Feb 23, 2014
Syncope (fainting) is one of the most common medical ailments encountered in clinical practice. Although frequently thought of as a condition with a neurological origin, it’s actually a cardiovascular problem - as such, a neurologic work-up is seldom rewarding. The two main causes of syncope are cardiac arrhythmias and neurocardiogenic (vasovagal, vasodepressor) syndromes. In both of these conditions, blood circulation to the brain is reduced, resulting in temporary loss of consciousness.
Among the arrhythmias causing syncope, tachycardias (fast heartbeats), particularly those of ventricular origin, rather than bradycardias (slow heartbeats) are more often the culprits. In most patients with any evidence of previously known heart disease, it is likely that their syncope is related to a cardiac arrhythmia, usually VT. This is a serious matter because in patients with syncope due to VT, it’s common for SCD to occur within the ensuing year, this should be preventable if the cause of the syncope is found and managed. All cardiac arrhythmias can be effectively controlled if proper diagnosis is made with the help of cardiac electrophysiologic studies. In general, if a slow heart beat is the problem it can be treated with a pacemaker. If rapid beating is discovered, the treatment will vary depending on the nature of the fast rhythm.
Another common cause of syncope/presyncope is neurocardiogenic (vasovagal) syndrome. This condition, known by physicians as "neurally mediated hypotension", is also referred to as "the fainting reflex", "vasodepressor syncope", "vasovagal syncope", or "autonomic dysfunction". In this condition blood vessels tend to expand, which leads to pooling of blood in the lower parts of the body. As a result, less blood reaches the brain and this causes fainting. The usual stimulus for this action resides in the nerves of the heart-hence the term neurocardiogenic. A head-up tilt test can uncover the underlying cause of the fainting in this syndrome. Neurocardiogenic syncope is usually treated with medications that reduce the probability of cardiac nerves triggering the cycle that leads to lightheadedness, dizziness or fainting.
Together, arrhythmias and neurocardiogenic syndromes account for more than 75% of the cases of unexplained fainting spells-so it’s important that the initial diagnostic work-up be designed to investigate these possibilities.
When Does Neurocardiogenic Syncope Lead to Symptoms?
Neurocardiogenic syncope occurs in predisposed individuals in the following settings:
after prolonged periods of quiet upright posture (such as standing in line)
after being in a warm environment (such as in hot summer weather, a hot crowded room, a hot shower or bath)
immediately after exercise
after emotionally stressful events (having blood drawn, being scared or anxious)
some individuals get symptoms soon after eating, when blood flow has shifted to the intestinal circulation during the process of digestion
We are all susceptible to fainting by activation of the vaso-vagal reflex that results in a lowered blood pressure, however, an individual’s susceptibility varies day to day based upon genetic make-up, dietary factors, psychological state, and triggers such as infection, dehydration, and alcohol intake.
Why Does an Upright Posture Trigger Neurocardiogenic Syncope?
When a normal individual stands up, gravity causes blood to pool in the legs, and return of blood to the heart is decreased. In order to compensate for this reduction, the body releases a surge of adrenaline (epinephrine). The heart beats faster and more forcefully, thereby pumping blood more efficiently to vital organs (especially the brain).
In an individual with neurocardiogenic syncope, the reduction of blood return triggers a miscommunication between the heart and the brain. Just when the heart needs to beat faster, the brain sends out a message that the heart rate should be slowed down, and that the blood vessels in the arms and legs should dilate. These actions take even more blood away from the central part of the circulation where it is needed. As a result, the individual feels lightheaded or may faint because not enough blood is getting to the brain. Fainting is helpful, in that it restores a person to the flat position, removing the pooling effect of gravity on the blood, and allowing more blood to return to the heart. Following the lightheadedness or syncope, most individuals feel tired and their mental abilities are somewhat foggy.
What Symptoms Does Neurocardiogenic Syncope Cause?
Individuals that are prone to neurocardiogenic syncope manifest a spectrum of symptoms ranging from fatigue, vague lightheadedness, recurrent dizziness, near fainting, palpitations, nausea, unexplained sweating, joint or muscle aches, to the most dramatic "the faint". Some people may only have one or more of these symptoms but never progress to fainting. Prolonged fatigue after a modest amount of physical activity is occasionally seen. This post-exertional fatigue can last 24-72 hours, and interferes with many daily activities.
Some develop worse fatigue after such activities as reading and concentrating, and this may be due to the fact that for some, the veins of the arms and legs dilate, thereby allowing more blood to pool, rather than constricting in response to mental tasks.
How is Neurocardiogenic Syncope Diagnosed?
Neurocardiogenic syncope cannot be detected in the office with a routine blood pressure or heart rate screening. The diagnosis can be made using a tilt table test. Since heart rate and blood pressure recordings are impractical during an actual episode, a test designed to provoke this episode in a controlled setting is used. A tilt table test allows careful measurement of the heart rate and blood pressure responses to the head-up position at a 70-degree angle, in an almost standing position.
Many people with neurocardiogenic syncope develop adaptations to keep from fainting, such as crossing their legs, fidgeting, or sitting or lying down when they get lightheaded or tired, but the tilt table test prohibits them from performing those natural defenses. As a result, lightheadedness, nausea, and fainting can be provoked during the tilt table test. Fatigue and malaise may occur for a few days after the test is performed. The test itself is safer than the actual episode in real life because the event is monitored carefully.
What Causes Neurocardiogenic Syncope?
The cause for neurocardiogenic syncope isn't well understood at present, but we suspect this condition has genetic origins in many people, because it is not uncommon to find several affected individuals in the same family. It is likely that we all could develop this neurally mediated drop in blood pressure provided that the conditions were sufficiently severe: for example, if we were dehydrated, were subjected to extremely prolonged periods of upright posture, or to very warm environments. The reflex response, which results in lowered blood pressure, simply occurs more easily and without an apparant trigger in susceptible individuals.
One of the most common and treatable problems identified in those with neurocardiogenic syncope is a low salt (sodium) intake in the diet. Salt helps us retain fluid in the blood vessels, and helps maintain a healthy blood pressure. For individuals with neurocardiogenic syncope, a low salt intake may move them from feeling good to developing the symptoms of fatigue and lightheadedness described earlier.
How is Neurocardiogenic Syncope Treated?
Neurocardiogenic syncope is most often treated with a combination of increased salt and water intake in conjunction with drugs that regulate blood pressure. It is important for patients to recognize potential triggers and heed warning signs. Treatment can broadly be divided into two categories:
1. General measures
The first step in treating this problem is to increase fluid intake. We cannot stress this enough. Patients who drink fluids regularly throughout the day seem to do better than those who don't take this task seriously.
If low salt intake is an issue, we recommend an increase in the amount of salt for patients to add to their food. For some individuals with mild symptoms, an increased intake of salt and fluids may be all that is needed. Most of those with chronic fatigue syndrome and more severe symptoms require one of several medications in addition to the increased salt and fluid intake. The increased salt and fluid intake continue regardless of which of these medications is added. To be successful, though, the increased salt intake must be accompanied by a sufficient increase in the intake of water and other fluids (minimum of 2 liters of fluid per day). Please contact your physician if you have high blood pressure.
Where practical, avoid circumstances that might bring on symptoms.
Shop at non-peak hours to avoid long lines
Take shorter showers and baths and aim for a cooler water temperature
Avoid saunas, hot tubs, and lying on a hot beach
Avoid standing still for prolonged periods in hot environments, and on very hot days
Flex your leg muscles and shift your weight when you are standing still, or better still, walk around.
Avoid alcohol because it leads to dilation of the veins and arteries, and this can steal blood away from the central circulation
Reduce caffeine intake
Certain postures and physical maneuvers are helpful in raising blood pressure when sitting for a prolonged time, mainly by helping use contraction of the leg muscles to pump blood back to the heart and by compressing the abdomen to reduce the amount of blood that pools in the intestinal circulation. The helpful maneuvers include:
standing with one's legs crossed
standing with one leg on a chair
bending forward from the waist (such as leaning over a shopping cart)
sitting in the knee-chest position
sitting in a low chair
leaning forward with hands on the knees when sitting
elevate the head of the bed slightly by 10-15o, a position that appears to help the body retain fluid at night rather than lose fluid into the urine
waist-high support hose can prevent some of the excessive pooling of blood in the legs (knee-high support socks may not work as well
Exercise is important in regaining the effects that fitness brings in counteracting neurocardiogenic syncope. Because exercise can initially make symptoms worse, it must be done carefully at first.
Medications are designed to make the patient more resistant to the same triggers, especially if they cannot be identified or eliminated. Some drugs work by allowing the kidneys to retain sodium and others block the body's response to adrenaline, which can kick-start the blood pressure abnormality. In addition, it is important to review your current medications with your doctor to ensure that these medications do not include drugs or vitamins that have the potential to make neurocardiogenic syncope worse.
The treatments require persistence, commitment and the willingness to try several possible drugs and combinations over an extended period of time. Because there is a risk of serious side effects with some of the drugs, such as elevated blood pressure, elevated sodium level, lowered potassium level, or depression, careful ongoing monitoring by a physician is required. Drugs that have been found to help are:
beta-blockers (e.g., atenolol)
methylphenidate (Ritalin), and
Your treating physician will work with you to determine the best possible drug or combination of drugs for you.
Does Treatment Cure the Problem?
No, treatment for neurocardiogenic syncope does not cure the problem. Rather, it helps control (minimize if not eliminate) symptoms and is aimed at improving quality of life. When medications are stopped and when salt intake is reduced, symptoms frequently reappear. Many of the adolescents and adults with the problem also have symptoms resurface or worsen at busy or stressful times (making an oral presentation in class). Many women describe a worsening of symptoms in the days around the start of a menstrual period.
The question of what happens over the long term has not been adequately studied, and the optimal duration of medical treatment is still being worked out. Unfortunately, despite appropriate doses of the available medications, some individuals with abnormal tilt table tests do not experience a marked improvement in symptoms, and some are intolerant of the medications. In such people, the realistic expectation may be reduction in frequency and severity of symptoms rather than their complete elimination. More research on this problem is ongoing.