September 20, 2019
Syncope (medicine)

Syncope (medicine)

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

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