a. Definition. Syncope is a transient loss of consciousness and postural tone that occurs because of transient global cerebral hypoperfusion. Typical characteristics of an episode of syncope include rapid onset and short duration of loss of consciousness followed by spontaneous complete recovery. Patients may experience a prodrome of lightheadedness, fatigue, weakness, nausea, or visual changes, but in some cases loss of consciousness can be sudden. Syncope should be differentiated from presyncope, dizziness, and vertigo—all of which do not result in loss of consciousness. Non–perfusion-related causes of alteration in consciousness such as seizures must be excluded. A careful history and examination for prodromal or postictal symptoms and rhythmic myoclonic activity is therefore required.
b. Epidemiology. Syncope is extremely common, accounting for approximately 6% of medical admissions and 3% of emergency department visits. The lifelong incidence approaches 50% in some groups.
B. Causes of Syncope. There are many causes of syncope, but the most important can easily be remembered using the mnemonic, “SYNCOPE.”
MNEMONIC: Causes of Syncope (“SYNCOPE”)
Vasovagal (The V looks like a Y. This is a type of neurally mediated syncope.)
Causes of syncope can also be categorized according to etiology following the European Society of Cardiology Classification system:
a. Reflex (neurally mediated) syncope
i. Vasovagal syncope is also known as “common faint” and is the most common cause of syncope in young patients resulting from reflex-mediated decrease in vascular tone (vasodepressor effect due to reduction of sympathetic tone) or heart rate (cardioinhibitory component due to exaggerated parasympathetic tone) or the combination. Common causes of vasovagal syncope include:
1. Vasovagal syncope mediated by emotional stress (e.g., fear, pain, blood phobia).
2. Vasovagal syncope mediated by orthostasis.
iii. Carotid sinus syncope is caused by carotid sinus sensitivity resulting in changes in autonomic tone.
b. Syncope due to orthostatic hypotension. This cause of syncope is more common in older adults. Normally with standing, systolic blood pressure (SBP) decreases by less than 15 mm Hg, whereas diastolic blood pressure (DBP) increases. In orthostatic hypotension, patients demonstrate a decrease in SBP that exceeds 20 mm Hg and concomitant decrease (not increase) in DBP. Causes of orthostatic hypotension include:
i. Autonomic failure can be seen with primary neurologic conditions (multiple-system atrophy, Parkinson’s disease, Lewy body dementia) as well as secondary causes of autonomic insufficiency (e.g., diabetes mellitus, amyloidosis).
ii. Medication/drug-induced orthostasis can be caused by a long list of medications, including but not limited to peripheral vasodilators, diuretics, psychiatric medications, cocaine, and alcohol.
iii. Hypovolemia can be caused by bleeding, gastrointestinal losses, and overdiuresis.
c. Cardiovascular syncope
i. Mechanical/obstructive disorders. Aortic, mitral or pulmonic valvular stenosis, hypertrophic cardiomyopathy, subvalvular/supravalvular stenosis, and atrial myxoma can interfere with cardiac output to precipitate syncope.
ii. Arrhythmias. Disorders that lead to bradycardia (e.g., sick sinus syndrome, second- and third-degree atrioventricular [AV] block) or tachycardia (e.g., ventricular fibrillation, ventricular tachycardia, torsades de pointes, supraventricular tachycardia, ion channel disorders) can also interfere with cardiac output and decrease cerebral perfusion.
iii. Other cardiovascular etiologies. Ischemic disorders can precipitate an episode of syncope through low cardiac output or arrhythmias. Aortic dissection can lead to syncope through cardiac tamponade from hemopericardium or acute cerebrovascular insufficiency. Other cardiovascular causes of syncope that should be considered include pulmonary hypertension, acute pulmonary embolism, subclavian steal syndrome, and cerebrovascular events, particularly those causing vertebrobasilar insufficiency.
d. Other conditions
i. Metabolic: hypoglycemia, severe hypoxemia.
ii. Psychogenic: a diagnosis of exclusion.
C. Approach to the Patient. The evaluation of a patient with syncope should occur in a rigorous, stepwise fashion to avoid missing life-threatening disease. The goals of the evaluation are not only to identify the exact etiology but also to determine whether the cause is cardiac or noncardiac given that cardiac syncope is associated with significantly worse prognosis.
a. History. A thorough history is the most important aspect of the evaluation and may establish the diagnosis in up to half of patients. The history should seek to determine the circumstances before or around the syncope event.
i. Reflex/situational. Was the episode preceded by urination, defecation, swallowing, coughing, exertion of arm muscles (subclavian steal), or manipulation of the neck (carotid sinus hypersensitivity)? A diagnosis of carotid sinus hypersensitivity is suggested by a history of the syncopal event occurring during situations of external carotid pressure such as shaving, tight collars, or neck movements. Testing for carotid sinus hypersensitivity should be done carefully after excluding significant carotid artery stenosis and only if the patient is monitored by EKG.
ii. Vasovagal. Did a painful or emotional stimulus precede the event? Common scenarios for vasovagal syncope include being in hot and crowded environments (parade, church, airplane, restaurant).
iii. Neurogenic. Were convulsions, bowel or bladder incontinence, or signs suggestive of a postictal state noted? Although seizure is not syncope, it could result in a loss of consciousness and must be considered in the differential diagnosis.
iv. Cardiac. A cardiac cause is more likely if the patient has any history suggestive of cardiac disease. Has the patient complained of feeling lightheaded during exercise (suggestive of an obstructive cause)? Has the patient complained of “palpitations” (suggestive of an arrhythmic cause)? Patients may also complain of symptoms suggestive of cardiac ischemia, including exertional chest pain or dyspnea.
v. Orthostatic hypotension. Does the patient report that he or she “got up too quickly?” Always check orthostatic vital signs in patients admitted with syncope. Orthostatic hypotension is defined by one of the following findings occurring within 2 to 5 minutes of the patient standing from a sitting position: (1) decrease in SBP of 20 mm Hg; (2) decrease in diastolic blood pressure of 10 mm Hg; (3) reflex tachycardia of 20 beats/min; or (4) symptoms of cerebral hypoperfusion.
vi. Psychogenic. A psychogenic cause for the syncope (e.g., hyperventilation) should be considered after all other causes have been excluded.
vii. Everything else. What prescription, over-the-counter, or illicit drugs might the patient have access to?
“Convulsive syncope:” uncommonly, syncope can be associated with muscular jerking or loss of bladder control, particularly if posture is maintained during the episode of syncope.
b. Physical examination can offer clues to the etiology of the syncopal event.
i. Vital signs. Is there evidence of orthostasis, tachycardia, bradycardia, or baseline hypotension? Disparities between upper extremities in blood pressure or pulse may be consistent with aortic dissection or subclavian steal syndrome. Hypoxemia may indicate pulmonary embolism.
ii. Neck. Auscultation of carotid bruits may reveal evidence of stenosis.
iii. Oral cavity. Inspection of a patient’s tongue may display lacerations associated with seizure activity.
iv. Cardiovascular. Auscultation of the heart may reveal an irregular rhythm (atrial fibrillation), systolic murmur (aortic stenosis or hypertrophic obstructive cardiomyopathy), diastolic murmur (mitral stenosis), a tumor plop (suggestive of atrial myxoma), or an S3 sound consistent with heart failure.
v. Pulmonary. Auscultation may reveal crackles consistent with pulmonary edema.
vi. Neurologic examination may display evidence of stroke or resolving transient ischemic attack (TIA).
c. Electrocardiogram (EKG). All patients should have an EKG, although fewer than 10% of the causes of syncope can be identified by this test. Look for evidence of acute or remote myocardial infarction, preexcitation syndromes, arrhythmias, a long QT interval, conduction system disease (i.e., bundle branch block), or findings consistent with hypertrophic cardiomyopathy (left ventricular hypertrophy).
d. Risk assessment. Patients should be classified into two groups: those with low risk features and no evidence of heart disease, and those who may have heart disease or findings suggestive of short-term high-risk etiology. High-risk features include:
1. Evidence of structural or ischemic heart disease.
2. Age greater than 60 years.
3. Syncope while supine or during exercise.
4. Palpitations at the time of syncope.
5. Syncope without prodrome.
6. Family history of sudden cardiac death.
7. High-risk EKG findings: nonsustained ventricular tachycardia, prolonged QT interval, findings suggestive of channelopathies (Brugada patterns, arrhythmogenic right ventricular cardiomyopathy), preexcitation.
ii. Low-risk features and no evidence of heart disease. Patients who fall in this category after a thorough history, physical examination, and EKG are at low risk for a cardiac cause; additional cardiac testing is usually not warranted.
iii. High-risk features or evidence of heart disease. Anyone who meets criteria concerning for possible high-risk etiology is included in this group. If there is suspicion of an ischemic or arrhythmic cause, hospital admission and EKG monitoring are indicated. Additional diagnostic tests to be considered include:
1. Ambulatory EKG monitoring. This test is widely used, but it establishes a diagnosis in only a small percentage of patients. Holter monitors, applied for 24–48 hours, can be considered if the patient reports frequent symptoms (daily). Event or loop recorders, often used for 2–4 weeks, may improve the diagnostic yield in case of less frequent symptoms. Like Holter monitors, an event recorder constantly monitors the heart rhythm but only records if the heart rate or rhythm meets certain preset parameters or the patient triggers the monitor to record in case of symptoms. Implantable loop records are long-term monitoring devices that are subcutaneously implanted and can be considered in patients with infrequent (less than once a month) and unexplained episodes of syncope.
2. Exercise treadmill testing can rule out exercise- or ischemia-induced syncope.
3. Echocardiography allows assessment of structural heart abnormalities including valvular disease as well as left ventricular size and function in addition to cardiomyopathies (hypertrophic cardiomyopathy), pulmonary hypertension, or rarely cardiac tumors (e.g., atrial myxoma).
4. Electrophysiologic (EP) studies are especially useful in patients at high risk for tachyarrhythmia (i.e., those with poor left ventricular function) when a diagnosis cannot be established using noninvasive methods. The yield of EP studies is lower in patients without structural heart disease and in those with bradyarrhythmias.
5. Tilt table test. Although useful in documenting vasovagal syncope, tilt table testing has poor specificity. If the clinical suspicion for vasovagal syncope is high, the utility of the tilt table test decreases substantially. Moreover, tilt table testing is not useful in guiding treatment changes after the diagnosis is established.
6. Neurologic and vascular imaging: carotid duplex or computed tomography (CT)/magnetic resonance (MR) angiography may be considered if a vascular etiology is highly suspected based on the history and clinical presentation. These tests should not be routinely ordered.
D. Treatment Is Cause Specific
a. Treatment of any correctable cardiac abnormality should be the first consideration (i.e., permanent pacemaker for patients with bradyarrhythmias, implantable cardiac defibrillators in patients with ventricular tachycardia, or valvular surgery for those with severe aortic stenosis).
b. Patients with frequent vasovagal syncope may benefit from a trial of midodrine, β-blockers, paroxetine, or disopyramide. In rare instances, patients with a significant cardioinhibitory component may benefit from permanent pacemaker placement. The most important component of treating vasovagal syncope is educating the patient about the condition, trigger avoidance, and reassurance.
c. Orthostatic hypotension is treated with volume resuscitation and discontinuation of culprit drugs. Rarely, support stockings, salt tablets, fludrocortisone, and midodrine may be added if autonomic insufficiency is present and disabling.
a. Medications, along with the use of alcohol or illicit drugs, should be reviewed carefully.
b. Education about likely precipitants or triggers can help prevent recurrences.
Suggested Further Readings
Linzer M, Yang EH, Estes NM, Wang P, Vorperian VR, Kapoor WN. Clinical guideline: diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Ann Intern Med 1997;126:989–96. (Classic Article.)Find this resource:
Linzer M, Yang EH, Estes NM, Wang P, Vorperian VR, Kapoor WN. Clinical guideline: diagnosing syncope. Part 2: Unexplained syncope. Ann Intern Med 1997;127:76–86. (Classic Article.)Find this resource:
Prandoni P, Lensing AW, Prins MH, et al. Prevalence of pulmonary embolism among patients hospitalized for syncope. N Engl J Med 2016;375:1524–31.Find this resource:
Puppala VK, Dickinson O, Benditt DG. Syncope: classification and risk stratification. J Cardiol 2014;63:171–7.Find this resource:
Sheldon RS, Grubb BP 2nd, Olshansky B, et al. 2015 Heart Rhythm Society expert consensus statement on the diagnosis and treatment of postural tachycardia syndrome, inappropriate sinus tachycardia, and vasovagal syncope. Heart Rhythm 2015;12:e41–63.Find this resource: