Vasovagal syncope

Vasovagal syncope is very common: the highest prevalence among teenagers, athletes, and the elderly. 

 

With a sufficient degree of stress it can be induced in more than 75% of healthy people.

 

It is not a predictor of adverse cardiovascular outcomes. 

 

Vasovagal syncope is a form of dysautonomia characterized by an inappropriate drop in blood pressure while in the upright position.

 

Vasovagal syncope occurs as a result of increased activity of the vagus nerve, the mainstay of the parasympathetic nervous system.

 

 Patients will feel sudden, unprovoked lightheadedness, sweating, changes in vision, and finally a loss of consciousness.

 

 Consciousness will often return rapidly once patient is lying down and the blood pressure returns to normal.

Consciousness is regained rapidly and then no neurologic sequele although it can result in head trauma and bone fractures.

The vasovagal reaction can be initiated by emotional, sensory, or hemodynamic stimuli, but triggers may not be apparent.

Rarely in older men, turning the neck can generate pressure in the carotid sinus and cause a vasovagal reaction.

The prodromal phase of the vasovagal syndrome usually lasts 30 seconds or longer, and sympathetic efferent  activation and epinephrine release can cause skin vasoconstriction, facial pallor, diaphoresis, piloerection, nausea and gastric discomfort.

These symptoms of autonomic activation are present in vasovagal syndrome, but not in efferent baroreflex failure.

With syncope efferent activity stops and norepinephrine levels fail to increase, but there is a marked increase in the release of epinephrine from the adrenal medulla.

When hypotension causes hypo perfusion of the brain lightheadedness, visual dimming, and muffled sounds occur.

Hyperventilation which begins in the prodromal phase, leads to hypocapnia with constricted cerebral vessels and exacerbated decrease in cerebral blood flow.

With a vasovagal reaction vasopressin is released, which can contribute to facial pallor and nausea.

Complications include injury from a fall.

Differential diagnosis includes: Arrhythmia, orthostatic hypotension, seizure, hypoglycemia.

Frequency of occurrence is > 1 per 1,000 people per year.

Reflex syncope is divided into three types: vasovagal, carotid sinus, and situational.

It is the most common type of syncope, making up more than 50% of all cases.

Vasovagal syncope is typically triggered by seeing blood, pain, emotional stress, or prolonged standing.

With vasovagal syncope cardiac output, venous return and blood pressure decrease.

Carotid sinus syncope is due to pressure on the carotid sinus in the neck, and involves the nervous system slowing the heart rate and dilating blood vessels resulting in low blood pressure and therefore not enough blood flow to the brain.

Diagnosis of carotid sinus syncope is based on symptoms after ruling out other possible causes.

Situational syncope is often triggered by urination, swallowing, or coughing.

Generally recovery occurs without specific treatment.

Management includes avoiding known triggers, adequate hydration, and exercise.

Medications that may be preventative include Midodrine, and fludrocortisone.

Typically a recurrent process and usually occurs when the predisposed person is exposed to a specific trigger.

Patients frequently experience early manifestations such as lightheadedness, nausea, the feeling of being hot or cold, sweating, ringing in the ears, an uncomfortable feeling in the heart, fuzzy thoughts, confusion, a slight inability to speak, weakness visual disturbances 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 of symptoms usually occurs when a person is sitting up or standing, and they may become more intense over several seconds-several minutes before the loss or impairment of consciousness.

With lost of consciousness, patient’s fall down and, when in this position, effective blood flow to the brain is immediately is restored, allowing the person to regain consciousness.

If the person’s head remains elevated above the trunk, a state similar to a seizure may result because of the inability of blood returning quickly to the brain.

Fainting occurs when there a loss of oxygen to the brain.

The autonomic nervous system action leads to loss of consciousness and may persist for several minutes.

Patients may be nauseated, pale, and diaphoretic for several minutes or hours.

Reflex syncope occurs in response to dysfunction of the heart rate and blood pressure regulating mechanisms.

When heart rate slows, blood pressure drops, and the resulting lack of blood to the brain causes fainting.

Typical triggers of vasovagal syncope include:

Prolonged standing

Emotional stress

Pain

The sight of blood

Situational syncope

Micturition syncope

Straining, such as to have a bowel movement

Coughing

Swallowing

Lifting a heavy weight

Carotid sinus syncope

Regardless of the trigger, the mechanism of syncope is similar, the nucleus tractus solitarii of the brain stem is directly or indirectly activated, enhancing the parasympathetic nervous system and the withdrawal of sympathetic nervous system tone.

The nucleus tractus solitarii activation causes a variety of responses, including a cardioinhibitory response, with a drop in heart rate and in contractility leading to a decrease in cardiac output that is significant enough to result in a loss of consciousness.

The cardioinhibitory response is thought to result primarily from enhancement in parasympathetic tone.

The vasodepressor response, caused by a drop in blood pressure without much change in heart rate, 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 the cardioinhibitory response and vasodepressor response

A number of other medical conditions may cause syncope:

lightheadedness, seizures, vertigo, and low blood sugar as other causes.

Diagnostic accuracy can often be improved by following diagnostic tests:

A tilt table test

Implantation of an insertable loop recorder

A Holter monitor or event monitor

An echocardiogram

An electrophysiology study

Treatment

The primary management focuses on avoidance of triggers, restoring blood flow to the brain during an episode, and measures that interrupt or prevent the pathophysiologic mechanisms.

The cornerstone of treatment is avoidance of triggers known to cause syncope in that person.

Exposure-based exercise therapy can reduce vasovagal syncope if the trigger is mental or emotional.

If a trigger is a specific drug, then avoidance is the only treatment.

Movement or crossing of legs, legs and tightening leg muscles may help to keep blood pressure from dropping

Before known triggering events, increasing consumption of salt and fluids and electrolytes to increase blood volume may be helpful.

If one experiences prodromal signs: they should lie down and raise their legs, or at least lower their head to increase blood flow to the brain.

Patients should try to relocate to a close by, safe, cushioned location in case of losing consciousness.

Graded compression stockings may be helpful.

Beta blockers (β-adrenergic antagonists) have been shown to be ineffective, and may cause the syncope by lowering the blood pressure and heart rate.

Effective medications include: CNS stimulants, fludrocortisone, midodrine, SSRIs, such as paroxetine or sertraline, and, adrenaline.

For the cardioinhibitory form of vasovagal syncope, a pacemaker may be beneficial or even curative.

Long-term therapy for vasovagal syncope include:

Preload agents

Vasoconstrictors

Anticholinergic agents

Negative cardiac inotropes

Central agents

Mechanical device

Discontinuation of medications known to lower blood pressure may be helpful, as antihypertensive drugs may worsen the syncope.

Brief periods of unconsciousness do no harm and are seldom symptoms of other disease.

The main danger is the risk of injury by falling while unconscious.

For some individuals medication is ineffective and they will continue to have fainting episodes.

Incidence of sudden death low at 0.8%.

Affects up to 40% of young adults, with predominance in women.

Cause suggested to be related to orthostatic venous pooling below the thorax leading to paradoxical activation of the cardio-neural inhibitory reflexes by underfilled ventricles.

Dilated inferior vena cava may indicate decreased abdominal venous tone and or increased compliance.

Exaggerated abdominal venous pooling during standing and subsequently orthostatic symptoms.

Relatively increased splanchic blood volume during tilt test in patients with this process.

Compression of abdomen more effective than compression of legs in preventing orthostatic symptoms in patients with orthostatic vasovagal syncope.