Syncope (medicine)
Syncope, commonly known as fainting or passing out, is a loss of consciousness and muscle strength characterized by a fast onset, short duration, and spontaneous recovery. It is caused by a decrease in blood flow to the brain, typically from low blood pressure. 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. Psychiatric causes can also be determined when a patient experiences fear, anxiety, or panic; particularly before a stressful event, usually medical in nature. When consciousness and muscle strength are not completely lost, it is called presyncope. It is recommended that presyncope be treated the same as syncope.
Causes range from non-serious to potentially fatal. There are three broad categories of causes: heart or blood vessel related; reflex, also known as neurally mediated; and orthostatic hypotension. 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. 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. Neurally mediated syncope occurs when blood vessels expand and heart rate decreases inappropriately. 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. Neurally mediated syncope may also occur when an area in the neck known as the carotid sinus is pressed. The third type of syncope is due to a drop in blood pressure when changing position, such as when standing up. This is often due to medications that a person is taking, but may also be related to dehydration, significant bleeding, or infection. There also seems to be a genetic component to syncope.
A medical history, physical examination, and electrocardiogram are the most effective ways to determine the underlying cause. The ECG is useful to detect an abnormal heart rhythm, poor blood flow to the heart muscle and other electrical issues, such as long QT syndrome and Brugada syndrome. Heart related causes also often have little history of a prodrome. 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. More specific tests such as implantable loop recorders, tilt table testing or carotid sinus massage may be useful in uncertain cases. Computed tomography is generally not required unless specific concerns are present. 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. Treatment depends on the underlying cause. Those who are considered at high risk following investigation may be admitted to hospital for further monitoring of the heart.
Syncope affects approximately three to six out of every thousand people each year. It is more common in older people and females. It is the reason for one to three percent of visits to emergency departments and admissions to hospitals. 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. Of those presenting with syncope to an emergency department, about 4% died in the next 30 days. The risk of a poor outcome, however, depends on the underlying cause.
Causes
Causes range from non-serious to potentially fatal. There are three broad categories of causes: heart or blood vessel related; reflex, also known as neurally mediated; and orthostatic hypotension. 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.There also seems to be a genetic component to syncope. A recent genetic study has identified the first risk locus for syncope and collapse. The lead genetic variant, residing at chromosome 2q31.1, is an intergenic variant approximately 250 kb downstream of the ZNF804A gene. The variant affected the expression of ZNF804A, making this gene the strongest driver of the association.
Neurally mediated syncope
or neurally mediated syncope occurs when blood vessels expand and heart rate decreases inappropriately leading to poor blood flow to the brain. This may occur from either a triggering event such as exposure to blood, pain, or strong feelings, or from a specific activity such as urination, vomiting, or coughing.Vasovagal syncope
Vasovagal 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 that all fall under the umbrella of vasovagal syncope related by the same central mechanism. First, the person is usually predisposed to decreased blood pressure by various environmental factors. A lower than expected blood volume, for instance, from taking a low-salt diet in the absence of any salt-retaining tendency, or heat causing vaso-dilation and worsening the effect of the relatively insufficient blood volume. 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 requirements because of the low blood volume or decreased return. A feedback response to the medulla is triggered via the afferent vagus nerve. The high sympathetic activity is thereby modulated by vagal outflow, leading to excessive slowing of heart rate. The abnormality lies in this excessive vagal response, causing loss of blood flow to the brain. The tilt-table test typically evokes the attack. Avoiding what provokes the syncope and possibly greater salt intake is often all that is needed.Associated symptoms may be felt in the minutes leading up to a vasovagal episode and are referred to as the prodrome. These consist of light-headedness, confusion, pallor, nausea, salivation, sweating, tachycardia, blurred vision, and a sudden urge to defecate, among other symptoms.
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 neurally mediated syncope. It is associated with any of the following: preceding or succeeding sleepiness, preceding visual disturbance, sweating, lightheadedness. The subject is usually but not always upright. The tilt-table test, if performed, is generally positive. It is relatively uncommon.
Another 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 they are 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.
Much of this pathway was discovered in animal experiments by Bezold in the 1860s. In animals, it may represent a defense mechanism when confronted by danger. A 2023 study identified neuropeptide Y receptor Y2 vagal sensory neurons and the periventricular zone as a coordinated neural network participating in the cardioinhibitory Bezold–Jarisch reflex regulating fainting and recovery.
Situational syncope
Syncope may be caused by specific behaviors, including coughing, urination, defecation, vomiting, swallowing, and following exercise. 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." Fainting can occur in "cough syncope" following severe fits of coughing, such as that associated with pertussis or "whooping cough". Neurally mediated syncope may also occur when an area in the neck known as the carotid sinus is pressed. A normal response to carotid sinus massage is a reduction in blood pressure and slowing of the heart rate. Especially in people with hypersensitive carotid sinus syndrome, this response can cause syncope or presyncope.Cardiac
Heart-related causes may include an abnormal heart rhythm, problems with the heart valves or heart muscle, or blockages of blood vessels from a pulmonary embolism or aortic dissection, among others.Cardiac arrhythmias
The most common cause of cardiac syncope is cardiac 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.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 originates 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 and defibrillation.
Long QT syndrome can cause syncope when it sets off ventricular tachycardia or torsades de pointes. The degree of QT prolongation determines the risk of syncope. Brugada syndrome also commonly presents with syncope secondary to arrhythmia.
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.