eMedicine Specialties > Cardiology > Arrhythmias

Syncope

Author: Jatin Dave, MD, MPH, Instructor, Department of Medicine, Department of Internal Medicine, Division of Aging, Harvard Medical School; Staff Physician, Brigham and Women's Hospital
Coauthor(s): John Michael Gaziano, MD, MPH, Associate Professor of Medicine, Harvard Medical School; Consulting Staff, Division of Aging, Brigham and Women's Hospital; Consulting Staff, Veterans Affairs Boston Healthcare System
Contributor Information and Disclosures

Updated: Jan 29, 2007

Introduction

Background

Syncope is defined as a transient self-limited loss of consciousness, usually leading to a fall. It is a subset of a broader range of conditions causing transient loss of consciousness. Syncope is a common medical problem accounting for up to 1% of emergency department visits and is the sixth leading cause of hospitalization for people older than 65 years.

Pathophysiology

Syncope results from a self-terminating inadequacy of global cerebral nutrient perfusion. In some patients, brainstem hypoxia triggers a posturing reflex that can appear like a seizure. A number of cardiac and noncardiac conditions can cause syncope (see Causes).

The most common type of syncope, neurocardiogenic syncope, is characterized by a sudden failure of the autonomic nervous system to maintain blood pressure to maintain cerebral perfusion.

Although the exact mechanism is not clear, one proposed mechanism is that in patients who are predisposed to have increased peripheral venous pooling, a sudden drop in preload results in a hypercontractile state. The forceful contraction stimulates mechanoreceptors, located primarily on the floor of the left ventricle. This mechanical activation results in neural traffic (falsely), mimicking hypertension and leading to sympathetic withdrawal and parasympathetic activation. The result is bradycardia (cardioinhibitory), vasodilatation (vasodepressor), or both (mixed response). Similar mechanoreceptors are also present in other parts of the body such as the bladder, rectum, esophagus, and lungs. Thus, other situational triggers to reflex syncope include micturition, defecation, deglutition, and cough.

As highlighted in a recent review by Hainsworth, "the trigger for the switch in autonomic response remains one of the unresolved mysteries in cardiovascular physiology."

Frequency

United States

Primary care physicians, cardiologists, and emergency department physicians frequently encounter patients with syncope. In the Framingham study, 822 (10.5%) of 7814 patients reported at least one syncopal event during the average follow up of 17 years. The incidence of new syncope was 6.2 per 1000 person-years. Assuming the constant incidence rate, a person living 70 years was estimated to have a 42% lifetime prevalence of syncope. The incidence rate is almost double in patients with cardiovascular disease compared with those without it.

Mortality/Morbidity

The prognostic significance of syncope depends on its cause (cardiac syncope with worse prognosis), the nature and severity of underlying structural heart disease, and the treatment initiated. Mortality is likely highest in patients with left ventricular dysfunction due to coronary artery disease or nonischemic cardiomyopathy. In these patients, syncope is frequently due to ventricular tachyarrhythmias. This risk is reduced substantially in patients treated with implanted cardioverter-defibrillators (ICDs). Even in patients with a benign cause of syncope, spells can result in significant injury, particularly in elderly persons.

In a recent study, mortality was about 30% higher among all participants with syncope than in those without syncope.

Race

No effect of race on the incidence of syncope is known.

Sex

Although earlier studies reported a slightly higher incidence of syncope in women compared with men, recent studies show similar incidence. A 72 per 1000 person-year incidence was noted in both men and women in a recent study based on the Framingham cohort.

Age

The incidence of syncope increases with age. Syncope is not uncommon in younger patients; neurally mediated (ie, neurocardiogenic) syncope accounts for most cases in younger patients. Occasionally, syncope in young patients presages a potentially life-threatening problem such as congenital long QT syndrome, Wolff-Parkinson-White (WPW) syndrome, Brugada syndrome, or hypertrophic cardiomyopathy.

Clinical

History

Patients with syncope may present with various complaints.

  • Patients may describe a syncopal episode in many ways, including blackout, dizzy spell, and seizure. Unexplained falls, particularly in elderly persons, also may be due to syncope.
  • Associated symptoms include palpitations, lightheadedness, diaphoresis, nausea and vomiting, warmth, chest pain, and shortness of breath.
  • Any history of focal neurologic symptoms or incontinence of bowel or bladder should also be sought.
  • Differentiating syncope from vertigo, in which a sensation of movement of either the patient or the surroundings transpires, is important. Vertigo usually reflects a neurologic or otolaryngologic problem.
  • Reports of eyewitnesses may be very helpful.
  • Triggers for the spells and a careful medication history, including over-the-counter and illicit drugs, should be sought.
  • The family history, particularly any family history of sudden death or syncope, should be reviewed, ie, the entire history is necessary.
  • The following clues suggest a higher risk of syncope and indicate that an expedient evaluation may be necessary:
    • Underlying structural heart disease, especially left ventricular dysfunction
    • Exertional syncope
    • Family history of sudden death
    • Significant traumatic injury due to loss of consciousness

Physical

A thorough physical examination should be performed on all patients who present with syncope.

  • Orthostatic vital signs at 1 and 3 minutes should be recorded.
  • The physician should look carefully for any cardiovascular or focal neurologic abnormalities.
  • Carotid sinus massage should be carefully performed during cardiac monitoring as long as carotid bruits or known carotid artery disease is not present.

Causes

Table 1. Causes of Syncope

Open table in new window

Table
CauseSymptomsPrognostic ImplicationApproximate Incidence Rate, %
CardiacVariableModerate-to-severe20
Reflex/orthostaticWarmth, nausea, diaphoresisBenign35
NeurologicSeizure, transient ischemic attack, focalModerate10
PsychiatricNo injuryBenign2
CauseSymptomsPrognostic ImplicationApproximate Incidence Rate, %
CardiacVariableModerate-to-severe20
Reflex/orthostaticWarmth, nausea, diaphoresisBenign35
NeurologicSeizure, transient ischemic attack, focalModerate10
PsychiatricNo injuryBenign2

Note that no diagnosis is determined in a significant fraction of patients presenting with syncope. Cardiac causes of syncope can be divided further into those related to structural heart disease and those related to a dysrhythmia.

Table 2. Cardiac Causes of Syncope

Open table in new window

Table
StructuralDysrhythmia
BradycardiaTachycardia
Aortic stenosisSick sinus syndromeVentricular tachycardia (VT)
Hypertrophic cardiomyopathyAtrioventricular (AV) blockVentricular fibrillation
Pulmonary embolusDrug-inducedTorsade de pointes VT
Pulmonary hypertension
Supraventricular tachycardia
Acute myocardial infarction
Atrial fibrillation/flutter
Tamponade

Aortic dissection

StructuralDysrhythmia
BradycardiaTachycardia
Aortic stenosisSick sinus syndromeVentricular tachycardia (VT)
Hypertrophic cardiomyopathyAtrioventricular (AV) blockVentricular fibrillation
Pulmonary embolusDrug-inducedTorsade de pointes VT
Pulmonary hypertension
Supraventricular tachycardia
Acute myocardial infarction
Atrial fibrillation/flutter
Tamponade

Aortic dissection

More on Syncope

Overview: Syncope
Differential Diagnoses & Workup: Syncope
Treatment & Medication: Syncope
Follow-up: Syncope
Multimedia: Syncope
References

References

  1. Brignole M, Alboni P, Benditt DG, et al. Guidelines on management (diagnosis and treatment) of syncope--update 2004. Europace. Nov 2004;6(6):467-537.

  2. Cannom DS. A critical appraisal of indications for the implantable cardioverter defibrillator (ICD). Clin Cardiol. May 1992;15(5):369-72. [Medline].

  3. Chen-Scarabelli C, Scarabelli TM. Neurocardiogenic syncope. BMJ. Aug 7 2004;329(7461):336-41.

  4. Connolly SJ, Sheldon R, Roberts RS, Gent M. The North American Vasovagal Pacemaker Study (VPS). A randomized trial of permanent cardiac pacing for the prevention of vasovagal syncope. J Am Coll Cardiol. Jan 1999;33(1):16-20. [Medline].

  5. Grubb BP, Kosinski DJ. Syncope resulting from autonomic insufficiency syndromes associated with orthostatic intolerance. Med Clin North Am. Mar 2001;85(2):457-72. [Medline].

  6. Kapoor WN. Syncope. N Engl J Med. Dec 21 2000;343(25):1856-62. [Medline].

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

  8. Linzer M, Yang EH, Estes NA 3rd, et al. Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Clinical Efficacy Assessment Project of the American College of Physicians. Ann Intern Med. Jun 15 1997;126(12):989-96. [Medline].

  9. Linzer M, Yang EH, Estes NA 3rd, et al. Diagnosing syncope. Part 2: Unexplained syncope. Clinical Efficacy Assessment Project of the American College of Physicians. Ann Intern Med. Jul 1 1997;127(1):76-86. [Medline].

  10. Soteriades ES, Evans JC, Larson MG. Incidence and prognosis of syncope. N Engl J Med. Sep 19 2002;347(12):878-85. [Medline].

  11. Sutton R, Brignole M, Menozzi C, et al. Dual-chamber pacing in the treatment of neurally mediated tilt-positive cardioinhibitory syncope: pacemaker versus no therapy: a multicenter randomized study. The Vasovagal Syncope International Study (VASIS) Investigators. Circulation. Jul 18 2000;102(3):294-9. [Medline].

Further Reading

Keywords

syncope, loss of consciousness, loss of postural tone, decreased cerebral perfusion, brainstem hypoxia, carotid sinus pressure, coronary artery disease, nonischemic cardiomyopathy, non-ischemic cardiomyopathy, ventricular tachyarrhythmia, congenital long QT syndrome, Wolff-Parkinson-White syndrome, WPW syndrome, Brugada syndrome, hypertrophic cardiomyopathy, syncopal episode, blackout, dizzy spell, seizure, dizziness, aortic stenosis, pulmonary embolus, pulmonary hypertension, acute myocardial infarction, acute MI, tamponade, aortic dissection, atrial fibrillation, atrial flutter, supraventricular tachycardia, SVT, torsades de pointes, ventricular tachycardia, VT, ventricular fibrillation, AV block, atrioventricular block, A/V block, A-V block, sick sinus syndrome, implanted cardioverter/defibrillators, ICDs

Contributor Information and Disclosures

Author

Jatin Dave, MD, MPH, Instructor, Department of Medicine, Department of Internal Medicine, Division of Aging, Harvard Medical School; Staff Physician, Brigham and Women's Hospital
Jatin Dave, MD, MPH is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Geriatrics Society, American Medical Association, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

John Michael Gaziano, MD, MPH, Associate Professor of Medicine, Harvard Medical School; Consulting Staff, Division of Aging, Brigham and Women's Hospital; Consulting Staff, Veterans Affairs Boston Healthcare System
John Michael Gaziano, MD, MPH is a member of the following medical societies: American College of Cardiology, American Geriatrics Society, American Heart Association, American Medical Association, and Gerontological Society of America
Disclosure: Nothing to disclose.

Medical Editor

Hanumant Deshmukh, MD †, Former Chief of Cardiology, Veterans Affairs Medical Center; Former Associate Professor, Department of Medicine, Rosalind Franklin University of Medicine and Science
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Brian Olshansky, MD, Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine
Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences
Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Reliant Grant/research funds Other; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Michael E Zevitz, MD, Assistant Professor of Medicine, Finch University of the Health Sciences, The Chicago Medical School; Consulting Staff, Private Practice
Michael E Zevitz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Medical Association, and Michigan State Medical Society
Disclosure: Nothing to disclose.

 
 
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