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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. 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".
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 older age. Estimates of lifetime incidence of at least one syncopal episode include 40 to 50 percent of the general population. Syncope comprises 1 to 3 percent of all attendances to emergency departments and 1 to 6 percent of all hospital admissions.
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 .
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 (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:
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.
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.
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."
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.
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.
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.
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.
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.
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.
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.
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).
For people with uncomplicated syncope (without seizures and a normal neurological exam) 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.
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.
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.
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.
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.
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.
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.
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