What is a Vasovagal Episode?
A vasovagal episode is an abnormal physiological response resulting in a symptomatic decline in heart rate and drop in blood pressure. An associated condition, termed a vasodepressor episode, is associated with a drop in blood pressure without a significant decline in heart rate. The term vasovagal episode is often used synonymously for both types of episodes. The symptoms associated with vasovagal/vasodepressor episodes may range from mild lightheadedness to total loss of consciousness.
Regulation of Heart Rate and Blood Pressure by the Autonomic Nervous System
Regulation of the heart rate (sinus node firing rate) as well as the blood pressure (through the degree of constriction of the blood vessels) is primarily under the control of the autonomic nervous system (ANS). The autonomic regulation of the heart rate and blood pressure is complicated and only the simplest overview is presented here.
There are two components to the autonomic nervous system: 1) the parasympathetic or vagal system and, 2) the sympathetic or adrenergic system. Activation of the vagal system causes the heart rate (sinus node firing rate) and blood pressure to decrease, while inhibition of the vagal system triggers an increase in heart (sinus) rate (and to a lesser degree blood pressure). On the other hand, activation of the adrenergic system results in an increase in heart rate (and to a lesser degree blood pressure), while a withdrawal of sympathetic tone leads to a decrease in heart rate and blood pressure. Even at rest or while sleeping, there are subtle moment-to-moment shifts in the heart rate and blood pressure as these two involuntary components of the nervous system "push & tug" on the sinus node firing rate and degree of constriction of the peripheral blood vessels. This system is designed to maintain blood pressure within a fairly narrow range, even during sleep, changes in posture, or reductions in blood volume (dehydration). For example, when a person lies in bed sleeping, it is unnecessary to have a high blood pressure and a fast heart rate. Therefore, the ANS responds by increasing parasympathetic (vagal) tone and reducing (withdrawing) sympathetic (adrenergic) tone. On the other hand, when playing tennis, the autonomic system responds by withdrawing parasympathetic tone and enhancing sympathetic tone, resulting in a faster heart rate and a higher blood pressure to ensure delivery of adequate oxygenated blood to all the muscles and organs working at a high level.
Cerebral Hypoperfusion and Syncope
Of crucial importance, the autonomic regulatory system is designed to ensure that the brain receives a steady and uninterrupted supply of oxygenated blood. A global disruption of blood supply to the brain (cerebral hypoperfusion) — even for only a few seconds — may cause dramatic symptoms, including lightheadedness, dizziness, transient partial loss of vision or hearing, and even complete loss of consciousness ("blackout" or "fainting"). The technical term for such a blackout spell is syncope (pronounced 'sink-oh-pee', with the emphasis on the "sink"). Syncope is defined as a transient loss of consciousness and postural tone that spontaneously resolves. Syncope can be very frightening and distressing to family, friends, or bystanders who witness the event. In fact, a complete fainting spell often prompts an emergency 911 call and a visit to the hospital. Fortunately, vasovagal episodes are only rarely serious or dangerous. In almost all cases, the episode quickly resolves without any permanent residual effects. Injury or permanent damage generally only occurs if the patient falls or has an automobile accident as a result of syncope.
Transient Autonomic Dysfunction Causes Vasovagal Episodes
A vasovagal episode is caused by an unexpected and unpredictable disruption of the autonomic regulation of heart rate and blood pressure. Specifically, a vasovagal episode results when blood vessels dilate and the heart rate slows, resulting in a drop in blood pressure. If the blood pressure decline is too steep and too prolonged, the loss of oxygenated blood supply to the brain may result in complete loss of consciousness (syncope), as noted above. If the drop in blood pressure is less severe, or if the patient is able to lie down quickly (putting the level of the brain at the same level as the heart), syncope can often be avoided. However, even in this case the patient may still feel very lightheaded as if fainting is imminent. Even if the patient is not able lie down, the sensation of lightheadedness or dizziness may last for many minutes without further progression of symptoms, or these symptoms may progress to a frank loss of consciousness. While vasovagal episodes may prompt a full-fledged blackout spell, often only a near-fainting episode occurs that resolves before a complete loss of consciousness occurs. Other symptoms often associated with vasovagal episodes include nausea, vomiting, and "cold sweats". Witnesses usually describe the person as looking as "white as a sheet". In cases of complete loss of consciousness, the person may have a brief episode of involuntary muscle jerking which is often mistaken for a seizure. While most vasovagal syncope is preceded by a prodrome (warning) of lightheadedness/dizziness and possibly nausea and sweating, many episodes occur without any significant warning symptoms.
The precise cause(s) for vasovagal episodes and vasovagal syncope are still unclear. However, evidence suggests that the mechanism responsible may be related to "confusion" occurring within the central regulatory center of the ANS. According to this theory, an internal or external trigger causes the ANS to inappropriately increase vagal activation and decrease adrenergic tone, even though the opposite should occur. There is evidence that the initial physiological event causing this subsequent abnormal cascade of events is a relative excess of adrenergic activity in the body (see figure below). The ANS central control center in the brainstem may sense this adrenergic excess as inappropriate and it responds by "telling" the vagal system to increase its activity while also rapidly withdrawing sympathetic tone. The net effect is that heart rate slows, the blood vessels dilate, and the blood pressure plummets. As a consequence, the patient may feel lightheaded or dizzy, or may completely lose consciousness, unless this abnormal cascade of events is terminated or reversed.
Possible mechanism responsible for vasovagal syncope.
In many cases a clear external trigger can be identified that precipitates the vasovagal spell. For example, many people may have experienced a vasovagal spell and fainting during a routine blood draw in the hospital or outpatient clinic. The trigger may be the fear of the needle, the pain of the needle stick, and possibly the emotional discomfort at seeing the site of their own blood. The relative excess of adrenergic activity in the body triggers an inappropriate enhancement of vagal activity and abrupt withdrawal of sympathetic tone. Unless this abnormal autonomic reflex is disrupted, the person may faint. Sometimes the episode can be aborted by the person if they get their head below the level of the their heart (lie down or put their head between their legs). Other triggers that may precipitate vasovagal episodes ion some people are anger, intense excitement or joy, work stress, pain, intense anxiety, or fear. In addition, eating, urinating, or having a bowel movement are also common causes of vasovagal episodes. The common denominator in these cases, is that these normal physiological activities may cause intense activation of the vagal nervous system. Vagal activation is required for digestion of food, or emptying the bowels or bladder. Fainting during urination is so common that it has been given its own unique name — micturition syncope.
Evaluation of Vasovagal Episodes
As mentioned above, vasovagal episodes and vasovagal syncope are rarely a serious medical condition. However, after suffering syncope, patients and family members are often concerned about the presence of a serious heart or brain condition, such as a dangerous cardiac arrhythmia, or a brain seizure disorder. This concern may prompt extensive testing by emergency or primary care physicians, including computed tomography (CT) or magnetic resonance imaging (MRI) scans, 24-hour ambulatory ECG monitoring, treadmill testing, echocardiography (ECHO), and electroencephalography (EEG) studies. Because vasovagal episodes are caused by a transient malfunction of the ANS, these studies are generally negative. There is no test that can reliably (with high sensitivity and specificity) detect this transient ANS dysfunction.
It cannot be emphasized enough that the diagnosis of vasovagal episodes rests squarely upon a precise verbal description of the event obtained from the patient or a witness. Particularly useful information includes a description of what happened immediately before the event, associated symptoms including nausea, vomiting, sweats, heart palpitations, lightheadedness, what was noted by bystanders or paramedics, and how the patient felt after they awoke (if complete fainting occurred). The type (or lack of) any injuries occurring during any fall should also be noted and investigated. Descriptions of the patient's appearance and, especially, reports by bystanders or paramedics of the patient's heart rate and blood pressure are uniformly valuable. A history of an identifiable trigger (as discussed above) such as urination or fear, is also helpful. Finally, a history of recurrence of these types of episodes over a period of time (even if the precise details of each event differ) usually confirms a benign cause consistent with a vasovagal mechanism.
In young and healthy people, the diagnosis can almost always be made solely from the verbal description provided by the patient and any witnesses. A normal Electrocardiography (ECG) and echocardiogram effectively eliminates the possibility of a serious cardiac arrhythmia — such as a Ventricular Tachyarrhythmias — causing the syncopal episode. Dangerous life-threatening ventricular tachyarrhythmias virtually never occur in a patient with a structurally normal heart and a normal ECG (including normal a QT interval). Other more benign cardiac arrhythmias, including Supraventricular Tachyarrhythmias, also rarely cause syncope. Patients with syncope due supraventricular tachycardia invariably have a history of recurrent episodes of abnormal fast heart rhythms and ECG documentation of supraventricular tachycardia. Tilt table testing (TTT) as been recommended by some as a helpful test for diagnosing vasovagal syncope. However, TTT has a low sensitivity and specificity and is not as useful in diagnosing a vasovagal cause as simply talking with the patient. At best, therefore, TTT functions as a test to confirm a diagnosis already made by interviewing the patient (and excluding a more serious cause possibly by obtaining an echocardiogram and ECG). Because of this, TTT rarely alters the treatment plan and its performance is usually unnecessary.
Treatment of Vasovagal Syncope
The cornerstone of treatment of vasovagal episodes is patient education, including reviewing much of the above discussion. In many cases, vasovagal episodes are sporadic isolated events, and no treatment is necessary. In addition, the condition appears to self-limited and usually lessens or completely resolves with age. For patients with recurrent episodes, two treatment plans are available. The first (non-medical) option involves behavior modification, retraining of the ANS, and eliminating (if possible) medications that may be contributing to syncope. Under this option, patients should be advised to avoid dehydration and known triggering events. The use of support stockings to minimize pooling of blood volume in the lower extremities may be therapeutic. There is now some evidence that the ANS may be "trained" to minimize vasovagal episodes. Specifically, standing upright with the patient's back leaning against a wall (with heals about 6 inches from the wall) for 15-30 minutes twice a day, may be useful at minimizing vasovagal episodes. Finally, eliminating offending agents that may be contributing to the events, such as alcohol, or therapeutic agents such as vasodilators (e.g., calcium channel blocking agents) or diuretics (e.g., furosemide or hydrochlorothiazide) may be valuable.
If medical therapy is required to treat recurrent, problematic vasovagal episodes, the first-line medication is usually beta-adrenergic blocking agents, such as atenolol or metoprolol. It seems paradoxical that a drug that causes beta-adrenergic blockade and actually slows heart rate would be therapeutic in a condition such as vasovagal syncope in which part of the mechanism is an inappropriately slow heart rate. However, as discussed above, the internal physiological trigger for the vasovagal episode may be an inappropriate excess of adrenergic tone. Beta-adrenergic blocking drugs, by inhibiting the triggering sympathetic activation, often can prevent the subsequent cascade of events (vasodilation and bradycardia) leading to characteristic symptoms of vasovagal episodes. Clearly, beta-adrenergic blockers are effective in reducing the incidence, or completely eliminating, vasovagal episodes in many patients; however, they are not effective in all individuals. Other agents that have been employed include vasoconstrictors (midodrine), vagolytic agents (probanthine, diisopyramide), or inhibitors of serotonin re-uptake (paroxitene). The inefficacy of multiple agents in some patients, suggests that the there may be various mechanisms responsible for vasovagal episodes and the simplified theoretical mechanism discussed above may not be cause in all patients. Rare patients remain refractory to all treatment options. In rare cases of malignant vasovagal syncope, associated with frequent episodes of prolonged Sinoatrial (SA) Node Dysfunction, treatment with Pacemakers may be required.