This allows blood to pool in your legs, which lowers your blood pressure. Combined, the drop in blood pressure and slowed heart rate quickly reduce blood flow to your brain, and you faint. You may not always be able to avoid a vasovagal syncope episode. If you feel like you might faint, lie down and lift your legs.
This allows gravity to keep blood flowing to your brain. If you can't lie down, sit down and put your head between your knees until you feel better. Mayo Clinic does not endorse companies or products. Advertising revenue supports our not-for-profit mission. This content does not have an English version. This content does not have an Arabic version.
Overview Vasovagal syncope vay-zoh-VAY-gul SING-kuh-pee occurs when you faint because your body overreacts to certain triggers, such as the sight of blood or extreme emotional distress.
Request an Appointment at Mayo Clinic. More Information Fainting during urination micturition syncope : What causes it? Simply put, neurocardiogenic syncope is a miscommunication between the heart, the blood vessels in the lower extremities, and the brain. There are multiple names for neurocardiogenic syncope. These include, but are not limited to: neurally mediated syncope, vasovagal syncope, vasodepressor syncope, and reflex syncope. It may also be referred to by the mechanism that causes the syncope, i.
Although the mechanism of neurocardiogenic syncope is not completely understood, it seems to be an exaggerated response to a compensatory mechanism which occurs when a person is in the upright position for a prolonged period of time.
It is quite normal for blood to pool in the lower extremities when a person is in an upright position. This will initially cause an increase in heart rate and slight decrease in blood pressure. Most people will compensate for these minor changes without feeling any different.
For patients with neurocardiogenic syncope, this triggers an exaggerated response. The lack of blood volume in the left ventricle, caused from the peripheral venous pooling, results in hypotension. The decrease in blood pressure will cause a response in the baroreceptors found in the aortic arch and carotid sinus, which will subsequently send signals to parts of the brain controlling the vagus nerve.
In addition, mechanoreceptors, otherwise known as C fibers, found in the heart are activated. The end result is even more severe hypotension and bradycardia.
This profound response leads to presyncope and eventually syncope. Although not a critical disease in itself, many patients may suffer from a variety of symptoms which vary in frequency and severity.
These symptoms not only are bothersome, but can lead to life-threatening injuries. A large number of these patients are evaluated following a motor vehicle accident secondary to a syncopal episode while driving. It is crucial to determine the etiology of syncope so that proper treatment can be instituted and injury to the patient or others is avoided. Performing a thorough history and physical can elicit invaluable information. Knowing the circumstances surrounding the patient s near syncopal or syncopal episode provides direction for workup.
Neurocardiogenic syncope often occurs in patients who are dehydrated. Dehydration may be a result of inappropriate fluid intake, excessive activity or perspiration, physical illness, excessive caffeine or excessive alcohol intake. Emotional stress and physical stress also may be precipitating factors. Position of the patient at the time of presyncope or syncope is also very helpful. A presyncopal or syncopal episode occurring as a result of neurocardiogenic syncope rarely occurs when a patient is supine.
Typically, these patients are either standing or sitting. A position with their feet below the level of the heart predisposes these patients to symptoms and possible loss of consciousness. Neurocardiogenic syncope used to be referred to as church syncope, because standing upright for prolonged periods of time in closed-in, warm environments such as church services frequently caused people to pass out.
Know the circumstances surrounding each episode. Premonitory symptoms vary in patients with neurocardiogenic syncope. Often these patients will have some type of warning prior to loss of consciousness. Symptoms include dizziness, warmth, diaphoresis, vision disturbances, nausea, or vomiting. Infrequently, patients may have abrupt loss of consciousness with no warning. Patients may have seizure activity associated with their loss of consciousness and are at times treated erroneously for a seizure disorder.
After regaining consciousness, many patients feel completely normal, although some continue to complain of headache or fatigue. When evaluating patients, probe into their childhood history as well.
Ask them if they recall having similar episodes when they were younger, and if so, what circumstances surrounded these episodes. Although they may have never actually lost consciousness before, many people can recall "dizzy spells" or near syncope at other times in their lives.
Patients that describe this type of scenario are often admitted for head up tilt testing. Head up tilt testing can be performed utilizing different methods. No matter which method is chosen by the physician, patients are asked not to take anything by mouth for at least six hours prior to the test.
Some physicians will order intravenous fluids to be administered. According to the ACC Expert Consensus Document, it is recommended that intravenous fluid replacement should be 75 milliliters for each hour of fasting.
However, some physicians prefer no fluid load prior to tilt testing. Passive tilt table testing is one method used to assess for neurocardiogenic or vasodepressor syncope.
Patients are brought into a dimly lit room and positioned on a tilt table that has a firm footrest. A minimum of two straps are used to restrain the patient in the event they lose consciousness and collapse. Patients are in a supine position while they are connected to a monitoring system s and blood pressure is checked. Patients will remain in this position for approximately 45 minutes, or until they become symptomatic.
Blood pressure and heart rate are monitored every three to five minutes. Isoproterenol is a common medication used for provocation of neurocardiogenic syncope. Specific Isoproterenol protocols vary from facility to facility. Isoproterenol may help elicit symptoms in patients that have had negative passive tilts. Postural Tachycardia Syndrome. Last updated: March 3, Accessed: March 2, Orthostatic hypotension.
Am Fam Physician. Am J Hypertens. Last updated: August 10, Pathophysiology and diagnosis of vertebrobasilar insufficiency: A review of the literature. Int Arch Otorhinolaryngol.
Reflex syncope. Last updated: August 14, Syncope: Evaluation and Differential Diagnosis.. Mellusi J. Differential diagnosis of syncope.. Anesth Prog. Heart 's inability to meet an increased oxygen demand e. Arrhythmogenic syncope. Sick sinus syndrome Ventricular tachycardia Atrioventricular block Supraventricular arrhythmias Adams-Stokes syndrome Torsades de pointes. Cardiovascular syncope. Structural outflow obstruction. Massive MI Aortic stenosis Mitral valve prolapse Atherosclerosis Pulmonary embolism Pulmonary hypertension Hypertrophic cardiomyopathy Severe asymmetric septal hypertrophy Cardiac tamponade.
Neurocardiogenic syncope subtype of vasovagal syncope. Prolonged standing and no compensatory heart rate acceleration. Common in younger patients unusual to have first episode after age 40 Can be recurrent.
Emotional syncope subtype of vasovagal syncope. Pain or emotional stress. Pain Fear Sight of blood Injury. Carotid sinus syndrome.
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