the leg, but not arm. this is believed to reflect peripheral sympathetic denervation in the lower limbs. people with hyperadrenergic pots show a marked increase of blood pressure and norepinephrine levels when standing, and are more likely to have from prominent palpitations, anxiety, and tachycardia. people with pots can be misdiagnosed with inappropriate sinus tachycardia (ist) as 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. treatment pots treatment involves using multiple methods in combination to counteract cardiovascular dysfunction, address symptoms, and simultaneously address any associated disorders. for most patients, water intake should be increased, especially after waking, in order to expand blood volume (reducing hypovolemia). eight to ten cups of water daily are recommended. increasing salt intake, by adding salt to food, taking salt tablets, or drinking sports drinks and other electrolyte solutions is an effective way to raise blood pressure by helping the body retain water. different physicians recommend different amounts of sodium to their patients. combining these techniques with gradual physical training enhances their effect. in some cases, when increasing oral fluids and salt intake is not enough, intravenous saline or the drug desmopressin is used to help increase fluid retention. large meals worsen symptoms for some people. these people may benefit from eating small meals frequently throughout the day instead. alcohol and food high in carbohydrates can also exacerbate symptoms of orthostatic hypotension. excessive consumption of caffeine beverages should be avoided, because they can promote urine production (leading to fluid loss) and consequently hypovolemia. exposure to extreme heat may also aggravate symptoms. prolonged physical inactivity can worsen the symptoms of pots. techniques that increase a person's capacity for exercise, such as endurance training or graded exercise therapy, can relieve symptoms for some patients. aerobic exercise performed for 20 minutes a day, three times a week, is sometimes recommended for patients who can tolerate it. exercise may have the immediate effect of worsening tachycardia, especially after a meal or on a hot day. in these cases, it may be easier to exercise in a semi-reclined position, such as riding a recumbent bicycle, rowing, or swimming. when changing to an upright posture, finishing a meal, or concluding exercise, a sustained hand grip can briefly raise the blood pressure, possibly reducing symptoms. compression garments can also be of benefit by constricting blood pressures with external body pressure. aggravating factors include exertion (81%), continued standing (80%), heat (79%), and after meals (42%). medication if nonpharmacological methods are ineffective, medication may be necessary. medications used may include beta blockers, pyridostigmine, midodrine, or fludrocortisone. as of 2013, no medication has been approved by the u.s. food and drug administration to treat pots, but a variety are used off-label. their efficacy has not yet been examined in long-term randomized controlled trials. fludrocortisone may be used to enhance sodium retention and blood volume, which may be beneficial not only by augmenting sympathetically mediated vasoconstriction, but also because a large subset of pots patients appear to have low absolute blood volume. while people with pots typically have normal or even elevated arterial blood pressure, the neuropathic form of pots is presumed to constitute a selective sympathetic venous denervation. in these patients the selective alpha-1 adrenergic receptor agonist midodrine may increase venous return, enhance stroke volume, and improve symptoms. midodrine should only be taken during the daylight hours as it may promote supine hypertension. sinus node blocker ivabradine can successfully restrain heart rate in pots without affecting blood pressure, demonstrated in approximately 60% of people with pots treated in an open-label trial of ivabradine experienced symptom improvement. pyridostigmine has been reported to restrain heart rate and improve chronic symptoms in approximately half of people. the selective alpha-1 agonist phenylephrine has been used successfully to enhance venous return and stroke volume in some people with pots. however, this medication may be hampered by poor oral bioavailability. pharmacologic treatments for postural tachycardia syndrome pots subtypes therapeutic action goal drug(s) neuropathic pots alpha-1 adrenergic receptor agonist constrict the peripheral blood vessels aiding venous return. midodrine splanchnic–mesenteric vasoconstriction splanchnic vasoconstriction octreotide hypovolemic pots synthetic mineralocorticoid forces the body to retain salt. increase blood volume fludrocortisone (florinef) vasopressin receptor agonist helps retain water, increase blood volume desmopressin (ddavp) hyperadrenergic pots beta-blockers (non-selective) decrease sympathetic tone and heart rate. propranolol (inderal) beta-blockers (selective) metoprolol (toprol), bisoprolol selective sinus node blockade directly reducing tachycardia. ivabradine alpha-2 adrenergic receptor agonist decreases blood pressure and sympathetic nerve traffic. clonidine, methyldopa anticholinesterase inhibitors splanchnic vasoconstriction. increase blood pressure. pyridostigmine other (refractory pots) psychostimulant improve cognitive symptoms (brain fog) modafinil central nervous system stimulant tighten blood vessels. increases alertness and improves brain fog. methylphenidate (ritalin, concerta) direct and indirect α1-adrenoreceptor agonist. increased blood flows ephedrine and pseudoephedrine norepinephrine precursor improve blood vessel contraction droxidopa (northera) alpha-2 adrenergic antagonist increase blood pressure yohimbine prognosis pots has a favorable prognosis when managed appropriately. symptoms improve within five years of diagnosis for many patients, and 60% return to their original level of functioning. approximately 90% of people with pots respond to a combination of pharmacological and physical treatments. those who develop pots in their early to mid teens will likely respond well to a combination of physical methods as well as pharmacotherapy. outcomes are more guarded for adults newly diagnosed with pots. some people do not recover, and a few even worsen with time. the hyperadrenergic type of pots typically requires continuous therapy. if pots is caused by another condition, outcomes depend on the prognosis of the underlying disorder. epidemiology the prevalence of pots is unknown. one study estimated a minimal rate of 170 pots cases per 100,000 individuals, but the true prevalence is likely higher due to underdiagnosis. another study estimated that there are at least 500,000 cases in the united states. pots is more common in women than men, with a female-to-male ratio of 4:1. most people with pots are aged between 20 and 40, with an average onset of 21. diagnoses of pots beyond age 40 are rare, perhaps because symptoms improve with age. as recently stated, up to one-third of pots patients also present with vasovagal syncope (vvs). this ratio is probably higher if pre-syncope patients, patients that report the symptoms of syncope without overt fainting, were included. given the difficulty with current autonomic measurements in quantitatively isolating and differentiating parasympathetic (vagal) activity from sympathetic activity without assumption or approximation, the current direction of research and clinical assessment is understandable: perpetuating uncertainty regarding underlying cause, prescribing beta-blockers and proper daily hydration as the only therapy, not addressing the orthostatic dysfunction as the underlying cause, and recommending acceptance and associated lifestyle changes to cope. direct measures of parasympathetic (vagal) activity obviates the uncertainty and lack of true relief of pots as well as vvs. for example, the hypothesis that pots is an auto-immune disorder may be an indication that a significant number of pots cases are indeed co-morbid with vvs. remember the parasympathetic nervous system is the memory for, and controls and coordinates, the immune system. if parasympathetic (vagal) over-, or prolonged-, activation is chronic then portions of the immune system may remain active beyond the limits of the infection. given that portions of the immune system are not of self, these portions remain active and continue to “feed.” once the only source of “feed” is self, the immune system begins to attack the host. this is the definition of autoimmune. this is a counter-hypothesis that may provide a simpler explanation with a more immediate plan for therapy and relief. for it may be that relieving the vagal over-activation, will retires the self-attacking portion of the immune system, thereby relieving the autoimmunity. another example may be “hyperadrenergic pots.” a counter hypothesis and perhaps a simpler explanation that leads to more direct therapy and improved outcomes is again the fact that pots and vvs may be co-morbid. it is well known that parasympathetic (vagal) over-activation may cause secondary sympathetic over-activation. without direct parasympathetic (vagal) measures, the resulting assumption is that the secondary sympathetic over-activation (the definition of “hyperadrenergic”) is actually the primary autonomic dysfunction. simply treating the (secondary) sympathetic over-activation may be just treating a symptom in these cases, which may work for a while but then the body compensates and more medication is needed or the patient become unresponsive and the permanent degraded lifestyles are considered the only option. again, this is unfortunate. given that cases of pots with vvs involves different portions of the nervous system (parasympathetic and sympathetic), and that both branches may be treated simultaneously, albeit differently, true relief of both conditions, as needed, is quite possible, and the cases of these newer hypothesized causes may be relieved with current, less expensive, and shorter-term therapy modalities. co-morbidities conditions that are commonly reported with pots include: migraine headaches (11–40%) ehlers–danlos syndrome (20–25%) fibromyalgia (11–20%) irritable bowel syndrome (7–30%) chronic fatigue syndrome (7–21%) mast cell activation disorder (6–9%) history in 1871, physician jacob mendes da costa described a condition that resembled the modern concept of pots. he named it irritable heart syndrome. cardiologist thomas lewis expanded on the description, coining the term soldier's heart because it was often found among military personnel. the condition came to be known as da costa's syndrome, which is now recognized as several distinct disorders, including pots. postural tachycardia syndrome was coined in 1982 in a description of a patient who had postural tachycardia, but not orthostatic hypotension. ronald schondorf and phillip a. low of the mayo clinic first used the name postural orthostatic tachycardia syndrome, pots, in 1993. notable cases 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. 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 responsibility to answer questions in parliament on the subjects of health and departmental business. when answering these questions, it is customary for ministers to sit when listening to the question and then to rise to give an answer from the despatch box, thus standing up and sitting down numerous times in quick succession throughout a series of questions. on 17 june 2019, she fainted during one of these questioning sessions after standing up from a sitting position four times in the space of twelve minutes, and it was suggested that her pots was a factor in her fainting. asked about the incident, she stated: "i was frustrated and embarrassed my body gave up on me at work ... but i am grateful it gives me a chance to shine a light on a condition many others are also living with."