• Clinical science

Syncope

Summary

Syncope is a sudden, completely reversible loss of consciousness secondary to an acute reduction of cerebral perfusion, which may last from several seconds up to minutes. The most frequent form is vasovagal syncope, which is triggered by emotional stress or prolonged standing, and may be diagnosed with the tilt table test. Orthostatic syncope may occur upon suddenly standing up after prolonged sitting or lying down. It is caused by a drop in blood pressure. This relatively benign cause may, however, lead to life-threatening injuries as a result of falls. A thorough medical investigation is necessary as syncopes may also be the result of a serious cardiovascular disorder (e.g., cardiac arrhythmia or valvular stenosis). The treatment strategy is dependent on the cause of the syncopes.

Clinical features

Thorough neurological and cardiopulmonary assessments, including pulse and blood pressure measurement in the supine, standing, and sitting positions, are crucial for identifying the underlying etiology!
References:[1][2]

Etiology

  • TLOC (transient loss of consciousness): temporary syncope of unknown origin
Overview of possible causes of syncopes
Pathophysiology Subtype Etiology Examples
Cardiac syncope
  • Heart's inability to meet an increased oxygen demand (e.g., during exertion)
  • reduced cerebral perfusion
Arrhythmogenic syncope Bradycardia/tachycardiaejection fraction
Cardiovascular syncope Structural outflow obstruction

Reflex syncope (Most common cause)

  • Neurally mediated syncope that can be due to parasympathetic hyperactivity (cardioinhibitory response), sympathetic hypoactivity (vasodepressor response), or a combination of both
  • vasodilatation (vasodepressor response) and/or bradycardia (cardioinhibitory response)
  • → reduced BP
  • reduced cerebral perfusion
Neurocardiogenic syncope (subtype of vasovagal syncope) Prolonged standing (and no compensatory heart rate acceleration)
  • Common in younger patients (unusual to have first episode after age 40)
  • Can be recurrent
Emotional syncope (subtype of vasovagal syncope) Pain or emotional stress
  • Pain
  • Fear
  • Sight of blood
  • Injury
Carotid sinus syndrome Increased carotid sinus sensitivity (frequently associated with arteriosclerotic changes in the carotid sinus) → systolic blood pressure when pressure is applied to the carotid sinus
  • Pressure on the carotid sinuses (e.g., during a massage, when shaving, tightening a necktie)
Other situational syncopes Vagotonic, peripheral vascular dilation
Orthostatic syncope (postural hypotension)
  • Standing up/postural change
  • insufficient counterregulation due to autonomic dysfunction (e.g. decreased baroreceptor sensitivity in the elderly)
  • reduced cerebral perfusion
Sympathotonic orthostatic hypotension When standing up: systolic blood pressure despite excessive sympathotonic counter regulation (significant heart rate increase) reduced cerebral perfusion
Asympathotonic orthostatic hypotension When standing up: systolic blood pressure without sympathotonic counterregulation (steady or even reduced heart rate) reduced cerebral perfusion
Postural tachycardia syndrome (PoTS, orthostatic intolerance) When standing up: no significant drop in blood pressure, but massive heart rate increase within 10 minutes of standing up

References:[3][4][1][5][2][6][7][8]

Differential diagnoses

Non-syncopal events Medical history and clinical features Diagnosis
Seizure
  • Abnormal EEG
  • Brain lesions visible in imaging (CT, MRI)
Subclavian steal syndrome
  • Occurs when straining the ipsilateral arm
  • Rare: complete loss of consciousness
  • Focal-neurological signs during an attack (e.g., double images, dysarthria)
Vertebrobasilar insufficiency
  • Drop attacks can be seen with a TIA in the vertebrobasilar circulation.
  • Other neurologic deficits will be seen as well.
Hypoglycemia
  • Diabetes
  • Clinical symptoms: symptoms of autonomic counterregulation (e.g., restlessness, sweating, pale skin)
  • ↓ Blood glucose
Craniocerebral injury
  • Pathology on imaging (CT, MRI)
Heatstroke
  • The body is unable to regulate the core body after it becomes elevated.
  • Syncope can precede exertional heatstroke.
Hyperventilation
Cryptogenic drop attacks
  • The cause of many falls, especially in older patients, remains elusive despite extensive diagnostic testing. These falls/attacks are called cryptogenic drop attacks.

References:[2][9]

The differential diagnoses listed here are not exhaustive.

Diagnostics

It is important to rule out life-threatening causes of syncope such as pulmonary embolism, hemorrhage, or serious cardiac conditions!
References:[4][1][2][10][11][12]

Treatment

  • Treat underlying condition
  • Vasovagal syncopes
    • Physiological counterstrategies: Crossing the legs, tensing muscles, lying down, and elevating the legs can reverse the syncope.
    • Avoid triggers
  • Orthostatic syncopes

References:[2]

Complications

References:[2]

We list the most important complications. The selection is not exhaustive.

  • 1. Benditt D. Syncope in adults: Clinical manifestations and diagnostic evaluation. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/syncope-in-adults-clinical-manifestations-and-diagnostic-evaluation. Last updated October 12, 2016. Accessed February 17, 2017.
  • 2. Morag R. Syncope. In: Syncope. New York, NY: WebMD. http://emedicine.medscape.com/article/811669. Updated January 13, 2017. Accessed March 15, 2017.
  • 3. Herold G. Internal Medicine. Cologne, Germany: Herold G; 2014.
  • 4. Agabegi SS, Agabegi ED. Step-Up To Medicine. Baltimore, MD, USA: Wolters Kluwer Health; 2015.
  • 5. Prandoni P, Lensing AWA, Prins MH, et al. Prevalence of Pulmonary Embolism among Patients Hospitalized for Syncope. N Engl J Med. 2016; 375: pp. 1524–1531. doi: 10.1056/NEJMoa1602172.
  • 6. Chen-Scarabelli C, Scarabelli TM. Neurocardiogenic syncope. BMJ. 2004; 329(7461): pp. 336–341. doi: 10.1136/bmj.329.7461.336.
  • 7. O’Mahony D. Pathophysiology of carotid sinus hypersensitivity in elderly patients. Lancet. 1995; 346(8980): pp. 950–952. doi: 10.1016/s0140-6736(95)91563-x.
  • 8. Kaufmann H, Freeman R. Postural Tachycardia Syndrome. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/postural-tachycardia-syndrome. Last updated March 3, 2015. Accessed March 2, 2018.
  • 9. Lima Neto A, Bittar R, Gattas G, et al. Pathophysiology and diagnosis of vertebrobasilar insufficiency: A review of the literature. Int Arch Otorhinolaryngol. 2016; 21(3): pp. 302–307. doi: 10.1055/s-0036-1593448.
  • 10. Bradley JG, Davis KA. Orthostatic hypotension. Am Fam Physician. 2003; 68(12): pp. 2393–2399. url: https://www.aafp.org/afp/2003/1215/p2393.html.
  • 11. Juraschek SP, Miller ER, Appel LJ. Orthostatic hypotension and symptoms in the AASK Trial. Am J Hypertens. 2018. doi: 10.1093/ajh/hpy010.
  • 12. Benditt D. Upright Tilt Table Testing in the Evaluation of Syncope. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/upright-tilt-table-testing-in-the-evaluation-of-syncope. Last updated August 10, 2017. Accessed March 2, 2018.
  • Olshansky B. Reflex syncope. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/reflex-syncope. Last updated August 14, 2014. Accessed February 17, 2017.
  • Runser LA, Gauer RL, Houser A. Syncope: Evaluation and Differential Diagnosis. Am Fam Physician. 2017; 95(5): pp. 303–312. pmid: 28290647.
  • Mellusi J. Differential diagnosis of syncope. Anesth Prog. 1967; 14(1): pp. 4–11. pmid: 5228333.
  • Stern SDC, Cifu AS, Altkorn D. Symptom to Diagnosis An Evidence Based Guide, Fourth Edition. McGraw-Hill Education / Medical; 2019.
last updated 09/15/2020
{{uncollapseSections(['E9b86D', 'B9bzpD', '99bNpD', '-9bDJD', '_9b5JD', 'ZCbZqD', '0CbeqD'])}}