Syncope

Douglas J Lanska MD FAAN MS MSPH (Dr. Lanska of the Great Lakes VA Healthcare System and the University of Wisconsin School of Medicine and Public Health has no relevant financial relationships to disclose.)
Originally released October 21, 1993; last updated May 1, 2017; expires May 1, 2020

This article includes discussion of syncope, faint, Stokes-Adams attack, transient loss of consciousness, and vasodepressor syncope. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

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” (Task Force for the Diagnosis and Management of Syncope et al 2009). 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” (Task Force for the Diagnosis and Management of Syncope et al 2009).

 

• 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” (Task Force for the Diagnosis and Management of Syncope et al 2009). 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, and psychogenic pseudosyncope (Task Force for the Diagnosis and Management of Syncope et al 2009).

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” (Task Force for the Diagnosis and Management of Syncope et al 2009).

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 (Task Force for the Diagnosis and Management of Syncope et al 2009).

Syncope may be classified as reflex (neurally mediated), secondary to orthostatic hypotension, or cardiac (cardiovascular) (Task Force for the Diagnosis and Management of Syncope et al 2009).

Reflex syncopes are a heterogeneous group of disorders mediated by cardiovascular reflexes that are inappropriately triggered, producing vasodilation and/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 (Task Force for the Diagnosis and Management of Syncope et al 2009). 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) (Task Force for the Diagnosis and Management of Syncope et al 2009). 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 (Kenny and McNicholas 2016). Situational syncopes are triggered by specific circumstances such as coughing/sneezing, 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.

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, beta-blockers, diuretics, phenothiazines, antidepressants), and volume depletion (eg, dehydration, hemorrhage, diarrhea, vomiting) (Task Force for the Diagnosis and Management of Syncope et al 2009).

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), pulmonary embolism, acute aortic dissection, and pulmonary hypertension (Task Force for the Diagnosis and Management of Syncope et al 2009). 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 (Kapoor et al 1983).

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