Roy Sucholeiki, MD,
Director, Comprehensive Seizure and Epilepsy
Program, The Neurosciences Institute at Central DuPage
Hospital
UCB
Pharma Honoraria Speaking and
teaching
Specialty Editor(s)
Florian P Thomas, MD, MA, PhD,
Drmed,
Director, Spinal Cord Injury Unit, St Louis
Veterans Affairs Medical Center; Director, National MS
Society Multiple Sclerosis Center; Professor, Department of
Neurology and Psychiatry, Associate Professor, Institute for
Molecular Virology, and Department of Molecular Microbiology
and Immunology, St Louis University
Nothing to disclose.
Francisco Talavera, PharmD, PhD,
Senior Pharmacy Editor,
eMedicine
Nothing to disclose.
Selim R Benbadis, MD,
Professor, Director of Comprehensive Epilepsy
Program, Departments of Neurology and Neurosurgery,
University of South Florida School of Medicine, Tampa General
Hospital
Nothing to disclose.
Spiros Manolidis, MD,
Associate Professor of Otolaryngology and
Neurological Surgery, Columbia University
Nothing to disclose.
Chief Editor
Robert A Egan, MD,
Director of Neuro-Ophthalmology, St Helena
Hospital
Nothing to disclose.
Background
Syncope is a term used to describe the loss of consciousness from temporary disruption of cerebral oxygenation. This is typically due to the interruption of blood flow to the brain, and the loss of consciousness usually lasts for less than 30 seconds. In lay terms, fainting is the equivalent descriptive term.
Patients who complain of dizziness, light-headedness, passing out, and/or blacking out must be questioned carefully to determine whether a true syncopal event has occurred. Other spells (eg, seizure, transient ischemic attack, cataplexy) may be similar, and a careful history often can clarify the condition and guide further evaluation and care. Syncope is a symptom of either cardiac or hemodynamic dysfunction and not a disease (or diagnosis).
The causes of syncope are many (see Causes). The 3 most important broad categories are the following: (1) decreased cardiac output secondary to intrinsic cardiac disease or clinically significant blood or volume loss; (2) decreased peripheral vascular resistance and/or venous return; and (3) clinically significant cerebrovascular disease that leads to compromise of cerebral perfusion. Regardless of the cause, all of these categories share a common factor, namely, disruption of adequate cerebral oxygenation resulting in a transient alteration of consciousness.
Syncope is common. However, exact rates are difficult to cite because of the many potential causes and varying history of the symptoms. Syncope accounts for 1-6% of admissions to hospitals and 1-3% of visits to emergency departments.
Mortality/Morbidity
In cases of syncope, morbidity parallels the cause. If an individual has had a simple case of fainting precipitated by specific circumstances and without sequelae, extensive workup may not be necessary. However, if the symptoms are recurrent or without clear provocation, cardiac, autonomic, or peripheral vascular dysfunction must be investigated and treated to prevent further events.
Patients may have physical injuries due to a fall, depending on how quickly the symptoms occur and the individual. For example, injuries are most likely in physically frail or elderly people.
Depending on the etiology, syncope may be a sign of serious underlying cardiovascular or cerebrovascular disease. A cardiac etiology is associated with more serious disease and carries a 20-30% mortality rate at 1 year. The mortality risk in noncardiac causes and idiopathic cases is approximately 5%.
Age
Syncope can occur in any age group, but the etiology varies by age. A young individual may have a syncopal attack with blood loss, dehydration, or hypoglycemia. Although these problems can occur in older individuals, additional medical problems could potentiate syncope. These problems may include congestive heart failure, autonomic instability, valvular heart disease, and cerebrovascular disease.
Regardless of the cause, patients with syncope present in a similar fashion. Vertigo is not a typical symptom of syncope. By definition, vertigo requires a sensation of spinning or movement that may indicate a cerebellar or vestibular problem. When patients use the term dizziness, the physician should thoroughly question the patient to clarify the symptom. The word dizzy or dizziness is ambiguous, and people can have vastly different meanings.
At the start of an episode, an individual feels a sense of uneasiness, progressing to unsteadiness, facial pallor, and perspiration; the vision can become darkened concentrically.
During this time, nausea and vomiting can occur.
Sighing can occur (an attempt to catch one's breath) because the person can have a feeling of shortness of breath.
All these symptoms occur in the presyncope stage and usually last for less than 1 minute before loss of consciousness occurs.
In cases of cardiac or carotid sinus syncope, the loss of consciousness can be rapid with little prodrome.
If the individual assumes a supine position during the presyncopal stage, syncope is often avoided because cerebral perfusion is restored. However, an attempt to rise too quickly may lead to another presyncopal episode.
The degree of altered consciousness varies from a static, dazed feeling to complete unconsciousness.
If unconsciousness lasts for more than 15-20 seconds, simple body and extremity jerks can be seen. This condition is termed convulsive syncope.
It should not be confused with seizures.
Unlike those associated with a seizure, the jerking motions are single and nonrhythmic.
During the syncopal period, the patient's systolic BP can be expected to be less than 60-80 mm Hg, and the patient's pulse may be thready.
Sphincteral tone is typically maintained.
Tongue biting of the type often noted with a generalized convulsion does not occur.
Once the patient is in the supine position, brain oxygenation is restored, and the patient regains consciousness.
The patient can usually recall the presyncopal symptoms that are critical to the diagnosis.
Falling may cause injury if the individual cannot protect himself. This is of particular concern in the elderly in whom the incidence of falls is already high.
Pulmonary embolism should be considered in the differential diagnosis, especially in the elderly
Because syncope is, by definition, a transient event, the general physical findings on initial presentation are usually normal. However, the following abnormalities can be noted:
Carotid bruits can indicate clinically significant cerebrovascular disease and an increased risk of stroke.
Abnormal heart sounds and/or an irregular heart rhythm might indicate a risk of decreased cardiac output.
Poor BP regulation may be present. Bedside testing of BP and heart rate with postural changes is imperative in the workup for syncope.
The patient's vital signs are assessed while he or she is supine and reassessed while the patient is standing.
If the systolic pressure decreases by more than 15 mm Hg, orthostatic hypotension can be diagnosed.
The heart rate is also measured. An increase is considered clinically significant if it is greater than 20 bpm while the patient is standing.
Peripheral neuropathy also suggests defective peripheral vascular tone caused by an autonomic neuropathy.
Neuropathy should be assessed by means of careful sensory and deep tendon reflex examination.
Abnormalities in light touch, vibration and proprioception, and pin-prick sensation and absent or sluggish deep tendon reflexes should be noted.
Syncope has many potential causes, some of which are challenging to diagnose.
Neurogenically mediated syncope: This can occur sporadically. However, familial dysautonomia with wild-type and mutations in IKBKAP mRNA has been described.
Vasodepressor or vasovagal causes
These are common etiologies in young people and are frequently associated with a precipitating circumstance, such as intense pain, emotion (eg, fear), the sight of blood, or having blood drawn.
The pathophysiology involves a sudden drop in peripheral vascular resistance and resultant hypotension coupled with bradycardia. The increased sympathetic activity induces perspiration, gastrointestinal (GI) motility, and occasionally vomiting.
Although the terms vasodepressor and vasovagal often are used synonymously, they indicate the involvement of different systems, with the latter referring to increased vagus-nerve efferent output with resulting bradycardia.
The term neurocardiogenic syncope suggests the hemodynamic stimulation of left ventricular mechanoreceptors, which can precipitate events leading to hypotension. This entity may be a separate mechanism for syncope.
Carotid sinus syncope
This results when the stretch receptors are activated and cause reflex hypotension (as opposed to only bradycardia).
The history is notable for the patient wearing a tight shirt collar and turning his or her head. Although carotid massage can reproduce the symptoms, carotid sonography must be performed first to rule out stenosis of the contralateral carotid, which indicates unilateral anterior blood supply to both hemispheres.
Carotid massage is contraindicated if plaque is present because it may theoretically liberate plaque debris and cause subsequent stroke.
Glossopharyngeal neuralgia
This is more common in men than in women and in those older than 40 years than in those younger, but is less common than trigeminal neuralgia.
Glossopharyngeal neuralgia is characterized by repeated, stabbing pain in the base of the tongue, tonsillar area, or pharyngeal area on 1 side of the throat. The pain can radiate to the angle of the jaw or ear.
These symptoms are due to involvement of the glossopharyngeal nerve. Because this cranial nerve can influence BP or heart rate, some patients may have cardiovascular symptoms, such as syncope.
Brugada syndrome
Patients can present with syncope.
Brugada syndrome is inherited in a dominant fashion and linked to mutations in SCN5A on chromosome 3.
On clinical evaluation, the heart is structurally normal but electrographic abnormalities may be present.
Sudden cardiac death is due to dysrhythmias.
The clinic features of Brugada syndrome can also be acquired by using drugs that can interfere with the ionic currents in the conduction system of the heart.
Micturition syncope: This is more common in older men than in other groups. It most often occurs at night when the patient stands up to urinate.
Cough syncope: This typically occurs in individuals with chronic obstructive pulmonary disease and usually follows a protracted bout of coughing.
Seizure: While seizures are one of the conditions that may resemble syncope, rarely they can be directly associated with syncope. This is the case with ictal bradycardia syndrome where seizures can produce symptomatic bradycardia and even asystole. This syndrome may be one of the causes of sudden unexpected death in epilepsy (SUDEP).
Swallow syncope: This is very rare. Bajwa et al reported a case of a 51-year-old man who experienced syncope with eating solid foods. Testing noted bradycardia with eating and he was treated with a pacemaker, which resolved the symptoms.[1]
Valsalva maneuver: A Valsalva maneuver (eg, as in straining to urinate) increases thoracic pressure and decreases venous return to the heart.
Postprandial syncope: This occurs in the elderly and is thought to be due to increase blood flow to the GI vasculature and an inability to compensate hemodynamically.
Impaired postural reflexes: These reflexes primarily include postural reflexes impaired by incompetence of the sympathetic nervous system, and they can be centrally or peripherally mediated. Centrally mediated findings are a feature of Parkinson disease, multisystem atrophy, Shy-Drager syndrome, and striatonigral degeneration. Although the most obvious symptoms involve abnormal motor control, the autonomic nervous system also can be involved severely. Postural BP regulation is typically defective, resulting in presyncope or syncope. The patient may have spinal disease or injury that affects the autonomic transmission of information. A stroke of the medulla or hypothalamus involving the relay nuclei that mediate autonomic activity may also be a cause.
Peripherally mediated findings are due to baroreceptor dysfunction and can be seen with peripheral neuropathies (eg, diabetes, amyloid, alcohol-related, Guillain-Barré syndrome), pure autonomic failure, and effects of drugs (eg, antihypertensives, tricyclics, phenothiazines, levodopa). The prognosis for patients with pure autonomic failure is more favorable than that of patients with multiple system atrophy.
Hemodynamic findings: Changes result from insufficient cardiac output or insufficient blood volume.
ECG should be performed in all patients to evaluate for current or past cardiac disease (eg, myocardial infarction, arrhythmia, conduction disturbances).
Complete electrolyte and chemistry panels are needed to evaluate for any contributing metabolic disorder (eg, hypoglycemia, dehydration).
Additional testing may be performed depending on the history and physical examination findings.
Prolonged cardiac monitoring, such as inpatient telemetry or Holter monitoring, should be considered if cardiac disease is suspected.
If monitoring is needed for longer than 24 hours then ambulatory continuous-loop recording permits monitoring for days to weeks.
Routine EEG is used to investigate a possible seizure disorder.
Prolonged ambulatory EEG or inpatient video-EEG monitoring may be indicated if the patient's history indicates a strong possibility of epilepsy.
Transthoracic and/or transesophageal echocardiography is ordered to evaluate cardiac output and valvular or wall-motion abnormalities.
Tilt-table testing may be needed to evaluate orthostatic hypotension. Tilt-table testing is an accurate method of assessing changes in BP and pulse with changes in position. The table is actually a bed that can be pivoted from a supine position to a standing position to enable precision measurements of BP and pulse in both. Tilt-table testing is generally available only in the cardiology departments of tertiary care centers or in autonomic testing laboratories of a neurology department.
Appropriate consultation should precede some of these additional tests.
Medical care depends on the etiology of the syncope.
If a serious cardiac or neurologic illness is suspected, admission to the hospital, where diagnostic testing can be performed in a monitored setting, may be warranted. This is particularly true if a patient presents to the emergency department.
If a patient is examined in an outpatient setting and if his or her history suggests a remote event, the workup may not be urgent and might be completed in an outpatient setting.
Pharmacotherapy is indicated when presyncope or syncope is recurrent and refractory to nonpharmacologic treatment. The choice of medication depends on the cause and the severity of the orthostatic hypotension in particular. Various medications for associated comorbidities, such as diabetes, hypertension, and cardiac abnormalities, may indirectly improve some symptoms of syncope.
Clinical Context:
Synthetic steroid with predominantly mineralocorticoid activity. Primary effects on renal distal tubules to enhance sodium reabsorption; also increases urinary excretion of potassium and hydrogen ions. Primary effects and similar actions on cation transport in other tissues appear to account for the spectrum of physiologic activities of mineralocorticoids. Maintains intravascular and extracellular volume. Available only as tab, which may be crushed.
For patients requiring parenteral mineralocorticoid therapy, high-dose hydrocortisone must be used. Dose determined by measuring BP (hypertension indicates overreplacement) and supine plasma renin activity (PRA). PRA suppression indicates overreplacement and elevation indicates underreplacement. Dosages vary considerably (50-500 mcg/d) and must be individualized. Dose adjustment typically not required in acute illness, though some advocate increasing dose in severe GI illness.
These agents improve the patient's hemodynamic status by increasing myocardial contractility and heart rate, increasing cardiac output. They also increase peripheral resistance by causing vasoconstriction. Increased cardiac output and increased peripheral resistance lead to increased BP.
Clinical Context:
Increases standing, sitting, and supine systolic and diastolic BP in patients with orthostatic hypotension of various etiologies. Standing systolic BP elevated by approximately 15-30 mm Hg at 1 h after 10-mg dose, with some effect for 2-3 h. No clinically significant effect on standing or supine pulse rates in patients with autonomic failure.
Clinical Context:
Central alpha-adrenergic agonist that stimulates alpha2-adrenoreceptors in brainstem and activates inhibitory neuron, decreasing vasomotor tone and heart rate. Used to control symptomatic hypertension; suggested if diastolic hypertension (>85 mm Hg) persists 30 min after diazepam administration.
Adams RD, Victor M, Ropper AH. Faintness and syncope. In: Adams RD, Victor M, Ropper AH, eds. Principles of Neurology. New York, NY: McGraw-Hill; 1997:367-79.
Drislane FW, Feske S. Transient events. In: Samuels MA, Feske S, et al, eds. Office Practice of Neurology. New York, NY: Churchill-Livingstone; 1996:111-4.
