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Found 6 results

  1. <p>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8924753&dopt=Abstract</p>
  2. edriscoll

    POTS: An overview

    An overview of Postural Orthostatic Tachycardia Syndrome Standing up is something most of us take for granted; we've been doing it since childhood. Our bodies automatically adjust to the pull of gravity by increasing vascular tone, heart rate, and cardiac output. Blood vessels contract, heart rates increase and our systolic blood pressure remains the same or decreases slightly while diastolic pressure increases slightly (Brunner & Suddarth, 2000, p. 546). Our bodies operate in perfect homeostasis and we stand up with little effort. However, the simple act of standing up can be a challenge for some people. There are disorders that affect the body's ability to appropriately adjust to the pull of gravity. When the body cannot effectively adjust to upright posture, a person is said to have orthostatic intolerance. Postural orthostatic tachycardia syndrome (POTS) is a disorder characterized by orthostatic intolerance. POTS is a disorder that is a part of the dysautonomia family of disorders. The criteria for diagnosis of POTS is: (1) a sustained increase in HR of at least 30 bpm within 10 minutes of standing (often with an absolute upright HR ≥ 120bpm); (2) in the absence of sustained orthostatic hypotension (drop in BP > 20/10mm Hg); (3) with symptoms of orthostatic intolerance for at least 6 months. In patients < 19 years of age, there is a higher HR threshold for POTS (increment  ≥40 bpm or absolute uprights HR  ≥ 120 bpm) due to physiological orthostatic tachycardia in adolescents and children (Singer et al., 2012) (Arnold, Ng, Raj, 2018) While the hallmark of POTS is an excessive heart rate increment upon standing, patients often exhibit numerous symptoms of autonomic nervous system dysregulation, and research by the Mayo Clinic suggests POTS is a limited autonomic neuropathy (Thieben, Sandroni, Sletten, Benrud-Larson, Fealey, Vernino, Lennon, Shen & Low, 2007). Many POTS symptoms seem to be caused by an imbalance of the Autonomic Nervous System's (ANS) control over blood flow. It is the autonomic nervous system (ANS) that regulates the needed adjustments in vascular tone, heart rate and blood pressure upon standing. Some of the messages coming from the autonomic nervous system tell the blood vessels to relax or tighten. In people with POTS, the system seems to be out of balance and blood is not going to the right place at the right time to do what the body needs (Fischer, 2007). The autonomic nervous system is responsible for regulating a multitude of organs and functions throughout the body. Some of these functions include temperature, respiration, pupil dilation and constriction, salivation and the digestive tract. A patient experiencing ANS dysregulation may experience abnormalities in the many organs and functions the ANS regulates. For example, around one third to one-half of POTS patients have digestive troubles (Fischer, 2007). The problem is that blood flow is not matching the need, so blood is not going to the right part of the intestinal system when it needs to. As a result, these people have trouble with nausea. For a smaller percentage of patients, the trouble is that there is too much blood in parts of the intestines. The body is attempting to digest food when there is no food to digest. This leads to cramping and colicky-like pains (Fischer, 2007). Patients commonly suffer from cognitive dysfunction, sleep disturbances and exercise intolerance. The symptoms can be exacerbated by numerous factors including dehydration, heat exposure, prolonged recumbency (resting, reclining), alcohol, menstruation, and acute exercise. Syncope (fainting) is not a predominant feature of POTS (only ~20–30% actually pass out, and this is usually thought to be due to vasovagal syncope) (Shen et al., 2017); however, many patients experience frequent pre-syncopal episodes that impair functional capacity. (Arnold, Ng, Raj, 2018) POTS can be categorized as primary, meaning it is idiopathic and not associated with other diseases, or secondary, meaning it is associated with a known disease or disorder (Grubb, Kanjwal & Kosinski, 2006). Common comorbidities include chronic fatigue syndrome, hypermobility type of Ehlers-Danlos syndrome, migraine, bowel irregularities, autoimmune disorders, and fibromyalgia(Garland et al., 2015). POTS is described as a clinical syndrome consisting of multiple heterogeneous disorders (disorders with diverse character). Some have taken to labeling "POTS Subtypes", with article published alluding to hyperadrenergic POTS ("Hyper POTS"), neuropathic POTS ("Neuro POTS"), or hypovolemic POTS. It is important to note that these subtypes do not all have standard definitions therefore there is a non-exclusivity of names with patients often having overlapping clinical features and symptoms that involve more than one subtype. Also, these subtypes do not have universally accepted definitions, so the labels can be misleading. "While one doctor may use the term "Hyper POTS" to refer to a specific set of findings, another doctor might think that it refers to a different set of findings. In theory, this could harm a patient's care. In our experience, these "subtype" labels are not clinically helpful." (Arnold, Ng, Raj 2018) People generally develop POTS after becoming sick with a virus, giving birth, or being exposed to great bodily stressors (i.e. surgery, trauma or chemotherapy). Some people have had POTS their entire lives. Teenagers sometimes develop the disorder during the years of rapid growth, and 75-80% of them can look forward to being asymptomatic when they reach adulthood (Grubb, Kanjwal & Kosinski, 2006). The symptoms of POTS are life-altering and debilitating at times. POTS patients use about three times more energy to stand than a healthy person (Grubb, 2002). It is as if these patients are running in place all the time. Activities such as housework, bathing, and even meals can exacerbate symptoms (Grubb, Kanjwal & Kosinski, 2006). Research shows that POTS patients' quality of life is similar to those with congestive heart failure and chronic obstructive pulmonary disease (Benrud-Larson, Dewar, Sandroni, Rummans, Haythornthwaite & Low, 2002) Twenty-five percent of people with POTS are disabled and unable to work (Goldstein, Robertson, Esler, Straus, & Eisenhofer, 2002). Most patients will have to make some lifestyle adjustments to cope with this disorder. It was once estimated that nearly 500,000 Americans had POTS, which made standing up a challenge (Robertson, 1999). However, with research advances and growing physician education, the number of people found to have POTS symptoms is steadily rising. It is now estimated that one out of every hundred teens has POTS (Fischer, 2007). The minimal requirements to detect POTS on initial evaluation are a detailed medical history, physical examination with orthostatic vitals and a resting 12-lead ECG (Sheldon et al, 2015) The medical history should document medications, other medical conditions including personal and family history of cardiac disease, joint hypermobility, autoimmunity or neurological disorders, and the nature of tachycardia including potential triggers, frequency, time of day, association with pre-syncopal or syncopal episodes, symptoms, and impact on daily activities. (Arnold, Ng, Raj 2018) POTS has a strong female predominance (4–5:1), and primarily affects women of childbearing age. Most patients present with POTS between 13 and 50 years of age, with a family history of orthostatic intolerance reported in approximately 13% of patients (Thieben et al., 2007).The onset can be sudden or gradual. The quantity and severity of symptoms vary from day to day. There are treatments for POTS symptoms which can be tailored to each individual patient, especially if an underlying cause is discovered. Researchers are attempting to identify and treat the mechanisms and causes of POTS. Studies show that most patients will eventually be able to stand up with fewer symptoms (Low, 2000). Most people with POTS can look forward to experiencing improvement with proper treatment. For more information on POTS, please view our other POTS links and resources. References 1. Amy C. Arnold, Jessica Ng, Satish Raj Postural tachycardia syndrome: Diagnosis, Physiology and Prognosis Autonomic Neuroscience, Vol 215 December 2018 https://doi.org/10.1016/j.autneu.2018.02.005 2. Benrud-Larson, L. M., Dewar, M. S., Sandroni, P., Rummans, T. A., Haythornthwaite, J. A., & Low, P. A. (2002, June). Quality of life in patients with postural tachycardia syndrome. Mayo Clinic Proceedings, 77, 531-537. Full text: http://www.mayoclinicproceedings.com/inside.asp? AID=112&UID= 3. Brunner, L. S. & Suddarth, D. S. (2000). Assessment of cardiovascular function. In S. C. Smeltzer & B. G. Bare (Eds.), Brunner and Suddarth's textbook medical-surgical nursing (pp. 532-563). Philadelphia, PA: Lippincott Williams and Wilkins. 4. Fischer, P. (2007). Postural orthostatic tachycardia syndrome. Mayo Clinic Podcast. http://www.podcastingnews.com/details/www. mayoclinic.org/rss/heart-podcast.xml/view.htm 5. Goldstein, D., Robertson, D., Esler, M., Straus, S., & Eisenhofer, G. (2002). Dysautonomias: clinical disorders of the autonomic nervous System. Ann Intern Med., 137, 753–763. Full Text 6. Grubb, B. P. (2000, July). Orthostatic intolerance. National Dysautonomia Research Foundation Patient Conference. Minneapolis, Minnesota. 7. Grubb, B. P. (2002, October). The heterogeneity of symptoms related to dysautonomia. Symposium conducted at the meeting of the National Dysautonomia Research Foundation Northwest Ohio Support Group. Toledo, Ohio. 8. Grubb B. P., Kanjwal, Y., & Kosinski, D. J. (2006). The postural tachycardia syndrome: A concise guide to diagnosis and management. J Cardiovasc Electrophysiol., 17, 108-112. 9. Grubb, B. P., & McMann, M. C. (2001). The Fainting Phenomenon: Understanding why people faint and what can be done about it. New York: Futura Publishing Company. 10. Low, P. A. (2000, July). Orthostatic intolerance. National Dysautonomia Research Foundation Patient Conference. Minneapolis, Minnesota. 11. Robertson, D. (1999). The epidemic of orthostatic tachycardia and orthostatic intolerance. The American Journal of the Medical Sciences, 317, 75- 77. 12. Thieben, M. J., Sandroni, P., Sletten, D. N., Benrud-Larson, L. M., Fealey, R. D., Vernino, S., Lennon, V. A., Shen, W. K., & Low, P. A., (2007). Postural orthostatic tachycardia syndrome: the Mayo Clinic experience. Mayo Clin. Proc. 82, (3), 308-313. Full Text
  3. the article says: "The next time you get your blood pressure checked, ask your health provider to take measurements on both arms. Having a difference in readings between arms could indicate a condition called peripheral artery disease, a narrowing of the blood vessels in the arms and legs that restricts blood flow to the heart and raises the risk of a heart attack and stroke." http://bostonglobe.com/lifestyle/health-wellness/2012/01/30/weekly-challenge-check-your-blood-pressure-both-arms/k1dGVXlGgDjNe0qIlQocCK/story.html
  4. Hi everyone, Sorry if this is something that's been discussed, but I couldn't find it in any past threads. I've recently started midodrine and noticed that my systolic blood pressure has risen from the low range (used to be 80-90 and is now 90-120), but my diastolic blood pressure is still pretty low (anywhere from 40s-60s). I know that diastolic bp is the pressure when your heart is not beating, but what does that mean as far as POTS and symptoms go? I have to say, I've felt different, but not exactly better on midodrine so far--it's almost like I have more nervous energy sometimes, but I still have the weakness, shakiness, dizziness, and overall fatigue/crappiness as usual! Also, I've seen posts about many people have LOW pulse pressure, but it would seem that mine is really pretty high since my diastolic is so low but my systolic is pretty normal. I guess I would be averaging a pulse pressure of about 60 now where it used to be more like 30. I guess I'm just trying to figure out what this change might indicate and if it's a sign that midodrine is helping or not. Does anyone else have this kind of bp reading, or could anyone tell me what it might indicate is going on? Thanks in advance!
  5. Hi Everyone, I've been researching and researching non-stop and I've read through everyone's issues, every Dysautonomia website and it's all lead me to this post. I have a theory I'm working on and discussing with some Dysautonomia doctors. My theory only relates to our symptoms in a secondary nature because there are many primary causes and bundled all together it's causing different type of Dysautonomia. My theory unfortunately does not lead to a cure or even a cause but I believe it can help many of use with better treatment. My Theory: Our Dysautonomia symptoms are the result of imbalances in our blood pressure either systemically (through our whole circulatory system http://en.wikipedia.org/wiki/Systemic_disease), localized blood pressure imbalances (isolated to one organ at a time http://en.wikipedia.org/wiki/Localized_disease) and in some cases the imbalance of blood pressure disseminates to other organs (starts in one but spreads to others http://en.wikipedia.org/wiki/Disseminated_disease). Explanation: Our Autonomic Nervous systems (ANS) ( Para and Sympathetic) control our "flight or fight (FoF)" response but they also control our blood pressure using arterial sympathetic tonus which is separate from our FoF response. Our two ANS systems basically play a ping pong match to keep everything stable. Depending on what organ of the body either one (Symp or Para) constrict or dilate. I pasted examples below from Wikipedia. You will see Mast Cells, Blood Vessels, Digestive tract, Endo and Urinary, etc... Basically all Dysautonomia patient symptom areas. Okay so that's the basics, here is the details. I believe that at the heart of our Dysautonomia symptoms are our Arteries. Depending what primary disease, illness, complication, whatever... they are effecting the pressure in our arteries. This pressure is then causing our symptoms. And depend what primary issue you have it can affect our pressure systemically, locally or by diffusion. I believe there are two keys to lowering our symptoms. 1. We find the primary disease and we treat it. Unfortunately it seems that most of our primary disease have very poor treatment options and just are rarely curable and sometimes hardly manageable. 2. Is we locate our blood pressure issue, especially if it is localized and we get doctors to treat specific local blood pressure issues. Here are some of the local blood pressure issues I've found thus far. A) Pulmonary Pressure- Breathing issues, faintness http://en.wikipedia.org/wiki/Pulmonary_hypertension Intercranial Pressure- Brain issues- may cause dizziness, nausua, headaches http://en.wikipedia.org/wiki/Intracranial_pressure C) Renovascular hypertensions- Kidney issues- http://en.wikipedia.org/wiki/Renovascular_hypertension These are just a few of the more prevalent localized BP issues but there are others. Treatment is not great for BP issues because most medicines operate on a systemic level and go into our entire blood stream. And if a patient is has Pulmonary Hypertension but has systemic Hypotension then anti hypertension meds will help the breathing issues but exacerbate the systemic Hypotension. The hope is that they find meds that are selective to certain organs. They do have such meds for certain treatments and they are called "selective." Also note worthy is that hypertension is related to Mitochondrial issues, Nitric Oxide issues, endothelium issues and a few more vascular issues. And there are new CT Scans (which I posted) that will help diagnose they BP issues in the future... http://en.wikipedia.org/wiki/Autonomic_nervous_system Blood vessels Target Sympathetic (adrenergic) Parasympathetic (muscarinic) vascular smooth muscle in general α1:[5] contracts; β2:[5] relaxes M3: relaxes [4] renal artery α1[6]: constricts --- larger coronary arteries α1 and α2[7]: constricts [4] --- smaller coronary arteries β2:dilates [8] --- arteries to viscera α: constricts --- arteries to skin α: constricts --- arteries to brain α1[9]: constricts [4] --- arteries to erectile tissue α1[10]: constricts M3: dilates arteries to salivary glands α: constricts M3: dilates hepatic artery β2: dilates --- arteries to skeletal muscle β2: dilates --- Veins α1 and α2 [11] : constricts β2: dilates --- [edit]Other Target Sympathetic (adrenergic) Parasympathetic (muscarinic) platelets α2: aggregates --- mast cells - histamine β2: inhibits --- [edit]Respiratory system Target Sympathetic (adrenergic) Parasympathetic (muscarinic) smooth muscles of bronchioles β2:[5] relaxes (major contribution) α1: contracts (minor contribution) M3:[5] contracts The bronchioles have no sympathetic innervation, but are instead affected by circulating adrenaline [4] [edit]Nervous system Target Sympathetic (adrenergic) Parasympathetic (muscarinic) Pupil dilator muscle α1: Contracts (causes mydriasis) - Iris sphincter muscle - M3: contracts (causes miosis) Ciliary muscle β2: relaxes (causes long-range focus) M3: contracts (causes short-range focus) [edit]Digestive system Target Sympathetic (adrenergic) Parasympathetic (muscarinic) salivary glands: secretions β: stimulates viscous, amylase secretions α1: stimulates potassium secretions M3: stimulates watery secretions lacrimal glands (tears) β: stimulates protein secretion [12] --- juxtaglomerular apparatus of kidney β1:[5] renin secretion --- parietal cells --- M1: Gastric acid secretion liver α1, β2: glycogenolysis, gluconeogenesis --- adipose cells β1,[5] β3: stimulates lipolysis --- GI tract (smooth muscle) motility α1, α2,[13] β2: decreases M3, (M1) [4]: increases sphincters of GI tract α1,[5] α2,[4] β2: contracts M3:[5] relaxes glands of GI tract no effect [4] M3: secretes [edit]Endocrine system Target Sympathetic (adrenergic) Parasympathetic (muscarinic) pancreas (islets) α2: decreases insulin secretion from beta cells, increases glucagon secretion from alpha cells M3[14][15]: increases secretion of both insulin and glucagon.[14][15] adrenal medulla N (nicotinic ACh receptor): secretes epinephrine and norepinephrine --- [edit]Urinary system Target Sympathetic (adrenergic) Parasympathetic (muscarinic) Detrusor urinae muscle‎ of bladder wall β2:[5] relaxes M3:[5] contracts internal urethral sphincter α1:[5] contracts M3:[5] relaxes [edit]Reproductive system Target Sympathetic (adrenergic) Parasympathetic (muscarinic) uterus α1: contracts (pregnant[4]) β2: relaxes (non-pregnant[4]) --- genitalia α1: contracts (ejaculation) M3: erection [edit]Integumentary system Target Sympathetic (muscarinic and adrenergic) Parasympathetic sweat gland secretions M:[5] stimulates (major contribution); α1: stimulates (minor contribution) --- arrector pili α1: stimulates --- [edit]References
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