics, antihypertensive medications, antipsychotic agents, barbiturates, beta blockers, bromocriptine, calcium channel blockerchlorpheniramine, cinnarizine, clonidine, desipramine, digoxin, diphenhydramine, diuretics, dothiepin, erectile dysfunction medications, Flurazepam, ganglionic blocker, hydralazine, hydroxyzine, L-dopa, nitrates, nortriptyline, opiates, phenothiazines, rizatriptan, tricyclic antidepressants, vasodilators
Ear Nose Throat No underlying causes
Endocrine No underlying causes
Environmental No underlying causes
Gastroenterologic Gastrointestinal bleeding
Genetic Channelopathy
Hematologic No underlying causes
Iatrogenic No underlying causes
Infectious Disease No underlying causes
Musculoskeletal/Orthopedic No underlying causes
Neurologic Carotid sinus hypersensitivity, dysautonomia, Lewy body dementia, multiple system atrophy, parkinson disease, seizure, spinal cord injury, subarachnoid hemorrhage, transient ischemic attack, vagal stimulation, vertebrobasilar insufficiency
Nutritional/Metabolic No underlying causes
Obstetric/Gynecologic No underlying causes
Oncologic Atrial myxoma, carcinoid syndrome
Ophthalmologic No underlying causes
Overdose/Toxicity No underlying causes
Psychiatric Anorexia nervosa, anxiety, emotional stress, hysterical faint, psychogenic pseudosyncope
Pulmonary Hypoxia
Renal/Electrolyte Uremia
Rheumatology/Immunology/Allergy Anaphylaxis, Takayasu's arteritis
Sexual No underlying causes
Trauma No underlying causes
Urologic No underlying causes
Miscellaneous Breath holding spells, choking game, cough, defecation, deglutition, drop attack, hair combing, heat illness, hyperventilation, hypocapnia, hypoglycemia, implanted cardioverter defibrillator malfunction, laughing, micturition, post-exercise, postprandial hypotension, prolonged bed rest, sneeze, significant blood loss, valsalva maneuver, vomiting, weightlifting

Causes in Alphabetical Order

Clinical test

The tilt table test is an evaluative clinical test to help identify presyncope or syncope.[19] A tilt angle of 60 and 70 degrees is optimal and maintains a high degree of specificity.[19] A positive sign with the tilt table test must be taken in context of patient history, with consideration of pertinent clinical findings before coming to a conclusion.


  1. Reeves, Alexander G. "Chapter 14: Evaluation of the Dizzy Patient". Disorders of the nervous system: a primer. Dartmouth Medical School. Retrieved 2012-01-06. Unknown parameter |coauthors= ignored (help)
  2. Armstead WM (2016). "Cerebral Blood Flow Autoregulation and Dysautoregulation". Anesthesiol Clin. 34 (3): 465–77. doi:10.1016/j.anclin.2016.04.002. PMC 4988341. PMID 27521192.
  3. 3.0 3.1 3.2 Shen WK, Sheldon RS, Benditt DG, Cohen MI, Forman DE, Goldberger ZD; et al. (2017). "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". J Am Coll Cardiol. 70 (5): e39–e110. doi:10.1016/j.jacc.2017.03.003. PMID 28286221.
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  7. Sheldon R, Rose S, Ritchie D, Connolly SJ, Koshman ML, Lee MA; et al. (2002). "Historical criteria that distinguish syncope from seizures". J Am Coll Cardiol. 40 (1): 142–8. doi:10.1016/s0735-1097(02)01940-x. PMID 12103268.
  8. Chen LY, Shen WK, Mahoney DW, Jacobsen SJ, Rodeheffer RJ (2006). "Prevalence of syncope in a population aged more than 45 years". Am J Med. 119 (12): 1088.e1–7. doi:10.1016/j.amjmed.2006.01.029. PMID 17145254.
  9. Soteriades ES, Evans JC, Larson MG, Chen MH, Chen L, Benjamin EJ; et al. (2002). "Incidence and prognosis of syncope". N Engl J Med. 347 (12): 878–85. doi:10.1056/NEJMoa012407. PMID 12239256.
  10. Kapoor WN (1990). "Evaluation and outcome of patients with syncope". Medicine (Baltimore). 69 (3): 160–75. doi:10.1097/00005792-199005000-00004. PMID 2189056.
  11. Sun BC, Emond JA, Camargo CA (2005). "Direct medical costs of syncope-related hospitalizations in the United States". Am J Cardiol. 95 (5): 668–71. doi:10.1016/j.amjcard.2004.11.013. PMID 15721118.
  12. Chen LY, Gersh BJ, Hodge DO, Wieling W, Hammill SC, Shen WK (2003). "Prevalence and clinical outcomes of patients with multiple potential causes of syncope". Mayo Clin Proc. 78 (4): 414–20. doi:10.4065/78.4.414. PMID 12683693.
  13. Kenny RA (2003). "Syncope in the elderly: diagnosis, evaluation, and treatment". J Cardiovasc Electrophysiol. 14 (9 Suppl): S74–7. doi:10.1046/j.1540-8167.14.s9.8.x. PMID 12950524.
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  15. Colman N, Nahm K, Ganzeboom KS, Shen WK, Reitsma J, Linzer M; et al. (2004). "Epidemiology of reflex syncope". Clin Auton Res. 14 Suppl 1: 9–17. doi:10.1007/s10286-004-1003-3. PMID 15480937.
  16. Rothman SA, Laughlin JC, Seltzer J, Walia JS, Baman RI, Siouffi SY; et al. (2007). "The diagnosis of cardiac arrhythmias: a prospective multi-center randomized study comparing mobile cardiac outpatient telemetry versus standard loop event monitoring". J Cardiovasc Electrophysiol. 18 (3): 241–7. doi:10.1111/j.1540-8167.2006.00729.x. PMID 17318994.
  17. Nishida, K.; Hirota, SK.; Tokeshi, J. (2008). "Laugh syncope as a rare sub-type of the situational syncopes: a case report". J Med Case Rep. 2: 197. doi:10.1186/1752-1947-2-197. PMID 18538031.
  18. Benbadis, SR.; Chichkova, R. (2006). "Psychogenic pseudosyncope: an underestimated and provable diagnosis". Epilepsy Behav. 9 (1): 106–10. doi:10.1016/j.yebeh.2006.02.011. PMID 16697264. Unknown parameter |month= ignored (help)
  19. 19.0 19.1 Natale, A., Akhtar, M., Jazayeri, M., Dhala, A., Blanck, Z., Deshpande, S., et al. (1995). Provocation of Hypotension During Head-Up Tilt Testing in Subjects With No History of Syncope or Presyncop. American Heart Association, (92), 54-58. doi: 10.1161/01.CIR.92.1.54; url:

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