Syncope is a sudden, brief loss of consciousness (LOC) with loss of postural tone followed, by definition, by spontaneous revival. Typically, the patient is pale, motionless, diaphoretic, and hypotensive, with cool extremities, a weak pulse, and shallow rapid breathing. Light-headedness and a sense of an impending faint without LOC (near-syncope) are usually considered with syncope because the causes are the same; when the patient is upright, syncope often follows (in orthostatic hypotension). Syncope and near-syncope are fairly common and recur in up to ¹⁄₃ of people. Although the cause is often benign, identifying the occasional life-threatening cause (eg, tachyarrhythmia, heart block) is important.

Pathophysiology and Etiology

Syncope results from global CNS dysfunction, which may have many causes. Typically, CNS dysfunction results from cerebral hypoperfusion. Cerebral hypoperfusion most commonly results from disorders that decrease cardiac output (CO). CO can be impaired by primary cardiac disorders or conditions that decrease venous return (eg, reflex-mediated vasomotor instability). Occasionally, cerebrovascular disorders cause hypoperfusion. In the elderly, syncope often has more than one cause.

Primary cardiac disorders

Mechanisms for decreased CO include outflow obstruction, diastolic filling disorders, arrhythmias, and less commonly, pump failure. Cardiac causes of syncope, unlike other causes, have a significant risk of sudden death. The risk is from the underlying disorder, not from syncope itself.

Cardiac outflow may be obstructed because of valvular stenosis (particularly aortic), hypertrophic cardiomyopathy, a defective prosthetic valve, or a pulmonary embolus. Intracardiac tumors (eg, atrial myxoma) or ball-valve thrombi can intermittently obstruct blood flow through the heart, sometimes only with certain changes in position. Exercise and hypovolemia exacerbate outflow obstruction (particularly in aortic stenosis and hypertrophic cardiomyopathy) and may precipitate syncope. Inotropic drugs also may trigger syncope in patients with hypertrophic cardiomyopathy.

Arrhythmias cause syncope when heart rate is too fast to allow adequate ventricular filling (eg > 150 to 180 beats/min) or too slow to provide adequate output (eg, < 30 to 35 beats/min). When other cardiovascular (eg, obstructive) disorders are present, less extreme heart rate changes may cause syncope.

Bradyarrhythmias that can cause syncope include sick sinus syndrome (with or without tachyarrhythmias) and high-grade atrioventricular block, especially when onset is abrupt. Although bradyarrhythmias develop at all ages, they are most common among the elderly, usually because of fibrosis of the conduction system (due to ischemia or age-related degeneration). Digoxin, β-blockers (including ophthalmic drops), Ca channel blockers, and other drugs may cause bradyarrhythmias and syncope.

Tachyarrhythmias may be of supraventricular or ventricular origin; they may result from ischemia, heart failure, cardiomyopathy, drug toxicity (quinidine syncope is best known), electrolyte abnormalities (eg, hypokalemia, hypomagnesemia), preexcitation, or other disorders.

Systolic or diastolic ventricular dysfunction (eg, in acute MI, myocarditis, or cardiac tamponade) may decrease CO, rarely causing syncope. Acute MI causes syncope usually only if arrhythmia or heart block (particularly common with inferior MI) is also present; syncope rarely results from ischemic ventricular dysfunction alone. However, syncope is the presenting symptom of MI in a few patients, particularly in the elderly.

Reflex-mediated vasomotor instability

Several stimuli can trigger a reflex-mediated withdrawal of sympathetic tone and increase in vagal tone, leading to neurally mediated (neurogenic) syncope. Predisposing factors may be involved.

Increased intrathoracic pressure (due to cough, straining to void or defecate, or another Valsalva maneuver) can limit venous return and increase vagal tone, resulting in decreased CO and syncope.

Strong emotion, pain, fear, sight of blood, or injury can produce strong vagal stimulation, causing vasovagal syncope. An initial increase in BP and heart rate is followed by an abrupt decrease in BP and sometimes heart rate. This form of syncope is common and benign; assuming a horizontal position results in complete recovery.

Carotid sinus pressure (due to inadvertent pressure on the neck or constricting clothing) can activate one or both carotid sinuses, causing peripheral vasodilation, hypotension, and syncope in people whose carotid sinuses are abnormally sensitive.

Swallowing sometimes produces syncope, usually in patients with an esophageal disorder (particularly structural abnormalities) and usually due to vasovagal reflex mechanisms inducing bradycardia and vasodilation.

Orthostatic hypotension

Orthostatic hypotension (see also Approach to the Cardiac Patient: Orthostatic Hypotension) results from failure of normal mechanisms to compensate for the temporary decrease in venous return after standing. Orthostatic hypotension is a common benign cause of syncope. Causes include autonomic dysfunction, cardiovascular disorders, and many drugs (see Table 6: Approach to the Cardiac Patient: Causes of Orthostatic Hypotension). Assuming a horizontal position results in complete recovery from syncope due to orthostatic hypotension.

Cerebrovascular disorders

Cerebral hypoperfusion may be caused by vascular insufficiency, especially in the posterior circulation. Because hypoperfusion must affect centrencephalic structures to cause LOC, most cerebrovascular disorders do not result in syncope. However, basilar artery ischemia, due to transient ischemic attack or migraine, can produce syncope, as can hyperventilation-induced CNS vasoconstriction. Rarely, vertebrobasilar insufficiency due to severe cervical arthritis or spondylosis causes syncope when the head is moved in certain positions.

Other causes

Patients with a conversion disorder may have hysterical fainting. Patients with an anxiety disorder may faint because of hyperventilation, in which hypocapnia-induced vasoconstriction reduces cerebral blood flow.

Severe anemia may result in inadequate oxygenation and syncope, as may Takayasu's arteritis (by impairing blood flow through the carotid arteries or vertebrobasilar system).

In the subclavian steal syndrome, subclavian artery stenosis proximal to the origin of the vertebral artery “steals” flow from the vertebral artery to supply the arm during exertion, causing syncope with an orthostatic component on standing.

Weight lifter's syncope, which is benign, involves several mechanisms. Hyperventilation before lifting causes hypocapnia, cerebral vasoconstriction, and peripheral vasodilation. The Valsalva maneuver of lifting decreases venous return and CO; squatting further impedes venous return and potentiates systemic vasodilation and decreased BP.

Standing for long periods without moving can cause venous pooling (with decreased venous return and inadequate cardiac filling), leading to syncope (parade ground syncope). This type of syncope occurs in healthy people and is benign.

Breath-holding spells in infants can cause syncope. In early pregnancy, syncope is common because of hormonal changes; it is somewhat less common later, occurring if the gravid uterus presses on the inferior vena cava and impairs venous return. Seizures, including febrile seizures in children, can cause LOC that may mimic syncope.

Evaluation

History and physical examination, with particular attention to cardiovascular abnormalities, suggest a cause in 40 to 50% of cases. Identification of syncope due to cardiac causes is important because sudden death is a risk.

LOC also occurs during seizures; these episodes are not considered syncope, although many patients who have had unwitnessed seizures are brought to the hospital for apparent syncope. Conversely, patients with syncope due to hypoperfusion often have brief (eg, < 5 sec) seizure activity, which should not be mistakenly attributed to a seizure disorder. Narcolepsy also may be mistaken for syncope, particularly at initial presentation.

History

Drugs used (particularly antihypertensives, diuretics, vasodilators, and antiarrhythmics with proarrhythmic or atrioventricular conduction-altering actions) must be identified.

The patient is asked to describe associated events and symptoms, which may aid diagnosis (see Table 7: Approach to the Cardiac Patient: Differentiating Syncope by Cause). Syncope that begins and ends suddenly and spontaneously is typical of cardiac causes, most commonly an arrhythmia. Syncope precipitated by unpleasant physical or emotional stimuli (eg, pain, fright), usually occurring in the upright position, and often preceded by vagally mediated warning symptoms (eg, nausea, weakness, yawning, apprehension, blurred vision, diaphoresis) suggests vasovagal syncope. Syncope that occurs most often when assuming an upright position (particularly in elderly patients after prolonged bed rest, in patients with severe varicose veins, or in patients taking certain drug classes) suggests orthostatic syncope. Syncope that occurs after standing for long periods without moving is usually due to venous pooling.

Table 7
Differentiating Syncope by Cause Feature Neurally Mediated Hypotension Arrhythmias Outflow Obstruction Seizures Sex Females more than males Males more than females Equal Equal Age < 55 yr > 54 yr Any age < 45 yr Frequency of episodes > 2 < 3 > 1 > 1 Triggers Standing, warm room, emotional upset Any setting Exercise Any setting Premonitory symptoms Palpitations, blurred vision, nausea, warmth, diaphoresis, light-headedness Usually none; sometimes palpitations, vertigo, or light-headedness Usually none; sometimes angina or dyspnea Sudden onset or brief aura (déjà vu, olfactory, gustatory, visual) Duration of loss of consciousness > 5 sec < 6 sec Brief (occasionally cardiac arrest and death) Longer: 1–5 min Observations during the event Pallor, diaphoresis, dilated pupils, slow pulse, low BP, sometimes incontinence, sometimes brief clonic movements Blue skin tone (no pallor); sometimes incontinence, brief clonic movements, or stertorous breathing Blue skin tone (no pallor), sometimes incontinence, sometimes brief clonic movements Blue face (no pallor), tonic/clonic movements, in-continence (common), frothing at the mouth, tongue biting, horizontal eye deviation, elevated pulse and BP Observations after the event Residual symptoms common (eg, prolonged fatigue in > 90%); quick, complete recovery of orientation Residual symptoms uncommon (unless unconsciousness is prolonged); quick, complete recovery of orientation Residual symptoms uncommon (unless unconsciousness is prolonged); quick, complete recovery of orientation Postictal state with prolonged confusion and somnolence; often aching muscles and headache

Syncope associated with dyspnea, tachypnea, chest discomfort, cyanosis, and hypotension may be due to pulmonary embolism and usually indicates massive pulmonary vascular obstruction. It may also be due to tension pneumothorax.

Syncope that begins gradually (with warning symptoms), resolves slowly, and is often preceded by paresthesias and chest discomfort suggests hyperventilation.

LOC that is abrupt in onset; is associated with muscular jerking or convulsions, incontinence, and tongue biting; and is followed by postictal confusion or somnolence suggests a seizure.

Physical examination

Postural changes in heart rate and BP suggest hypovolemia or other causes of orthostatic hypotension. A carotid bruit or diminished carotid pulse suggests cerebral ischemia. A harsh, late-peaking, basal murmur radiating to the carotid arteries suggests aortic stenosis; a systolic murmur that increases with the Valsalva maneuver and disappears with squatting suggests hypertrophic cardiomyopathy. A click and murmur heard earlier in systole and more prominently during standing indicate mitral valve prolapse, suggesting the cause is an arrhythmia. Further evaluation is needed for suspected hemorrhage, other causes of hypovolemia, or a focal CNS disorder.

Asking the patient to hyperventilate or applying carotid sinus pressure (to detect carotid sinus hypersensitivity) may reproduce symptoms. Carotid sinus pressure requires ECG monitoring and should not be applied bilaterally.

If observed by the clinician, hysterical fainting can be distinguished from syncope because consciousness is not lost (although some patients are excellent mimics), heart rate and BP remain normal, and pallor and diaphoresis are absent.

Testing

Resting ECG is done for all patients. The ECG may reveal arrhythmia, a conduction abnormality, ventricular hypertrophy, preexcitation, QT prolongation, pacemaker malfunction, myocardial ischemia, or MI. If there are no clinical clues, measuring cardiac markers and obtaining ECGs to rule out MI in older patients plus Holter ECG monitoring for at least 24 h is prudent. Any detected arrhythmia must be associated with altered consciousness to be implicated as the cause, but most patients do not experience syncope during monitoring. An event recorder may be useful if warning symptoms precede syncope.

If possible, pulse oximetry should be done during or immediately after an episode to identify hypoxemia (which may indicate pulmonary embolism). If hypoxemia is present, a lung scan or other test for pulmonary embolism is indicated (see Pulmonary Embolism (PE): Diagnosis). Other laboratory tests are done based on clinical suspicion; reflexively obtained laboratory panels are of little use. Hct is measured if anemia is suspected; electrolytes are measured, particularly if hypokalemia or hypomagnesemia is suspected. Cardiac markers (eg, serum troponin, CPK-MB) are measured if acute MI is suspected.

In general, if syncope results in an injury or is recurrent, more intensive evaluation for the cause is warranted. Injury is less likely when the cause of syncope is benign, because LOC is slightly slower than when the cause is cardiac.

Patients with arrhythmia, myocarditis, or ischemia should be evaluated as inpatients. Others may be evaluated as outpatients.

Echocardiography is indicated for patients with exercise-induced syncope, cardiac murmurs, or suspected intracardiac tumors.

Exercise or pharmacologic stress testing is done when intermittent myocardial ischemia is suspected. A signal-averaged ECG may identify predisposition to ventricular arrhythmias in patients with ischemic heart disease or post-MI patients.

Tilt table testing is done if history and physical examination indicate vasodepressor or other reflex-induced syncope (see Cardiovascular Tests and Procedures: Tilt Table Testing). It is also used to evaluate exercise-induced syncope if echocardiography or exercise stress testing is negative.

Invasive electrophysiologic testing is considered if noninvasive testing does not identify arrhythmia in patients with unexplained recurrent syncope; a negative response defines a low-risk subgroup with a high rate of remission of syncope. The role of electrophysiologic testing is controversial in other patients. Exercise testing is less valuable, unless physical activity precipitated syncope.

EEG is warranted if a seizure disorder is suspected; CT and MRI of the head and brain are indicated only if signs and symptoms suggest a focal CNS disorder or an intracranial process.

Prognosis and Treatment

For young people who have syncope of unknown cause but no cardiovascular disorder, the prognosis is favorable; elaborate evaluation is rarely required. Syncope is more likely to be due to a significant disorder in elderly than in younger patients. For patients with coronary artery disease, myocarditis, hypertrophic cardiomyopathy, aortic stenosis, or known ventricular arrhythmias, syncope denotes a poor prognosis.

Placing the patient in a horizontal position with legs elevated typically ends the syncopal episode. If the patient sits upright too rapidly, syncope may recur; propping the patient upright or transporting the patient in an upright position may prolong cerebral hypoperfusion and prevent recovery.

Further treatment depends on the cause. Hypertrophic cardiomyopathy causing obstruction is treated with β-blockers, verapamil, or septal myomectomy; these treatments and amiodarone may alleviate associated arrhythmias.

Bradyarrhythmias may require pacemaker implantation; tachyarrhythmias require specific drug therapy, radioablation, or surgical correction. Ventricular arrhythmias may require implantable defibrillators. Carotid sinus hypersensitivity may require pacemaker insertion for bradyarrhythmias or carotid sinus radiation to alleviate the vasodepressor component. Hypovolemia, anemia, an electrolyte abnormality, and drug toxicity are treated. For aortic stenosis, aortic valve surgery may be done. It is not contraindicated by older age.

Last full review/revision November 2005