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  • Updated 05.15.2024
  • Released 10.21.1993
  • Expires For CME 05.15.2027

Syncope

Introduction

Overview

Syncope is a specific category of transient loss of consciousness that is “due to transient global cerebral hypoperfusion [and is] characterized by rapid onset, short duration, and spontaneous complete recovery” (188). Narrowing of the field of vision and loss of color vision (graying out) occur, followed by complete loss of vision, loss of consciousness, turning up of the eyeballs, and, possibly, myoclonic jerks. Although the treatment of neurologic or cardiac syncope aims at the underlying cause, the primary treatment of neurovascular syncope consists of patient education and instruction in reasonable precautions.

Key points

• Syncope is a specific category of transient loss of consciousness that is “due to transient global cerebral hypoperfusion [and is] characterized by rapid onset, short duration, and spontaneous complete recovery” (188).

• Syncope is a prevalent disorder, accounting for 3% to 5% of emergency department visits and 1% to 3% of hospital admissions.

• Syncope may be confused with seizure, cryptogenic drop attacks, migraine, basilar thrombosis, or metabolic disturbances.

• Unlike true episodes of syncope, episodes of pseudosyncope are not associated with compromised cerebral circulation.

Historical note and terminology

Transient loss of consciousness. Transient loss of consciousness (TLOC) is an umbrella term that encompasses “all disorders that are characterized by self-limited loss of consciousness” (188). The 2018 Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology operationally defines transient loss of consciousness as “a state of real or apparent [loss of consciousness] with loss of awareness, characterized by amnesia for the period of unconsciousness, abnormal motor control, loss of responsiveness, and a short duration” (40). Unfortunately, many papers inappropriately equate transient loss of consciousness with syncope, distorting estimates of frequency, and generating confusing conclusions and misleading or incorrect recommendations for assessment and management. Categories of nontraumatic transient loss of consciousness include syncope, epileptic seizures, psychogenic pseudosyncope, and psychogenic nonepileptic seizures (188; 40).

Syncope. Syncope is a specific category of transient loss of consciousness that is “due to transient global cerebral hypoperfusion [and is] characterized by rapid onset, short duration, and spontaneous complete recovery” (188; 40). The 2018 Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology noted that low blood pressure and global cerebral hypoperfusion are “the central final common pathway of syncope” (40). Loss of consciousness will be produced by a sudden cessation of cerebral blood flow for as short as 6 to 8 seconds, or a systolic blood pressure of 50 to 60 mm Hg at the heart level (corresponding to 30 to 45 mm Hg at the brain level in the upright position) (40).

Presyncope. Presyncope and near syncope are terms used “to describe a state that resembles the prodrome of syncope but which is not followed by [loss of consciousness],” although whether the mechanisms involved are the same as in syncope is not entirely clear (188).

Classification and pathophysiology of syncope. Syncope may be classified as reflex (neurally mediated), secondary to orthostatic hypotension, or cardiac (cardiovascular) (188; 40).

Blood pressure is the product of cardiac output and total peripheral vascular resistance. Causes of low total peripheral resistance include: (1) decreased reflex activity causing vasodilatation through withdrawal of sympathetic vasoconstriction as in the vasodepressive type of reflex syncope; (2) a functional impairment of the autonomic nervous system as may occur with various drugs; and (3) a structural impairment of the autonomic nervous system from primary or secondary autonomic failure (40). Causes of low cardiac output include (1) reflex bradycardia, known as cardioinhibitory reflex syncope; (2) cardiovascular causes, eg, arrhythmia, structural disease including pulmonary embolism, and pulmonary hypertension; (3) inadequate venous return due to volume depletion or venous pooling; and (4) chronotropic and inotropic incompetence through autonomic failure (40).

Reflex syncope. Reflex syncopes are a heterogeneous group of disorders mediated by cardiovascular reflexes that are inappropriately triggered, producing vasodilation or bradycardia, with a resultant fall in both blood pressure and cerebral perfusion. Reflex syncopes can be classified as vasovagal, situational, carotid sinus, and atypical (188; 40). Vasovagal syncopes are the most common reflex syncopes and include the common faint; they are often triggered by emotional distress, fear, pain, and instrumentation (eg, blood draw) (188; 40). Atypical vasovagal syncope may be associated with a short or absent prodrome and amnesia for loss of consciousness, thus, increasing the possibility of misdiagnosis with nonsyncopal falls (92). Situational syncopes are triggered by specific circumstances such as coughing/sneezing, hiccupping, swallowing, defecation, visceral pain, micturition (or immediately postmicturition), postexercise, postprandial, and weightlifting; they are often forms of reflex syncope, but may not be, or can be multifactorial in causation (188; 40; 208).

Patients with reflex syncope have lower 24-hour systolic blood pressure but higher 24-hour diastolic blood pressure and more frequent daytime systolic blood pressure drops less than 90 mmHg than individuals without syncope (155; 165).

Vestibular syncope. Vestibular syncope is a neurally mediated reflex syncope associated with a sudden hemodynamic change during vertigo. This sudden hemodynamic change can be arterial hypertension triggered by a false downward inertial cue or hypotension driven by a false upward inertial cue. The pathomechanism of syncope is thought to be an interaction between the vestibulo-sympathetic reflex and the baroreflex, which have different operating mechanisms and action latencies; however, the central vestibular system, which estimates gravity orientation and inertia motion, may also play an important role (47). In addition, orthostatic hypotension is present in about 20% of patients with vestibular syncope. Vestibular syncope has most often been reported with Meniere disease, but other vestibular disorders, including benign paroxysmal positioning vertigo, may also be responsible (145; 147; 146; 96; 47). Vestibular syncope is separate from the otolithic crises (also called “otolithic catastrophe” or "Tumarkin attacks") that patients with Meniere disease experience as a sensation of suddenly being thrown to the ground without warning.

Orthostatic hypotension. Syncope due to orthostatic hypotension may result from primary autonomic failure (eg, pure autonomic failure, multisystem atrophy, Parkinson disease, Lewy body dementia), secondary autonomic failure (eg, alcoholism, diabetes mellitus, spinal cord injury), drugs (eg, alcohol, vasodilators, alpha-blockers, beta-blockers, diuretics, phenothiazines, antidepressants), and volume depletion (eg, dehydration, hemorrhage, diarrhea, vomiting) (188; 40; 129; 150; 175).

Cardiovascular syncope. Cardiac (cardiovascular) syncope may result from bradycardia (eg, sinus node dysfunction including bradycardia/tachycardia syndrome, atrioventricular conduction system disease, and implanted device malfunction), tachycardia (supraventricular or ventricular), structural heart disease (eg, aortic stenosis, acute myocardial ischemia or infarction, hypertrophic cardiomyopathy, atrial myxoma, pericardial tamponade), and cardiopulmonary conditions and disorders of the great vessels, (eg, pulmonary embolism, acute aortic dissection, and pulmonary hypertension) (188; 40). The cardiac subtype is also likely to yield the highest rate of electrocardiographic abnormality. A cardiac cause of syncope is an independent predictor of sudden death, and mortality rates are higher in patients with cardiac syncope compared with those of noncardiac or unknown origin (88).

In a study of 95 patients with pacemakers, half (49%) had experienced syncope in the past 12 months (156). In 100 documented episodes of syncope, vasovagal syncope was diagnosed in 49%, whereas 17% of episodes were linked with cardiac-related causes, 11% with unknown causes, and 9% with pacemaker failure. New York Heart Association (NYHA) Functional Class II had a significantly higher risk of developing syncope. Even though half of the cases had neurogenic syncope, a careful evaluation is clearly warranted because of the significant frequency of life-threatening etiologies in this group.

Examples of syncope from diseases of the great vessels or cerebrovascular disease include some cases of subclavian steal syndrome (especially with coexistent cerebrovascular disease) (70; 141; 174; 44; 59; 138; 57; 94; 104; 114; 177; 122) and bilateral Eagle syndrome with bilateral carotid artery compression with certain head positions (186). However, in patients without focal neurologic symptoms and signs, syncope from diseases of the great vessels or cerebrovascular disease is extremely rare.

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