AUTHOR AND EDITOR INFORMATION

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• Follow-up
• Miscellaneous
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INTRODUCTION

Section 2 of 11  

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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

Section 3 of 11  

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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

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

DIFFERENTIALS

Section 4 of 11  

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Other Problems to be Considered

The history findings usually allow differentiation of syncope from the following conditions:

Vertigo: A sensation of movement of the patient and/or the surroundings, vertigo is usually caused by a neurologic or otolaryngologic problem. Most commonly, the abnormality is in the inner ear. Vertigo may be reproduced with the Parinet maneuver.

Seizure: Epileptic disorders are caused by excessive electrical activity in the cortex or other area of the brain. Partial complex seizures may cause loss of consciousness without marked motor activity. Grand mal seizures are characterized by tonic-clonic motor activity. On the other hand, syncope can be accompanied by tonic posturing due to brainstem hypoxia. Syncope is rarely accompanied by incontinence or a prolonged period of confusion following the event (ie, postictal confusion).

Transient ischemic attack: While a vertebrobasilar transient ischemic attack can cause loss of consciousness, this is unusual in the absence of other vertebrobasilar symptoms (eg, dysarthria, difficulty swallowing).

Narcolepsy: This is an extreme tendency to fall asleep during the day. A patient who is found to have unexpectedly fallen asleep is sometimes diagnosed with syncope.

Pseudosyncope: This is a functional or psychiatric disorder, in which episodes are fabricated or faked.

Cataplexy: This rare condition is characterized by transient loss of postural tone without loss of consciousness.

WORKUP

Section 5 of 11  

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Lab Studies

• See Image 1 for an algorithm for the evaluation of syncope.
• No laboratory studies are routinely obtained in patients with syncope. Instead, tests should be ordered if they are indicated clinically. For example, perform (1) a serum electrolyte evaluation if concerned about dehydration, (2) a digoxin level measurement if the patient is on this medication, or (3) thyroid studies in patients with bradycardia.

Imaging Studies

• No imaging studies are routinely obtained in patients with syncope. Tests should be ordered if indicated clinically, especially in patients suspected of having cerebrovascular causes for loss of consciousness.
• A transthoracic echocardiogram is useful to screen for structural heart disease such as left ventricular dysfunction, aortic stenosis, and hypertrophic cardiomyopathy. An echocardiogram should be performed if any suggestion of structural heart disease is present, if the patient is not young, or if the history findings are inconsistent with neurocardiogenic syncope.

Other Tests

• Additional work-up based on the suspected etiology from history and physical examination may include the following:
• • Cardiac causes - Electrocardiogram, exercise stress test, and echocardiogram followed by electrophysiological study in selected patients
  • Neurally mediated syncope - Carotid sinus message in appropriate patients, tilt table test
  • Unexplained syncope - Start with a carotid sinus message (if not contraindicated) and tilt table test followed by echocardiogram
• Electrocardiogram: A resting ECG should be performed on all patients who present with syncope. Relevant abnormalities include long QT syndrome, ventricular preexcitation, signs of ischemia/infarction, Brugada syndrome, and the suggestion of right ventricular cardiomyopathy.
• Exercise stress test: Stress testing should not be performed routinely in patients with syncope; testing should be performed only if coronary artery disease is suggested or if the syncope occurs during or after exercise. In the latter case, an echocardiogram should be performed first to exclude significant aortic stenosis and hypertrophic cardiomyopathy.
• Ambulatory monitoring: External endless loop recording is generally more useful than Holter monitoring because of the relative infrequency of syncopal episodes.
• Implantable loop recorder: For patients with extremely infrequent episodes, a device may be implanted subcutaneously that records (1) episodes of bradycardia and tachycardia and (2) patient-activated events for up to a year.
• Head-up tilt test: This noninvasive test assesses a patient's tendency for neurocardiogenic or vasovagal syncope. Protocols vary; one representative protocol includes tilting the patient at a 70° angle for 30 minutes. If the response after a baseline tilt is negative, it is typically repeated during pharmacologic provocation (eg, isoproterenol infusion, nitroglycerin). Several positive responses are possible with head-up tilt testing. A cardioinhibitory response involves severe bradycardia. In a vasodepressor response, the degree of hypotension is out of proportion to any bradycardia induced because of profound vasodilatation. Frequently, the response is mixed.
• Electrophysiologic study: Invasive electrophysiologic (EP) testing helps assess a patient's propensity for bradyarrhythmias and tachyarrhythmias. The yield on EP testing is greatest when evaluating the risk of ventricular tachyarrhythmias in patients with ischemic cardiomyopathy. The yield is lower in patients with nonischemic cardiomyopathy or possible bradycardia.
• Neurologic testing: Although brain MRI/CT scan, carotid studies, and electroencephalograms are performed frequently in patients with syncope, the yield on these studies is extremely low in patients who do not have focal neurologic deficits or witnessed seizure activity.

Procedures

• Diagnostic EP studies may be necessary.

TREATMENT

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Medical Care

The treatment strategy in patients with syncope depends entirely on the level of certainty of the symptom's etiology, an estimate of recurrence of symptoms, an estimation of potential risk with future recurrence, and the occupation of the patient.

• Neurocardiogenic (vasovagal or reflex) syncope
• • A number of therapeutic strategies are available.
  • Patients with rare episodes with a specific trigger (eg, drawing blood) generally do not require specific therapy.
  • In some patients with more frequent symptoms, nonpharmacologic measures may be adequate. These include fluid and sodium loading, avoidance of triggering situations (eg, hot tubs), support stockings to reduce venous pooling, and others. Discontinuation of offending medications (eg, nitrates) that are not necessary also may be helpful.
  • Drug therapy for patients with neurocardiogenic syncope may include beta-blockers, selective serotonin reuptake inhibitors, fludrocortisone, midodrine, theophylline, disopyramide, scopolamine, and hyoscyamine.
  • Permanent pacemakers have been shown to be effective in patients whose syncope is refractory and has a significant cardioinhibitory component. Pacemakers are frequently useful in patients with carotid sinus hypersensitivity.
• Orthostatic hypotension
  • In younger patients, orthostatic hypotension may be reflective of a dysautonomia.
  • In elderly patients, orthostatic hypotension may be due to other medical conditions such as diabetes mellitus or medications. Nonpharmacologic measures, such as dangling the legs over the side of the bed before slowly arousing and use of support stockings, may be helpful.
  • In young patients and in those without a history of hypertension, fluid and sodium expansion may improve symptoms; fludrocortisone and midodrine are frequently helpful in this setting.
  • If hypertension is present, modification of the medical regimen may improve symptomatic orthostasis. Blood pressure must be monitored carefully if therapy with fludrocortisone or midodrine is undertaken.
• Bradyarrhythmias: Unless the sinus node or AV conduction abnormality is attributable to a medication that can be discontinued safely, a permanent pacemaker is generally indicated for patients with symptomatic bradycardia.
• Ventricular tachyarrhythmias
• • In patients with significant structural heart disease, ventricular tachyarrhythmias are possible potentially life-threatening causes of syncope. In these patients, the documentation of a sustained episode of VT, ventricular fibrillation, or EP testing results documenting a high risk for ventricular tachyarrhythmias is generally an indication for ICD implantation.
  • For patients in whom ICD implantation is not appropriate or desired, medical therapy with amiodarone is also an option.
• Supraventricular tachycardia: In patients with supraventricular tachycardia causing syncope or patients with preexcitation (WPW syndrome) and syncope, radiofrequency catheter ablation is generally suggested.
• Structural heart disease: For patients with syncope attributable to structural heart disease (eg, aortic stenosis, hypertrophic cardiomyopathy, pulmonary hypertension), treatment is generally directed at the underlying organic cardiovascular condition.

Surgical Care

Pacemakers and ICDs are frequently implanted in patients with syncope.

• Pacemaker implantation
• • Pacemakers are implanted in patients with syncope due to bradyarrhythmias (sinus node dysfunction or AV block).
  • Pacemakers may be of benefit in patients with refractory neurally mediated (ie, reflex or vasovagal) syncope with a prominent cardioinhibitory component, but this remains controversial.
• ICD implantation
• • ICDs are implanted in patients with syncope in whom ventricular tachyarrhythmias are determined to have caused the syncope or in those who have structural heart disease and a high risk for life-threatening ventricular arrhythmias, but they are generally not implanted to prevent syncope.
  • Patients with idiopathic VT and cardiac arrest due to WPW syndrome are not treated with ICDs. Patients with idiopathic VT may be treated with drugs or catheter ablation; the prognosis is excellent if the heart is structurally normal. Patients with WPW syndrome and syncope (or sudden death) should undergo EP studies and radiofrequency catheter ablation.

Consultations

Patients with recurrent syncope or syncope in the setting of significant structural heart disease should generally be referred to a cardiac electrophysiologist.

Diet

Dietary recommendations depend on the underlying conditions. Patients with neurocardiogenic syncope in the setting of structurally normal hearts are generally recommended to increase their intake of fluid and sodium. Dehydration predisposes patients to vasovagal episodes.

Activity

Activity recommendations depend on the patient's underlying conditions. For patients with recurrent syncope, working at heights, scuba diving, and driving are generally proscribed until the syncope is treated successfully. In some US states, physicians are required to report patients with syncope to the state's drivers' license bureau.

MEDICATION

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Pharmacologic therapy is used most commonly in patients with neurally mediated (ie, vasovagal) syncope.

Drug Category: Beta-adrenergic blocking agents

May help block the vasovagal reflex by their negative inotropic effects.

Drug Category: Selective serotonin reuptake inhibitors

May be effective in patients with neurally mediated syncope, although the reason for this is not clear.

Drug Category: Corticosteroids

Can be of benefit in patients with neurally mediated syncope and syncope due to orthostatic hypotension.

Drug Category: Alpha-adrenergic agonists

Peripherally acting alpha-agonists can be of benefit in patients with neurally mediated syncope and syncope due to orthostatic hypotension.

Drug Category: Methylxanthines

May be of benefit in patients with neurally mediated syncope.

Drug Category: Class IA antiarrhythmic agents

Negative inotropic agents may be of benefit in patients with neurally mediated syncope.

Drug Category: Anticholinergic agents

May be of benefit in patients with neurally mediated syncope.

FOLLOW-UP

Section 8 of 11  

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• Follow-up
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Further Inpatient Care

• Patients treated with ICDs or pacemakers require follow-up care at regular intervals.
• Patients with neurocardiogenic syncope require clinical follow-up observation to assess response to therapy.
• Results from follow-up tilt testing are not necessarily predictive of the clinical response to medical therapy; therefore, follow-up tilt testing is not generally recommended.
• Patients with structural heart disease require follow-up care as dictated by the specific heart disease.

Further Outpatient Care

• Patients treated for neurocardiogenic syncope are generally observed clinically.
• Repeat tilt testing has not been established to firmly predict clinical response to therapy.

In/Out Patient Meds

• See Medication.

Transfer

• Patients with syncope in the setting of structural heart disease should be transferred to facilities with EP laboratories because ventricular arrhythmias may be causing the episodes.

Deterrence/Prevention

• Nonpharmacologic therapies may be of benefit in patients with neurally mediated syncope. These include salt and fluid loading, compression stockings, sleeping with the head of the bed elevated, moving slowly from a lying to a standing position, and avoiding triggers (eg, hot tubs, prolonged standing in a warm room).

Complications

• Syncope due to bradyarrhythmia (primarily complete AV block) and ventricular tachyarrhythmia can be important clues to the underlying, potentially life-threatening problem. With any type of syncope, even if the cause is benign (eg, orthostatic, vasovagal), the potential exists for significant trauma, which can be devastating, particularly in elderly persons (eg, hip fracture).

Patient Education

• Patient education should focus on pathophysiologic issues and nonpharmacologic issues.
• For excellent patient education resources, visit eMedicine's Brain and Nervous System Center and Heart Center. Also, see eMedicine's patient education articles Fainting and Supraventricular Tachycardia.

MISCELLANEOUS

Section 9 of 11  

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• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• In some US states, syncope is a medical condition that is reportable to the state's drivers' license bureau. Physicians are urged to understand the laws of the state(s) in which they practice. Even in states in which reporting of syncope is not mandatory, recommending that patients not drive, and documenting this recommendation, are prudent. Regulations regarding commercial drivers and pilots are more stringent.

Special Concerns

• Syncope during pregnancy is frequently attributed to orthostatic hypotension and/or inferior vena cava compression by the gravid uterus, but patients should be evaluated carefully for other potentially life-threatening causes of syncope in this age group (eg, long QT syndrome, hypertrophic cardiomyopathy, WPW syndrome).
• Syncope in pediatric patients is frequently ascribed to epilepsy, even if the workup findings are negative. Pediatric patients should be assessed carefully for potentially life-threatening causes of syncope in this age group (eg, long QT syndrome, hypertrophic cardiomyopathy, WPW syndrome). Because many of these syndromes are familial, careful attention to the family history is imperative.
• Syncope in elderly persons can have devastating consequences, even if the etiology is benign (eg, orthostatic hypotension). Trauma due to syncope can include hip and other fractures, which can cause substantial morbidity and mortality. Thus, an aggressive workup of syncope is frequently warranted in elderly persons.

MULTIMEDIA

Section 10 of 11  

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• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  An algorithm for the evaluation of syncope.
	View Full Size Image
Media type:  Graph

REFERENCES

Section 11 of 11

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• 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.
• Cannom DS. A critical appraisal of indications for the implantable cardioverter defibrillator (ICD). Clin Cardiol. May 1992;15(5):369-72. [Medline].
• Chen-Scarabelli C, Scarabelli TM. Neurocardiogenic syncope. BMJ. Aug 7 2004;329(7461):336-41.
• 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].
• 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].
• Kapoor WN. Syncope. N Engl J Med. Dec 21 2000;343(25):1856-62. [Medline].
• Kapoor WN. Current evaluation and management of syncope. Circulation. Sep 24 2002;106(13):1606-9.
• 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].
• 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].
• Soteriades ES, Evans JC, Larson MG. Incidence and prognosis of syncope. N Engl J Med. Sep 19 2002;347(12):878-85. [Medline].
• 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].

Article Last Updated: Jan 29, 2007