Syncope, 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 that most often results from hypotension.
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.
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, loss of hearing, loss of pain and
feeling, 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". There are three broad categories of syncope:
cardiogenic, reflex 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 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.
Etymology The term is derived from the Late Latin syncope,
from Ancient Greek συγκοπή, from σύν and κόπτειν.
Differential diagnosis Central nervous system ischaemia
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 .
Vertebro-basilar arterial disease 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
Vasovagal syncope, one of the most common types, may occur in scary, embarrassing or
uneasy situations, or during blood drawing, coughing, urination or defecation. 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. 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. It is associated with any of the
following: preceding or succeeding sleepiness, preceding visual disturbance, 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, or acute fear, the vaso-motor centre demands an increased pumping action
by the heart. This is set in motion via the adrenergic outflow from the brain, but the
heart is unable to meet requirement because of the low blood volume, or decreased return.
The high 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 in the 1860s. In animals, it may represent a defence mechanism when
confronted by danger. 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.
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.
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.
Deglutition syncope 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." Cardiac
Cardiac arrhythmias 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 and VT. 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. 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. Obstructive cardiac lesion
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 can occur during pulmonary embolism.
Rarely, cardiac tumors such as atrial myxomas can also lead to syncope.
Structural cardiopulmonary disease 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, some of the most important are hypertrophic cardiomyopathy, acute aortic
dissection, pericardial tamponade, pulmonary embolism, aortic stenosis, and pulmonary hypertension.
Other cardiac causes 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 and cardiomyopathy can also
result in syncope. Various medications, such as β-blockers,
may cause bradycardia induced syncope. Blood pressure
Orthostatic 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 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, 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 or in neurological diseases.
Other causes 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.
More serious causes of fainting include cardiac conditions such as an 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. 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
For people with uncomplicated syncope computed tomography or MRI is not indicated. Likewise,
using carotid ultrasonography on the premise of identifying carotid artery disease as a
cause of syncope also is not indicated. Although sometimes investigated as a cause of syncope,
carotid artery problems are unlikely to cause that condition.
A hemoglobin count may indicate anemia or blood loss. However, this has been useful
in only about 5% of patients evaluated for fainting.
An electrocardiogram 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.
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.
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 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. The San Francisco syncope rule however
was not validated by subsequent studies. Management
Recommended acute treatment of vasovagal and orthostatic 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
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, but it was fashionable for women to affect an aristocratic frailty and create
a scene by fainting at a dramatic moment. Some individuals occasionally or frequently
play the "fainting 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. See also
Voodoo death References
Further reading 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
2004 European Society of Cardiology Guidelines on Management of Syncope.
Dysautonomia International [1] Dysautonomia Information Network
Tilt table test The San Francisco syncope rule