firewatcher

You could certainly do "tilt training," as long as you are allowed to get out of bed. That would at least prevent the cardiac atrophy portion of your rest. You simply stand still against a wall, or in front of a chair and allow your POTSiness to do the rest... Of course you sit down if you feel dizzy or pre-syncopal! There were several posts on tilt training in the past if you look for them. Being upright may be enough to keep you from getting the cardiac atrophy portion of deconditioning.

I actually wasn't thinking of rowing, but there are many other exercises that you can do supine that will get your HR up, but no stress your groin injury. You could get a set of pedals (like the physical therapists have) and pedal/cycle from a seated position, Pilates, arm exercises, etc. The article actually seemed to state that fluid was as important as exercise in maintaining conditioning. You may have to see a physical therapist anyway, so why wait? Good Luck!

J Appl Physiol. 2012 May;112(10):1735-43. Epub 2012 Feb 16. Effect of rowing ergometry and oral volume loading on cardiovascular structure and function during bed rest. Hastings JL, Krainski F, Snell PG, Pacini EL, Jain M, Bhella PS, Shibata S, Fu Q, Palmer MD, Levine BD. Source Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas and. Abstract This study examined the effectiveness of a short-duration but high-intensity exercise countermeasure in combination with a novel oral volume load in preventing bed rest deconditioning and orthostatic intolerance. Bed rest reduces work capacity and orthostatic tolerance due in part to cardiac atrophy and decreased stroke volume. Twenty seven healthy subjects completed 5 wk of -6 degree head down bed rest. Eighteen were randomized to daily rowing ergometry and biweekly strength training while nine remained sedentary. Measurements included cardiac mass, invasive pressure-volume relations, maximal upright exercise capacity, and orthostatic tolerance. Before post-bed rest orthostatic tolerance and exercise testing, nine exercise subjects were given 2 days of fludrocortisone and increased salt. Sedentary bed rest led to cardiac atrophy (125 ± 23 vs. 115 ± 20 g; P < 0.001); however, exercise preserved cardiac mass (128 ± 38 vs. 137 ± 34 g; P = 0.002). Exercise training preserved left ventricular chamber compliance, whereas sedentary bed rest increased stiffness (180 ± 170%, P = 0.032). Orthostatic tolerance was preserved only when exercise was combined with volume loading (-10 ± 22%, P = 0.169) but not with exercise (-14 ± 43%, P = 0.047) or sedentary bed rest (-24 ± 26%, P = 0.035) alone. Rowing and supplemental strength training prevent cardiovascular deconditioning during prolonged bed rest. When combined with an oral volume load, orthostatic tolerance is also preserved. This combined countermeasure may be an ideal strategy for prolonged spaceflight, or patients with orthostatic intolerance. PMID: 22345434 [PubMed - in process] Perhaps with something extra to expand your volume and some bedbound exercise to regularly get your heartrate up you won't atrophy as quickly.

There is this article: http://www.ncbi.nlm.nih.gov/pubmed/22575480 "The clinical symptoms related to NCS almost disappeared at 3 months after the treatment. All stents were patent at the duplex scan examination, without restenosis, and no secondary recurrence of the symptoms occurred at the end of the follow-up. CONCLUSIONS: Endovascular treatment is a safe, effective, and very minimally invasive technique that provides good long-term patency rates for patients with NCS, and under the premise morphologic measurements, 14-mm-diameter, 60-mm-long self-expanding stents should be first considered for Chinese patients with NCS."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2878259/ Mayo clinic article on nutcracker syndrome..."The frequency and severity of the syndrome vary from asymptomatic microhematuria to severe pelvic congestion.30,33 Although some patients have severe and persistent symptoms, many, especially children, are asymptomatic.30,34,35 Symptoms are often aggravated by physical activity22 and commonly include hematuria, pain or gonadal vein syndrome,36 varicocele,8,22,36,37 orthostatic proteinuria,19,38-46 and orthostatic intolerance.5,47..."

No clue!

Again, there was a recent article out of Vanderbilt on this one. http://www.ncbi.nlm.nih.gov/pubmed/21509337 Dysautonomians/Dysautonomiacs can have several sleep disturbances: obstructive apnea, central apnea, circadian rhythm disruption, and many others. I know that my sleep improved dramatically once the sympathetic overdrive was better controlled. With all the norepinephrine/epinephrine running through the system, it was like trying to sleep while being chased by a bear! There was just no way, the slightest noise would wake me...if I slept at all. Make sure you get a good sleep specialist, not just some pulmonologist looking for apnea. My sleep doc is one of my favorites and also one of my best advocates. He has told me that my symptoms will probably improve once I can sleep better (once the kids leave home,) but until then things will just be rough!

Clin Sci (Lond). 2012 Feb;122(4):183-92. doi: 10.1042/CS20110200. Neurohumoral and haemodynamic profile in postural tachycardia and chronic fatigue syndromes. Okamoto LE, Raj SR, Peltier A, Gamboa A, Shibao C, Diedrich A, Black BK, Robertson D, Biaggioni I. Source Vanderbilt Autonomic Dysfunction Center, Vanderbilt University School of Medicine, Nashville, TN, U.S.A. Abstract Several studies recognized an overlap between CFS (chronic fatigue syndrome) and POTS (postural tachycardia syndrome). We compared the autonomic and neurohormonal phenotype of POTS patients with CFS (CFS-POTS) to those without CFS (non-CFS-POTS), to determine whether CFS-POTS represents a unique clinical entity with a distinct pathophysiology. We recruited 58 patients with POTS, of which 47 were eligible to participate. A total of 93% of them reported severe fatigue [CIS (Checklist of Individual Strength), fatigue subscale >36], and 64% (n=30) fulfilled criteria for CFS (CFS-POTS). The prevalence of CFS symptoms (Centers for Disease Control and Prevention criteria) was greater in the CFS-POTS group, but the pattern of symptoms was similar in both groups. Physical functioning was low in both groups (RAND-36 Health Survey, 40±4 compared with 33±3; P=0.153), despite more severe fatigue in CFS-POTS patients (CIS fatigue subscale 51±1 compared with 43±3; P=0.016). CFS-POTS patients had greater orthostatic tachycardia than the non-CFS-POTS group (51±3 compared with 40±4 beats/min; P=0.030), greater low-frequency variability of BP (blood pressure; 6.3±0.7 compared with 4.8±1.0 mmHg2; P=0.019), greater BP recovery from early to late phase II of the Valsalva manoeuvre (18±3 compared with 11±2 mmHg; P=0.041) and a higher supine (1.5±0.2 compared with 1.0±0.3 ng/ml per·h; P=0.033) and upright (5.4±0.6 compared with 3.5±0.8 ng/ml per h; P=0.032) PRA (plasma renin activity). In conclusion, fatigue and CFS-defining symptoms are common in POTS patients. The majority of them met criteria for CFS. CFS-POTS patients have higher markers of sympathetic activation, but are part of the spectrum of POTS. Targeting this sympathetic activation should be considered in the treatment of these patients. PMID: 21906029 [PubMed - indexed for MEDLINE] PMCID: PMC3203411 Free PMC Article

The doctor has to suspect this to look for it. An abdominal ultrasound while standing and supine looks like the diagnostic test to evaluate for this.

Behav Brain Funct. 2011 Oct 27;7:46. Autonomic nervous alterations associated with daily level of fatigue. Tanaka M, Mizuno K, Yamaguti K, Kuratsune H, Fujii A, Baba H, Matsuda K, Nishimae A, Takesaka T, Watanabe Y. Source Department of Physiology, Osaka City University Graduate School of Medicine, Osaka, Japan. masa-t@msic.med.osaka-cu.ac.jp Abstract BACKGROUND: Fatigue is a common symptom in both sick and healthy people. We examined autonomic nervous alterations associated with fatigue to clarify the mechanisms underlying fatigue. METHODS: The study group consisted of 19 healthy participants who performed a 2-back test for 30 min as a fatigue-inducing mental task session. Before and after the session, they completed the advanced trail making test (ATMT) for 30 min for mental fatigue evaluation, subjective scales to measure fatigue sensation, and underwent electrocardiography to allow assessment of autonomic nerve activities. RESULTS: After the fatigue-inducing task, the total error counts on the ATMT tended to increase (P = 0.076); the ATMT for total trial counts (P = 0.001), the subjective level of fatigue (P < 0.001), and the % low-frequency power (%LF) (P = 0.035) increased significantly; and the % high-frequency power (%HF) decreased compared with before the fatigue-inducing task although this did not reach the statistical significance (P = 0.170). Although LF measured in absolute units did not change significantly before and after the fatigue-inducing task (P = 0.771), and HF measured in absolute units decreased after the task (P = 0.020). The %LF and LF/HF ratio were positively associated with the daily level of fatigue evaluated using Chalder's fatigue scale. In addition, %HF was negatively associated with the fatigue score. CONCLUSIONS: Increased sympathetic activity and decreased parasympathetic activity may be characteristic features of both acute and daily levels of fatigue. Our findings provide new perspectives on the mechanisms underlying fatigue. PMID: 22032726 [PubMed - indexed for MEDLINE] PMCID: PMC3214128 Free PMC Article

Best Pract Res Clin Rheumatol. 2011 Apr;25(2):141-54. Central pain mechanisms in chronic pain states--maybe it is all in their head. Phillips K, Clauw DJ. Source University of Michigan, Ann Arbor, MI, United States. kphill@med.umich.edu Abstract Mechanisms underlying chronic pain differ from those underlying acute pain. In chronic pain states, central nervous system (CNS) factors appear to play particularly prominent roles. In the absence of anatomical causes of persistent pain, medical sub-specialities have historically applied wide-ranging labels (e.g., fibromyalgia (FM), irritable bowel syndrome, interstitial cystitis and somatisation) for what now is emerging as a single common set of CNS processes. The hallmark of these 'centrally driven' pain conditions is a diffuse hyperalgesic state identifiable using experimental sensory testing, and corroborated by functional neuroimaging. The characteristic symptoms of these central pain conditions include multifocal pain, fatigue, insomnia, memory difficulties and a higher rate of co-morbid mood disorders. In contrast to acute and peripheral pain states that are responsive to non-steroidal anti-inflammatory drugs (NSAIDs) and opioids, central pain conditions respond best to CNS neuromodulating agents, such as serotonin-norepinephrine reuptake inhibitors (SNRIs) and anticonvulsants. Copyright © 2011 Elsevier Ltd. All rights reserved. PMID: 22094191 [PubMed - indexed for MEDLINE] PMCID: PMC3220875

World J Pediatr. 2012 May;8(2):116-22. Epub 2012 May 10. Newly-identified symptoms of left renal vein entrapment syndrome mimicking orthostatic disturbance. Koshimichi M, Sugimoto K, Yanagida H, Fujita S, Miyazawa T, Sakata N, Okada M, Takemura T. Source Department of Pediatrics, Kinki University School of Medicine, Osaka, Japan. Abstract BACKGROUND: In addition to the urinary abnormalities, symptoms of left renal vein entrapment between the aorta and superior mesenteric artery (left renal vein entrapment syndrome, LRVES) may include abdominal and flank pain as well as chronic fatigue. We investigated various LRVES symptoms in this study. METHODS: In 53 pediatric LRVES patients treated at our department, 22 had a score of 5 points or higher on orthostasis. Initial evaluation of LRVES by abdominal ultrasonography showed a stenotic-to-prestenotic vein diameter ratio of 0.2 or less. Definitive diagnosis was made by computed tomography and magnetic resonance angiography. Cortisol, catecholamine (CA), and brain natriuretic peptide (BNP) were also measured. RESULTS: The frequency of LRVES was 2.5 times higher in girls than in boys. Low or very low body mass indexes were seen in both sexes. The most common initial finding was urine abnormalities, followed by dizziness and malaise. In 6 patients, orthostasis precluded school attendance. Ten patients had orthostasis scores above 12. Patients unable to attend school had either low levels of plasma or urinary cortisol. Midodrine significantly decreased orthostasis scores. Some patients required treatment with fludrocortisone. Plasma CA, renin, and BNP levels were all normal. CONCLUSIONS: Locally excessive venous pressure may cause reversible adrenal dysfunction with transitory Addisonian symptoms. Children with cryptogenic malaise or severe orthostasis should be evaluated for LRVES. PMID: 22573421

I have read several articles that postulate that the fatigue is as central as the nervous system itself. Our nervous system is hypersensitive to pain and fatigue, so that what a "normal" person would feel/respond to is bone-crushing for us. We also cannot marshall the correct bodily responses to recover properly since our bodies are always in "crisis"/fight or flight mode. There is also a non-restorative sleep aspect to dysautomia/POTS, where even if we slept all day it isn't the same as eight hours of "normal" sleep. I know that a great deal of my fatigue is from pain and circadian rhythm disruption. I am not as tired when I can sleep to my own schedule.

Br J Psychiatry. 2012 Apr 26. [Epub ahead of print] Brain structure and joint hypermobility: relevance to the expression of psychiatric symptoms. Eccles JA, Beacher FD, Gray MA, Jones CL, Minati L, Harrison NA, Critchley HD. Source Brighton and Sussex Medical School, and Sussex Partnership National Health Service (NHS) Foundation Trust, Sussex Education Centre, Hove. Abstract Joint hypermobility is overrepresented among people with anxiety and can be associated with abnormal autonomic reactivity. We tested for associations between regional cerebral grey matter and hypermobility in 72 healthy volunteers using voxel-based morphometry of structural brain scans. Strikingly, bilateral amygdala volume distinguished those with from those without hypermobility. The hypermobility group scored higher for interoceptive sensitivity yet were not significantly more anxious. Our findings specifically link hypermobility to the structural integrity of a brain centre implicated in normal and abnormal emotions and physiological responses. Our observations endorse hypermobility as a multisystem phenotype and suggest potential mechanisms mediating clinical vulnerability to neuropsychiatric symptoms. PMID: 22539777

Here is a nice article explaining chronic illness and life insurance: http://www.investopedia.com/articles/pf/08/get-life-insurance.asp#axzz1ua5BTEY5 There is a huge difference between life insurance and health insurance, so your chances are better at getting life insurance since POTS is not supposed to shorten your lifespan (just your quality of life. ) Before you go off and get life insurance though, you need to ask yourself WHY you need it! Do you have small children or an income that would need to be replaced if you die? If you have no dependants, you probably don't need insurance! It may be expensive if you do need it and the underwriting will be tough (expects lots of paperwork and medical exams) but if your POTS just makes you miserable and does not put you at risk (and you can prove that) then you may be able to get it. There are policies out there specifically for the chronically ill, but they are usually low value, short term policies (which may be all you need.) Good luck and keep us posted as to what you find out.

BTW- my endo did an aldosterone/renin test, but did not follow proper protocols, so the test was not accurate. IF you know what tests you are having, research them yourself so that you know how to give the best samples!

My Endocrinologist was very good; he did orthostatic vitals on me during my first appointment and got me on the path to diagnosis. Generally, an Endo will want fasting bloodwork to start to check for blood sugar and other wonkiness that would be obvious. I was scheduled for several other tests within two weeks and given detailed instructions on how to prepare: cortisol, Lh/Fsh, estradiol, catecholamines, TSH, T4, thyroid antibodies, etc. Your symptoms will give him more of an idea what to look for. Be prepared to give a LOT of blood! I gave 17 vials in one day...I looked like I'd been attacked by a stapler wielding vampire! Have someone go with you for your fasting labs and testing, believe me, you don't want to drive after these. Good luck!

DDAVP is often given to children for bedwetting. The rationale behind the safety of doing this is that they won't drink anything once in bed, and it will allow the kidneys to retain water/concentrate urine until morning when that water is shed/dumped. DDAVP has several issues, mostly dealing with electrolyte issues due to over-drinking while the drug is active (hyponatremia) since desmopressin causes the kidney to retain water only and not sodium. I take dDAVP twice a day with a "dumping" period for several hours in the afternoon, this preserves and readjusts my electrolyte balance. I can lose up to 6 lbs of water during this time. The only negative effects that I had were when I first started taking it and was used to fluid loading. I've been on it since 2008 without bad side effects, at first I would have calf cramps and other electrolyte related issues until I "got the feel" for when to drink. I have been tested (correctly) several times for ADH levels and mine are not detectible, but the test is notoriously innaccurate; it is not a test that just any lab can do. If you take this drug, you need to be monitored closely by a doctor until you get an accurate measure of how much you can drink and what goes on in your body. I had blood-work done twice a day for several days over several weeks to make sure that my serum sodium levels were OK.

Diabetes Insipidus is not the same as Diabetes Mellitus. DI is a pituitary disorder where the kidneys do not concentrate urine due to a lack/lack of response to the pituitary hormone vasopressin. I would discuss it with your endocrinologist before you try it since the extra volume could possibly mess with your blood sugar levels. I can't take aspirin because of kidney issues, but my blood is measureably too thick (high serum osmolality/ high hematocrit.) DDAVP can cause a lot of side effects due to possible volume overload and resulting hyponatremia (low serum sodium,) so it needs to be monitored closely. I had blood tests done twice a day for several days when I first started taking it to make sure that I was not over-drinking. Does your doc think that your dysautonomia is due to your diabetes?

IF your heart rate issue is directly due to the hypovolemia, then a volume expander like dDAVP should lower it...BUT, it has no direct effect on the nervous system or heart muscle to lower HR. I have unconfirmed (just missing the official volume test) hypovolemia due to (questionable) partial diabetes insipidus and my orthostatic HR change is almost normal when my volume status is up; but it does nothing for exertional tachycardia.

I did those ropes...once. That kind of intense cardio will cause me to grey-out/black-out within two minutes. I am much better at strength training/Pilates. If I start feeling that way, I slowly cool down, continuing to move until I feel OK. I get the shaking too, it definitely signifies that I "overdid" it!

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3326904/?tool=pubmed This article points to some intriguing connections between the RAS and migraine (which is now classified as an autonomic disorder.)

Can J Physiol Pharmacol. 2012 Apr 18. [Epub ahead of print] Glutamate and GABA in the medial amygdala induce selective central sympathetic/parasympathetic cardiovascular responses. Neckel H, Quagliotto E, Casali KR, Montano N, Dal Lago P, Rasia-Filho AA. Source a Department of Basic Sciences, Federal University of Health Sciences of Porto Alegre, RS 90050-170, Brazil. Abstract Glutamate and γ-aminobutyric acid (GABA) participate in central cardiovascular control, and are found in the rat posterodorsal medial amygdala (MePD), an area of the forebrain that modulates emotional/social behaviors. Here we tested whether these neurotransmitters in the MePD could change the basal activity, chemoreflex, and baroreflex cardiovascular responses in awake rats. Power spectral analysis and symbolic analysis were used to evaluate these responses. Microinjections of saline, glutamate (2 µg), or GABA (61 ng or 100 µg; n = 5-7 rats per group) did not affect basal parameters or chemoreflex responses. However, baroreflex responses showed marked changes. Glutamate increased power spectral and symbolic sympathetic indexes related to both cardiac and vascular modulations (P < 0.05). In turn, the displacement of the baroreflex half-maximal heart rate (HR) response was associated with a GABA (61 ng) mediated decrease in the upper plateau (P < 0.05). Administration of GABA (61 ng, but not 100 µg) also increased HR variability (P < 0.05), in association with parasympathetic activation. These data add novel evidence that the MePD can promote selective responses in the central regulation of the cardiovascular system, i.e., glutamate in the MePD evoked activation of a central sympathetic reflex adjustment, whereas GABA activated a central parasympathetic one. PMID: 22512449 [PubMed - as supplied by publisher]

"My question is this: Are ALL forms of POTS "cured" with exercise and does it take it away forever or do you have to continue the exercise forever?" The anecdotal answer would probably be no, and yes, you have to exercise regularly for the rest of your life. Exercise can TREAT POTS, but it is not the CURE in some cases. I follow a POTS blog and this woman was a huge promoter of the exercise protocol; she relapsed when she stopped exercising. She also ended up having MCAS and having an anaphylactic reaction during exercise. Dr. Levine has been looking into the difference between fainting during and after exercise, and he states that there is a BIG difference (http://www.ncbi.nlm.nih.gov/pubmed/22386295 .) I am one of these; I don't get syncopal until I exert myself. He is also studying how to best treat forced, sedentary rest. This is from his latest article on it, and may help you: J Appl Physiol. 2012 Feb 16. [Epub ahead of print] The Effect of Rowing Ergometry and Oral Volume Loading on Cardiovascular Structure and Function During Bed Rest. Hastings JL, Krainski F, Snell PG, Pacini E, Jain M, Bhella PS, Shibata S, Fu Q, Palmer MD, Levine BD. Abstract Objective: This study examined the effectiveness of a short duration but high intensity exercise countermeasure in combination with a novel oral volume load in preventing bed rest deconditioning and orthostatic intolerance. Background: Bed rest reduces work capacity and orthostatic tolerance due in part to cardiac atrophy and decreased stroke volume. Methods: 27 healthy subjects completed 5 weeks of -6° head down bed rest. 18 were randomized to daily rowing ergometry and biweekly strength training, while 9 remained sedentary. Measurements included cardiac mass, invasive pressure-volume relations, maximal upright exercise capacity, and orthostatic tolerance. Prior to post-bed rest orthostatic tolerance and exercise testing, 9 exercise subjects were given 2 days of fludrocortisone and increased salt. Results: Sedentary bed rest led to cardiac atrophy (125±23 vs 115±20 g; P<0.001), however exercise preserved cardiac mass (128±38 vs 137±34 g; P=0.002). Exercise training preserved LV chamber compliance, while sedentary bed rest increased stiffness (180±170%, P=0.032). Orthostatic tolerance was preserved only when exercise was combined with volume loading (-10 ± 22%, P=0.169), but not with exercise (-14 ± 43%, P=0.047) or sedentary bed rest (-24 ± 26%, P=0.035) alone. Conclusions: Rowing and supplemental strength training prevents cardiovascular deconditioning during prolonged bed rest. When combined with an oral volume load, orthostatic tolerance is also preserved. This combined countermeasure may be an ideal strategy for prolonged spaceflight, or patients with orthostatic intolerance. PMID: 22345434

I got this a lot when I started exercising and before my diagnosis. I took my BP immediately after walking and it was commonly 88/80. My doctor at the time said that this wasn't possible and that my BP cuff was broken. I went out and bought another and it read exactly the same! My new/diagnosing doc explained it very nicely: when you exercise, your blood vessels dilate and the blood is moved into the muscles. When you stop, your vessels are still dilated, but the heart is not having to keep up with the muscular demand, so the blood is "pooling" in the muscle and not in the circulatory system so you become pseudo-hypovolemic (at least in my case.) So my BP actually was 88/80 and he was shocked that I could even see well enough to read the cuff! Needless to say, I was dizzy and feeling weird! I "fixed" this by slowing down gradually and then laying down for 10-15 minutes after every "workout" so that my BP and HR would normalize without sacrificing the blood to my brain.