Syncope is a sudden, brief loss of consciousness with loss of postural tone followed by spontaneous revival. The patient is motionless and limp and usually has cool extremities, a weak pulse, and shallow breathing. Sometimes brief involuntary muscle jerks occur, resembling a seizure.
Near-syncope is light-headedness and a sense of an impending faint without loss of consciousness. It is usually classified and discussed with syncope because the causes are the same.
Seizures can cause sudden loss of consciousness but are not considered syncope. However, seizures must be considered in patients presenting for apparent syncope because history may be unclear or unavailable, and some seizures do not cause tonic-clonic convulsions. Furthermore, a brief (< 5 second) seizure sometimes occurs with true syncope.
Diagnosis depends on a careful history, eyewitness accounts, or fortuitous examination during the event.
Pathophysiology of Syncope
Most syncope results from insufficient cerebral blood flow. Some cases involve adequate flow but with insufficient cerebral substrate (oxygen, glucose, or both).
Insufficient cerebral blood flow
Most deficiencies in cerebral blood flow result from decreased cardiac output (CO).
Decreased CO can be caused by
Cardiac disorders that obstruct outflow
Cardiac disorders of systolic dysfunction
Cardiac disorders of diastolic dysfunction
Arrhythmias (too fast or too slow)
Conditions that decrease venous return
Outflow obstruction can be exacerbated by exercise, vasodilation, and hypovolemia (particularly in aortic stenosis and hypertrophic cardiomyopathy), which may precipitate syncope.
Arrhythmias cause syncope when the heart rate is too fast to allow adequate ventricular filling (eg > 150 to 180 beats/minute) or too slow to provide adequate output (eg, < 30 to 35 beats/minute).
Venous return can be decreased by hemorrhage, increased intrathoracic pressure, increased vagal tone (which can also decrease heart rate), and loss of sympathetic tone (eg, from drugs, carotid sinus pressure, autonomic dysfunction). Syncope involving these mechanisms (except for hemorrhage) is often termed vasovagal or neurocardiogenic and is common and benign.
Orthostatic hypotension, a common benign cause of syncope, results from failure of normal mechanisms (eg, sinus tachycardia, vasoconstriction, or both) to compensate for the temporary decrease in venous return that occurs with standing.
Cerebrovascular disorders (eg, strokes, transient ischemic attacks) rarely cause syncope because most of them do not involve the centrencephalic structures that must be affected to cause loss of consciousness. However, basilar artery ischemia, due to transient ischemic attack, stroke, or migraine, may cause syncope. Rarely, patients with severe cervical arthritis or spondylosis develop vertebrobasilar insufficiency with syncope when the head is moved in certain positions.
Insufficient cerebral substrate
The central nervous system (CNS) requires oxygen and glucose to function. Even with normal cerebral blood flow, a significant deficit of either will cause loss of consciousness . In practice, hypoglycemia is the primary cause because hypoxia rarely develops in a manner causing abrupt loss of consciousness (other than in flying or diving incidents). Loss of consciousness due to hypoglycemia is seldom as abrupt as in syncope or seizures because warning symptoms occur (except in patients taking beta-blockers); however, the onset may be unclear to the examiner unless the event was witnessed.
Etiology of Syncope
Causes are usually classified by the mechanism (see table Some Causes of Syncope).
The most common causes are
Vasovagal (neurocardiogenic)
Idiopathic
Many cases of syncope never have a firm diagnosis but lead to no apparent harm. A smaller number of cases have a serious cause, usually cardiac.
Evaluation of Syncope
Evaluation should be done as soon as possible after the event. The more remote the syncopal event, the more difficult the diagnosis. Information from witnesses is quite helpful and best obtained as soon as possible.
History
History of present illness should ascertain events leading up to the syncope, including the patient’s activity (eg, exercising, arguing, in a potentially emotional situation), position (eg, lying or standing), and, if standing, for how long. Important associated symptoms immediately before or after the event include whether there was a sense of impending loss of consciousness, nausea, sweating, blurred or tunnel vision, tingling of lips or fingertips, chest pain, or palpitations. Length of time recovering should also be ascertained. Witnesses, if any, should be sought and asked to describe events, particularly the presence and duration of any seizure activity.
Review of systems should ask about any areas of pain or injury, episodes of dizziness or near-syncope upon arising, and episodes of palpitations or chest pain with exertion. Patients should be asked about symptoms suggesting possible causes, including bloody or tarry stools, heavy menses (anemia); vomiting, diarrhea, or excess urination (dehydration or electrolyte abnormalities); and risk factors for pulmonary embolism (recent surgery or immobilization, known cancer, previous clots or hypercoagulable state).
Past medical history should ask about previous syncopal events, known cardiovascular disease, and known seizure disorders. Drugs used should be identified (particularly antihypertensives, diuretics, vasodilators, and antiarrhythmics—see table Some Drug Causes of Syncope). Family history should note presence at a young age of heart disease or sudden death in any family member.
Physical examination
Vital signs are essential. Heart rate and blood pressure are measured with the patient supine and after 3 minutes of standing. Pulse is palpated for irregularity.
General examination notes patient’s mental status, including any confusion or hesitancy suggesting a postictal state and any signs of injury (eg, bruising, swelling, tenderness, tongue bite).
The heart is auscultated for murmurs; if present, any change in the murmur with a Valsalva maneuver, standing, or squatting is noted.
Careful evaluation of the jugular venous waves (see figure Normal jugular vein waves) while palpating the carotid or auscultating the heart may allow diagnosis of an arrhythmia if an ECG is not available. For example, cannon "a" waves occur when the atria contraction takes place against a closed tricuspid valve and indicate atrial-ventricular dissociation.
Abdomen is palpated for tenderness, and a rectal examination is done to check for gross or occult blood.
A neurologic examination is done to identify any focal abnormalities, which suggest a central nervous system cause (eg, seizure disorder).
Red flags
Certain findings suggest a more serious etiology:
Syncope during exertion
Multiple recurrences within a short time
Heart murmur or other findings suggesting structural heart disease (eg, chest pain)
Older age
Significant injury during syncope
Family history of sudden unexpected death, exertional syncope, or unexplained recurrent syncope or seizures
Interpretation of findings
Although the cause is often benign, it is important to identify the occasional life-threatening cause (eg, tachyarrhythmia, heart block) because sudden death is a risk. Clinical findings (see table Some Causes of Syncope) help suggest a cause in 40 to 50% of cases. A few generalizations are useful.
Benign causes often lead to syncope.
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 or in patients taking drugs in certain classes) suggests orthostatic syncope.
Syncope that occurs after standing for long periods without moving is usually due to venous pooling.
Dangerous causes are suggested by red flag findings.
Syncope with exertion suggests cardiac outflow obstruction or exercise-induced arrhythmia. Such patients sometimes also have chest pain, palpitations, or both. Cardiac findings may help identify a cause. 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.
Syncope that begins and ends suddenly and spontaneously is typical of cardiac causes, most commonly an arrhythmia.
Syncope while lying down also suggests an arrhythmia because vasovagal and orthostatic mechanisms do not cause syncope in the recumbent position.
Syncope accompanied by injury during the episode increases the likelihood of a cardiac cause or seizure, and therefore the event is of greater concern. The warning signs and slower loss of consciousness that accompany benign vasovagal syncope somewhat reduce the likelihood of injury.
Loss of consciousness during a seizure or postictal confusion can sometimes be confused with syncope, but muscular jerking or convulsions that last more than a few seconds, incontinence, drooling, or tongue biting, if present, usually point to a seizure.
Testing
Testing typically is done.
ECG
Pulse oximetry
Sometimes echocardiography
Sometimes tilt table testing
Blood tests only if clinically indicated
Central nervous system imaging rarely indicated
In general, if syncope results in an injury or is recurrent (particularly within a brief period), more intensive evaluation is warranted. Cardiac and brain imaging are not done unless indicated by clinical findings (suspected cardiac etiology or neurologic deficits).
Patients with suspected arrhythmia, myocarditis, or ischemia should be evaluated as inpatients. Others may be evaluated as outpatients.
ECG is done for all patients. The ECG may reveal arrhythmia, a conduction abnormality, ventricular hypertrophy, pre-excitation, QT prolongation, pacemaker malfunction, myocardial ischemia, or myocardial infarction. If the diagnosis is questionable after this basic evaluation, measuring cardiac markers and obtaining serial ECGs to rule out MI in older patients plus ECG monitoring for at least 24 hours are prudent. Any detected arrhythmia must be associated with altered consciousness in order to be implicated as the cause, but most patients do not experience syncope during monitoring. On the other hand, the presence of symptoms in the absence of rhythm disturbance helps rule out a cardiac cause. An event recorder (which can record cardiac rhythm for longer periods) may be useful if warning symptoms precede syncope. A signal-averaged ECG may identify predisposition to ventricular arrhythmias in patients with ischemic heart disease or in post-myocardial infarction patients. If syncopal episodes are infrequent (eg, < 1/month), an implantable loop recorder can be used for longer term recording. This device continuously records the rhythm and can be interrogated by an external machine that allows the cardiac rhythm to be printed.
Pulse oximetry should be done during or immediately after an episode to identify hypoxemia (which may indicate pulmonary embolism). If hypoxemia is present, CT angiography is indicated to rule out pulmonary embolism.
Laboratory tests are done based on clinical suspicion; reflexively obtained laboratory panels are of little use. However, all females of childbearing age should have a pregnancy test. Hematocrit is measured if anemia is suspected. Electrolytes are measured only if an abnormality is clinically suspected (eg, by symptoms or drug use). Serum troponin is measured if acute myocardial infarction is suspected.
Echocardiography is indicated for patients with clinically unexplained syncope, exercise-induced syncope, cardiac murmurs, or suspected intracardiac tumors (eg, those with positional syncope).
Tilt table testing may be done if history and physical examination indicate vasodepressor or other reflex-induced syncope. It is also used to evaluate exercise-induced syncope if echocardiography or exercise stress testing is negative.
Stress testing (exercise or pharmacologic) is done when intermittent myocardial ischemia is suspected. It is often done for patients with exercise-induced symptoms. Exercise testing is less valuable unless physical activity precipitated syncope.
Invasive electrophysiologic testing is considered if noninvasive testing does not identify arrhythmia in patients with any of the following:
Unexplained recurrent syncope
Unexplained red flag findings
Ischemic cardiomyopathy, non-ischemic cardiomyopathy, and adult congenital disease, or unexplained syncope that does not otherwise meet criteria for an ICD used for primary prevention
A negative response defines a low-risk subgroup with a high rate of remission of syncope. The use of electrophysiologic testing is controversial in other patients.
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.
Treatment of Syncope
Tachyarrhythmias are treated; a direct-current synchronized shock
Placing the patient in a horizontal position with legs elevated typically ends the syncopal episode if life-threatening disorders are ruled out. 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.
Specific treatment depends on the cause and its pathophysiology. Driving and use of machinery should be prohibited until the cause is determined and treated.
Geriatrics Essentials: Syncope
The most common cause of syncope in older adults is postural hypotension due to a combination of factors. Factors include rigid, noncompliant arteries, reduced skeletal muscle pumping of venous return due to physical inactivity, and degeneration of the sinoatrial node and conduction system due to progressive structural heart disease.
In older adults, syncope often has more than one cause. For example, the combination of taking several heart and blood pressure drugs and standing in a hot church during a long or emotional service may lead to syncope even though no single factor might cause syncope.
Key Points
Syncope results from global central nervous system dysfunction, usually resulting from insufficient cerebral blood flow.
Most syncope results from benign causes.
Some less common causes involve cardiac arrhythmia or outflow obstruction and are serious or potentially fatal.
Vasovagal syncope usually has an apparent trigger, warning symptoms, and a few minutes or longer of postrecovery symptoms.
Syncope due to cardiac arrhythmias typically occurs abruptly and with quick recovery.
If a benign etiology is not clear, driving and use of machinery should be prohibited until the cause is determined and treated—the next manifestation of an unrecognized cardiac cause may be fatal.
Treatment is directed at the underlying disorder.
More Information
Primary Writing Committee, Sandhu RK, Raj SR, et al: Canadian Cardiovascular Society Clinical Practice Update on the Assessment and Management of Syncope. Can J Cardiol 36(8):1167–1177, 2020. doi: 10.1016/j.cjca.2019.12.023
