Neurally Mediated Hypotension
NEURALLY MEDIATED HYPOTENSION AND ITS TREATMENT
Neurally Mediated Hypotension Working Group
Johns Hopkins Hospital
Revised January 1997
What is neurally mediated hypotension?
Neurally mediated hypotension is also known by the following names: the fainting reflex, neurocardiogenic syncope, vasodepressor syncope, the vaso-vagal reflex, and autonomic dysfunction. Hypotension is the formal medical term for low blood pressure, and syncope is the term for fainting. Neurally mediated hypotension occurs when there is an abnormal reflex
interaction between the heart and the brain, both of which usually are structurally normal.
When does neurally mediated hypotension lead to symptoms?
Neurally mediated hypotension occurs in susceptible individuals in the following settings:
-after prolonged periods of quiet upright posture (such as standing in line, standing in a shower, or even sitting up for long periods),
We are all susceptible to activation of the vaso-vagal reflex that results in a lowered blood pressure (NMH), but each person's susceptibility is affected by his or her genetic make-up, dietary factors, psychological make-up, and acute triggers such as infection and allergy. The clinical problem of NMH occurs when there is sufficiently early triggering of this
reflex to cause symptoms.
-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 (seeing blood or gory scenes, 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.
How does upright posture lead to these problems?
After a normal individual stands up, blood pools in the legs through the effect of gravity. To compensate for the lower amount of blood returning to the heart immediately after standing, the body has a surge of adrenaline (epinephrine). This adrenaline surge leads to a faster heart rate and to
more vigorous heart beats (a familiar feeling we all experience when we are frightened, for example). The faster heart rate and more vigorous heart contractions allow the reduced amount of blood returning to the heart to be pumped more efficiently to vital organs (especially the brain).
In individuals with neurally mediated hypotension, there is a "miscommunication" between the heart and the brain. Just when the heart needs to beat faster, (to pump blood to the brain and prevent fainting), the brain sends out the 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. In response, individuals feel 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.
Which symptoms can be caused by the neurally mediated hypotension?
Recurrent lightheadedness and fainting are common symptoms, as is an unusual difficulty with prolonged fatigue after a modest amount of physical activity. This post-exertional fatigue can last 24-72 hours, and interferes with many daily activities.
We have also observed that chronic fatigue, muscle aches (or fibromyalgia), headaches, and mental confusion can be prominent symptoms of neurally mediated hypotension even in individuals who do not faint. The mental confusion takes the form of difficulty concentrating, staying on task, paying
attention, or finding the right words. Some describe being in a "mental fog". It appears that as long as the fainting reflex is activated whenever the person stands or sits upright for a period of time, then the blood pressure is improperly regulated, and these symptoms are the result. 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 neurally mediated hypotension diagnosed?
Neurally mediated hypotension cannot be detected with a routine blood pressure or heart rate screening. The diagnosis can be made using a prolonged standing test or more commonly using a tilt table test. Many hospitals and academic centers throughout the world perform tilt table testing. It 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. The usual reason for performing a tilt table test in the past had been for the evaluation of recurrent fainting. Many people with neurally mediated hypotension 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 often occur during the tilt table test. Fatigue and malaise often occur for a few days after the test is performed.
What causes neurally mediated hypotension?
The answer to this question isn't well understood at present, but we suspect neurally mediated hypotension has genetic origins in many people, because it is not uncommon for us to find several individuals with neurally medaited hypotension in the same family. No gene for this condition has been identified. It is likely that we all could develop neurally mediated hypotension provided that the conditions were sufficiently severe: for example, if we did not take in enough fluids or salt, 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 at
an earlier point in some individuals.
One of the most common, and treatable problems identified in those with neurally mediated hypotension 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. Salt has received bad press in the last couple of decades because a *high* salt diet in some individuals with high or high-normal blood pressure can contribute to further elevations in blood
pressure, and thereby to heart disease and stroke. This has led to general health recommendations to "cut down on salt." As we are finding, this general recommendation isn't right for all people.
An average adult blood pressure is 120/70, and a blood pressure is considered elevated if it is above 140/90. Individuals can have neurally mediated hypotension at a wide range of resting blood pressures. It may be slightly more common in those whose systolic blood pressure [the top number]
is in the 90-110 range, but we also see it in those whose resting blood pressure is high. For individuals with neurally mediated hypotension, a low salt intake may be unhealthy, and may move them from feeling good to developing the symptoms of fatigue and lightheadedness described earlier. In experimental work earlier this century, severe short term salt depletion led
to fatigue and mental dulling in the adult research subjects.
How is neurally mediated hypotension treated?
Neurally mediated hypotension is most often treated with a combination of increased salt and water intake in conjunction with drugs that regulate blood pressure. 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 neurallly mediated hypotension worse.
We want to emphasize, however, that the treatments require persistence, commitment and the willingness to try several possible drugs and combinations over an extended perios of time. Because there is a risk of serious side effects with some of the drugs such as elevated blood pressure, elevated
sodium levels, lowered potassium levels, or depression, careful monitoring by a physician is required. Among the drugs that have been found to help improve tilt table responses in patients are fludrocortisone (Florinef), beta-blockers (e.g., atenolol), disopyramide (Norpace), fluoxetine (Prozac), sertraline (Zoloft), ephedrine, pseudoephedrine, theophylline, methylphenidate (Ritalin), and midodrine. Your treating physician should work with you to determine the best possible combination for your personal situation. In general, however, the first step in treating this problem is to increase fluid intake. We cannot stress this enough. Our patients who have discovered the importance of drinking fluids regularly throughout the day seem to do better than those who don't take this task seriously.
For those who have been on a low salt intake we recommend an increase in the amount of salt they add to their food. The Appendix to this document contains a list of high salt foods, but specific foods are now conveniently labeled with sodium content for you to check. For some mildly affected individuals, 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 a day). The Appendix also describes some of the drugs used for treating neurally mediated hypotension.
Does treatment cure the problem?
It needs to be emphasized that, when successful, the medications for neurally mediated hypotension do not *cure* the problem. Rather, they help control symptoms. 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, having company over for Thanksgiving, rushing for a meeting on a hot day and forgetting to drink). Many women describe a worsening of symtoms 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 for neurally mediated hypotension, some individuals with abnormal tilt table
tests do not experience an improvement in symptoms, and some are intolerant of the medications. This emphasizes the need for more research on this problem. Many women who have NMH describe an improvement in symptoms when they have been pregnant, and often describe pregnancy as the time when they felt "the best ever." The improvement may be due to an expansion of blood
volume that occurs with pregnancy.
What other things can I do to get better?
Where practical, avoid circumstances which might bring on symptoms. For example, 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. You may also want to avoid alcohol because it often leads to dilation of the veins, and this can "steal" blood away from the central circulation. Most with neurally mediated hypotension are quite intolerant of alcohol. Caffeine intake (including caffeine in soft drinks) affects some people with NMH in an adverse way, so examine whether caffeine is helping you or making symptoms worse.
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. Dr. Wouter Wieling in Amsterdam and his colleagues have emphasized the importance of these small changes, as even a small increase in
blood pressure can help maintain an adequate blood flow to the brain. Many patients have adopted these postures without knowing why. The helpful
maneuvers include:
-standing with one's legs crossed
Some of these are less conspicuous than others. Sitting in a low chair (such as a camping stool) is helpful because it causes the legs to be brought up toward the abdomen, and probably reduces the amount of blood pooling in the intestinal circulation. For similar reasons, avoid sitting in a high chair
with the legs dangling freely, as there is no resistance to blood pooling unless the muscles are actively contracting. One young woman found she could sit longer without symptoms if she put her feet on a low foot rest (this probably required more leg muscle contraction than regular sitting, and may have also compressed the abdomen better).
-squatting
-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.
We have adopted another recommendation from the Dutch group, namely to elevate the head of the bed slightly by 10-15 degrees, a position that appears to help the body retain fluid at night rather than lose fluid into the urine. Depending on one's level of comfort with this form of dress, 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), as can garments that increase abdominal compression (these work by preventing excessive amounts of blood pooling in the intestinal circulation).
Exercise is important in regaining the effects that fitness beings in counteracting NMH. Because exercise can make NMH sumptsoms worse in the period before effective treatment of the NMH has been found, it must be done carefully at first. When you and your doctor feel you are ready, begin a regular regimen of exercise, finding something that does not make you lightheaded and doing it for brief periods at first, increasing gradually but relentlessly. For example, one girl who had been ill for several years began doing better once two of the NMH medications were working for her. She began on a treadmill, but this made her lightheaded, so she switched to a reclining
exercise bike. Although she started with only 2 minutes a day, she increased this in small increments and was up to 30 minutes 3 times a week after about three months. Remember to warm up slowly before, and cool down gradually after exercise.
Attention to other medical conditions is crucial to ensuring that the NMH treatments are as effective as they can be. In particular, preventing activation of even mild asthma and allergies has been important in keeping our patients from developing a worsening of symptoms. Endometriosis in women with lower abdominal pain can aggravate NMH, as can sinusitis, anxiety
disorders, infections of any sort, and all of these need appropriate medical attention when present. Allergies to food proteins (most commonly cow's milk protein) have been identified by our colleague Dr. Kevin J. Kelly (now at Christopher's Hospital in Philadephia) as being common in those with NMH, and
substantial improvements can result from strict exclusion of offending foods. Given the potential dangers of unsupervised diets, be sure to discuss these issues with your doctor.
Again, we want to emphasize strongly that a key part of the therapy is to increase fluid intake. Those who force themselves to drink extra fluids every couple of hours seem to do better than those who aren't as serious about increasing their fluid intake. Keep in mind that prolonged periods of sleeping (more than 12 hours) may interfere with your ability to attend to
your fluid needs on as regular a basis as would be ideal.
Peter C. Rowe, MD, Department of Pediatrics
Hugh Calkins, MD, Department of Medicine
Jean Kan, MD, Department of Pediatrics
John Flynn, MD, Department of Medicine
Sally Snader, RN
Karen DeBusk, RN
Johns Hopkins Hospital, © January 1997
See also the Johns Hopkins information on
medications used for treating NMH and dietary recommendations for NMH
I have had Chronic Fatigue Syndrome since March 1997. Although I sometimes feel dizzy and/or light-headed, I have never fainted. Several doctors dismissed the idea of my taking a tilt table test as unnecessary. In March 1999, one doctor finally recommended the test. I welcomed the opportunity to take the test, but I really didn't think the result would be abnormal.
My test was handled by the University of California at Irvine Medical Group. The staff was wonderful. My one grievance is that they would not allow my husband to stay in the room during the test. While he waited outside, I was strapped to the table and connected to machines. The nurse explained the entire procedure to me, including the discomforts I might feel. As soon as the doctor arrived, we began the test.
At first, I simply felt the weakness and fatigue of standing. I tried continually talking with the nurse to distract myself. I also held my head down and kept my eyes shut. After a few minutes, I began to feel nauseous. Then, I looked up and saw only a blur of grey and white. I informed the staff that I was feeling sick, and they all gathered around me. I didn't know what was happening. I was shaking and sweating, feeling sick and ready to pass out. The doctor checked my vital signs. Then, he quickly lowered me and told me the test was over; my results were abnormal.
The experience was rather quick, but it was quite traumatic. I had to wait a while before I could even sit up. After a few more minutes, I was able to get dressed, and my husband helped me to our car. When we got home, I went to bed and slept. It took my body over a week to fully recover. My best advice to anyone preparing to take this test is (1) try to stay relaxed and just get through it; and (2) do not drive yourself! You will be exhausted after the test, and this exhaustion may last several days.
Procedure in detail: following informed consent, the patient is brought to the cardiac electrophysiologic laboratory. She is placed on the table; an iv was started in the right antecubital fossa. Her vital signs were monitored and were shown to be stable over five minutes. Heart rate was 72 and regular in sinus rhythm, blood pressure 115/60. The patient was then elevated to an 80 degree head upright tilt position. Within the first minute, the heart rate increased from 70 to 95, blood pressure changed from 115/60 to 120/60. The patient had no symptoms. Over the next five minutes, the heart rate gradually increased from 95 up to 120, blood pressure remained in the relatively narrow range and was essentially unchanged. Suddenly, the patient felt nauseated and faint like. At that time, the blood pressure dropped precipitously to 50/30 and the heart rate dropped to 50 in a junctional rhythm. The patient was then brought back down to a supine position, her legs were elevated and the patient recovered relatively uneventfully within a couple of minutes. Finally the heart rate and blood pressure returned to normal, heart rate was 62 and regular in sinus rhythm, blood pressure was 120/60.
In conclusion, Karen had the precipitation of neurally mediated syncope within the first eight minutes of the test, she developed hypotension and junctional rhythm and responded to standing upright.
DATE OF PROCEDURE: 04/22/1999
Home --
Photo Gallery --
Sign Guestbook --
Send Email
Get your own Free Home Page