Syncope: A Merck Manual of Patient Symptoms podcast
Syncope is a sudden, brief loss of consciousness (LOC) 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 LOC. It is usually classified and discussed with syncope because the causes are the same.
Seizures can cause sudden LOC 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 sec) seizure sometimes occurs with true syncope.
Diagnosis depends on a careful history, eyewitness accounts, or fortuitous examination during the event.
Most syncope results from insufficient cerebral blood flow. Some cases involve adequate flow but with insufficient cerebral substrate (O2, 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
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/min) or too slow to provide adequate output (eg, < 30 to 35 beats/min).
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 (see Orthostatic Hypotension).
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 produce LOC. However, basilar artery ischemia, due to transient ischemic attack 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 CNS requires O2 and glucose to function. Even with normal cerebral blood flow, a significant deficit of either will cause LOC. In practice, hypoglycemia is the primary cause because hypoxia rarely develops in a manner causing abrupt LOC (other than in flying or diving incidents). LOC due to hypoglycemia is seldom as abrupt as in syncope or seizures because warning symptoms occur (except in patients taking β-blockers); however, the onset may be unclear to the examiner unless the event was witnessed.
Causes are usually classified by the mechanism (see Table 8: Some Causes of Syncope).
The most common causes are
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.
|PrintOpen table in new window
|PrintOpen table in new window
|Some Drug Causes of Syncope
Amiodarone, other rate-limiting drugs
Ca channel blockers (not dihydropyridines)
Any antiarrhythmic drug that prolongs repolarization (eg, procainamide, disopyramide)
Most antihypertensives (rarely β-blockers)
Antipsychotics (mainly phenothiazines)
Nitrates (with or without a phosphodiesterase inhibitor for erectile dysfunction)
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 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 LOC, 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—Table 9: Some Drug Causes of Syncope). Family history should note presence at a young age of heart disease or sudden death in any family member.
Vital signs are essential. Heart rate and BP are measured with the patient supine and after 3min 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 (Fig. 1: Normal jugular vein waves.) while palpating the carotid or auscultating the heart may allow diagnosis of an arrhythmia if an ECG is not available.
Some clinicians carefully apply unilateral carotid sinus pressure during ECG monitoring with the patient supine to detect bradycardia or heart block, suggesting carotid sinus hypersensitivity. Carotid sinus pressure should not be applied if a carotid bruit is present.
Abdomen is palpated for tenderness, and a rectal examination is done to check for gross or occult blood.
A full neurologic examination is done to identify any focal abnormalities, which suggest a CNS cause (eg, seizure disorder).
Certain findings suggest a more serious etiology:
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 8: 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.
LOC that is abrupt in onset; is associated with muscular jerking or convulsions that last more than a few seconds, incontinence, drooling, or tongue biting; and is followed by postictal confusion or somnolence suggests a seizure.
Red flag findings suggest a dangerous cause.
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. Because vasovagal and orthostatic mechanisms do not cause syncope in the recumbent position, syncope while lying down also suggests an arrhythmia.
If the patient is injured during the episode of syncope, the likelihood of a cardiac cause or seizure is somewhat greater, and therefore the event is of greater concern. The warning signs and slower LOC that accompany benign vasovagal syncope somewhat reduce the likelihood of injury.
Testing typically is done.
In general, if syncope results in an injury or is recurrent (particularly within a brief period), more intensive evaluation is warranted.
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 MI. If there are no clinical clues, measuring cardiac markers and obtaining serial ECGs to rule out MI in older patients plus ECG monitoring for at least 24 h 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 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-MI patients. If syncopal episodes are infrequent (eg, < 1/mo), an implantable loop recorder can be used for longer term recording.
Pulse oximetry should be done during or immediately after an episode to identify hypoxemia (which may indicate pulmonary embolism). If hypoxemia is present, CT or a lung scan 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. Hct 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 MI is suspected.
Echocardiography is indicated for patients with 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.
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 use 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.
In witnessed syncope, pulses are checked immediately. If the patient is pulseless, CPR is begun and cardiac resuscitation is done. If pulses are present, severe bradycardia is treated with atropine or external transthoracic pacing. Isoproterenol can be used to maintain adequate heart rate while a temporary pacemaker is placed.
Tachyarrhythmias are treated (see also Palpitations); a direct-current synchronized shock is quicker and safer for unstable patients. Inadequate venous return is treated by keeping the patient supine, raising the legs, and giving IV normal saline. Tamponade is relieved by pericardiocentesis. Tension pneumothorax requires insertion of a pleural cannula and drainage. Anaphylaxis is treated with parenteral epinephrine.
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.
The most common cause of syncope in the elderly 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 the elderly, syncope often has more than one cause. For example, the combination of taking several heart and BP 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.
Last full review/revision August 2014 by Lyall A. J. Higginson, MD
Content last modified August 2014