Lavina Malhotra, MD
Stephen F. Schaal, MD
Subha V. Raman, MD
DESCRIPTION 
Syncope is a transient loss of consciousness (LOC) due to transient global cerebral hypoperfusion characterized by rapid onset, short duration, and spontaneous complete recovery.
- Clinical characteristics:
- The onset of syncope may either be abrupt or subacute with or without prodromal symptoms. The patient may only recall “passing out,” while someone who observed the event may provide more detailed information. Thus, a thorough history involves both the patient and any observers the patient wishes to include in the interview.
PATHOPHYSIOLOGY
Neurally Mediated Syncope (NMS)
In neurocardiogenic syncope, which usually occurs with normal cardiac function, reflective changes in heart rate or BP fail to appropriately maintain cardiac output; this may include an abnormal fall in heart rate or BP or simply a failure to adequately augment these parameters. Vasodepressor syncope occurs with a situational stimulus (blood draw, unpleasant surprise) and likely has similar pathophysiology. These are the most common forms of syncope.
Arrhythmia
Arrhythmias induce hemodynamic impairment causing a critical decrease in cardiac output and cerebral blood flow. Syncope often has multiple contributory factors such as the heart rate, type of arrhythmia (supraventricular or ventricular), left ventricular function, and adequacy of vascular compensation. Bradyarrhythmias in particular should be considered in elderly patients with resting bradycardia or atrioventricular conduction disease. Atrial fibrillation can be an important cause. Several drugs can also cause brady- and tachyarrhythmia. Many antiarrhythmic drugs can cause bradycardia as a consequence of their specific effect on sinus node function or AV conduction. Syncope due to torsade de pointes is not uncommon, especially in women, and is caused by drugs prolonging the QT interval. It is particularly frequent in patients affected by the long QT syndrome. QT-prolonging drugs belong to different categories, i.e., antiarrhythmics, vasodilators, psychotropics, antimicrobials, non-sedating antihistamines, etc.
Structural Disease
Structural cardiovascular disease can cause syncope when circulatory demands overweigh the impaired ability of the heart to increase its output. In conditions with a fixed or a dynamic obstruction to the left ventricular outflow such as hypertrophic cardiomyopathy or severe aortic stenosis, syncope results from obstruction to cardiac output. Any mechanical obstruction to cerebral blood flow may produce syncope in a similar mechanism; less frequent causes include ascending aortic dissection flap or occlusion of the left ventricular outflow tract by a dislodged left atrial myxoma.
[Outline]
Initial evaluation consists of careful history, physical examination including orthostatic BP measurements and an ECG. Other less specific tests such as neurological evaluation or blood test are only indicated when there is a suspicion of non-syncopal transient LOC. The following questions should be answered: Was seizure activity present? Was somnolence present after syncope? Was the LOC transient with rapid onset and short duration? Was the recovery spontaneous, complete, and without sequel? And did the patient lose postural tone? Neurally mediated syncope is suspected in the absence of any heart disease; long history of recurrent syncope; prodrome of nausea and vomiting; occurrence after sudden, unexpected, or unpleasant sight, sound, smell, or pain and with head rotation or pressure on carotid sinus (as in tumors, shaving, and tight collars). Orthostatic hypotension is often considered a cause of syncope if it occurs after standing up; temporal relationship with start or changes of dosage of vasodepressive drugs leading to hypotension; standing after exertion and presence of autonomic neuropathy or Parkinsonism. Clinical features that suggest a diagnosis on initial evaluation are presence of definite structural heart disease, family history of unexplained sudden death or channelopathy, sudden onset of palpitation immediately followed by syncope and abnormal ECG findings (bifascicular block, Mobitz I second-degree AV block, sinus bradycardia, right bundle branch blocks (BBB) pattern, Q waves suggesting myocardial infarction, etc.).
DIAGNOSTIC TESTS AND INTERPRETATION
An array of diagnostic tests is available. Appropriate selection of any test should be guided by individual patient assessment, as typically the history provides sufficient information to obtain at least a tentative diagnosis in most cases.
Carotid Sinus Massage (CSM)
CSM is performed to evaluate patients with suspected carotid sinus hypersensitivity (CSH). This test may be performed at the bedside with patients in the supine or upright positions under continuous ECG and BP monitoring. CSH is diagnosed when CSM causes a >3 second pause, a >50 mm Hg fall in systolic BP or both, associated with presyncope and/or syncope. CSM should not be performed in patients with a history of recent transient ischemic attack or stroke or on a carotid artery that had a significant bruit or known stenosis.
Tilt Testing
Patients with a suspicion of orthostatic or vasodepressor syncope undergo this test. Patients are placed on a tilt table and then tilted upward at angles between 60 and 80 degrees for 30 to 40 minutes with regular monitoring of clinical response, BP and heart rates. This test promotes venous pooling in the lower extremities and provokes vasovagal response through the Bezold–Jarisch mechanism leading to bradycardia and hypotension. Pharmacologic provocation with sublingual nitroglycerine, Isuprel or adenosine triphosphate infusion is occasionally administered during this test. Symptomatic hypotension without bradycardia is indicative of orthostatic syncope.
Exercise Stress Test
Exercise stress testing in patients with syncope is performed to identify coronary artery disease and exercise-induced cardiac arrhythmias such as sinus node dysfunction, AV block, or tachycardia. This testing is particularly helpful in patients with syncope during activity or exercise.
ECG Monitoring
- ECG monitoring is indicated for diagnosing intermittent bradycardia and tachyarrhythmia. The gold standard for diagnosis of syncope is when a correlation between the symptoms and a documented arrhythmia is recorded. The choice of outpatient cardiac monitoring is based on the frequency of syncope. In patient monitoring (in bed or telemetry) is warranted only when the patient is at high risk for a life-threatening arrhythmia. ECG monitoring is helpful in almost all instances of syncope and particularly indicated in patients with palpitations.
- The Holter monitor is an external device that is used to monitor the ECG tracing continuously for a period of 24 hours or longer. It may be of value of the symptoms are very frequent and to differentiate patients with psychogenic pseudo-syncope. Holter monitoring may also reveal QT interval changes, T wave alternans or ST changes.
- Longer term monitoring such as with external loop or implantable devices should occur when there is a high suspicion of arrhythmia as a cause of syncope.
Echocardiogram
Structural heart diseases that predispose patients to syncope can be effectively evaluated by echocardiography. This test provides diagnostic and prognostic information with assessment of parameters such as cardiac size, left ventricular function, wall motion, and valvular heart disease. Transesophageal echocardiography, CT, and MRI may be performed in selected cases (e.g., aortic dissection and hematoma, pulmonary embolism, cardiac masses, pericardial and myocardial diseases, and congenital anomalies of coronary arteries).
Electrophysiology
The electrophysiologic study (EPS) is an invasive procedure that is recommended when cardiac arrhythmias are suspected to be the cause of syncope and noninvasive diagnostic studies are not conclusive. It is indicated in patients who have unexplained syncope in the presence of impaired left ventricular function or structural heart disease. The EPS involves placing catheters inside the heart with conduction system measurements and arrhythmia provocation. In patients with BBB, Brugada syndrome, arrhythmogenic right ventricular cardiomyopathy (ARVC) and hypertrophic cardiomyopathy, EPS should be considered when noninvasive tests have failed to make the diagnosis.
DIFFERENTIAL DIAGNOSIS
Establishing that syncope occurred is usually straightforward, the patient will say, “I passed out.” Distinguishing near-syncope from vertigo or non-specific neurologic syndromes may be more challenging. The history from the patient or an observer will allow the clinician to distinguish vestibular phenomena from true syncope. In eliciting a history of tonic–clonic movements or incontinence, keep in mind that seizure-like activity may ensue from syncope of any etiology, but focal neurologic signs should prompt consideration of a primary neurologic disorder. Identifying other autonomic disturbances raises the possibility of diseases such as Shy-Drager syndrome, Parkinson's disease, and diabetic neuropathy. Volume depletion due to any cause may predispose a susceptible patient to syncopal episodes. Neurological evaluation is indicated in patients in whom transient LOC is suspected to be epilepsy.
[Outline]
The goals in treating patients with syncope should include: Limiting physical injuries, preventing recurrences, and prolonging survival.
NMS:
- Patient education is an important part of the treatment of NMS. Educating patients about mechanism and avoidance may reduce the incidence of such episodes. Medical treatment for NMS includes avoiding dehydration, physical counterpressure maneuvers (PCM) at the onset of prodrome (lying down with their feet popped up, squatting, isometric hand gripping, arm tensing, and leg crossing), increasing the intravascular volume by oral or intravenous fluids and dietary salt, wearing support hose, and physical tilt training. Some patients may require pharmacotherapy, such as volume expanders (fludrocortisones), beta blockers, and vasoconstrictors. Randomized controlled trials have demonstrated no clear clinical benefit of these agents, and the patient should be warned of possible side effects of hypertension (dietary salt, fludrocortisones, or urinary retention or urgency).
- Cardiac pacing is rarely considered in NMS unless symptoms are refractory.
Orthostatic Syncope
The treatment of orthostatic syncope consists of education regarding aggravating factors for orthostatic syncope, non-pharmacologic and pharmacologic corrections of hypovolemia, and autonomic imbalance. The non-pharmacologic approach focuses on making slow and careful changes in position, adequate hydration and salt intake, increasing intravascular volume, wearing support hose, and a routine exercise program. The patients may also benefit from PCM, tilt training, and sleeping with the head of the bed elevated to 20 to 25 cm to increase fluid volume. Pharmacotherapy with volume expanders or vasoconstrictors (Fludrocortisones and Midodrine) may be prescribed for severe symptoms of orthostasis.
Cardiac Arrhythmia-Related Syncope
- Cardiac pacing: Cardiac pacemaker therapy is indicated and has proved highly effective in patients with sinus node dysfunction when bradyarrhythmia has been demonstrated as cause for syncope (symptom—ECG correlation). Syncope and second degree Mobitz II, advanced or complete AV block, BBB and positive electrophysiological study are all indications for cardiac pacing.
- Catheter ablation: In patients with paroxysmal AV nodal reciprocating tachycardia, AV reciprocating tachycardia or typical atrial flutter associated with syncope, catheter ablation is first-choice treatment. However, patients with onset of rapid atrial fibrillation, the decision should be individualized. The role of drug therapy is limited.
- Antiarrhythmic drug therapy: Antiarrhythmic drug therapy including rate control drugs is indicated in patients with syncope due to onset of rapid atrial fibrillation.
- Implantable cardioverter defibrillator: ICD should be considered in patients with documented ventricular tachycardia, structural heart disease and inherited cardiomyopathies or channelopathies.
Unexplained Syncope in Patients with High Risk of Sudden Cardiac Death (SCD)
Unexplained syncope with a high risk of SCD is seen in the following groups: Hypertrophic cardiomyopathies, ARVC, inherited cardiac ion channel abnormalities, long QT syndromes, and Brugada syndrome. All should be evaluated by a cardiologist with expertise in these syndromes.
Driving
The American Heart Association established driving guidelines related to arrhythmias that may affect consciousness were later amended to include drivers with ICD insertion for primary prevention. Two groups of drivers are defined: Private and commercial. Drivers of taxicabs, small ambulances, and other vehicles form an intermediate category. Data suggest that the risk for a motor vehicle accident related to syncope is low. The efficacy of drug therapy for NMS remains inconclusive, and repeat tilt-table testing to assess therapy has no predictive value. There is no evidence that allowing three asymptomatic months to elapse provides assurance that syncope will not recur. Driving recommendations should be prescribed in conjunction with the collaborating physician or cardiologist.
IN-PATIENT CONSIDERATIONS
Admission Criteria
Any episode of syncope resulting in significant harm to the patient mandates inpatient evaluation. Furthermore, patients with structural heart disease and syncope probably should be admitted to a telemetry ward given the risk of sudden death. On the other hand, a young person with a clearly identified reversible precipitant such as dehydration or presumed vasodepressor (neurocardiogenic) syncope could be managed as an outpatient in the absence of high-risk features.
[Outline]
FOLLOW-UP RECOMMENDATIONS
Patient Monitoring
Patient monitoring is indicated particularly if an arrhythmic cause is suspected but a diagnosis has not been made.
PATIENT EDUCATION
Symptoms of noncardiac syncope are briefly outlined at this NIH website: http://www.ninds.nih.gov/health_and_medical/disorders/syncope_doc.htm
PROGNOSIS
Two important elements should be considered with the risk stratification of syncope: The risk of death and life-threatening events and the risk of recurrence and physical injury associated with syncope. Structural heart disease and primary electrical disease are associated with poor prognosis, conversely young patients affected by reflex syncope have excellent prognosis. The number of episodes of syncope during life is the strongest predictor of recurrence. Recurrent syncope may be associated with bone fractures and soft tissue injuries. Morbidity is particularly high in elderly and ranges from loss of confidence, depressive illness and fear of falling to fractures and subsequent institutionalization. Nonetheless recurrent syncope is comparable with chronic illnesses as it significantly impairs the quality of life.
[Outline]
