Syncope (/ˈsɪŋkəpi/ SING-kə-pee), also known as fainting or passing out, is defined as a short loss of consciousness and muscle strength, characterized by a fast onset, short duration, and spontaneous recovery. It is due to a decrease in blood flow to the entire brain usually from low blood pressure. Some causes have prodromal symptoms before the loss of consciousness occurs. These symptoms may include light headedness, sweating, pale skin, blurred vision, nausea, vomiting, and feeling warm among others. Syncope may also be associated with a short episode of muscle twitching. If a person does not completely lose consciousness and muscle strength it is referred to as presyncope. It is recommended that presyncope be treated the same as syncope.[1]

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 or strong feelings or a specific activity such as urination, vomiting, or coughing. This type of syncope may also occur when an area in the neck known as the carotid sinus is pressed. The final type of syncope is due to a drop in blood pressure from standing up. This is often due to medications that a person is taking but may also be related to dehydration, significant bleeding or infection.[1]

A medical history, physical examination, and electrocardiogram (ECG) are the most e ective ways to figure out the underlying cause. The ECG is useful to detect an abnormal heart rhythm, poor blood flow to the heart muscle, and other electrical issue such as long QT syndrome and Brugada’s. 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. Computer tomography (CT) is generally not required unless specific concerns are present. Other causes of

similar symptoms that should be considered including 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.[1]

Syncope a ects about three to six out of every thousand people each year.[1] 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 hospital. 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 life.[2] Of all those with syncope about 4% die in the next 30 days.[1] The risk of a bad outcome, however, depends very much on the underlying cause.[3]

1 Etymology

The term is derived from the Late Latin syncope, from Ancient Greek συγκοπή (sunkopē), from σύν (sin, “together, thoroughly”) and κόπτειν (koptein, “strike, cut o ”).

2 Di erential diagnosis

2.1 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 e ect combined with the following collapse can make a strong and dramatic impression on bystanders.

The weakness of the legs causes most su erers to sit or lie down if there is time to do so. This may avert a complete collapse, but whether the su erer sits down or falls down, the result of an ischaemic episode is a posture in which