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Lawrence Family Vision Clinic, 3111 W 6th St # a, Lawrence, Ks 66049

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Status in which a change from lying to standing causes an abnormally large increase in heart rate

Medical status

Postural orthostatic tachycardia syndrome
Other names Postural tachycardia syndrome (POTS)
Dependent Acrocyanosis in a Norwegian 33-year old male POTS patient.jpg
Acrocyanosis in a male Norwegian POTS patient.
Specialty Cardiology, Neurology
Symptoms More oftentimes with continuing: lightheadedness, problem thinking, tachycardia, weakness,[i] palpitations, heat intolerance, acrocyanosis
Usual onset Most common (modal) age of onset is fourteen years[2]
Duration > half dozen months[3]
Causes Antibodies confronting the Blastoff ane adrenergic receptor and muscarinic acetylcholine M4 receptor[four] [5] [six]
Risk factors Family history[1]
Diagnostic method An increase in heart charge per unit by xxx beats/min with standing[1]
Differential diagnosis Dehydration, heart problems, adrenal insufficiency, epilepsy, parkinson disease[7]
Treatment Avoiding factors that bring on symptoms, increasing dietary common salt and h2o, compression stockings, practise, medications[1]
Medication Beta blockers, Ivabradine, midodrine, and fludrocortisone.[1]
Prognosis ~90% better with treatment,[eight] 25% of patients unable to work[nine]
Frequency ~ 500,000 (US)[vii]

Postural orthostatic tachycardia syndrome (POTS) is a condition in which a change from lying to continuing causes an abnormally large (or college than normal) increase in heart beat rate.[1] This occurs with symptoms that may include lightheadedness, trouble thinking, blurred vision, or weakness.[1] Other normally associated conditions include Ehlers–Danlos syndrome, mast cell activation syndrome, irritable bowel syndrome, indisposition, chronic headaches, chronic fatigue syndrome, and fibromyalgia.[1] It can exist treated with lifestyle changes such as increasing fluid and common salt intake, compression stockings, rising slowly later lying downward, fugitive prolonged bedrest, and medication.

Causation [edit]

The causes of POTS are varied.[x] Frequently, it begins after a viral infection, surgery, or pregnancy.[eight] Hazard factors include a family history of the condition.[1] Diagnosis in adults is based on an increase in eye rate of more than 30 beats per minute within x minutes of standing up that is accompanied by symptoms.[one] Low claret pressure with standing, even so, may non occur.[1] Other conditions which can cause like symptoms, such as aridity, centre problems, adrenal insufficiency, epilepsy, and parkinson disease, must not be present.[vii]

Treatment may include fugitive factors that bring on symptoms, increasing dietary common salt and h2o, small and frequent meals,[11] abstention of immobilization,[11] pinch stockings, exercise program, and medications.[12] [13] [ane] [fourteen] Medications used may include beta blockers,[15] pyridostigmine,[xvi] midodrine[17] or fludrocortisone.[1] More fifty% of people whose status was triggered by a viral infection become better inside five years.[eight] Well-nigh 80% have symptomatic improvement with treatment, but 25 pct of patients are still unable to work.[ix] [eight] Retrospective studies has shown that five years after diagnosis nineteen% had a full resolution of symptom.[18]

Information technology is estimated that 500,000 people are afflicted in the United States.[xix] The average age of onset is 20 years one-time, and information technology occurs near five times more than often in females.[one]

Signs and symptoms [edit]

In adults, the primary manifestation is an increase in eye charge per unit of more 30 beats per minute inside 10 minutes of continuing up.[1] [20] The resulting heart charge per unit is typically more than than 120 beats per infinitesimal.[1] For people anile betwixt 12 and 19, the minimum increase for diagnosis is 40 beats per infinitesimal.[21] This is known as orthostatic (upright) tachycardia (fast heart rate). It occurs without whatever coinciding drop in blood pressure, every bit that would indicate orthostatic hypotension.[xx] Certain medications to treat POTS may crusade orthostatic hypotension. It is accompanied by other features of orthostatic intolerance—symptoms that develop in an upright position and are relieved by reclining.[20] These orthostatic symptoms include palpitations, light-headedness, chest discomfort, shortness of breath,[20] nausea, weakness or "heaviness" in the lower legs, blurred vision, and cerebral difficulties.[1] Symptoms may be exacerbated with prolonged sitting, prolonged standing, alcohol, heat, exercise, or eating a big meal.[ citation needed ]

In upwards to one third of people with POTS,[ane] fainting occurs in response to postural changes or exercise.[22] Migraine-like headaches are common, sometimes with symptoms worsening in an upright position (orthostatic headache).[22] 40–50% of patients with POTS develop acrocyanosis of extremities, a blood-red-purple color in the legs and/or hands when they stand up (indicative of blood pooling).[23] [22] [24] 48% of people with POTS written report chronic fatigue and 32% written report sleep disturbances.[25] [26] [27] [28] Others exhibit simply the cardinal symptom of orthostatic tachycardia.[22] Boosted signs and symptoms are varied, and may include excessive sweating, a lack of sweating, heat intolerance, digestive issues such as bloating, nausea, indigestion, constipation, and diarrhea, a flu-like feeling, coat-hanger pain, forgetfulness, brain fog, and presyncope.[29]

Brain fog [edit]

Ane of the about disabling and prevalent symptoms in POTS is "encephalon fog",[30] a term used by patients to describe the cognitive difficulties they experience. In one survey of 138 POTS patients, brain fog was divers as "forgetful" (91%), "difficulty thinking" (89%), and "difficulty focusing" (88%). Other common description was "Difficulty processing what others say" (80%), Confusion (71%), Lost (64%), and "Thoughts moving besides speedily" (40%)[31] The same survey described the most common triggers of brain fog to be fatigue (91%), lack of sleep (90%), prolonged standing (87%) and dehydration (86%).[ citation needed ]

Neuropsychological testing has shown that a POTS-patient has reduced attention (Ruff 2&7 speed and WAIS-III digits forward), short-term retention (WAIS-III digits back), cognitive processing speed (Symbol digits modalities test) and executive function (Stroop word color and trails B).[32] [33] [34]

A potential cause for encephalon fog is a decrease in cerebral blood flow (CBF), especially in upright position.[35] [36] [37]

Another theory is that interoception of excessive autonomic activeness causes interoceptive prediction errors (PE) to occur.[38] A prediction fault is the mismatch between a prior expectation and reality.[39] This would cause anxiety which so overwhelms the consciousness of POTS-patient causing cognitive-affective symptoms. This so makes them predisposed to response-focused emotion regulation (ER) instead of an ancestor-focused ER.[38] [40] [41] [42]

Causes [edit]

The symptoms of POTS tin be caused by several distinct pathophysiological mechanisms.[20] These mechanisms are poorly understood,[21] and tin can overlap, with many people showing features of multiple POTS types.[20] Many people with POTS showroom depression blood volume (hypovolemia), which can decrease the rate of blood flow to the heart.[twenty] To compensate for this, the center increases its cardiac output past beating faster,[43] leading to the symptoms of presyncope and reflex tachycardia.[20]

In the thirty% to 60% of cases classified as hyperadrenergic POTS, norepinephrine levels are elevated on standing,[1] often due to hypovolemia or partial autonomic neuropathy.[20] A smaller minority of people with POTS take (typically very high) standing norepinephrine levels that are elevated even in the absence of hypovolemia and autonomic neuropathy; this is classified as cardinal hyperadrenergic POTS.[twenty] [24] The high norepinephrine levels contribute to symptoms of tachycardia.[20] Some other subtype, neuropathic POTS, is associated with denervation of sympathetic nerves in the lower limbs.[xx] In this subtype, it is thought that dumb constriction of the blood vessels causes claret to pool in the veins of the lower limbs.[1] Heart rate increases to compensate for this blood pooling.[44]

In up to 50% of cases, there was an onset of symptoms following a viral illness.[45] Information technology may too be linked to vaccination, physical trauma, concussion, pregnancy, or surgery.[46] [11] [22] It is believed that these events could act as a trigger for an autoimmune response that result in POTS.[47]

POTS is more common in females than males. It has too been shown to be linked in patients with acute stressors such every bit pregnancy, contempo surgery, or contempo trauma. POTS also has been linked to patients with a history of autoimmune diseases,[46] irritable bowel syndrome, anemia, hyperthyroidism, fibromyalgia, diabetes, amyloidosis, sarcoidosis, systemic lupus erythematosus, and cancer. Genetics likely plays a part, with one study finding that one in eight POTS patients reported a history of orthostatic intolerance in their family.[43]

Associated Co-morbidities[2] [48]
Migraine headaches (11-40%)
Ehlers–Danlos syndrome (twenty-25%)
Fibromyalgia (xi-20%)
Irritable bowel syndrome (seven-xxx%)
Chronic fatigue syndrome (7-21%)
Mast prison cell activation disorder (6-nine%)

Autoimmunity [edit]

There is an increasing number of studies indicating that POTS is an autoimmune illness.[46] [49] [fifty] [four] [51] [52] A high number of patients has elevated levels of autoantibodies against the adrenergic alpha 1 receptor and against the muscarinic acetylcholine M4 receptor.[53] [5] [54]

Especially elevations of adrenergic α1 receptor is associated with symptoms severity in patients with POTS.[53]

Secondary [edit]

If POTS is caused by another condition, it may exist classified equally secondary POTS.[viii] Chronic diabetes mellitus is one common crusade.[viii] POTS tin besides be secondary to gastrointestinal disorders that are associated with low fluid intake due to nausea or fluid loss through diarrhea, leading to hypovolemia.[1] Systemic lupus erythematosus and other autoimmune diseases have as well been linked to POTS.[46]

In that location is a subset of patients who present with both POTS and mast jail cell activation syndrome (MCAS), and it is non all the same clear whether MCAS is a secondary crusade of POTS or simply comorbid, however, treating MCAS for these patients can significantly improve POTS symptoms.[12]

POTS can besides co-occur in all types of Ehlers–Danlos syndrome (EDS),[22] a hereditary connective tissue disorder marked by loose hypermobile joints prone to subluxations and dislocations, pare that exhibits moderate or greater laxity, easy bruising, and many other symptoms. A trifecta of POTS, EDS, and Mast Cell Activation Syndrome (MCAS) is becoming increasingly more common, with a genetic mark common among all three atmospheric condition.[55] [56] [57] [58] POTS is also often accompanied by vasovagal syncope, with a 25% overlap existence reported.[59] At that place are some overlaps between POTS and chronic fatigue syndrome, with bear witness of POTS in 10–20% of CFS cases.[60] [59] Fatigue and reduced practise tolerance are prominent symptoms of both conditions, and dysautonomia may underlie both conditions.[59]

POTS tin can sometimes exist a paraneoplastic syndrome associated with cancer.[61]

There are case reports of people developing POTS and other forms of dysautonomia post-COVID.[62] [63] [64] [65] [66] [67] [68] [69] [70] [71] There is no good big-scale empirical evidence nevertheless to prove a connection, so for now the evidence is preliminary .[72]

Diagnosis [edit]

POTS is virtually commonly diagnosed by a cardiologist (41%), cardiac electrophysiologist (15%), or Neurologist (19%).[2] The boilerplate number of physicians seen earlier receiving diagnosis is vii, and the average delay before diagnosis is 4.7 years.[2]

Diagnostic criteria [edit]

A POTS diagnosis requires the following characteristics:[73]

  • For patients age 20 or older, increase in heart rate ≥30 bpm within 10 minutes of upright posture (tilt test or standing) from a supine position
    • For patients historic period 12–xix, heart rate increase must be >40 bpm[21]
  • Associated with related symptoms that are worse with upright posture and that improve with recumbence
  • Chronic symptoms that have lasted for longer than six months
  • In the absenteeism of other disorders, medications, or functional states that are known to predispose to orthostatic tachycardia

Autoantibodies against One thousand-protein coupled receptor [edit]

Measurement of 1000 protein–coupled receptor activity may be used as a diagnostic tool in the near time to come.[53]

Orthostatic intolerance [edit]

An increment in centre charge per unit upon moving to an upright posture is known as orthostatic (upright) tachycardia (fast heart rate). It occurs without any coinciding drop in claret pressure, as that would indicate orthostatic hypotension.[twenty] Certain medications to treat POTS may cause orthostatic hypotension. It is accompanied by other features of orthostatic intolerance—symptoms that develop in an upright position and are relieved past reclining.[20] These orthostatic symptoms include palpitations, low-cal-headedness, chest discomfort, shortness of breath,[20] nausea, weakness or "heaviness" in the lower legs, blurred vision, and cognitive difficulties.[1]

Differential diagnoses [edit]

A variety of autonomic tests are employed to exclude autonomic disorders that could underlie symptoms, while endocrine testing is used to exclude hyperthyroidism and rarer endocrine conditions.[22] Electrocardiography is commonly performed on all patients to exclude other possible causes of tachycardia.[1] [22] In cases where a particular associated condition or complicating cistron are suspected, other non-autonomic tests may be used: echocardiography to exclude mitral valve prolapse, and thermal threshold tests for small-scale-fiber neuropathy.[22]

Testing the cardiovascular response to prolonged head-up tilting, exercise, eating, and heat stress may help determine the best strategy for managing symptoms.[22] POTS has likewise been divided into several types (see § Causes), which may benefit from singled-out treatments.[74] People with neuropathic POTS show a loss of sweating in the anxiety during sweat tests, as well every bit impaired norepinephrine release in the leg,[75] but not arm.[1] [74] [76] This is believed to reflect peripheral sympathetic denervation in the lower limbs.[75] [77] [1] People with hyperadrenergic POTS evidence a marked increase of blood pressure and norepinephrine levels when standing, and are more likely to suffer from prominent palpitations, feet, and tachycardia.[78] [79] [45] [74]

People with POTS can be misdiagnosed with inappropriate sinus tachycardia every bit they present similarly. One distinguishing feature is those with POTS rarely exhibit >100 bpm while in a supine position, while patients with IST often have a resting heart rate >100 bpm. Additionally patients with POTS display a more pronounced change in heart rate in response to postural change.[8]

Treatment [edit]

POTS handling involves using multiple methods in combination to counteract cardiovascular dysfunction, address symptoms, and simultaneously address whatsoever associated disorders.[22] For about patients, water intake should exist increased, peculiarly after waking, in lodge to expand claret volume (reducing hypovolemia).[22] Eight to 10 cups of water daily are recommended.[12] Increasing salt intake, past calculation salt to food, taking common salt tablets, or drinking sports drinks and other electrolyte solutions is an effective way to enhance blood pressure by helping the body retain h2o. Different physicians recommend different amounts of sodium to their patients.[80] Combining these techniques with gradual physical training enhances their upshot.[22] In some cases, when increasing oral fluids and salt intake is not plenty, intravenous saline or the drug desmopressin is used to help increment fluid retentivity.[22] [24]

Big meals worsen symptoms for some people. These people may do good from eating small meals frequently throughout the day instead.[22] Alcohol and nutrient high in carbohydrates can also exacerbate symptoms of orthostatic hypotension.[21] Excessive consumption of caffeine beverages should be avoided, because they can promote urine production (leading to fluid loss) and consequently hypovolemia.[22] Exposure to extreme estrus may likewise aggravate symptoms.[12]

Aggravating factors[81]
Exertion (81%)
Continued continuing (80%)
Heat (79%)
After meals (42%)

Prolonged concrete inactivity can worsen the symptoms of POTS.[22] Techniques that increase a person'southward chapters for practise, such as endurance training or graded practice therapy, tin relieve symptoms for some patients.[22] Aerobic practice performed for 20 minutes a day, iii times a week, is sometimes recommended for patients who can tolerate information technology.[80] Exercise may have the immediate consequence of worsening tachycardia, peculiarly after a repast or on a hot solar day.[22] In these cases, information technology may be easier to practise in a semi-reclined position, such as riding a recumbent cycle, rowing, or swimming.[22]

When changing to an upright posture, finishing a meal, or terminal do, a sustained hand grip tin briefly heighten the blood force per unit area, maybe reducing symptoms.[22] Compression garments can also be of benefit by constricting blood pressures with external torso pressure.[22]

Medication [edit]

If nonpharmacological methods are ineffective, medication may be necessary.[22] Medications used may include beta blockers, pyridostigmine, midodrine,[82] or fludrocortisone.[83] [i] As of 2013, no medication has been canonical by the U.Due south. Food and Drug Administration to care for POTS, but a variety are used off-label.[12] Their efficacy has non yet been examined in long-term randomized controlled trials.[12]

Fludrocortisone may exist used to enhance sodium memory and blood volume, which may be beneficial not only past augmenting sympathetically-mediated vasoconstriction, only also because a large subset of POTS patients announced to have depression absolute blood volume.[84]

While people with POTS typically have normal or even elevated arterial blood pressure level, the neuropathic class of POTS is presumed to found a selective sympathetic venous denervation.[84] In these patients the selective Blastoff-1 adrenergic receptor agonist midodrine may increase venous return, enhance stroke volume, and better symptoms.[84] Midodrine should merely be taken during the daylight hours as information technology may promote supine hypertension.[84]

Sinus node blocker Ivabradine tin can successfully restrain heart rate in POTS without affecting blood force per unit area, demonstrated in approximately 60% of people with POTS treated in an open up-label trial of ivabradine experienced symptom comeback.[85] [86] [84]

Pyridostigmine has been reported to restrain middle rate and improve chronic symptoms in approximately one-half of people.[12]

The selective alpha-1 agonist phenylephrine has been used successfully to heighten venous return and stroke volume in some people with POTS.[87] Notwithstanding, this medication may exist hampered past poor oral bioavailability.[88]

Pharmacologic treatments for postural tachycardia syndrome
POTS subtypes Therapeutic action Goal Drug(s)
Neuropathic POTS Alpha-one adrenergic receptor agonist Constrict the peripheral claret vessels aiding venous return. Midodrine[17] [89] [xc] [91]
Splanchnic–mesenteric vasoconstriction Splanchnic vasoconstriction Octreotide[92] [93]
Hypovolemic POTS Synthetic mineralocorticoid Forces the body to retain table salt. Increase claret volume Fludrocortisone (Florinef)[94] [95]
Vasopressin receptor agonist Helps retain water, Increase blood book Desmopressin (DDAVP) [96]
Hyperadrenergic POTS beta-blockers (Non-Selective) Decrease sympathetic tone and centre charge per unit. Propranolol (Inderal)[97] [98] [99]
beta-blockers (Selective) Metoprolol (Toprol),[89] [100] Bisoprolol[101] [94]
Selective sinus node blockade Directly reducing tachycardia. Ivabradine[85] [86] [102] [103] [104]
blastoff-two adrenergic receptor agonist Decreases blood pressure and sympathetic nerve traffic. Clonidine,[12] Methyldopa[12]
Anticholinesterase inhibitors Splanchnic vasoconstriction. Increment blood pressure. Pyridostigmine[xvi] [105] [106]
Other (Refractory POTS) Psychostimulant Improve cognitive symptoms (Brain Fog) Modafinil[107] [108]
Cardinal nervous system stimulant Tighten blood vessels. Increases alertness and improves brain fog. Methylphenidate (Ritalin, Concerta)[109]
Straight and indirect α1-adrenoreceptor agonist. Increased claret flows Ephedrine and pseudoephedrine[110]
Norepinephrine precursor Improve blood vessel contraction Droxidopa (Northera)[110] [111]
Alpha-2 adrenergic antagonist Increase blood pressure Yohimbine[112]

Prognosis [edit]

POTS has a favorable prognosis when managed appropriately.[22] Symptoms improve within 5 years of diagnosis for many patients, and 60% return to their original level of performance.[22] Approximately 90% of people with POTS reply to a combination of pharmacological and physical treatments.[eight] Those who develop POTS in their early on to mid teens during a flow of rapid growth will most likely see consummate symptom resolution in two to 5 years.[113] Outcomes are more than guarded for adults newly diagnosed with POTS.[43] Some people exercise not recover, and a few even worsen with time.[eight] The hyperadrenergic type of POTS typically requires continuous therapy.[8] If POTS is acquired by another condition, outcomes depend on the prognosis of the underlying disorder.[8]

Epidemiology [edit]

The prevalence of POTS is unknown.[22] One written report estimated a minimal charge per unit of 170 POTS cases per 100,000 individuals, simply the true prevalence is likely higher due to underdiagnosis.[22] Another study estimated that there are at least 500,000 cases in the United States.[seven] POTS is more mutual in women than men, with a female person-to-male ratio of 4:one.[74] [114] About people with POTS are anile between 20 and forty, with an average onset of 21.[2] [74] Diagnoses of POTS beyond age xl are rare, perhaps because symptoms improve with age.[22]

History [edit]

In 1871, physician Jacob Mendes Da Costa described a condition that resembled the modern concept of POTS. He named information technology irritable middle syndrome.[22] Cardiologist Thomas Lewis expanded on the description, coining the term soldier's center because it was often found among military personnel.[22] The status came to be known as Da Costa syndrome,[22] which is now recognized equally several singled-out disorders, including POTS.[ citation needed ]

Postural tachycardia syndrome was coined in 1982 in a description of a patient who had postural tachycardia, but not orthostatic hypotension.[22] Ronald Schondorf and Phillip A. Low of the Mayo Clinic first used the proper name postural orthostatic tachycardia syndrome, POTS, in 1993.[22] [115]

Notable cases [edit]

British politician Nicola Blackwood revealed in March 2015 that she had been diagnosed with Ehlers–Danlos syndrome in 2013 and that she had later been diagnosed with POTS.[116] She was appointed Parliamentary Under-Secretary of State for Life Science by Prime Minister Theresa May in 2019 and given a life peerage that enabled her to take a seat in Parliament. As a junior minister, it is her responsibleness to respond questions in parliament on the subjects of Wellness and departmental business. When answering these questions, it is customary for ministers to sit when listening to the question and then to rising to give an answer from the despatch box, thus standing up and sitting downwards numerous times in quick succession throughout a series of questions. On 17 June 2019, she fainted during i of these questioning sessions after standing up from a sitting position iv times in the space of twelve minutes,[117] and it was suggested that her POTS was a factor in her fainting. Asked nearly the incident, she stated: "I was frustrated and embarrassed my body gave up on me at work...Just I am grateful it gives me a chance to shine a light on a condition many others are as well living with."[118]

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  117. ^ "Hospitals: Listeria: Volume 798". hansard.parliament.uk. Firm of Lords Hansard. 17 June 2019. Retrieved 2 September 2020. Baroness Blackwood of North Oxford makes four speeches (thus standing up iv times) between 5:52 PM and vi:04 PM.
  118. ^ "House of Lords collapse 'no big deal'". BBC News. 25 June 2019. Retrieved 25 June 2019.

Farther reading [edit]

  • Kress Southward (2018). Ability Over POTS. Bookbaby. ISBN978-ane-5439-0681-iii.
  • Goldstein DS (2016). Principles of Autonomic Medicine (PDF).
  • Freeman M (2015). The Dysautonomia Projection. Bardolf. ISBN978-1-938842-24-5.

External links [edit]

claylockonamind.blogspot.com

Source: https://en.wikipedia.org/wiki/Postural_orthostatic_tachycardia_syndrome

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