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What I am meaning is : Do you have to frequently explain how your feeling because YOU DON'T Look SICK OR Has your illness taken a toll on your appearance and you Don't recognize yourself anymore (And you always say to yourself in the mirror WHAT HAS HAPPENED ?

I was noticing changes I've been experiencing since I became sick, and was wondering is this a invisible condition or have you all noticed changes within yourselves also.

Hi, I have constant extreme fatigue I feel Very unrefreshed in the A.M 10-11am is when I wake and quite mentally alert and the more I stay upright the more brain fog I get along with weakness (like I can't lift anything over a few lbs) but I can grip very well. I stay up all day and by midnight my body feels like I will not survive (like I'm gonna die) and I crash into a deep sleep and the cycle repeats all over again the next day. I'm beginning to hate everyday because I know what to expect, I have to push myself all the time if not I'd would be bedridden and my kids would be neglected. How long can I really go on??.... This Extreme Fatigue has been daily for over a year!!!!!!I wish someone would help me Mae

I'm a smoker have been for 12 years I wanna quit thats my next mission. Mae

Dear Kanasgirl, I am a mother of 2 small children 2 and 1 , I fully understand how you feel its very overwhelming the crying and the constant dependency can and does take its toll of OUR health even healthy people would feel this to a point, but it is worse for us because we are in constant recovery stage I hear the crying day and night and on top of that I have a very stressful marriage with many many issues in which I am crying when the kids are not!!!! I feel like I'm hanging from a cliff every day with a racing heart and numb ringertips I pray alot thats all I have I have no one to help me and I can't afford getting outside help so I just keep my faith and pray that I become stronger and I look forward to the school age days until then I try to get a schedule going and take it day by day. Mae ****** you can message me anytime

This was one of my scary symptoms I have been dealing with this spontaneous numbness&tingling for years now but it use to happen when I was pregnant or right after but I get it now if I lay to long on one side, Hold my arms up or elevate my legs to long. I was really worried when I had an MRI and they put that triangular cushion under your knees when she took it from under me and I went to stand up my legs were so heavy numb tingling and like jello and I was shaking rubbing and trying to get it to just go away finally it did about 1/2 hour later . Every time I get this I try massaging de-elevating and range of motion exercises and it does pass. Mae

Hello, I asked this question because the my POTS symptoms seemed to be getting more cope-able, so I decided to have " A beer" after about 3 sips I was very hot alittle woozy and then I manage to drink 1/2 the beer . I felt so tired all the veins in my hands were very plump like my B/p was on the rise. I went to lay down and feel asleep I woke up about an hour later in a Extreme panic state heart racing numbness in arms and face and was terrified . I drank 2 bottles of water and craved something sweet and it finally passed . This was a bad experience and I use to be a drinker you know like a six pack or sometimes 12 and sometimes it seemed alcohol didn't have any effect on me. But this is an absolute intolerance for me. I never wanna feel that again. I didn't have hangover feeling this time, but all the other times I ever drank I had very bad hangover with the extreme anxiety for the whole next day along with vomiting faintness all the rest. Thanks for all replies Mae

Can you describe your symptoms from consuming a small amount of alcohol?

I used KAVA KAVA and thats when I had the most heart palps and bad chest pains you could actually see my heart beat fluttering in my chest! I was using it for anxiety problems which it did help that, but the heart problems were too extreme and was DX at that time with MVP and years later was told I didn't have MVP no longer. Mae

Hello all, I have been battling this illness and have gone from doctor to doctor and praying many times a day to just send me to a doctor that will tell me whats wrong and believe me. I do only receive medicaid and the doctors I've seen wanted to refer me to MAYO but I could never afford it, so I called Cleveland clinic after the doctors here locally wouldn't give me the proper referral and they said they wouldn't see me with no referral and they couldn't talk about financial arrangements because it was against the law to accept money from someone on medicaid . I was at a loss along with this illness I was having family problems and at a deep deep depression I felt like giving up totally. The phone rang about an hour ago it was Cleveland clinic with no referral the administrator approved me being seen next month ITS A BLESSING truely its unbelievable you wouldn't believe how I'm feeling I WILL FINALLY GET THE ANSWER and I now know for a fact GOD is listening and it happens in his time. Maybe I sound alittle dramatic but I have truely witnessed a miracle right in my own life . Cleveland Clinic knew nothing of me ,except trying to get an appointment and the basic insurance information .... I guess the moral of my short stories is keep faith and keep praying because anything is possible . God bless everyone and HE truely hears you through all your suffering. Mae

Sorry no help here I have the same problem....????

Hi, I have never been able to work and never knew why I've been hired by many but whenever I'd start after about 2 hours the lighting and standing ,seemed to cause many symptoms and I would fight the feeling to finish the shift and I'd actually force myself to go for a few months then I just couldn't take it no more. I would say I've worked 3 years in total my whole life and I'm 30. I do receive disability which I immediately (3 months) due to my lack of employment history past doctors visits with these bizarre symptoms and was DX with generalized anxiety disorder and depression which I believe was a misdiagnosis of POTS. Mae

I choose Brain fog if I could think clearly then I would be able to handle the rest . I am or was a very strong person that could handle any obstacle in life but when you feel like your working with half a brain I feel hopeless. Mae

Thank you all I will get the test results I am sitting here with tears in my eyes this has been so hard and I am glad I do have support here, I have to stay positive its affecting me pretty bad, which you all have probally been where I am right now. I stayed on the TT for 30 minutes while HE read a magazine He wouldn't have known if I had POTS even if it was written on my forehead. Besides that my resting heartrate which I've been tracking for months is always 75-80 today it was 95 just because I was scared and dehydrated ,it goes up everyday from 75-80 to 120-135. And them poking with that IV needle and pushing it around in my veins 4 times was crazy and I always have an easy time with blood drawns well them getting them in my veins. Well girls I have to relax my 2 year old has to have dental surgery tomorrow 6 am and thats pretty stressful and thats very very early so I better get off this computer I did find some intresting article on POTS don't know if you all have seen it already but I copied it and it is kinda long but it makes me keep fighting to find the right doctor to get my DX. Talk more 2morrow The Postural Tachycardia Syndrome (POTS): Pathophysiology, Diagnosis & Management Satish R Raj, MD MSCI Autonomic Dysfunction Center, Division of Clinical Pharmacology, Departments of Medicine & Pharmacology, Vanderbilt University, Nashville, Tennessee, USA Address for correspondence: Satish R Raj MD MSCI, AA3228 Medical Center North, Vanderbilt University, 1161 21st Avenue South Nashville, TN, 37232-2195, USA. E-mail: satish.raj@vanderbilt.edu This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. References AbstractPostural tachycardia syndrome (POTS), characterized by orthostatic tachycardia in the absence of orthostatic hypotension, has been the focus of increasing clinical interest over the last 15 years 1. Patients with POTS complain of symptoms of tachycardia, exercise intolerance, lightheadedness, extreme fatigue, headache and mental clouding. Patients with POTS demonstrate a heart rate increase of ≥30 bpm with prolonged standing (5-30 minutes), often have high levels of upright plasma norepinephrine (reflecting sympathetic nervous system activation), and many patients have a low blood volume. POTS can be associated with a high degree of functional disability. Therapies aimed at correcting the hypovolemia and the autonomic imbalance may help relieve the severity of the symptoms. This review outlines the present understanding of the pathophysiology, diagnosis, and management of POTS. References IntroductionPostural tachycardia syndrome (POTS), characterized by orthostatic tachycardia in the absence of orthostatic hypotension, has been the focus of increasing clinical interest over the last 15 years [1]. Patients with POTS complain of symptoms of tachycardia, exercise intolerance, lightheadedness, extreme fatigue, headache and mental clouding. This disorder is not new [2], but has gone by many different names over the last 150 years, including mitral valve prolapse syndrome, neurocirculatory asthenia, orthostatic tachycardia, and orthostatic intolerance [3,4]. An advantage of the name postural tachycardia syndrome (POTS) is that it focuses attention on the sympathetic activation which characterizes the disorder. This review outlines the present understanding of the pathophysiology, diagnosis, and management of POTS. References Physiology of Upright PostureAssumption of the upright posture requires prompt physiological adaptation to gravity. There is an instantaneous descent of ~500 ml of blood from the thorax to the lower abdomen, buttocks, and legs. In addition, there is a 10-25% shift of plasma volume out of the vasculature and into the interstitial tissue [5]. This shift decreases venous return to the heart, resulting in a transient decline in both arterial pressure and cardiac filling. This has the effect of reducing the pressure on the baroreceptors, triggering a compensatory sympathetic activation that results in an increase in heart rate and systemic vasoconstriction (countering the initial decline in blood pressure). Hence, assumption of upright posture results in a 10-20 beat per minute increase in heart rate, a negligible change in systolic blood pressure, and a ~5 mmHg increase in diastolic blood pressure. Top Pathophysiology of Orthostatic DysregulationFailure of the regulatory mechanism to respond properly may lead to either orthostatic hypotension, as is seen in autonomic failure, or orthostatic tachycardia, as is seen in POTS. Orthostatic hypotension is defined as a fall in pressure on standing of more than 20/10 mmHg. However, it is common in patients with autonomic failure for the decline to be much greater than this, which may result in loss of consciousness soon after standing. On the other hand, in POTS, blood pressure is typically maintained on standing or may even increase. Heart rate rises more than 30 bpm and symptoms reminiscent of impaired cerebral perfusion may develop. References Clinical Presentation of Postural Tachycardia Syndrome (POTS)Diagnostic Criteria & Common Clinical Features POTS is defined (Table 1) as the presence of symptoms of orthostatic intolerance for at least 6 months accompanied by a heart rate increase of at least 30 beats/min within 5-30 minutes of assuming an upright posture. This should occur in the absence of orthostatic hypotension (a fall in blood pressure >20/10 mmHg). The syndrome must occur in the absence of prolonged bed rest, medications that impair autonomic regulation (such as vasodilators, diuretics, antidepressants or anxiolytic agents), or any other chronic debilitating disorders that might cause tachycardia (such as dehydration, anemia or hyperthyroidism). It is important to recognize that this syndrome is typically disabling. Hence, the mere observation of orthostatic tachycardia is not, by itself, sufficient to make the diagnosis of POTS. Table 1 Criteria for the Postural Tachycardia Syndrome Symptoms include mental clouding (?brain fog?), blurred or tunneled vision, shortness of breath, palpitation, tremulousness, chest discomfort, headache, lightheadedness and nausea. While pre-syncope is common in these patients, only a minority (~30%) actually pass out. The chest pains are almost never due to coronary artery obstruction, but are sometimes associated with electrocardiographic changes in the inferior leads, particularly when upright [6]. Many patients complain of significant exercise intolerance and extreme fatigue. Even activities of daily living, such as bathing or housework, may greatly exacerbate symptoms with resultant fatigue. This can pose significant limitations on their functional capacity. The disorder primarily affects women of child-bearing age. The female:male ratio is 4:1. The reason for the strong female predominance is not known, but it should be noted that orthostatic tolerance is reduced in normal healthy females [7]. Others disorders such as autoimmune diseases and irritable bowel syndrome are seen commonly in patients with POTS, and also have higher prevalence in women. Patients frequently report that their symptoms began following acute stressors such as pregnancy, major surgery, or a presumed viral illness, but in others cases, symptoms develop more insidiously. About 80% of female patients report an exacerbation of symptoms in the pre-menstrual phase of their ovulatory cycle (unpublished data). Gazit et al. have also reported an association between joint hypermobility and POTS [8]. Many patients have bowel irregularities and have been co-diagnosed with irritable bowel syndrome, and some have abnormalities of sudomotor regulation [9]. Psychological Profile in POTS Patients with POTS are sometimes clinically diagnosed as having anxiety disorders such as panic disorder. Indeed, patients demonstrate elevated scores on the Beck Anxiety Inventory [10] (23?10 vs. 7?8; P<0.001), a commonly used instrument that quantifies the magnitude of anxiety symptoms [11]. Unfortunately, this questionnaire includes somatic anxiety symptoms (such as palpitation) which can result from a hyperadrenergic state such as is seen in POTS. When a newer, cognitive-based measure of anxiety (the Anxiety Sensitivity Index [12]) is used, there was a trend toward less anxiety in the patients with POTS than the general population (15?10 vs. 19?9; P=0.063) [11]. Thus, much of the anxiety attributed to patients with POTS might be due to a misinterpretation of their physical symptoms. We did find that patients with POTS often have diminished attention and concentration compared to matched healthy volunteers [11]. Using the Inattention score from the Connors Adult ADHD Rating Scale [13], the patients with POTS scored significantly higher than did the normal control subjects. Physical Findings in POTS The most striking physical feature of POTS is the severe tachycardia that develops on standing from a supine position. Blood pressure and heart rate must be measured in both postures and should be taken not only immediately after standing but also at 2, 5 and 10 minutes as occasional patients have a delayed tachycardia [14]. Normal subjects commonly develop a transient tachycardia within the 1st minute of standing that should not be mistaken for POTS. A sustained heart rate increase ≥30 beats per minute is considered diagnostic of orthostatic tachycardia (Figure 1). The systolic blood pressure should not fall by more than 20 mmHg, and in many cases it will actually increase with standing. Recent data suggests that there may be a significant circadian variability in the orthostatic tachycardia seen in patients with POTS [15]. In a cohort of 17 patients with POTS, the orthostatic tachycardia was greater in the morning than in the evening (38?4 bpm vs. 27?3 bpm; P<0.001), while there was no diurnal difference in the orthostatic change in blood pressure. These data suggest that to optimize diagnostic sensitivity, postural vital signs should be performed in the morning. Figure 1 Hemodynamics with Upright Posture in POTS Cardiac auscultation may reveal a murmur of mitral valve prolapse, but significant mitral regurgitation is unusual. A striking physical feature of POTS is the dependant acrocyanosis that occurs in 40-50% of patients with POTS (Figure 2). These patients experience a dark red-blue discoloration of their legs, which are cold to the touch. This can extend from the feet to above the level of the knees. The reasons underlying this phenomenon are not clear. The current data suggest that the problem is not due to increased pooling in the venous capacitance vessels, but rather due to decreased blood flow in the skin [16,17]. Figure 2 Acrocyanosis in POTS Laboratory Abnormalities in POTS Some authors advocate the use head-up tilt table testing as a standardized method to assess an individual's response to a change in posture [1]. The patient is positioned on a standard tilt table and following baseline measurements of blood pressure and heart rate, the patient is inclined to a 70-degree head-up angle. Blood pressure and heart rate are then measured either continuously or at least every 12 minutes. The orthostatic tachycardia is often measured in a similar fashion to the standing test, with a similar threshold used to diagnose orthostatic tachycardia (an increase of ≥30 bpm) [1]. However, the physiology in response to passive standing on a tilt table (with the legs still) is not the same as?active standing? where the patient must support their own weight and maintain their balance. The latter requires use of the ?skeletal muscle pump? and mimics real life, while the tilt table does not. For this reason Streeten et al. use similar criteria for orthostatic tachycardia (>27 bpm), but only with active standing [18]. In a recent study, we compared the orthostatic heart rate response of these 2 methods, and found that the tilt table test was associated with an increased orthostatic tachycardia in both patients with POTS and control subjects [19]. While both tests were sensitive for the diagnosis of POTS with a 30 bpm threshold for orthostatic tachycardia, the stand test had a specificity of 79% compared to only 23% for the tilt table test.POTS patients should have only sinus tachycardia. An electrocardiogram should be done routinely to rule out the presence of an accessory bypass tract or any abnormalities of cardiac conduction. A Holter monitor might prove useful to exclude a re-entrant dysrhythmia, especially if the patient gives a history of paroxysmal tachycardia with a sudden onset and sudden offset. Other tests such as echocardiograms are only required in individual cases when there is doubt about the structural integrity of the heart. We often measure plasma norepinephrine levels in both a supine and standing position (at least 15 minutes in each position prior to blood sampling). The supine norepinephrine is often high normal in patients with POTS, while the upright norepinephrine is usually elevated (>600 pg/ml), a reflection of the exaggerated neural sympathetic tone that is present in these patients while upright. Tests of autonomic nervous system function typically show intact or exaggerated autonomic reflex responses. These patients often have preserved vagal function as reflected by their sinus arrhythmia ratio in response to deep breathing. They often have a vigorous pressor response to the Valsalva maneuver, with an exaggerated blood pressure recovery and overshoot both before and after release [20]. The blood volume is low in many patients with POTS [5]. This can be objectively assessed with nuclear medicine tests to directly measure either the plasma volume or the red cell volume. This knowledge may help to focus the treatment plan. Some patients with POTS have co-existent complaints of episodic flushing. In about half of these cases there is an associated mast cell activation disorder [20]. This can be diagnosed by collecting urine from individual 2-4 hour voids following a severe flushing spell for determination of methylhistamines. References Differential DiagnosisThe clinical picture of POTS can be confused with pheochromocytoma because of the paroxysms of hyperadrenergic symptoms. Patients with pheochromocytoma are more likely to have symptoms while lying down than POTS patients, and often have much higher plasma norepinephrine levels. The diagnosis of pheochromocytoma is made by assessment of plasma or urinary metanephrines [21]. There is commonly some confusion between neurally mediated syncope and POTS. There is a clinical overlap between the 2 disorders, such that about 30% of patients with POTS also have neurally mediated syncope. Nonetheless, most patients with POTS do not faint. Almost all patients with POTS also have associated fatigue. The reasons are not entirely clear. In some patients, but not all, the fatigue improves with pharmacological control of the orthostatic tachycardia. Some patients with POTS have symptomatic overlap with chronic fatigue syndrome. References Pathophysiology of POTSTachycardia and asthenia on standing is a final common pathway of many pathophysiological processes. POTS is therefore best viewed as a syndrome rather than a disease. Many disorders with a common key clinical presentation (the orthostatic tachycardia) have been described. Over the last decade, much has been learned about specific forms or sub-types within POTS, although a simple test to categorize the individual patient remains elusive. We discuss here the common POTS phenotypes including neuropathic POTS and central hyperadrenergic POTS (Figure 3). Figure 3 Pathophysiological Schema in POTS Neuropathic POTS Considering that POTS patients have high plasma NE levels, it would seem paradoxical that a neuropathy is proposed as an underlying process. Yet some of them have a form of dysautonomia, with preferential denervation of sympathetic nerves innvervating the lower limbs [22-24]. There have been several findings consistent with this hypothesis. The results of sudomotor axon reflex testing [22] and galvanic skin stimulation [23] support this as well as skin biopsy results [25]. Further, these patients have been found to be hypersensitive to infusions of norepinephrine and phenylephrine into veins of the foot, despite high circulating plasma norepinephrine concentrations [24]. This suggests that there is a denervation hypersensitivity of the leg veins. Using a segmental norepinephrine spillover approach, Jacob et al. [26] demonstrated that patients with POTS had normal sympathetic neuronal norepinephrine release in their arms, but less norepinephrine release (and thus less sympathetic activation) in their lower body. Hypovolemia & Blood Volume Regulation Many patients with POTS have low plasma volumes [27,28], but not all. To determine if hypovolemia existed in an unselected group of POTS patients, we studied 15 patients with POTS (not selected for blood volume) and 14 control subjects [5]. Plasma volume was measured using 131I labeled human serum albumin using a dye dilution technique, and compared to the predicted blood volume for each individual, based upon their height, weight, and gender. As can be seen in Figure 4, the control subjects did not have a significant plasma volume deficit (0.8?2.5%). In contrast, the patients with POTS had a plasma volume deficit of 12.8?2.0% (P<0.001). Figure 4 Blood Volume Deviation in POTS The renin-angiotensin-aldosterone system plays a key role in the neurohormonal regulation of plasma volume in humans. Plasma renin activity and angiotensin II would be expected to increase in response to hypovolemia in order to promote blood volume expansion. Angiotensin II promotes sodium and water retention directly by stimulating sodium resorption in the proximal tubules, and indirectly by stimulating aldosterone secretion. Patients with orthostatic tachycardia who were also hypovolemic have low levels of standing plasma renin activity and aldosterone compared to normovolemic patients [21,22]. This is true in both supine (190?140 pM vs. 380?230 pM; P=0.017) and upright posture (480?290 pM vs. 810?370 pM; P=0.019). One would have expected a compensatory increase in both plasma renin activity and aldosterone given the hypovolemia in these patients. This low level of plasma renin activity and aldosterone is a paradox that remains unexplained. These data suggest that abnormalities in the renin-angiotensin-aldosterone axis might have a role in the pathophysiology of POTS by contributing to hypovolemia and impaired sodium retention. Such hypovolemia could be accounted for by a neuropathic process involving the kidney. A significant modulator of renin release is the sympathetic nervous system. Thus perturbations in the renin-aldosterone system might result from partial sympathetic denervation involving the kidney. Central Hyperadrenergic POTS As a part of the definition, POTS is associated with a hyperadrenergic state (Table 1). In many such cases, the hyperadrenergic state is secondary to a partial dysautonomia or hypovolemia. There are some cases, however, in which the primary underlying problem seems to be excessive sympathetic discharge. These patients often have extremely high levels of upright norepinephrine. While we require the upright norepinephrine level to be >600 pg/ml for the diagnosis of POTS, the hyperadrenergic subgroup often has upright norepinephrine level >1000 pg/ml and it is occasionally >2000 pg/ml. These patients sometimes have large increases in blood pressure on standing, indicating that baroreflex buffering is somehow impaired. Central hyperadrenergic POTS in its most florid form is much less common than neuropathic POTS, comprising only ~10% of patients. Thus therapy in these cases usually targets a decrease in sympathetic tone both centrally and peripherally. Central sympatholytics such as methyldopa or clonidine can be used. Peripheral beta-adrenergic blockade may be better tolerated by these patients than by those with neuropathic POTS. Norepinephrine Transporter Deficiency A specific genetic abnormality has been identified in a kindred with hyperadrenergic POTS [30]. These individuals have a single point mutation in the norepinephrine transporter (NET). The resultant inability to adequately clear norepinephrine produces a state of excessive sympathetic activation in response to a variety of sympathetic stimuli. While rare, this mutation has taught us much about the importance of a functional NET. Although functional NET mutations might be infrequent, pharmacological NET inhibition is very common. Many antidepressant and attention deficit medications work at least in part through inhibition of NET. This includes traditional drugs such as tricyclic antidepressants, and newer medications which are pure NET inhibitors (e.g. atomoxetine or reboxetine). Both we [31] and others [32] have found that pharmacological NET inhibition can recreate an orthostatic tachycardia phenotype in susceptible healthy volunteer subjects. Yohimbine, a central alpha-2 antagonist that will also increase synaptic norepinephrine, can also cause orthostatic tachycardia [33]. Mast Cell Activation Some patients with POTS have co-existent mast cell activation. These patients have episodic flushing and abnormal increases in urine methylhistamine (the primary urinary metabolite of histamine) [20]. Methylhistamine should ideally be measured in 2 hour aliquots at the time of a flushing episode and not just in a random 24 hour period. Other associated symptoms include shortness of breath, headache, lightheadedness, excessive diuresis, and gastrointestinal symptoms such as diarrhea, nausea, and vomiting. Flushing can be triggered by long-term standing, exercise, premenstrual cycle, meals, and sexual intercourse. These patients often have a hyperadrenergic response to posture, with both orthostatic tachycardia and hypertension. They demonstrate a vigorous sympathetic vasopressor response during the Valsalva maneuver with a blood pressure overshoot in late phase II and an exaggerated phase IV blood pressure overshoot. It is not clear if mast cell activation, releasing vasoactive mediators, represents the primary event in these patients or if sympathetic activation, through release of norepinephrine, neuropeptide Y and ATP, is the cause of mast cell activation [34]. In these patients, beta-adrenergic antagonists can actually trigger an episode and worsen symptoms. Centrally acting agents to decrease the sympathetic nervous system discharge (e.g. methyldopa or clonidine) may prove effective. Alternatively, treatment could target mast cell mediators with a combination of antihistamines (H1- and H2-antagonists) and with the cautious use of non-steroidal agents (high dose aspirin) in refractory cases. References Non-Pharmacological Treatment of POTSNo therapy is successful for all patients with POTS. Initial efforts should focus on identifying and treating any reversible causes. Potentially contributory medications (especially vasodilators, diuretics, and drugs that inhibit NET) should be withdrawn. If a patient has been through prolonged bedrest, their symptoms will gradually improve as they recondition themselves to upright posture. Treatment should be optimized for any chronic disease that is present. If there is clear evidence of a re-entrant supraventricular arrhythmia, then this should be treated, including with radiofrequency ablation as appropriate. However, radiofrequency sinus node modification for the sinus tachycardia of POTS is not recommended. This often makes the patient?s symptoms worse (and occasionally the patient becomes pacemaker dependent). Specific therapies are summarized in Table 2. Table 2 Treatments for the Postural Tachycardia Syndrome It is important to educate the patient about the nature of the disorder. The patient should avoid aggravating factors such as dehydration, and extreme heat. In order to ensure adequate hydration, we ask our patients to consume 8-10 cups of water daily and to rapidly drink 16 fl oz of water to lower their heart rates [35]. In addition, they are asked to aggressively increase their sodium intake up to 200 mEq/day. This is often hard to achieve without NaCl tablets 1 gm/tablet TID with meals. Elastic support hose can help to minimize the degree of peripheral venous pooling and enhance venous return. We recommend 30-40 mmHg of counter-pressure and they should come up to the waist. If the stockings are only knee-high, a line of edema can form just above the stockings. Their use can be limited by their tolerability as the stockings can be hot, itchy and uncomfortable. Exercise (both aerobic and resistance training) is also encouraged and has been shown to be beneficial [36]. In addition to reversing any ?deconditioning?, this intervention can also increase blood volume. Vigorous exercise may acutely worsen symptoms and may even result in prolonged fatigue. It is important that patients start slowly and remain within range of their ?target heart rate? in the early stages to avoid symptoms that might discourage further exercise. Acute blood volume expansion is effective at controlling the heart rate and acutely improving symptoms. Jacob et al. [37] found that 1 liter of physiological saline infused intravenously over 1 hour decreased the orthostatic tachycardia from 33?5 bpm before the infusion to 15?3 bpm immediately following the infusion. The physiological saline was more effective at heart rate control than were treatments with either an alpha-1 agonist or an alpha-2 agonist. This treatment is not practical on a day to day basis as a medical setting is required to insert the intravenous catheter and infuse the saline. Recently, there have been reports of patients having regular saline infusions, typically 1 liter of normal saline every other day or every day. Many report an improvement in symptoms. However, there are not yet objective data to substantiate such benefit. Further, there is a risk of vascular access complications or infection. At this time, such therapy for patients with POTS should be considered cautiously. References Pharmacological Treatment of POTSNo medicines are approved by the United States Food and Drug Administration for the treatment of POTS. Thus all agents are used for this disorder are ?off label?. Furthermore, there are no pharmacological agents that have been tested in a long-term properly powered randomized clinical trial. In patients in whom the presence of hypovolemia is either known or strongly suspected, fludrocortisone (an aldosterone analogue) is often used. Through enhanced sodium retention, it should expand the plasma volume, although there is a paucity of data regarding the exact mechanisms of action. Although fairly well tolerated, side effects can include hypokalemia, hypomagnesemia, worsening headaches, acne, and fluid retention with edema. Another volume expanding agent that may be helpful for short-term use is oral vasopressin (DDAVP). This agent causes the kidney to retain free water, but not sodium. Potential side effects include hyponatremia, edema and headache. Erythropoietin has occasionally proven useful in patients with POTS who are refractory to other forms of therapy. While the primary mode of action is likely an increase in intravascular volume via its increase in red cell mass, erythropoietin also appears to have a direct vasoconstrictive effect, possibly through enhanced red cell mediated nitric oxide scavenging [38]. Treatment with erythropoietin has many drawbacks including the significant expense and the need for subcutaneous administration. Central sympatholytic medications are often useful and well tolerated in patients with the central hyperadrenergic form of POTS, but may not be as well tolerated in neuropathic POTS. Clonidine is an alpha 2 agonist that acts centrally to decrease sympathetic nervous system tone. Clonidine, at doses of 0.05 mg to 0.2 mg PO BID, can stabilize heart rate and blood pressure in patients with a large amount of postganglionic sympathetic involvement. Unfortunately, it can also cause drowsiness, fatigue and worsen the mental clouding of some patients. Methyldopa, a false neurotransmitter, is sometimes more successful in controlling symptoms in these patients at doses of 125 mg to 250 mg PO TID [39]. When used in low doses, beta-adrenergic antagonists can be useful. We typical use propranolol 10-20 mg PO BID-QID. While this dose range is small, such doses can often have a significant impact on heart rate control, and higher doses are often not tolerated due to hypotension and fatigue. Since a failure of vascular resistance may be an integral part of neuropathic POTS, vasoconstrictors such as midodrine (an alpha-1 agonist) can be employed [40]. Some patients cannot tolerate this agent due to the unpleasant sensation of scalp tingling or goosebumps. Midodrine can also cause hypertension. We recently reported that an unselected group of patients seen in our inpatient research unit were given a trial of the acetylcholinesterase inhibitor pyridostigmine. By increasing the levels of synaptic acetylcholine at both the autonomic ganglia and the peripheral muscarinic parasympathetic receptors, pyridostigmine significantly restrained the heart rate in response to standing in our patients with POTS. We prescribe pyridostigmine 30mg to 60 mg PO TID alone or in combination with low dose propranolol. Pyridostigmine can enhance bowel motility, so it is not always well tolerated in patients with diarrhea-predominant irritable bowel syndrome symptoms. While most of the treatments discussed above have focused on the control of heart rate, many patients are also greatly troubled by mental clouding. Modafinil, a stimulant whose mechanism is not yet clear, has been used in some patients with resulting improvement in alertness. However, caution is advised as it may aggravate the orthostatic tachycardia [41]. Top ConclusionsPOTS is a disorder of the autonomic nervous system in which many symptoms can be treated. The cardinal manifestation is symptomatic orthostatic tachycardia. The disorder can produce substantial disability among otherwise healthy people. Patients with POTS demonstrate a heart rate increase of ≥30 bpm with prolonged standing (5-30 minutes), often have high levels of upright plasma norepinephrine, and many patients have a low blood volume. Therapies aimed at correcting the hypovolemia and the autonomic imbalance may help relieve the severity of the symptoms. Continued research is vital to better understand this disorder and to differentiate its various subtypes.

Thank you Thankful. So how do I really get a DX of POTS??? I am so very fed up with all this

Well I wasn't to happy with my visit. I 1st told the tech I do not want the med because I'm very sensitive to meds she said she understood and said let the doc know in the mean time they had to poke me 4 times for an iv line I was so dehydrated and I was extremely nervous so while laying my heart was 95 which is not normal for me and I was shaking . The doc came in and I told him I was uncomfortable with taking the med He replied I don't need a back seat driver to tell me how to do a procedure and this is how I do it, if you don't want me to do my job then I will not test....I told him well won't you be able to see the change in vitals with the position changes and I also said other docs and clinics don't use meds . He turned his back and looked at me and said fine I'll do it but you need to see someone else for another opinion. I was so mad!!!! so when they tilted me my heart only jumped and stayed 120's and B/P never dropped . I told them I have only passed out one time ever I always feel faint( but don't pass out) Anyway the test was over and he said it was negative and walked out. Can someone please answer this does it take a positive TTT for POTS? and can you have POTS without B/P problems or have drop in B/P occasionally? Thanks Mae I'm so so so depressed

Hi, my symptoms well the extreme symptoms started after the birth of my last baby. Shortness of breath which I never had before delivery I have had many tests and this was the last stop (dysautonomia) but before this condition I had something called Postpartum cardiomyopathy (weakness of the heart muscle) that cardio said it could have caused the Shortness of breath but that recovered pretty quickly but the shortness of breath has stayed . It could be something hormonal theres so much to rule out. But good luck and congrats. Mae

I get tachy every time I stand does that mean I won't need an injection? I'm terrified I'm gonna refuse it anyway but will that affect my results? Have any of you not had to have the injection and could you explain exactly what you went through. Thanks Mae

All4family, I get this way also and it happens almost daily especially if I don't get sleep and wake before 10 am OR try to live a normal life. Its bad when I walk around in public and have to interact like after a doc visit speaking to a receptionist I'm totally GONE and don't even know what to say and I have to depend on my husband to finish. I never go out alone unless I feel really good which is maybe twice a month . It makes me feel like I'm in another world, I honestly thought I had brain cancer or something severe, but it goes away once I lay down at least an hour and even better if I just go to bed for the night and I wake with a new brain. There have been many nights I've been so bad with symptoms I really didn't think I'd wake up but anyway I'm still here ....and your not alone with this PROBLEM for sure! Mae

I noticed the past few warm days (warmer in my house anything above 70 degrees) I don't have pooling and I feel very overheated and much much dizzier , nausea, faintness and the pooling is gone and I'm kinda pale dull looking and like I can't move unless I have alot of effort and bad concentration.So I turned on the air and the pooling came back and so is everything else my thinking and energy is what it was not much, but better than with the warmth in the house . Is this common I mean I know what heat intolerance is but a few degrees above 70 does me in....... Mae

Thank you all, I guess a doc that knows about it its a good thing but he seems to just not care like its no big deal!!! Yes I do have the monitor on as we speak and I will have TTT either wednesday or friday of next week I just wish he could of been alittle nicer and more informational, but from coming to this site I probally know as much as he does LOL Mae**** and yes maybe he will take me more serious after the results of these tests fingers crossed

Hi, I will soon be going to Cleveland clinic if you don't mind me asking about Insurance stuff? Did you have to pay or deal with medicaid from another state or do you know if they have financial assistants? And how long was the visit just 1 day or longer? Thanks Mae

Hey all, I went to the doc today and I'll go step by step and tell me what you all think..... He asked questions about my heart symptoms I have occasional palps and pains sometimes it feels like it skips. I told him I'm like on a rocking boat all the time unless laying down. He asked if I'd bring past echos and stress tests, and told me to wear the 24 halter and TTT next week and prescribed compression hoses. He checked my B/P sitting was 120/80 standing it told me jump up and do standing B/P HE said it didn't drop he checked it without any time in between I mean SECONDS!!!! He was about to leave the room and I said Do you even specialize in dysautonomia because he never brought it up okay .... he said Yes I know of it I use to run the dysautonomia lab in Ohio do you just want me to send you to Cleveland Clinic? I looked at him dumbfounded and was lost for a minute I said well you don't treat it? or DX it? He said I do heart surgery and work on the hearts electrical system I said well ummmmm does dysautonomia affect the heart ??? He again said you want me to send to Clev. clinic I looked at my husband and was about to BREAK DOWN CRY FLIP OUT and I said JUST DO THE TESTS YOU CAN DO I don't have insurance to just go to that clinic and I've been to 20 something doctors in the past year and I'm really sick of going through this I said your the doctor I came for Medical advise and your asking me what I wanna do . He said we are just human being we don't walk on water we are not GOD . I was speechless , basically this doc once was a doctor that specialized In dysautonomia and lost all interested he wants to do these tests and send me on my way. I felt uncomfortable and questioning myself was this a blessing to get this doc because he does know about this condition and he knows the doc in Cleveland personally or should I feel like this man is a Quack and a jerk and he had very bad bed side manner. It kinda seemed like if thats what I have no big deal you don't need HEART surgery your wasting my time. Anyway good thing is since I have this monitor on I have had some palps so I won't look like a hypo and it will record my rapid rate right????? Well there was my little story it just seemed so weird to me And he cared nothing about any of my other symptoms! Mae

I voted weight loss. I was losing weight rapidly when symptoms worsen thoughout the month and gain when symptoms are milder. So through the month I can go from 103 to 96 every single month and never above 103. and I'm 5'3 Mae

Thanks sorry to sound so dramatic LOL I am alittle bit !!!!! I'll stay calm though