|Synonyms||Vasovagal episode, vasovagal response, neurocardiogenic syncope|
Vasovagal syncope is a sudden brief loss of consciousness (syncope) due to activation of the vagus nerve. This activation may occur due to triggers, such as the sight of blood or emotional distress. The underlying mechanism involves the sudden drop in blood pressure. It is the most common type of fainting.
There are different syncope syndromes that fall under the umbrella of vasovagal syncope. The common element among these conditions is the central mechanism which may lead to the loss of consciousness. The differences among them are in the factors that trigger this mechanism.
Signs and symptoms
Episodes of vasovagal syncope are typically recurrent and usually occur when the predisposed person is exposed to a specific trigger. Before losing consciousness, the individual frequently experiences early signs or symptoms such as lightheadedness, nausea, the feeling of being extremely hot or cold (accompanied by sweating), ringing in the ears, an uncomfortable feeling in the heart, fuzzy thoughts, confusion, a slight inability to speak or form words (sometimes combined with mild stuttering), weakness and visual disturbances such as lights seeming too bright, fuzzy or tunnel vision, black cloud-like spots in vision, and a feeling of nervousness can occur as well. The symptoms may become more intense over several seconds to several minutes before the loss of consciousness (if it is lost). Onset usually occurs when a person is sitting up or standing.
When people lose consciousness, they fall down (unless prevented from doing so) and, when in this position, effective blood flow to the brain is immediately restored, allowing the person to regain consciousness. If the person does not fall into a fully flat, supine position, and the head remains elevated above the trunk, a state similar to a seizure may result from the blood's inability to return quickly to the brain, and the neurons in the body will fire off and generally cause muscles to twitch very slightly but mostly remain very tense. Fainting occurs with a loss of oxygen to the brain.
The autonomic nervous system's physiological state (see below) leading to loss of consciousness may persist for several minutes, so
- If sufferers try to sit or stand when they wake up, they may pass out again
- The person may be nauseated, pale, and sweaty for several minutes or hours
Vasovagal syncope occurs in response to a trigger due to dysfunction of the heart rate and blood pressure regulating mechanism. When heart rate slows, blood pressure drops, and the resulting lack of blood to the brain causes fainting and confusion.
Typical triggers for vasovagal episodes include:
- Prolonged standing or upright sitting
- After or during urination (micturition syncope)
- Straining, such as to have a bowel movement or during vomiting
- Standing up very quickly (orthostatic hypotension)
- During or post-biopsy procedures
- Stress directly related to trauma
- Postural orthostatic tachycardia syndrome (POTS). Multiple chronic episodes are experienced daily by many patients diagnosed with this syndrome. Episodes are most commonly manifested upon standing up.
- Any painful or unpleasant stimuli, such as:
- Severe menstrual cramps
- Sensitivity to pain
- Arousal or stimulants (e.g. sex, tickling, or adrenaline)
- Sudden onset of extreme emotions
- Lack of sleep
- Being exposed to high temperatures
- Food poisoning (e.g. Salmonella, etc)
- Random onsets due to nerve malfunctions
- Pressing upon certain places on the throat, sinuses, and eyes (also known as vagal reflex stimulation when performed clinically)
- Use of certain drugs that affect blood pressure, such as cocaine, alcohol, marijuana, inhalants, and opioids
- The sight of blood
- Serotonin level or SSRI medications
- Low blood sugar (less common)
- Time varying magnetic field (i.e. transcranial magnetic stimulation)
- Insertion of an intrauterine device (IUD)
Regardless of the trigger, the mechanism of syncope is similar in the various vasovagal syncope syndromes. The nucleus tractus solitarii of the brainstem is activated directly or indirectly by the triggering stimulus, resulting in simultaneous enhancement of parasympathetic nervous system (vagal) tone and withdrawal of sympathetic nervous system tone.
This results in a spectrum of hemodynamic responses:
- On one end of the spectrum is the cardioinhibitory response, characterized by a drop in heart rate (negative chronotropic effect) and in contractility (negative inotropic effect) leading to a decrease in cardiac output that is significant enough to result in a loss of consciousness. It is thought that this response results primarily from enhancement in parasympathetic tone.
- On the other end of the spectrum is the vasodepressor response, caused by a drop in blood pressure (to as low as 80/20) without much change in heart rate. This phenomenon occurs due to dilation of the blood vessels, probably as a result of withdrawal of sympathetic nervous system tone.
- The majority of people with vasovagal syncope have a mixed response somewhere between these two ends of the spectrum.
One account for these physiological responses is the Bezold-Jarisch reflex.
In addition to the mechanism described above, a number of other medical conditions may cause syncope. Making the correct diagnosis for loss of consciousness is one of the most difficult challenges that a physician can face. The core of the diagnosis of vasovagal syncope rests upon a clear description by the patient of a typical pattern of triggers, symptoms, and time course.
In patients with recurrent vasovagal syncope, diagnostic accuracy can often be improved with one of the following diagnostic tests:
- A tilt table test (results should be interpreted in the context of patients' clinical presentations and with an understanding of the sensitivity and specificity of the test)
- Implantation of an insertable loop recorder
- A Holter monitor or event monitor
- An echocardiogram
- An electrophysiology study
Treatment for vasovagal syncope focuses on avoidance of triggers, restoring blood flow to the brain during an impending episode, and measures that interrupt or prevent the pathophysiologic mechanism described above.
- The cornerstone of treatment is avoidance of triggers known to cause syncope in that person. However, a new development in psychological research has shown that patients show great reductions in vasovagal syncope through exposure-based exercises with therapists if the trigger is mental or emotional, e.g., sight of blood. However, if the trigger is a specific drug, then avoidance is the only treatment.
- Because vasovagal syncope causes a decrease in blood pressure, relaxing the entire body as a mode of avoidance is not favorable. A patient can move or cross his/her legs and tighten leg muscles to keep blood pressure from dropping so drastically before an injection.
- Before known triggering events, the affected person may increase consumption of salt and fluids to increase blood volume. Sports drinks or drinks with electrolytes may be particularly helpful.
- Discontinuation of medications known to lower blood pressure may be helpful, but stopping antihypertensive drugs can also be dangerous in some people. Taking antihypertensive drugs may worsen the syncope, as the hypertension may have been the body's way to compensate for the low blood pressure.
- Patients should be educated on how to respond to further episodes of syncope, especially if they experience prodromal warning signs: they should lie down and raise their legs, or at least lower their head to increase blood flow to the brain. At the very least, upon the onset of initial symptoms the patient should try to relocate to a 'safe', perhaps cushioned, location in case of losing consciousness. Positioning themselves in a way where the impact from falling or collapsing would be minimized is ideal. The 'safe' area should be within close proximity, since, time is of the essence and these symptoms usually climax to loss of consciousness within a matter of minutes. If the individual has lost consciousness, he or she should be laid down with his or her head turned to the side. Tight clothing should be loosened. If the inciting factor is known, it should be removed if possible (for instance, the cause of pain).
- Wearing graded compression stockings may be helpful.
- There are certain orthostatic training exercises which have been proven to improve symptoms in people with recurrent vasovagal syncope. A technique called "Applied Tension" which involves learning to tense the muscles in the torso, arms, and legs is effective for vasovagal syncope.
- Certain medications may also be helpful:
- Beta blockers (β-adrenergic antagonists) were once the most common medication given; however, they have been shown to be ineffective in a variety of studies and are thus no longer prescribed. In addition, they may cause the syncope by lowering the blood pressure and heart rate.
- Medications which may be effective include: CNS stimulants fludrocortisone, midodrine, SSRIs such as paroxetine or sertraline, disopyramide, and, in health-care settings where a syncope is anticipated, atropine epinephrine (adrenaline).
- For people with the cardioinhibitory form of vasovagal syncope, implantation of a permanent pacemaker may be beneficial or even curative.
Types of long-term therapy for vasovagal syncope include
- Preload agents
- Anticholinergic agents
- Negative cardiac inotropes
- Central agents
- Mechanical device
|This section needs expansion. You can help by adding to it. (January 2009)|
Brief periods of unconsciousness do no harm and are seldom symptoms of disease.
The main danger of vasovagal syncope (or dizzy spells from vertigo) is the risk of injury by falling while unconscious. Medication therapy could possibly prevent future vasovagal responses; however, for some individuals medication is ineffective and they will continue to have fainting episodes.
- Roemheld Syndrome
- Postural orthostatic tachycardia syndrome
- Orthostatic hypotension
- Orthostatic intolerance
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