Vasovagal syncope

Signs and symptoms

Episodes of vasovagal syncope are typically recurrent and usually occur when the predisposed person is exposed to a specific trigger. Prior to 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 (tinnitus), an uncomfortable feeling in the heart, fuzzy thoughts, confusion, a slight inability to speak/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 last for a few seconds before the loss of consciousness (if it is lost), which typically happens when the person is sitting up or standing.

When sufferers pass out, 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

Cause

Vasovagal syncope occurs in response to a trigger, with a corresponding malfunction in the parts of the nervous system that regulate heart rate and blood pressure. 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

Stress

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:

Trauma (such as hitting one's funny bone)

Watching or experiencing medical procedures (such as venipuncture or injection)

High pressure on or around the chest area after heavy exercise

Severe menstrual cramps

Sensitivity to pain

Arousal or stimulants, e.g. sex, tickling, or adrenaline

Sudden onset of extreme emotions

Lack of sleep

Hunger

Coughing

Being exposed to high temperatures

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 opiates

The sight of blood

Serotonin level / SSRI

Swallowing

(Less commonly) Low blood sugar

Time varying magnetic field (e.g., transcranial magnetic stimulation)

IUD insertion

Pathophysiology

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:

1. 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.
2. 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 vasodilation, probably as a result of withdrawal of sympathetic nervous system tone.
3. 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.

Diagnosis

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. It is also pertinent to differentiate lightheadedness, seizures, vertigo, and hypoglycemia as other causes.

In patients with recurrent vasovagal syncope, diagnostic accuracy can often be improved with one of the following diagnostic tests:

1. 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)
2. Implantation of an insertable loop recorder
3. A Holter monitor or event monitor
4. An echocardiogram
5. An electrophysiology study

Treatment

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 patient 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. 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

Vasoconstrictors

Anticholinergic agents

Negative cardiac inotropes

Central agents

Mechanical device

Prognosis

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.