| ICD-10 | R55 |
|---|---|
| ICD-9 | 780.2 |
| DiseasesDB | 27303 |
| eMedicine | med/3385 ped/2188 emerg/876 |
| MeSH | D013575 |
Syncope ( /ˈsɪŋkəpi/ sing-kə-pee), the medical term for fainting, is precisely 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.
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". Abdominal discomfort prior to loss of consciousness may be indicative of seizure which should be considered different than syncope.[1]
There are two broad categories of syncope, cardiogenic or reflex syncope 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 which are made evident by 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 loop recorders may be necessary in clinically uncertain cases.
Syncope does not occur with hypoxia which can lead to death by suffocation and does not fulfill the definition of syncope above. Syncope needs to be distinguished from coma or cerebrovascular accident which can include persistent states of loss of consciousness.
Although syncope may cause physical injury such as head trauma, it is specifically not directly caused by head trauma (concussion) or by a seizure disorder which may also produce short-lived unconsciousness unless these are also associated with globally reduced brain blood flow. Syncope is extraordinarily common occurring for the most part in two age ranges: the teen age years, and during older age. Estimates of lifetime incidence of at least one syncopal episode include 40-50% of the general populace.
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The central ischaemic response is triggered by an inadequate 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—one of the most common types—may occur in scary, embarrassing or uneasy situations, or during blood drawing, coughing, urination or defecation. Other types include postural syncope (caused by a changing in body posture), cardiac syncope (due to heart-related conditions), and neurological syncope (due to neurological conditions). There are many other causes of syncope, including low blood-sugar levels and lung disease such as emphysema and a pulmonary embolus. The cause of the fainting can be determined by a doctor using a complete history, physical, and various diagnostic tests.
The vasovagal type 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-dilatation 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 would be, what might seem to be counterintuitive, 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 liaise closely 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 [1].
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.[2]
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."[3]
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.
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.[1]
Aortic stenosis and mitral stenosis are the most common examples. Aortic stenosis presents with repeated episodes of syncope. 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 which may occur 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.
Various medications, such as β-blockers, may cause bradycardia induced syncope.[1]
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).
Factors that influence fainting are fasting long hours, taking in too little food and fluids, low blood pressure, hypoglycemia, growth spurts, physical exercise in excess of the energy reserve of the body, 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.
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.
If one is suffering from syncope, there are many underlying causes that may be contributing to the episodes. It is important to understand that there is no master list of tests that are currently being used to diagnose the underlying cause(s). However, there are some common diagnostic tests for fainting.
A hemoglobin count may indicate anemia or blood loss. However, this has been shown to be useful in only about 5% of patients being evaluated for fainting.[4]
An electrocardiogram (ECG) records the electrical activity of the heart. It is estimated that from 20%-50% of patients will 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.[5]
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 14 to 18 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.
The San Francisco syncope rule was developed to isolate patients who have higher risk for a serious cause of syncope. Anyone with high risk criteria needs to be further investigated. They are summed up by the CHESS mnemonic: congestive heart failure, hematocrit <30%, electrocardiogram abnormality, shortness of breath, or systolic blood pressure <90 mm Hg.[6]
Recommended treatment 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. As the dizziness and the momentary blindness passes, the person may experience a brief period of visual disturbances in the form of phosphenes, sudden sore throat, nausea, and general shakiness. 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.
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.[7]
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