ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Syncope in adults: Epidemiology, pathogenesis, and etiologies

Syncope in adults: Epidemiology, pathogenesis, and etiologies
Literature review current through: Aug 2023.
This topic last updated: Aug 25, 2022.

INTRODUCTION — Syncope is a clinical syndrome in which transient loss of consciousness (TLOC) is caused by a period of inadequate cerebral nutrient flow, most often due to diminished blood flow resulting from an abrupt drop of systemic blood pressure. Typically, the hypotensive event is of relatively brief duration (8 to 10 seconds) and, in syncope, is by definition spontaneously self-limited.

Loss of postural tone is an expected outcome with loss of consciousness, and, consequently, syncope usually is associated with collapse, which can trigger injury due to a fall (such as may occur if the person is standing) or other type of accident (eg, if syncope occurs while driving or during use of factory machinery). Recovery from true syncope is usually complete and rapid, with episodes rarely lasting more than a minute or two. Longer periods of real or apparent loss of consciousness suggest that the event is not syncope or is not syncope alone (eg, syncope resulting in a head injury [concussion], thereby prolonging the event).

True syncope has many possible causes (table 1), but is only one of the many potential causes of TLOC. Examples of nonsyncopal causes of TLOC, or apparent TLOC, include seizure disorders, traumatic brain injury (eg, concussion), intoxications, metabolic disturbances, and conversion disorders (eg, psychogenic "pseudosyncope" or "pseudoseizures"). Distinguishing these other conditions from true syncope may be challenging, but is crucial in order to determine appropriate management. Unfortunately, and inappropriately, true syncope and other TLOC events are often considered as one category both in clinical practice and in some published literature, thereby undermining the determination of an accurate diagnosis.

The epidemiology, pathogenesis, and etiologies of syncope will be reviewed here. The clinical manifestations, diagnostic evaluation, and management of syncope is discussed in detail separately. (See "Syncope in adults: Clinical manifestations and initial diagnostic evaluation" and "Syncope in adults: Management and prognosis".)

EPIDEMIOLOGY — Syncope/collapse is a common clinical problem, with a lifetime prevalence in the population as a whole of approximately 20 percent [1,2].

In the Framingham Heart study, 822 of 7814 individuals (11 percent) who were followed for an average of 17 years reported an apparent syncopal episode [3]. However, given advances in the evaluation of patients with suspected syncope, the applicability of the Framingham data requires reevaluation given the manner in which syncope and the causal "diagnosis" was established. The study did not use the current definition of syncope (ie, self-limited inadequate cerebral perfusion). As a result, the report inevitably combined syncope and nonsyncopal collapse, and some seizures may also have been included. Also, the cause of syncope in the Framingham population was, at best, inferential. As an example, a diagnosis of "cardiac syncope" was based on the presence of cardiac disease, not a documented connection to the symptoms as currently required. Despite these limitations, the Framingham data provide a useful population estimate of syncope/collapse, and are largely consistent with a later study [1].

In a retrospective community-based study of more than 1900 adults from Olmsted county, Minnesota, aged ≥45 years (47 percent male, mean age 62 years), 364 individuals (19 percent) reported having experienced syncope [1]. Nearly 50 percent of these individuals had subsequent recurrences of syncope, which may have been related to their mean age of 62.

The occurrence of syncope versus age has been reported as roughly bimodal, with a peak in late adolescence to early adulthood (mostly vasovagal in origin) and a second peak later in older age, with a sharp rise after age 70 years (figure 1). In younger patients, reflex syncope (particularly vasovagal faints) overwhelmingly predominates in terms of cause. Reflex faints also remain common as patients age, but, in older adult patients, disease-related abnormalities may not only predispose to transient hypotensive events (eg, arrhythmias, orthostatic hypotension) but may also impair the ability to respond to physiologic stresses that would ordinarily not cause syncope [4].

Syncope/collapse appears to be slightly more common among females depending upon the population studied [1,3]. Variation in the reported rates of syncope in different studies is due to varying study populations, definitions of syncope, and diagnostic methods and criteria. Males, however, are more likely than females to have a cardiac cause of syncope, presumably due to greater risk of cardiovascular disease in males [3,5].

Syncope/collapse is also a common clinical complaint of patients treated in the emergency department and is the source for a significant number of hospital admissions. Between 1 and 3 percent of all emergency department visits, and 1 percent of all hospital admissions, are related to syncope [6-8]. In general, approximately 35 percent of patients who present to the emergency department with syncope/collapse are admitted to hospital. This later proportion is substantially greater than is essential, and efforts have been directed to reducing admission rates. In particular, emergency department-based scoring systems are evolving to facilitate decisions regarding hospital admission versus outpatient evaluation of patients presenting with apparent transient loss of consciousness (TLOC). The OESIL score and the Canadian Syncope Risk Score are typical well-studied examples of tools that physicians may use to help facilitate the decision-making process [9,10]. (See "Approach to the adult patient with syncope in the emergency department", section on 'Risk stratification'.)

In regard to reducing hospital admission rates, a 2018 report shows a trend reduction of hospital admission for syncope in the United States, possibly due to greater use of short-term observation or outpatient care; nonetheless, the overall cost of care continues to rise [11]. Among 282,311 United States patients (54 percent female; median age 72 years) with a primary diagnosis of syncope identified from the 2013 to 2014 Nationwide Readmissions Database, 9.3 percent were re-admitted within 30 days; predictors of readmission primarily centered around medical co-morbidities (eg, heart failure [HF], atrial fibrillation, COPD, diabetes) and longer initial hospital stays (>3 days) [12]. (See "Approach to the adult patient with syncope in the emergency department".)

Determining the cause of syncope is important for both prognostic and therapeutic reasons. Several large studies have assessed the causes for syncope [3,13-16]. In general, vasovagal attacks are the most common cause of syncope in all age groups, followed by orthostatic syncope and then cardiac arrhythmias.

Vasovagal syncope (also known as the "common" or "innocent" faint), a type of reflex (neurally-mediated) syncope, is the most common cause of TLOC in all age groups, particularly in patients without apparent cardiac or neurologic disease. In contrast to vasovagal syncope, carotid sinus hypersensitivity is much more common in older patients (mostly males), especially those with atherosclerotic vascular disease.

A pooled analysis of five population-based studies including 1002 patients with presumed syncope between 1984 and 1990 found that arrhythmias were responsible for 14 percent of syncope cases (range 4 to 38 percent in different studies) [15].

Orthostatic hypotension accounted for 8.6 and 9.9 percent of syncope cases among individuals in the Framingham cohort, respectively, and for 8 percent of cases in the five pooled cohort studies (table 2 and table 3) [3,15]. However, the frequency of orthostatic hypotension increases substantially in older populations in whom treatment with antihypertensive drugs and diuretics is common.

The cause of syncope/collapse is unknown in approximately one-fifth to one-third of cases (table 2 and table 3), but the number of cases with undetermined causes is falling as more physicians are developing expertise in the syncope/collapse evaluation and diagnostic tools are improving. As an example, arrhythmias that may be the etiology of a significant proportion of unexplained syncopal events are now more readily detected by a variety of wearable and insertable ambulatory electrocardiogram (ECG) recorders [17,18]. (See 'Causes of syncope' below.)

Cardiovascular disease is a major risk factor for syncope. The age-adjusted incidence rate for apparent syncope among participants with cardiovascular disease was almost twice that of participants without cardiovascular disease in the Framingham cohort (10.6 versus 6.4 per 1000 person-years) [3]. Nonetheless, reflex syncope (particularly vasovagal syncope) is the most common cause of syncope overall. (See 'Reflex syncope' below.)

CAUSES OF SYNCOPE — In the evaluation of a patient with transient loss of consciousness (TLOC) in whom syncope is suspected, the clinician must necessarily consider and exclude conditions that mimic TLOC/syncope but are not true syncope. The most common of these conditions are seizures, sleep disturbances, accidental falls, and some psychiatric conditions (eg, conversion reactions resulting in psychogenic pseudo-syncope, or as preferred by many neurologists, nonepileptic seizures, also called psychogenic pseudoseizures). These conditions are discussed in detail separately. (See "Classification of sleep disorders" and "Psychogenic nonepileptic seizures: Etiology, clinical features, and diagnosis" and "Evaluation and management of the first seizure in adults".)

The possible causes of TLOC resulting in true syncope are generally grouped into several major categories (table 1):

Reflex syncope (neurally-mediated)

Orthostatic syncope

Cardiac (arrhythmias and structural cardiopulmonary disease)

Reflex syncope accounts for the vast majority of cases in younger individuals, and approximately 50 percent of cases in older patients. As individuals age, orthostatic and cardiac causes increase in frequency.

Reflex syncope — Reflex syncope comprises a number of related conditions in which neural reflexes modify heart rate and blood pressure inappropriately, resulting in syncope or near-syncope. The most well-known of these conditions is vasovagal syncope, otherwise known as the common faint. Other types of neurally-mediated reflex syncope include carotid sinus syncope as well as syncope triggered by micturition, defecation, swallowing, or coughing. (See "Reflex syncope in adults and adolescents: Clinical presentation and diagnostic evaluation", section on 'Types of reflex syncope' and "Carotid sinus hypersensitivity and carotid sinus syndrome".)

Orthostatic (postural) hypotension — Orthostatic (postural) hypotension, defined as a decrease in systolic blood pressure of at least 20 mmHg, or in diastolic blood pressure of at least 10 mmHg upon assuming upright posture, is another common cause of near-syncope and syncope. Orthostatic syncope occurs most often following movement from lying or sitting to a standing position. Orthostatic (postural) hypotension is often considered as being either immediate or delayed.

Immediate orthostatic hypotension – Many healthy individuals experience a minor form of orthostatic change in blood pressure when rising abruptly from a supine or seated position, and need to support themselves momentarily, a condition referred to as immediate orthostatic hypotension (OH). Immediate OH usually occurs within 10 seconds of movement to standing and is fully resolved 10 to 20 seconds later.

Delayed orthostatic hypotension – Delayed or "classic" orthostatic hypotension refers to episodes of near-syncope or syncope that occur after the affected individual has been upright for some period of time (usually one to several minutes). Such episodes are generally more worrisome, as the patient may be unprepared to protect themselves from the hazards of a fall and risk of injury.

The major causes of orthostatic hypotension associated with syncope include (see "Mechanisms, causes, and evaluation of orthostatic hypotension"):

Decreased intravascular volume, as may occur with inadequate fluid intake, excessive fluid loss in hot, dry environments or with exercise, or the result of diuretics or as a consequence of losses associated with certain gastrointestinal disorders.

Drug effects, especially antidepressants (tricyclics, phenothiazine) and antihypertensive agents (beta and alpha blockers, hydralazine, angiotensin converting enzyme inhibitors, ganglionic blockers), particularly vasodilators, including calcium channel blockers and nitrates (more commonly observed in older adults). Other drugs that may cause orthostatic hypotension include opiates and bromocriptine.

Primary autonomic insufficiency or failure (including pure autonomic failure, multiple system atrophy, Parkinson disease, and others).

Secondary autonomic insufficiency (eg, diabetes mellitus and amyloidosis).

Alcohol consumption which impairs vasoconstriction [19].

Aging is associated with an increased prevalence of orthostatic hypotension [20]. One contributory mechanism may be attenuation of the vestibulo-sympathetic reflex [21].

The greatest risk of orthostatic hypotension resulting in syncope is in older frail individuals, patients on multiple vasodilating and/or diuretic drugs, those who have underlying medical problems causing autonomic failure (eg, diabetes, certain nervous system diseases), and persons who are dehydrated (eg, hot environments, inadequate fluid intake). (See "Mechanisms, causes, and evaluation of orthostatic hypotension".)

Cardiac arrhythmias — Cardiac arrhythmias may cause syncope or near-syncope if the heart rate is either too slow or too fast to permit maintenance of an adequate cardiac output and systemic arterial pressure. Bradycardia resulting from prolonged sinus pauses, high grade atrioventricular (AV) block, or at the termination of an atrial tachyarrhythmia may cause syncope and near-syncope. Similarly, syncope or near-syncope may occur at the onset of an episode of tachycardia in which a fall in cardiac output cannot be adequately compensated for by vascular constriction. Although an arrhythmic etiology for syncope is often suspected clinically, the culprit arrhythmia frequently may be difficult to diagnose since most are paroxysmal and infrequent. Long-term ambulatory ECG monitoring is often essential. (See "Syncope in adults: Clinical manifestations and initial diagnostic evaluation" and "Ambulatory ECG monitoring".)

The most common arrhythmic causes of syncope include:

AV block – High grade (ie, complete or Mobitz type II second degree) AV block may trigger syncope (an event previously termed a Stokes-Adams attack). Conversely, Mobitz type I (Wenckebach) second degree AV block is usually benign and not associated with syncope. When Mobitz type II second degree or third degree AV block is present in conjunction with syncope, a permanent pacemaker is indicated. (See "Syncope in adults: Management and prognosis", section on 'Arrhythmias' and "Second-degree atrioventricular block: Mobitz type II" and "Third-degree (complete) atrioventricular block".)

Cardiac pauses – Cardiac pauses may be caused by intrinsic or drug-induced sinus pauses or prolonged recovery times after spontaneous termination of an episode of atrial fibrillation or flutter or other supraventricular tachycardia. (See "Sinus node dysfunction: Clinical manifestations, diagnosis, and evaluation".)

Ventricular tachyarrhythmias – Syncope resulting from ventricular tachycardia (VT) occurs most commonly in the setting of structural heart disease, particularly coronary heart disease. Patients with dilated cardiomyopathy and some congenital myopathic processes (eg, hypertrophic cardiomyopathy [HCM], arrhythmogenic right ventricular cardiomyopathy) are also prone to have VT presenting with syncope. In addition, an unusual form of VT, torsades de pointes, may cause syncope in patients with either the congenital or acquired forms of long QT syndrome. In addition, there has been substantial expansion of knowledge into other genetic cardiac ion channel diseases. While relatively rare, conditions such as Brugada syndrome, catecholaminergic polymorphic VT (CPVT), and others need to be considered as part of the syncope/collapse differential diagnosis. Finally, ventricular fibrillation is not often a cause of syncope as it only rarely is self-terminating [22]. In nearly all cases, this rhythm disturbance causes cardiac arrest and death. (See "Ventricular arrhythmias: Overview in patients with heart failure and cardiomyopathy" and "Congenital long QT syndrome: Epidemiology and clinical manifestations" and "Acquired long QT syndrome: Definitions, pathophysiology, and causes".)

Ventricular bigeminy – Ventricular bigeminy, with ventricular premature beats occurring every other beat, may occasionally be associated with hypotension, bradycardia, and near syncope, though full syncope with loss of consciousness is exceedingly rare. Syncope occurs primarily in patients with an underlying sinus bradycardia or those with advanced heart disease and significant left ventricular dysfunction. Ventricular bigeminy typically is associated with in ineffective cardiac output of the premature beats, thereby diminishing overall cardiac output.

Supraventricular tachyarrhythmias – Supraventricular tachyarrhythmias are only rarely associated with syncope [23]. Syncope may occur at the onset of the arrhythmia as impaired vasomotor function may be responsible for syncope due to delayed vasoconstrictive compensation. In some cases, the cause may be due to neurally-mediated (neurocardiogenic) responses rather than a direct result of the tachycardia [24-26]. In others, concomitant drug therapy (eg, vasodilators) may undermine compensatory vascular response.

Individuals with underlying heart disease (eg, previous myocardial infarction [MI], valvular heart disease), a channelopathy (eg, long QT syndrome, Brugada syndrome), HCM, congenital heart disease, or significant vascular disease are at greatest risk for syncope due to a tachyarrhythmia (usually VT). In contrast to patients who have vasovagal or other causes of syncope, an arrhythmic cause of syncope often occurs without warning. This is particularly true of the bradyarrhythmias and, in addition to reporting no warning symptoms, the patient may also suffer an injury with the event. Patients with a tachyarrhythmia may report having palpitations but may also have syncope without warning symptoms.

An abrupt change in heart rate, as occurs during the initiation of many arrhythmias, can cause TLOC. The blood pressure may precipitously decline, especially in an upright position, causing TLOC if a prompt compensatory vasopressor response (which may be blunted by antihypertensive or HF medications) does not occur. Then, gradually, with augmentation in sympathetic nervous system activation and elevation of catecholamine levels triggered by systemic hypotension, vasoconstriction and increased ventricular contractility restores adequate cerebral blood flow.

The hemodynamic stability resulting from any arrhythmia is also influenced by other factors including rate, ventricular function or presence of coronary or valvular heart disease, body position, medications, and baroreceptor sensitivity [27,28].

Structural cardiac or cardiopulmonary disease — The presence of heart disease has been shown to be an independent predictor of cardiac cause of syncope, with a sensitivity of 95 percent and a specificity of 45 percent; by contrast, the absence of heart disease excludes a cardiac cause of syncope in 97 percent of patients [29].

Structural cardiac or cardiopulmonary diseases that may lead to syncope due to inadequate cardiac output include cardiac valvular disease (particularly aortic stenosis), HCM, atrial myxoma, pulmonary embolus, pulmonary hypertension, pericardial tamponade, acute MI/ischemia, and acute aortic dissection. Channelopathies such as long QT syndrome, Brugada syndrome, CPVT, and others that are less frequent should also be included here, although the "structural" disease is at the cellular level.

Patients with an underlying cardiovascular cause of syncope have higher rates of sudden cardiac death (SCD) and all-cause mortality than those with a noncardiovascular cause of syncope. The mortality rate in patients with cardiovascular disease after five years of follow-up has been reported to approach 50 percent, with a 30 percent incidence of death in the first year (figure 2) [3,6,30,31]. Mortality in these patients is in large part due to the severity of the underlying cardiovascular disease.

Syncope may be caused by obstruction to blood flow due to cardiovascular abnormalities, the most frequent being aortic stenosis and HCM. Less common conditions include pulmonic stenosis, idiopathic pulmonary arterial hypertension, atrial myxomas, and pulmonary embolism.

Aortic stenosis – Aortic stenosis rarely presents with syncope unless the valve is critically stenotic. Syncope in patients with aortic stenosis is often associated with exertion. In most such cases, syncope results from an inability to produce a compensatory increase in cardiac output (due to the obstruction), which normally occurs in response to exercise-induced peripheral vasodilation [32,33]. Patients with syncope and severe aortic stenosis have a high mortality if untreated; aortic valve replacement is generally indicated in such patients. (See "Clinical manifestations and diagnosis of aortic stenosis in adults", section on 'Dizziness and syncope' and "Natural history, epidemiology, and prognosis of aortic stenosis" and "Indications for valve replacement for high gradient aortic stenosis in adults".)

Hypertrophic cardiomyopathy – Syncope may occur in up to 25 percent of patients who have HCM and may be due to dynamic left ventricular outflow tract (LVOT) obstruction or other causes. LVOT obstruction can intensify with postural changes, hypovolemia, or drugs. Multiple mechanisms may lead to syncope in patients with HCM and LVOT obstruction, notably including the LVOT obstruction itself (leading to reduced cardiac output) and VT. Syncope in patients with HCM is discussed in detail separately. (See "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation", section on 'Syncope'.)

Myocardial ischemia – VT and bradyarrhythmias secondary to myocardial ischemia are infrequent causes of syncope, accounting for only 1 percent of cases [34]. Although patients who are admitted to the hospital with syncope are commonly evaluated for acute coronary syndrome (myocardial infarction or unstable angina), generally, only a limited evaluation for acute coronary syndrome is required, as discussed separately. (See "Syncope in adults: Clinical manifestations and initial diagnostic evaluation", section on 'Approach to initial evaluation'.)

Other causes – Pulmonary embolism, severe pulmonic stenosis, idiopathic pulmonary arterial hypertension, and atrial myxomas are all rare causes of syncope due to obstruction of blood flow [35]. (See "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism", section on 'History and examination'.)

Cerebrovascular disease — Atherosclerotic disease of the cerebral arteries is almost never the cause of true syncope, as the brain has a very redundant blood supply. Instead, stroke and transient ischemia attacks cause focal neurologic deficits that do not recover rapidly or, in most cases, completely. As examples:

If the posterior cerebral circulation is impaired (vertebrobasilar artery insufficiency), symptoms such as dizziness are more apt to occur than syncope. Other causes of syncope should be excluded in patients with syncope and suspected vertebrobasilar ischemia.

If the anterior circulation is compromised, a focal neurologic deficit and not a global decrease in consciousness will occur.

The rare exception in which syncope can occur is with severe obstructive four vessel cerebrovascular disease; however, other neurologic findings are likely to occur prior to the loss of consciousness in these patients. (See "Vertebral artery revascularization".)

A vascular steal syndrome occurs when the arterial circulation to the arm is blocked proximally, resulting in a shunt of blood through the cerebrovascular system that supplies both parts of the brain and the arm. Impairment in brain perfusion during arm exercise may cause loss of consciousness. Vertebrobasilar steal is typically associated with vertigo, diplopia, blurred vision, cranial nerve dysfunction, drop attacks (sudden fall without loss of consciousness), and syncope. (See "Upper extremity atherosclerotic disease" and "Subclavian steal syndrome", section on 'Clinical features' and "Subclavian steal syndrome", section on 'Definition and physiology'.)

SYNCOPE OF UNKNOWN ORIGIN — When the initial evaluation, including history, physical examination, and ECG, are completely nondiagnostic, the patient is considered to have syncope/collapse of unknown origin/cause. Importantly, as was noted above, in many instances, apart from not knowing the cause, it may not be clear that the patient has experienced true syncope. The published literature often misses this point and syncope and nonsyncope collapse are, as a result, inappropriately combined; as noted earlier, lumping these conditions together complicates our understanding of the epidemiology and prognosis associated with such patients. (See 'Epidemiology' above.)

Leaving aside the uncertainty regarding combining true syncope and nonsyncopal causes of collapse (eg, accidents, seizures), approximately one-fifth to one-third of cases in the literature have been identified as having syncope from "unknown causes." However, identification of this group is problematic given limitations in diagnostic discrimination of causes. As an example, in the Framingham Heart Study cited above, the group identified as having syncope of "unknown" origin likely included individuals with a mixed group of conditions in which benign and not-so-benign diagnoses could not be sorted out given the limited diagnostic data available to Framingham investigators [3]. In more contemporary practice, however, with the increasingly broader availability of specialized syncope/collapse clinics, the frequency of "unexplained" transient loss of consciousness is diminishing and may be closer to 10 percent [36,37].

CAUSES OF NONSYNCOPAL ATTACKS — Episodes that may be confused with syncope include disorders without impairment of consciousness and disorders with partial or complete loss of consciousness (table 4). These disorders should be considered and excluded as part of the initial evaluation of the transient loss of consciousness (TLOC)/collapse patient (which includes a thorough history, physical examination, ECG, and selected additional testing on a case by case basis) (algorithm 1).

Seizures – Seizures are the probable cause in 5 to 15 percent of apparent TLOC/collapse episodes [3,15,34,38]. They can mimic syncope, especially when the seizure is atypical and not associated with tonic-clonic movements, the seizure is not observed, or a complete/detailed history cannot be obtained (table 5). Another potentially confounding factor is that loss of cerebral blood flow due to any cause of syncope can result in a myoclonic jerking that nonexpert witnesses may conclude is an epileptic state. As an example, the initiation of a rapid ventricular tachycardia may be associated with impaired cerebral blood flow, followed within seconds by movements that might (although only rarely) appear to the lay bystander or inexperienced medical practitioner to be tonic-clonic activity. This apparent seizure activity is associated with brain wave slowing, not epileptiform spikes, on the electroencephalogram. One distinguishing feature is that patients with seizures rarely have an abrupt complete recovery. Instead, the postictal state is characterized by a slow complete recovery. Other important clues, if present, are evidence of soft tissue injury at multiple sites due to tonic-clonic movements during the seizure. (See "Evaluation and management of the first seizure in adults".)

Psychogenic pseudo-syncope and nonepileptic "seizures" – Conversion disorders can mimic syncope or seizures and have been termed in some literature as psychogenic nonepileptic seizures (but are better called psychogenic pseudosyncope or psychogenic pseudoseizures, the distinction being whether the patient manifests jerky movements suggesting a seizure to untrained bystanders). These conditions, diagnosed in approximately 1 percent of patients referred to a syncope/collapse clinic, are usually distinguished by having multiple recurrences of apparent collapse, prolonged duration of apparent TLOC (often many minutes), absence of physical injury, and absence of evidence pointing toward a cause for syncope or evidence of seizure activity [39-41]. (See "Psychogenic nonepileptic seizures: Etiology, clinical features, and diagnosis".)

Metabolic and/or toxic abnormalities – Metabolic or toxic abnormalities are rarely associated with an abrupt onset or complete brisk recovery; syncope is therefore rare in this setting. Hypoglycemia and encephalitis can cause coma, stupor, and confusion, but rarely the transient loss of consciousness characteristic of syncope. Although metabolic abnormalities (such as hypoglycemia or hypoxia) infrequently cause syncope, they can cause impaired consciousness that may be difficult to distinguish from syncope. Metabolic abnormalities, anemia, and hypovolemia can be effectively managed by specific therapy to correct these abnormalities.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Syncope".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword[s] of interest.)

Basics topic (see "Patient education: Syncope (fainting) (The Basics)")

Beyond the Basics topic (see "Patient education: Syncope (fainting) (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Epidemiology – Syncope is a common clinical problem, which is one of the many causes of transient loss of consciousness (TLOC). Syncope has a lifetime prevalence in the population as a whole of approximately 20 percent. Syncope is responsible for between 1 and 3 percent of all emergency department visits and 1 percent of all hospital admissions. (See 'Epidemiology' above.)

Causes – The possible causes of TLOC resulting in true syncope are generally grouped into four major categories (table 1): reflex syncope (neurally-mediated), orthostatic syncope, cardiac arrhythmias, and structural cardiopulmonary disease. (See 'Causes of syncope' above.)

Causes of nonsyncopal attacks – In the evaluation of a patient with TLOC in whom syncope is suspected, the clinician must necessarily consider and exclude conditions that mimic TLOC/syncope but are not true syncope (algorithm 1). The most common of these conditions are seizures, sleep disturbances, accidental falls, and some psychiatric conditions (eg, conversion reactions resulting in psychogenic nonepileptic seizures, previously called psychogenic pseudoseizures). (See 'Causes of nonsyncopal attacks' above and "Evaluation and management of the first seizure in adults" and "Classification of sleep disorders" and "Psychogenic nonepileptic seizures: Etiology, clinical features, and diagnosis".)

Atherosclerotic disease of the cerebral arteries is almost never the cause of true syncopal symptoms, as the brain has a very redundant blood supply. Instead, stroke and transient ischemia attacks cause focal neurologic deficits that do not recover rapidly or completely. (See 'Cerebrovascular disease' above.)

Syncope of unknown origin – When the initial evaluation, including history, physical examination, and ECG, is nondiagnostic in a patient with suspected syncope, the patient is considered to have syncope with an unexplained diagnosis (ie, syncope of unknown origin). The frequency of an "unknown" cause was previously approximately one-third of cases, but is now closer to 10 percent as syncope experts and specialized syncope diagnostic clinics have become more widely available. As a rule, syncope of unknown cause is generally associated with a good prognosis, suggesting that most are likely "reflex" in origin. (See 'Syncope of unknown origin' above.)

  1. Chen LY, Shen WK, Mahoney DW, et al. Prevalence of syncope in a population aged more than 45 years. Am J Med 2006; 119:1088.e1.
  2. Shen WK, Sheldon RS, Benditt DG, et al. 2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines, and the Heart Rhythm Society. J Am Coll Cardiol 2017.
  3. Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med 2002; 347:878.
  4. Lipsitz LA. Syncope in the elderly. Ann Intern Med 1983; 99:92.
  5. Freed LA, Eagle KA, Mahjoub ZA, et al. Gender differences in presentation, management, and cardiac event-free survival in patients with syncope. Am J Cardiol 1997; 80:1183.
  6. Kapoor WN. Evaluation and outcome of patients with syncope. Medicine (Baltimore) 1990; 69:160.
  7. Manolis AS, Linzer M, Salem D, Estes NA 3rd. Syncope: current diagnostic evaluation and management. Ann Intern Med 1990; 112:850.
  8. Costantino G, Sun BC, Barbic F, et al. Syncope clinical management in the emergency department: a consensus from the first international workshop on syncope risk stratification in the emergency department. Eur Heart J 2016; 37:1493.
  9. Colivicchi F, Ammirati F, Melina D, et al. Development and prospective validation of a risk stratification system for patients with syncope in the emergency department: the OESIL risk score. Eur Heart J 2003; 24:811.
  10. Zimmermann T, du Fay de Lavallaz J, Nestelberger T, et al. International Validation of the Canadian Syncope Risk Score : A Cohort Study. Ann Intern Med 2022; 175:783.
  11. Anand V, Benditt DG, Adkisson WO, et al. Trends of hospitalizations for syncope/collapse in the United States from 2004 to 2013-An analysis of national inpatient sample. J Cardiovasc Electrophysiol 2018; 29:916.
  12. Kadri AN, Abuamsha H, Nusairat L, et al. Causes and Predictors of 30-Day Readmission in Patients With Syncope/Collapse: A Nationwide Cohort Study. J Am Heart Assoc 2018; 7:e009746.
  13. Alboni P, Brignole M, Menozzi C, et al. Diagnostic value of history in patients with syncope with or without heart disease. J Am Coll Cardiol 2001; 37:1921.
  14. Mathias CJ, Deguchi K, Schatz I. Observations on recurrent syncope and presyncope in 641 patients. Lancet 2001; 357:348.
  15. Linzer M, Yang EH, Estes NA 3rd, et al. Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Clinical Efficacy Assessment Project of the American College of Physicians. Ann Intern Med 1997; 126:989.
  16. Linzer M, Yang EH, Estes NA 3rd, et al. Diagnosing syncope. Part 2: Unexplained syncope. Clinical Efficacy Assessment Project of the American College of Physicians. Ann Intern Med 1997; 127:76.
  17. Olshansky B, Mazuz M, Martins JB. Significance of inducible tachycardia in patients with syncope of unknown origin: a long-term follow-up. J Am Coll Cardiol 1985; 5:216.
  18. Benditt DG, Adkisson WO, Sutton R, et al. Ambulatory diagnostic ECG monitoring for syncope and collapse: An assessment of clinical practice in the United States. Pacing Clin Electrophysiol 2018; 41:203.
  19. Narkiewicz K, Cooley RL, Somers VK. Alcohol potentiates orthostatic hypotension : implications for alcohol-related syncope. Circulation 2000; 101:398.
  20. Rutan GH, Hermanson B, Bild DE, et al. Orthostatic hypotension in older adults. The Cardiovascular Health Study. CHS Collaborative Research Group. Hypertension 1992; 19:508.
  21. Ray CA, Monahan KD. Aging attenuates the vestibulosympathetic reflex in humans. Circulation 2002; 105:956.
  22. Kontny F, Dale J. Self-terminating idiopathic ventricular fibrillation presenting as syncope: a 40-year follow-up report. J Intern Med 1990; 227:211.
  23. Benditt DG. Syncope risk assessment in the emergency department and clinic. Prog Cardiovasc Dis 2013; 55:376.
  24. Leitch JW, Klein GJ, Yee R, et al. Syncope associated with supraventricular tachycardia. An expression of tachycardia rate or vasomotor response? Circulation 1992; 85:1064.
  25. Doi A, Miyamoto K, Uno K, et al. Studies on hemodynamic instability in paroxysmal supraventricular tachycardia: noninvasive evaluations by head-up tilt testing and power spectrum analysis on electrocardiographic RR variation. Pacing Clin Electrophysiol 2000; 23:1623.
  26. Brembilla-Perrot B, Beurrier D, Houriez P, et al. Incidence and mechanism of presyncope and/or syncope associated with paroxysmal junctional tachycardia. Am J Cardiol 2001; 88:134.
  27. Hamer AW, Rubin SA, Peter T, Mandel WJ. Factors that predict syncope during ventricular tachycardia in patients. Am Heart J 1984; 107:997.
  28. Landolina M, Mantica M, Pessano P, et al. Impaired baroreflex sensitivity is correlated with hemodynamic deterioration of sustained ventricular tachycardia. J Am Coll Cardiol 1997; 29:568.
  29. Menozzi C, Brignole M, Garcia-Civera R, et al. Mechanism of syncope in patients with heart disease and negative electrophysiologic test. Circulation 2002; 105:2741.
  30. Kapoor W, Karpf M, Levey GS. Issues in evaluating patients with syncope. Ann Intern Med 1984; 100:755.
  31. Krahn AD, Andrade JG, Deyell MW. Selecting appropriate diagnostic tools for evaluating the patient with syncope/collapse. Prog Cardiovasc Dis 2013; 55:402.
  32. Grech ED, Ramsdale DR. Exertional syncope in aortic stenosis: evidence to support inappropriate left ventricular baroreceptor response. Am Heart J 1991; 121:603.
  33. Goliasch G, Kammerlander AA, Nitsche C, et al. Syncope: The Underestimated Threat in Severe Aortic Stenosis. JACC Cardiovasc Imaging 2019; 12:225.
  34. WAYNE HH. Syncope. Physiological considerations and an analysis of the clinical characteristics in 510 patients. Am J Med 1961; 30:418.
  35. Badertscher P, du Fay de Lavallaz J, Hammerer-Lercher A, et al. Prevalence of Pulmonary Embolism in Patients With Syncope. J Am Coll Cardiol 2019; 74:744.
  36. Kenny RA, Brignole M, Dan GA, et al. Syncope Unit: rationale and requirement--the European Heart Rhythm Association position statement endorsed by the Heart Rhythm Society. Europace 2015; 17:1325.
  37. Brignole M, Moya A, de Lange FJ, et al. 2018 ESC Guidelines for the diagnosis and management of syncope. Eur Heart J 2018; 39:1883.
  38. Sheldon R, Rose S, Ritchie D, et al. Historical criteria that distinguish syncope from seizures. J Am Coll Cardiol 2002; 40:142.
  39. Heyer GL, Harvey RA, Islam MP. Comparison of Specific Fainting Characteristics Between Youth With Tilt-Induced Psychogenic Nonsyncopal Collapse Versus Reflex Syncope. Am J Cardiol 2017; 119:1116.
  40. Walsh KE, Baneck T, Page RL, et al. Psychogenic pseudosyncope: Not always a diagnosis of exclusion. Pacing Clin Electrophysiol 2018; 41:480.
  41. Tannemaat MR, van Niekerk J, Reijntjes RH, et al. The semiology of tilt-induced psychogenic pseudosyncope. Neurology 2013; 81:752.
Topic 1049 Version 37.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟