"Syncopy" redirects here. For the motion picture company, see Syncopy Films.
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This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (October 2011) |
Syncope (medicine)
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| ICD-10 |
R55 |
| ICD-9 |
780.2 |
| DiseasesDB |
27303 |
| MedlinePlus |
003092 |
| eMedicine |
med/3385 ped/2188 emerg/876 |
| MeSH |
D013575 |
Syncope (// SING-kə-pee), the medical term for fainting or passing out, is defined as a transient loss of consciousness and postural tone, characterized by rapid onset, short duration, and spontaneous recovery, due to global cerebral hypoperfusion (low blood flow to the brain) that most often results from hypotension (low blood pressure). This definition of syncope differs from others by including the cause of unconsciousness, i.e. transient global cerebral hypoperfusion. Without that addition, the definition of syncope would include disorders such as epileptic seizures, concussion or cerebrovascular accident and syncope is distinguished from coma, which can include persistent states of unconsciousness. This confusion still occurs in some literature.
Many forms of syncope are preceded by a prodromal state that often includes dizziness and loss of vision ("blackout") (temporary), loss of hearing (temporary), loss of pain and feeling (temporary), nausea and abdominal discomfort, weakness, sweating, a feeling of heat, palpitations and other phenomena, which, if they do not progress to loss of consciousness and postural tone are often denoted "presyncope".[1] Abdominal discomfort prior to loss of consciousness may be indicative of seizure, which is different than syncope.[2]
There are three broad categories of syncope, cardiogenic, reflex (i.e. neurally mediated) and orthostatic hypotension, which underlie most forms of syncope. Cardiogenic forms are more likely to produce serious morbidity or mortality and require prompt or even immediate treatment. Although cardiogenic syncope is much more common in older patients, an effort to rule out arrhythmic, obstructive, ischemic, or cardiomyopathic causes of syncope and circulatory inadequacy is mandatory in each patient.
Variants of reflex syncope often have characteristic histories, including precipitants and time course. These become evident through skilled history-taking. Thus, the clinical history is the foremost tool used in the differential diagnosis of syncope. Physical examination, and electrocardiogram are part of the initial evaluation of syncope and other more specific tools such as implantable loop recorders may be necessary in clinically uncertain cases.
Syncope is extraordinarily common, occurring for the most part in two age ranges: the teenage years, and during older age. Estimates of lifetime incidence of at least one syncopal episode include 40 to 50 percent of the general populace. Syncope comprises 1 to 3 percent of all attendances to emergency departments and 1 to 6 percent of all hospital admissions.[3][4]
Contents
- 1 Etymology
- 2 Differential diagnosis
- 2.1 Central nervous system ischaemia
- 2.1.1 Vertebro-basilar arterial disease
- 2.2 Vasovagal
- 2.2.1 Deglutition (Swallowing) syncope
- 2.3 Cardiac
- 2.3.1 Cardiac arrhythmias
- 2.3.2 Obstructive cardiac lesion
- 2.3.3 Structural cardiopulmonary disease
- 2.3.4 Other cardiac causes
- 2.4 Blood pressure
- 2.5 Other causes
- 3 Diagnostic approach
- 3.1 San Francisco syncope rule
- 4 Management
- 5 Society and culture
- 6 References
- 7 Further reading
- 8 External links
Etymology[edit]
The term is derived from the Late Latin syncope, from Ancient Greek συγκοπή (sunkopē), from σύν (sin, "together, thoroughly") and κόπτειν (koptein, "strike, cut off").
Differential diagnosis[edit]
Central nervous system ischaemia[edit]
The central ischaemic response is triggered by an inadequate supply of oxygenated blood in the brain.
The respiratory system may contribute to oxygen levels through hyperventilation, though a sudden ischaemic episode may also proceed faster than the respiratory system can respond. These processes cause the typical symptoms of fainting: pale skin, rapid breathing, nausea and weakness of the limbs, particularly of the legs. If the ischaemia is intense or prolonged, limb weakness progresses to collapse. An individual with very little skin pigmentation may appear to have all color drained from his or her face at the onset of an episode. This effect combined with the following collapse can make a strong and dramatic impression on bystanders.
The weakness of the legs causes most sufferers to sit or lie down if there is time to do so. This may avert a complete collapse, but whether the sufferer sits down or falls down, the result of an ischaemic episode is a posture in which less blood pressure is required to achieve adequate blood flow. It is unclear whether this is a mechanism evolved in response to the circulatory difficulties of human bipedalism or merely a serendipitous result of a pre-existing circulatory response[citation needed].
Vertebro-basilar arterial disease[edit]
Arterial disease in the upper spinal cord, or lower brain, causes syncope if there is a reduction in blood supply, which may occur with extending the neck or after drugs to lower blood pressure.
Vasovagal[edit]
Main article: Vasovagal syncope
Vasovagal (situational) syncope, one of the most common types, may occur in scary, embarrassing or uneasy situations, or during blood drawing, coughing ("cough syncope"), urination ("micturition syncope") or defecation ("defecation syncope"). Vasovagal syncope can be considered in two forms:
- Isolated episodes of loss of consciousness, unheralded by any warning symptoms for more than a few moments. These tend to occur in the adolescent age group, and may be associated with fasting, exercise, abdominal straining, or circumstances promoting vaso-dilation (e.g., heat, alcohol). The subject is invariably upright. The tilt-table test, if performed, is generally negative.
- Recurrent syncope with complex associated symptoms. This is so-called neurally mediated syncope (NMS). It is associated with any of the following: preceding or succeeding sleepiness, preceding visual disturbance ("spots before the eyes"), sweating, light-headedness. The subject is usually but not always upright. The tilt-table test, if performed, is generally positive.
A pattern of background factors contributes to the attacks. There is typically an unsuspected relatively low blood volume, for instance, from taking a low-salt diet in the absence of any salt-retaining tendency. Heat causes vaso-dilation and worsens the effect of the relatively insufficient blood volume. That sets the scene, but the next stage is the adrenergic response. If there is underlying fear or anxiety (e.g., social circumstances), or acute fear (e.g., acute threat, needle phobia), the vaso-motor centre demands an increased pumping action by the heart (flight or fight response). This is set in motion via the adrenergic (sympathetic) outflow from the brain, but the heart is unable to meet requirement because of the low blood volume, or decreased return. The high (ineffective) sympathetic activity is always modulated by vagal outflow, in these cases leading to excessive slowing of heart rate. The abnormality lies in this excessive vagal response. The tilt-table test typically evokes the attack.
Much of this pathway was discovered in animal experiments by Bezold (Vienna) in the 1860s. In animals, it may represent a defence mechanism when confronted by danger ("playing possum"). This reflex occurs in only some people and may be similar to that described in other animals.
The mechanism described here suggests that a practical way to prevent attacks might seem counter-intuitive—specifically to block the adrenergic signal with a beta-blocker. A simpler plan might be to explain the mechanism, discuss causes of fear, and optimise salt as well as water intake.[citation needed]
Psychological factors also have been found to mediate syncope. It is important for general practitioners and the psychologist in their primary care team to work closely together, and to help patients identify how they might be avoiding activities of daily living due to anticipatory anxiety in relation to a possible faint and the feared physical damage it may cause. Fainting in response to a blood stimulus, needle or a dead body are common and patients can quickly develop safety behaviours to avoid any recurrences of a fainting response. See link for a good description of psychological interventions and theories.[5]
An evolutionary psychology view is that some forms of fainting are non-verbal signals that developed in response to increased inter-group aggression during the paleolithic. A non-combatant who has fainted signals that she or he is not a threat. This would explain the association between fainting and stimuli such as bloodletting and injuries seen in blood-injection-injury type phobias such as trypanophobia as well as the gender differences.[6]
Deglutition (Swallowing) syncope[edit]
Syncope may occur during deglutition. Manisty et al. note: "Deglutition syncope is characterised by loss of consciousness on swallowing; it has been associated not only with ingestion of solid food, but also with carbonated and ice-cold beverages, and even belching."[7]
Cardiac[edit]
Cardiac arrhythmias[edit]
Most common cause of cardiac syncope. Two major groups of arrhythmias are bradycardia and tachycardia. Bradycardia can be caused by heart blocks. Tachycardias include SVT (supraventricular tachycardia) and VT (ventricular tachycardia). SVT does not cause syncope except in Wolff-Parkinson-White syndrome. Ventricular tachycardia originate in the ventricles. VT causes syncope and can result in sudden death. Ventricular tachycardia, which describes a heart rate of over 100 beats per minute with at least three irregular heartbeats as a sequence of consecutive premature beats, can degenerate into ventricular fibrillation, which requires DC cardioversion.[citation needed]
Typically, tachycardic generated syncope is caused by a cessation of beats following a tachycardic episode. This condition, called tachycardia-bradycardia syndrome, is usually caused by sinoatrial node dysfunction or block or atrioventricular block.[2]
Obstructive cardiac lesion[edit]
Aortic stenosis and mitral stenosis are the most common examples. Aortic stenosis presents with repeated episodes of syncope. A pulmonary embolism can cause obstructed blood vessels. High blood pressure in the arteries supplying the lungs (pulmonary artery hypertension) can occur during pulmonary embolism. Rarely, cardiac tumors such as atrial myxomas can also lead to syncope.
Structural cardiopulmonary disease[edit]
These are relatively infrequent causes of faints. The most common cause in this category is fainting associated with an acute myocardial infarction or ischemic event. The faint in this case is primarily caused by an abnormal nervous system reaction similar to the reflex faints. In general, faints caused by structural disease of the heart or blood vessels are particularly important to recognize, as they are warning of potentially life-threatening conditions. Among other conditions prone to trigger syncope (by either hemodynamic compromise or by a neural reflex mechanism, or both), some of the most important are hypertrophic cardiomyopathy, acute aortic dissection, pericardial tamponade, pulmonary embolism, aortic stenosis, and pulmonary hypertension.
Other cardiac causes[edit]
Sick sinus syndrome, a sinus node dysfunction, causing alternating bradycardia and tachycardia. Often there is a long pause asystole between heartbeat.
Adams-Stokes syndrome is a cardiac syncope that occurs with seizures caused by complete or incomplete heart block. Symptoms include deep and fast respiration, weak and slow pulse and respiratory pauses that may last for 60 seconds.
Aortic dissection (a tear in the aorta) and cardiomyopathy can also result in syncope.[8]
Various medications, such as β-blockers, may cause bradycardia induced syncope.[2]
Blood pressure[edit]
Orthostatic (postural) hypotensive faints are as common or perhaps even more common than vasovagal syncope. Orthostatic faints are most often associated with movement from lying or sitting to a standing position.
Apparently healthy individuals may experience minor symptoms ("lightheadedness", "greying-out") as they stand up if blood pressure is slow to respond to the stress of upright posture. If the blood pressure is not adequately maintained during standing, faints may develop. However, the resulting "transient orthostatic hypotension" does not necessarily signal any serious underlying disease.
The most susceptible individuals are elderly frail individuals, or persons who are dehydrated from hot environments or inadequate fluid intake. More serious orthostatic hypotension is often the result of certain commonly prescribed medications such as diuretics, β-adrenergic blockers, other anti-hypertensives (including vasodilators), and nitroglycerin. In a small percentage of cases, the cause of orthostatic hypotensive faints is structural damage to the autonomic nervous system due to systemic diseases (e.g., amyloidosis or diabetes) or in neurological diseases (e.g., Parkinson's disease).
Other causes[edit]
Factors that influence fainting are fasting long hours, taking in too little food and fluids, low blood pressure, hypoglycemia, high g-force, emotional distress, and lack of sleep. Orthostatic hypotension caused by standing up too quickly or being in a very hot room can also cause fainting. The classic example of a combination of these is seen in the frequent fainting by medical students in the operating theatre during observation of surgery.[9]
More serious causes of fainting include cardiac (heart-related) conditions such as an abnormal heart rhythm (an arrhythmia), wherein the heart beats too slowly, too rapidly, or too irregularly to pump enough blood to the brain. Some arrhythmias can be life-threatening. Other important cardio-vascular conditions that can be manifested by syncope include subclavian steal syndrome and aortic stenosis.
Fainting can also occur following the severe fits of coughing associated with pertussis or "whooping cough."
Diagnostic approach[edit]
For people with uncomplicated syncope (without seizures and a normal neurological exam) computed tomography or MRI is not indicated.[10] Likewise, using carotid ultrasonography on the premise of identifying carotid artery disease as a cause of syncope also is not indicated.[11] Although sometimes investigated as a cause of syncope, carotid artery problems are unlikely to cause that condition.[11]
A hemoglobin count may indicate anemia or blood loss. However, this has been useful in only about 5% of patients evaluated for fainting.[12]
An electrocardiogram (ECG) records the electrical activity of the heart. It is estimated that from 20%-50% of patients have an abnormal ECG. However, while an ECG may identify conditions such as atrial fibrillation, heart block, or a new or old heart attack, it typically does not provide a definite diagnosis for the underlying cause for fainting.[13]
Sometimes, a Holter monitor may be used. This is a portable ECG device that can record the wearer's heart rhythms during daily activities over an extended period of time. Since fainting usually does not occur upon command, a Holter monitor can provide a better understanding of the heart's activity during fainting episodes.
The Tilt table test is performed to elicit orthostatic syncope secondary to autonomic dysfunction (neurogenic).
For patients with more than two episodes of syncope and no diagnosis on “routine testing”, an insertable cardiac monitor might be used. It lasts 28–36 months. Smaller than a pack of gum, it is inserted just beneath the skin in the upper chest area. The procedure typically takes 15 to 20 minutes. Once inserted, the device continuously monitors the rate and rhythm of the heart. Upon waking from a “fainting” spell, the patient places a hand held pager size device called an Activator over the implanted device and simply presses a button. This information is stored and retrieved by their physician and some devices can be monitored remotely.
San Francisco syncope rule[edit]
The San Francisco syncope rule was developed to isolate people who have higher risk for a serious cause of syncope. High risk is anyone who has: congestive heart failure, hematocrit <30%, electrocardiograph abnormality, shortness of breath, or systolic blood pressure <90 mm Hg.[14] The San Francisco syncope rule however was not validated by subsequent studies.[15]
Management[edit]
Recommended acute treatment of vasovagal and orthostatic (hypotension) syncope involves returning blood to the brain by positioning the person on the ground, with legs slightly elevated or leaning forward and the head between the knees for at least 10–15 minutes, preferably in a cool and quiet place. For individuals who have problems with chronic fainting spells, therapy should focus on recognizing the triggers and learning techniques to keep from fainting. At the appearance of warning signs such as lightheadedness, nausea, or cold and clammy skin, counter-pressure maneuvers that involve gripping fingers into a fist, tensing the arms, and crossing the legs or squeezing the thighs together can be used to ward off a fainting spell. After the symptoms have passed, sleep is recommended. If fainting spells occur often without a triggering event, syncope may be a sign of an underlying heart disease. In case syncope is caused by cardiac disease, the treatment is much more sophisticated than that of vasovagal syncope and may involve pacemakers and implantable cardioverter-defibrillators depending on the precise cardiac cause.
Society and culture[edit]
Fainting in women was a commonplace trope or stereotype in Victorian England and in contemporary and modern depictions of the period. This may have been partly due to genuine ill-health (the respiratory effects of corsets are frequently cited), but it was fashionable for women to affect an aristocratic frailty and create a scene by fainting at a dramatic moment.[citation needed]
Some individuals occasionally or frequently play the "fainting game" (also referred to in the US as the "choking game"), which involves the deliberate induction of syncope via voluntary restriction of blood flow to the brain, an action that can result in acute or cumulative brain damage and even death.[16]
References[edit]
- ^ Reeves, Alexander G; Rand S. Swenson. "Chapter 14: Evaluation of the Dizzy Patient". Disorders of the nervous system: a primer. Dartmouth Medical School. Retrieved 2012-01-06.
- ^ a b c Freeman, Roy (2011). "Chapter 20: Syncope". In Longo, Dan L.; Kasper, Dennis L.; Jameson, J. Larry; Fauci, Anthony S.; Hauser, Stephen L.; Loscalzo, Joseph. Harrison's Principles of Internal Medicine (Textbook) (18th ed.). New York, NY: The McGraw-Hill Companies. pp. 171–177. ISBN 978-0-07-174889-6.
- ^ Ruwald MH, Hansen ML, Lamberts M, et al. (October 2012). "The relation between age, sex, comorbidity, and pharmacotherapy and the risk of syncope: a Danish nationwide study". Europace 14 (10): 1506–14. doi:10.1093/europace/eus154. PMID 22588456.
- ^ Sun BC, Emond JA, Camargo CA (October 2004). "Characteristics and admission patterns of patients presenting with syncope to U.S. emergency departments, 1992-2000". Acad Emerg Med 11 (10): 1029–34. doi:10.1197/j.aem.2004.05.032. PMID 15466144. .
- ^ Gaynor D, Egan J (2011). "Vasovagal syncope (the common faint): what clinicians need to know". The Irish Psychologist 37 (7): 176–9. hdl:10147/135366.
- ^ Bracha HS (July 2006). "Human brain evolution and the 'Neuroevolutionary Time-depth Principle:' Implications for the Reclassification of fear-circuitry-related traits in DSM-V and for studying resilience to warzone-related posttraumatic stress disorder". Prog. Neuropsychopharmacol. Biol. Psychiatry 30 (5): 827–53. doi:10.1016/j.pnpbp.2006.01.008. PMID 16563589.
- ^ Manisty C, Hughes-Roberts Y, Kaddoura S (July 2009). "Cardiac manifestations and sequelae of gastrointestinal disorders". Br J Cardiol 16 (4): 175–80. Retrieved 11 May 2013.
- ^ Nallamothu BK, Mehta RH, Saint S, et al. (October 2002). "Syncope in acute aortic dissection: diagnostic, prognostic, and clinical implications". Am. J. Med. 113 (6): 468–71. doi:10.1016/S0002-9343(02)01254-8. PMID 12427495.
- ^ Jamjoom AA, Nikkar-Esfahani A, Fitzgerald JE (2009). "Operating theatre related syncope in medical students: a cross sectional study". BMC Med Educ 9: 14. doi:10.1186/1472-6920-9-14. PMC 2657145. PMID 19284564.
- ^ Moya A, Sutton R, Ammirati F, et al. (November 2009). "Guidelines for the diagnosis and management of syncope (version 2009)". Eur. Heart J. 30 (21): 2631–71. doi:10.1093/eurheartj/ehp298. PMC 3295536. PMID 19713422.
- ^ a b American Academy of Neurology (February 2013), "Five Things Physicians and Patients Should Question", Choosing Wisely: an initiative of the ABIM Foundation (American Academy of Neurology), retrieved August 1, 2013 , which cites
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- Strickberger, S. A.; Benson, D. W.; Biaggioni, I.; Callans, D. J.; Cohen, M. I.; Ellenbogen, K. A.; Epstein, A. E.; Friedman, P.; Goldberger, J.; Heidenreich, P. A.; Klein, G. J.; Knight, B. P.; Morillo, C. A.; Myerburg, R. J.; Sila, C. A.; American Heart Association Councils On Clinical Cardiology (2006). "AHA/ACCF Scientific Statement on the Evaluation of Syncope: From the American Heart Association Councils on Clinical Cardiology, Cardiovascular Nursing, Cardiovascular Disease in the Young, and Stroke, and the Quality of Care and Outcomes Research Interdisciplinary Working Group; and the American College of Cardiology Foundation: In Collaboration with the Heart Rhythm Society: Endorsed by the American Autonomic Society". Circulation 113 (2): 316–327. doi:10.1161/CIRCULATIONAHA.105.170274. PMID 16418451. edit
- Moya, A.; European Society of Cardiology (ESC); Sutton, R.; European Heart Rhythm Association (EHRA); Ammirati, F.; and Heart Rhythm Society (HRS); Blanc, J.-J.; Endorsed by the following societies; Brignole, M.; European Society of Emergency Medicine (EuSEM); Moya, J. B.; European Federation of Internal Medicine (EFIM); Sutton, J.-C.; European Union Geriatric Medicine Society (EUGMS); Ammirati, J.; Blanc, K.; European Neurological Society (ENS); Brignole, A.; European Federation of Autonomic Societies (EFAS); Dahm, M.; Deharo, M.; Gajek, T.; Gjesdal, R. R.; Krahn, F.; Massin, A.; Pepi, J. G.; Pezawas, E. P.; Ruiz Granell, W.; Sarasin, H.; Ungar, D. G. et al. (2009). "Guidelines for the diagnosis and management of syncope (version 2009): The Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology (ESC)". European Heart Journal 30 (21): 2631–2671. doi:10.1093/eurheartj/ehp298. PMC 3295536. PMID 19713422. edit
- NICE (August 2010), Transient loss of consciousness in adults and young people (CG109), NICE, retrieved 24 October 2013
- ^ Grubb (2001) p.83
- ^ Grubb (2001) pp.83-84
- ^ Quinn J, McDermott D, Stiell I, Kohn M, Wells G (May 2006). "Prospective validation of the San Francisco Syncope Rule to predict patients with serious outcomes". Ann Emerg Med 47 (5): 448–54. doi:10.1016/j.annemergmed.2005.11.019. PMID 16631985. Lay summary – Journal Watch (July 21, 2006).
- ^ Birnbaum A, Esses D, Bijur P, Wollowitz A, Gallagher EJ (August 2008). "Failure to validate the San Francisco Syncope Rule in an independent emergency department population". Ann Emerg Med 52 (2): 151–9. doi:10.1016/j.annemergmed.2007.12.007. PMID 18282636.
- ^ "'Choking Game' Becoming Deadly Fad For Adolescents". WJZ-TV Baltimore. 2005-11-04. Archived from the original on 2007-12-19. Retrieved 2008-02-13.
Further reading[edit]
- Grubb, Blair P. The Fainting Phenomenon; Understanding Why People Faint and What to Do About It. 2001. 2nd ed. New York: Blackwell Publishing, 2007
External links[edit]
- 2004 European Society of Cardiology Guidelines on Management (Diagnosis and Treatment) of Syncope.
- Dysautonomia International[1]
- Dysautonomia Information Network
- Tilt table test
- The San Francisco syncope rule
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Symptoms and signs: cognition, perception, emotional state and behaviour (R40–R46, 780.0–780.5, 781.1)
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| Cognition |
Alteration of
consciousness |
- Confusion (Delirium)
- Somnolence
- Obtundation
- Stupor
- Unconsciousness
- Syncope
- Coma
- Persistent vegetative state
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| Fainting/Syncope |
- Carotid sinus syncope
- Heat syncope
- Vasovagal episode
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| Other |
- Amnesia
- Anterograde amnesia
- Retrograde amnesia
- Dizziness
- Vertigo
- Presyncope/Lightheadedness
- Disequilibrium
- Convulsion
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|
|
| Emotional state |
- Anxiety
- Irritability
- Hostility
- Suicidal ideation
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|
| Behavior |
|
|
Perception/
sensation
disorder |
- Olfaction : Anosmia
- Hyposmia
- Dysosmia
- Parosmia
- Phantosmia
- Hyperosmia
- Taste: Ageusia
- Hypogeusia
- Dysgeusia
- Parageusia
- Hypergeusia
- Hallucination: Auditory hallucination
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dsrd (o, p, m, p, a, d, s), sysi/epon, spvo
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proc (eval/thrp), drug (N5A/5B/5C/6A/6B/6D)
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