Definition and Overview
Vasovagal syncope (VVS) is a representative form of neurally mediated syncope in which bradycardia and vasodilation occur simultaneously due to excessive activity of the vagus nerve, resulting in a temporary decrease in cerebral blood flow and loss of consciousness. Syncope is a type of transient loss of consciousness. It is caused by global cerebral hypoperfusion and is characterized by complete spontaneous recovery.
VVS is the most common type of syncope, accounting for approximately 56-66% of all syncope causes. According to the 2018 European Society of Cardiology (ESC) syncope guidelines, approximately 40% of the general population experiences syncope at least once in their lifetime, and more than half of these are estimated to be due to vasovagal mechanisms. The annual incidence rate is approximately 6.2 cases per 1,000 population, and it accounts for approximately 1-3% of emergency room visits.
VVS can occur at any age, but its first onset is most common between the ages of 10 and 30. Women have a slightly higher incidence than men, and in older people, it is important to differentiate it from orthostatic hypotension. VVS itself is a benign disease that is not life-threatening, but repeated occurrences are accompanied by a risk of trauma and a decrease in quality of life. Sheldon et al. (2006), approximately 25% of VVS patients experienced recurrence within 5 years.
Mechanism of occurrence
The core mechanism of VVS is the Bezold-Jarisch reflex. This reflex is a process in which the normal autonomic response is excessively activated, causing a paradoxical drop in blood pressure and bradycardia.
Normally, when standing up, about 500 to 800 mL of blood moves to the lower extremities and internal blood vessels by gravity. In response, baroreceptors activate the sympathetic nerves and increase heart rate and peripheral vascular resistance to maintain blood pressure. In VVS, this compensation mechanism is reversed.
If standing upright continues, venous return decreases and ventricular filling decreases. As the relatively empty ventricle contracts excessively, mechanoreceptors on the ventricular wall are stimulated. When this signal is transmitted to the vasomotor center of the medulla oblongata through vagal afferent fibers, the sympathetic nerve is suddenly inhibited and the parasympathetic nerve (vagus nerve) becomes hyperactive.
As a result, the heart rate rapidly decreases (bradycardia), peripheral blood vessels dilate, and blood pressure drops rapidly. When cerebral blood flow decreases below a critical level, loss of consciousness occurs. Fainting occurs when blood flow to the brain is completely blocked for about 6 to 8 seconds.
Depending on the reaction pattern of VVS, it is classified into three types:
- Vasodepressor type: The main mechanism is a decrease in blood pressure, and the heart rate decrease is slight.
- Cardioinhibitory type: bradycardia or asystole is the main mechanism. Cardiac arrest lasting longer than 3 seconds may be observed.
- Mixed type: Both a decrease in blood pressure and bradycardia appear significantly. This is the most common type in clinical practice.
Recently, the role of the upper central nervous system, including the cerebral cortex, insular cortex, and amygdala, has also been receiving attention. It is interpreted that the reason emotional stress or pain causes fainting is because a downward signal is transmitted from the cerebral cortex to the autonomic nerve center in the medulla oblongata.
trigger
VVS is often triggered by specific situations or stimuli. The main triggering factors are:
Factors associated with standing include standing for long periods of time, standing in hot environments, crowded spaces, and prolonged immobility during church or school assemblies. A typical example is the phenomenon of soldiers or students collapsing while in line.
Factors related to emotions and pain include blood sampling, injections, witnessing surgery, extreme pain, fear, and anxiety. Fainting during blood draw is a typical case of VVS.
Physical factors include dehydration, excessive sweating, drinking too much, fasting for long periods of time, lack of sleep, and overwork. Fainting after a hot bath or sauna also occurs through the VVS mechanism due to vasodilation.
Situational syncope caused by specific movements such as urination, defecation, coughing, and swallowing is also included in neuromediated syncope in a broad sense. Fainting due to carotid sinus hypersensitivity occurs when pressure is applied to the neck and is more common in older men.
symptoms
Symptoms of VVS are divided into three stages: prodromal phase, syncopal phase, and recovery phase.
prodromal symptoms
It is a warning symptom that appears seconds to minutes before syncope occurs. Prodromal symptoms precede approximately 70-80% of VVS patients. Typical symptoms include lightheadedness, blurred or dark vision, nausea, diaphoresis, pallor, tinnitus or hearing loss, tingling in the extremities, and general weakness. As the heart rate decreases and blood pressure decreases, the extremities become cold and yawning occurs.
If prodromal symptoms are recognized early, syncope can be prevented by sitting or lying down, so prodromal recognition training is a key element in patient education.
Syncopal phase
When cerebral blood flow decreases below a critical level, loss of consciousness occurs. Most fainting caused by VVS recovers spontaneously within a few seconds to 1 minute. During syncope, muscle tone is lost and the person collapses, and may be accompanied by brief rigidity or myoclonic jerks. This may be confused with epilepsy, but the convulsive movements in VVS are secondary to cerebral hypoperfusion and are essentially different from epilepsy.
During syncope, transient bradycardia or cardiac arrest (asystole) lasting more than 3 seconds may be observed. According to the 2018 ESC guidelines, cardiac arrest lasting more than 3 seconds is recorded in approximately 40 to 50% of VVS patients during a tilt-table test.
convalescence
When you switch to a lying position, blood flow to the brain is restored and consciousness returns. After recovery, general fatigue, headache, nausea, etc. may last from a few minutes to several hours. Even after regaining consciousness, getting up too quickly can cause fainting again, so get enough rest.
diagnosis
In the diagnosis of VVS, history taking is the most important, and the tilt table test is the standard diagnostic tool.
history taking
Systemically identify typical triggers (prolonged standing, pain, heat, emotional stress, etc.), the presence of prodromal symptoms, syncope patterns, and recovery process. Important information includes the starting position of the syncope (standing or sitting), witness statements, duration of the syncope, whether it was accompanied by convulsions, and status after recovery. Be sure to check family history, history of heart disease, and medication history.
The 2018 ESC guidelines stated that typical VVS can be diagnosed based on history alone. This applies to cases where typical triggering factors and prodromal symptoms are present, organic heart disease is excluded, and there are no neurological abnormalities.
Standing tilt table inspection
After the patient lies down on the examination table, the patient is tilted at an angle of 60 to 70 degrees for 20 to 45 minutes to continuously measure changes in blood pressure and heart rate. If syncope is reproduced during the test and a drop in blood pressure and bradycardia are confirmed, the test is judged positive. If there is no response in the basic test, a drug provocation test is performed using sublingual administration of nitroglycerin or intravenous isoproterenol.
The sensitivity of the tilt-table test is reported to be approximately 61-69%, and the specificity is approximately 93%. Because reproducibility is not perfect, a negative test does not rule out VVS.
Differential diagnosis
The most important thing in diagnosing syncope is ruling out cardiac syncope. Cardiogenic syncope is caused by arrhythmia, structural heart disease, aortic stenosis, etc., and unlike VVS, it can be life-threatening. It is diagnosed through 12-lead electrocardiogram (ECG), echocardiography, and 24-hour electrocardiogram monitoring (Holter monitoring).
Differentiating it from epilepsy is also important. The convulsive syncope accompanying VVS can be confused with epileptic seizures, but in VVS, brief convulsions appear after loss of consciousness, and postictal confusion is absent or very brief.
Orthostatic hypotension, carotid sinus hypersensitivity, and psychogenic pseudosyncope are also subject to differentiation.
treatment
Non-pharmacological treatment is the primary treatment for VVS, and drug treatment and device treatment are considered for recurrent syncope.
Patient education and trigger avoidance
The starting point of treatment is to clearly explain to the patient that VVS is a benign disease that is not life-threatening. This education alone reduces anxiety and lowers the recurrence rate in many patients. Identify individual triggers and guide them to avoid them. Avoid standing for long periods of time, hot environments, dehydration, and excessive drinking.
physical counter pressure method
It is an isometric muscle contraction exercise performed when prodromal symptoms are felt. These include leg crossing with tensing, arm tensing with handgrip, and squatting. van Dijk et al. (2006), in a randomized controlled trial, physical counterpressure significantly reduced the rate of VVS recurrence. The 2018 ESC guidelines recommended physical counterpressure as Class I (recommendation level) for VVS patients with prodromal symptoms.
Water and salt intake
It is recommended to consume 2 to 3 liters of water and 6 to 10 g of salt per day. Sufficient water and salt intake increases circulating blood volume and improves venous return when standing. A quick drink of 500 mL of water (water bolus) when waking up in the morning can also temporarily increase blood pressure.
standing training
Tilt training involves leaning your back against a wall and standing twice a day for 20 to 30 minutes each time. The purpose is to gradually strengthen the autonomic tolerance to standing, and there are reports that if practiced consistently, the rate of syncope recurrence can be reduced by about 40-50%. However, some say that long-term effects are limited due to low patient compliance.
medication
Consider pharmacological treatment for recurrent VVS that is not controlled by non-pharmacological treatment. To date, there are limited drugs that have consistently proven effective against VVS.
Midodrine is an alpha-1 adrenergic receptor agonist that maintains blood pressure by constricting peripheral blood vessels. Some studies have confirmed its effectiveness in reducing syncope recurrence.
Fludrocortisone is a mineralocorticoid that increases blood volume by promoting sodium and water retention. In the POST 2 study, fludrocortisone significantly reduced VVS recurrence.
Beta-blockers were widely prescribed in the past, but Sheldon et al. (2006) in the POST study (Prevention of Syncope Trial), metoprolol did not show a significant difference in preventing VVS recurrence compared to placebo. However, a subgroup analysis was reported showing that it may be effective in patients over 42 years of age.
pacemaker insertion
Implantation of a permanent pacemaker may be considered in cardiosuppressive VVS that does not respond to drug treatment and has documented cardiac arrest. The 2018 ESC guidelines recommended a dual-chamber pacemaker as Class IIa in patients over 40 years of age, with recurrent syncope, and with symptom-related cardiac arrest of more than 3 seconds recorded on an implantable loop recorder.
Progress and prognosis
VVS mostly has a benign course. The mortality rate of VVS patients without organic heart disease is no different from that of the general population. However, recurrence is common, and the recurrence rate within one year after the first syncope is reported to be approximately 25-35%. The more frequent syncope occurs and the younger it occurs for the first time, the higher the risk of recurrence.
Recurrent VVS has a significant impact on quality of life. It may be accompanied by restrictions on occupational activities, prohibition of driving, social withdrawal, anxiety, and depression. When fainting, secondary trauma such as head trauma, tooth damage, or fractures caused by a fall cannot be ignored. In elderly patients, femur fracture due to a fall is a factor that increases morbidity and mortality.
In long-term follow-up studies, a significant proportion of VVS patients show a natural decrease in the frequency of syncope over time. In particular, VVS that occurs in adolescence often resolves spontaneously in adulthood.
life guide
Daily life management to reduce recurrence of VVS is the core of treatment.
Aim for water intake of 2 to 3 liters per day, and it is effective to drink enough right after waking up in the morning and before meals. Consume 6-10g of salt per day, but only if you do not have high blood pressure or kidney disease. Avoid excessive consumption of caffeine or alcohol as they can cause dehydration.
In situations where you have to stand for a long time, cross your legs, shift your weight from side to side, or repeat movements that strengthen your calf muscles. Avoid standing in an immobile position with your knees straight. In hot environments, be especially careful about hydration and avoid prolonged exposure.
When waking up in the morning, avoid getting up quickly. Stay in the sitting position on the bed for 1-2 minutes and then stand up slowly. Wearing compression stockings (30-40mmHg) helps maintain blood pressure by reducing venous retention in the lower extremities.
Regular aerobic exercise improves cardiovascular function and autonomic nervous system control. Moderate-intensity exercise (brisk walking, cycling, swimming, etc.) 3-5 times a week, 30-45 minutes per session is recommended. Drink plenty of water when exercising and avoid strenuous exercise while dehydrated.
In situations that may cause syncope, such as blood sampling or dental procedures, inform the medical staff in advance of your history of VVS and have the patient undergo the procedure lying down or in a semi-recumbent position.