Syncope (medicine)

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For other uses, see Syncope.
"Fainting" redirects here. For other uses, see Faint.
"Passing out" redirects here. For the completion of a military course, see Passing out (military).

Syncope

Other names Fainting, passing out, swooning

A 1744 oil painting by Pietro Longhi called Fainting

 /ˈsɪŋkəpi/ SING-kə-pee
Pronunciation

Specialty Neurology, cardiology

Symptoms Loss of consciousness and muscle strength[1]

Usual onset Fast onset[1]

Duration Short duration[1]

Types Cardiac, reflex, orthostatic hypotension[1]

Causes Decrease in blood flow to brain[1]

Diagnostic method Medical history, physical

examination, electrocardiogram[1]
 Treatment Based on underlying cause[2]

Prognosis Depends on underlying cause[2]

Frequency ~5 per 1,000 per year[1]

Syncope, also known as fainting, is a loss of consciousness and muscle strength characterized by
a fast onset, short duration, and spontaneous recovery.[1] It is caused by a decrease in blood flow to
the brain, typically from low blood pressure.[1] There are sometimes symptoms before the loss of
consciousness such as lightheadedness, sweating, pale skin, blurred vision, nausea, vomiting, or
feeling warm. Syncope may also be associated with a short episode of muscle twitching.[1] When
consciousness and muscle strength are not completely lost, it is called presyncope.[1] It is
recommended that presyncope be treated the same as syncope.[1]
Causes range from non-serious to potentially fatal.[1] There are three broad categories of
causes: heart or blood vessel related, reflex also known as neurally mediated, and orthostatic
hypotension.[1] Issues with the heart and blood vessels are the cause in about 10% and typically the
most serious while neurally mediated is the most common.[1] Heart related causes may include
an abnormal heart rhythm, problems with the heart valves or heart muscle and blockages of blood
vessels from a pulmonary embolism or aortic dissection among others.[1] Neurally mediated syncope
occurs when blood vessels expand and heart rate decreases inappropriately.[1] This may occur from
either a triggering event such as exposure to blood, pain, strong feelings or a specific activity such
as urination, vomiting, or coughing.[1] This type of syncope may also occur when an area in the neck
known as the carotid sinus is pressed.[1] The third type of syncope is due to a drop in blood pressure
from standing up.[1] This is often due to medications that a person is taking but may also be related
to dehydration, significant bleeding or infection.[1]
A medical history, physical examination, and electrocardiogram (ECG) are the most effective ways
to determine the underlying cause.[1] The ECG is useful to detect an abnormal heart rhythm, poor
blood flow to the heart muscle, and other electrical issue such as long QT syndrome and Brugada
syndrome.[1] Heart related causes also often have little history of a prodrome.[1] Low blood pressure
and a fast heart rate after the event may indicate blood loss or dehydration, while low blood oxygen
levels may be seen following the event in those with pulmonary embolism.[1] More specific tests such
as implantable loop recorders, tilt table testing or carotid sinus massage may be useful in uncertain
cases.[1] Computed tomography (CT) is generally not required unless specific concerns are
present.[1] Other causes of similar symptoms that should be considered
include seizure, stroke, concussion, low blood oxygen, low blood sugar, drug intoxication and some
psychiatric disorders among others.[1] Treatment depends on the underlying cause.[1] Those who are
considered at high risk following investigation may be admitted to hospital for further monitoring of
the heart.[1]
Syncope affects about three to six out of every thousand people each year.[1] It is more common in
older people and females.[3]It is the reason for one to three percent of visits to emergency
departments and admissions to hospital.[3] Up to half of women over the age of 80 and a third of
medical students describe at least one event at some point in their lives.[3] Of those presenting with
syncope to an emergency department, about 4% died in the next 30 days.[1] The risk of a poor
outcome, however, depends very much on the underlying cause.[2]

Contents

 1Differential diagnosis
o 1.1Central nervous system ischemia
 o 1.2Vasovagal
o 1.3Cardiac
o 1.4Blood pressure
o 1.5Other causes
 2Diagnostic approach
o 2.1Imaging
o 2.2San Francisco syncope rule
o 2.3Differential diagnosis
 3Management
 4Society and culture
o 4.1Etymology
 5See also
 6References
 7External links

Differential diagnosis[edit]
Central nervous system ischemia[edit]
The central ischemic 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 is one of the most common types which may occur in response to
any of a variety of triggers, such as scary, embarrassing or uneasy situations, during blood drawing,
or moments of sudden unusually high stress. There are many different syncope syndromes which all
fall under the umbrella of vasovagal syncope related by the same central mechanism, such as
urination ("micturition syncope"), defecation ("defecation syncope"), and others related to trauma and
stress.
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 neurally mediated syncope
(NMS). It is associated with any of the following: preceding or succeeding sleepiness, preceding
visual disturbance ("spots before the eyes"), sweating, lightheadedness. The subject is usually
but not always upright. The tilt-table test, if performed, is generally positive. It is relatively
uncommon.
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. 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").
Avoiding what brings on the syncope and possibly greater salt intake is often all that is needed.[4]
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 needle
phobia 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]

Syncope from bradycardia

Cardiac arrhythmias[edit]
The most common cause of cardiac syncope is cardiac arrhythmia (abnormal heart rhythm) wherein
the heart beats too slowly, too rapidly, or too irregularly to pump enough blood to the brain. Some
arrhythmias can be life-threatening.
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 is rapidly fatal without cardiopulmonary resuscitation (CPR) and defibrillation.[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.[8]
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 and is
the cause of syncope in less than 1% of people who present to the emergency
department.[9][10] Rarely, cardiac tumors such as atrial myxomas can also lead to syncope.
Structural cardiopulmonary disease[edit]
These are relatively infrequent causes of fainting. 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 heartbeats.
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.
Subclavian steal syndrome arises from retrograde (reversed) flow of blood in the vertebral artery or
the internal thoracic artery, due to a proximal stenosis (narrowing) and/or occlusion of the subclavian
artery.
Aortic dissection (a tear in the aorta) and cardiomyopathy can also result in syncope.[11]
Various medications, such as beta blockers, may cause bradycardia induced syncope.[8]
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, standing up too quickly, or being in a very hot room. 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.[12]
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, low blood sugar, high g-force, emotional distress, and lack of sleep.
One theory in evolutionary psychology is that fainting at the sight of blood might have evolved as a
form of playing dead which increased survival from attackers and might have slowed blood loss in a
primitive environment.[13] "Blood-injury phobia", as this is called, is experienced by about 15% of
people.[14]
Fainting can occur in "cough syncope" following severe fits of coughing, such as that associated
with pertussis or "whooping cough."[15]

Diagnostic approach[edit]
A hemoglobin count may indicate anemia or blood loss. However, this has been useful in only about
5% of people evaluated for fainting.[16]
An electrocardiogram (ECG) records the electrical activity of the heart. It is estimated that from 20%-
50% of people 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.[17]
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 people 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-sized 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.
Imaging[edit]
For people with uncomplicated syncope (without seizures and a normal neurological
exam) computed tomography or MRI is not generally indicated.[18][19] Likewise, using carotid
ultrasonography on the premise of identifying carotid artery disease as a cause of syncope also is
not indicated.[20] Although sometimes investigated as a cause of syncope, carotid artery problems are
unlikely to cause that condition.[20] Additionally an electroencephalogram (EEG) is generally not
recommended.[21]
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 mmHg.[22] The
San Francisco syncope rule however was not validated by subsequent studies.[23]
Differential diagnosis[edit]
Other diseases which mimic syncope include seizure, low blood sugar, and certain types of stroke.
While these may appear as "fainting", they do not fit the strict definition of syncope being a sudden
reversible loss of consciousness due to decreased blood flow to the brain.

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.
Falling-out is a culture-bound syndrome primarily reported in the southern United States and
the Caribbean.
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.[24]