Medicine:Orthostatic hypotension

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Short description: Drop in blood pressure when standing up or sitting down
"Head rush" redirects here. For the television science series, see Head Rush (TV series).
Orthostatic hypotension
Other namesOrthostasis (elliptical jargon), postural hypotension, positional hypotension, neurogenic orthostatic hypotension
SpecialtyCardiology, neurology
SymptomsSymptoms that are worse when sitting or standing and improve when lying down, including lightheadedness, vertigo, tinnitus, slurred speech, confusion, coathanger pain in neck and shoulders, grayed or blurred vision, severe fatigue, fainting or near fainting
ComplicationsCumulative brain damage, possibility of injury or death from falls
Diagnostic methodIn-office (lie down for at least 20 minutes, take BP; stand for 3 minutes, take BP), or tilt-table testing by an autonomic specialist
TreatmentIdentify and treat causes (medications, dehydration), midodrine, compression garments, bed tilting
PrognosisDepends on frequency, severity, and underlying cause; neurogenic orthostatic hypotension is a chronic, debilitating, and often progressively fatal condition[1]

Orthostatic hypotension, also known as postural hypotension[2] or commonly known as headrush[3], is a medical condition wherein a person's blood pressure drops (hypotension) when they are standing up (orthostasis) or sitting down. Primary orthostatic hypotension is also often referred to as neurogenic orthostatic hypotension.[4] The drop in blood pressure may be sudden (vasovagal orthostatic hypotension), within 3 minutes (classic orthostatic hypotension) or gradual (delayed orthostatic hypotension).[5] It is defined as a fall in systolic blood pressure of at least 20 mmHg or diastolic blood pressure of at least 10 mmHg after 3 minutes of standing. It occurs predominantly by delayed (or absent) constriction of the lower body blood vessels, which is normally required to maintain adequate blood pressure when changing the position to standing. As a result, blood pools in the blood vessels of the legs for a longer period, and less is returned to the heart, thereby leading to a reduced cardiac output and inadequate blood flow to the brain.

Very mild occasional orthostatic hypotension is common and can occur briefly in anyone, although it is prevalent in particular among the elderly and those with known low blood pressure. Severe drops in blood pressure can lead to fainting, with a possibility of injury. Moderate drops in blood pressure can cause confusion/inattention, delirium, and episodes of ataxia. Chronic orthostatic hypotension is associated with cerebral hypoperfusion that may accelerate the pathophysiology of dementia.[6] Whether it is a causative factor in dementia is unclear.[7]

The numerous possible causes for orthostatic hypotension include certain medications (e.g. alpha blockers), autonomic neuropathy, decreased blood volume, multiple system atrophy, and age-related blood-vessel stiffness.

Apart from addressing the underlying cause, orthostatic hypotension may be treated with a recommendation to increase salt and water intake (to increase the blood volume), wearing compression stockings, and sometimes medication (fludrocortisone, midodrine, or others). Salt loading (dramatic increases in salt intake) must be supervised by a doctor, as this can cause severe neurological problems if done too aggressively.

Anatomy and physiology

To maintain sufficient blood pressure, the body has several compensatory mechanisms. Baroreceptors, a kind of mechanoreceptors, play a crucial role in conveying data about blood pressure in the autonomic nervous system. The data is conveyed to regulate the peripheral resistance and heart output, keeping blood pressure within an established normal limit.[8] There are two kinds of baroreceptors: high-pressure arterial baroreceptors and low-pressure volume receptors, both activated by the stretching of vessel walls.[8] Arterial baroreceptors are situated in the carotid sinuses and the aortic arch, while the low-pressure volume receptors, known as cardiopulmonary receptors, are in the atria, ventricles, and pulmonary vasculature.[8] Arterial baroreceptors detect changes in blood pressure and transmit this information to the brainstem, the nucleus of the solitary tract, which modulates the activity of the autonomic nervous system (ANS).[9] This results in decreased blood pressure, which leads to an increase in heart rate.[9] What's more, the venoarteriolar axon reflex, which results in the constriction of arterial flow to muscles, skin, and adipose tissue also helps stabilize blood pressure.[9]

Signs and symptoms

Orthostatic hypotension is characterized by symptoms that occur after standing (from lying or sitting), particularly when done rapidly. Many report lightheadedness (a feeling that one might be about to faint), sometimes severe, or even actual fainting with associated fall risk.[10][11][12] With chronic orthostatic hypotension, the condition and its effects may worsen even as fainting and many other symptoms become less frequent. Generalized weakness or tiredness may also occur. Some also report difficulty concentrating, blurred vision, tremulousness, vertigo, anxiety, palpitations (awareness of the heartbeat), unsteadiness, feeling sweaty or clammy, and sometimes nausea. A person may look pale.[13] Some people may experience severe orthostatic hypotension with the only symptoms being confusion or extreme fatigue. Chronic severe orthostatic hypotension may present as fluctuating cognition/delirium. Women who are pregnant are also susceptible to orthostatic hypotension.[14][15][16][17]

Associated diseases

The disorder may be associated with Addison's disease, atherosclerosis (build-up of fatty deposits in the arteries), diabetes, pheochromocytoma, porphyria,[18] long COVID,[19][20] and certain neurological disorders, including autoimmune autonomic ganglionopathy, multiple system atrophy, and other forms of dysautonomia. It is also associated with Ehlers–Danlos syndrome and anorexia nervosa. It is also present in many patients with Parkinson's disease or Lewy body dementias resulting from sympathetic denervation of the heart or as a side effect of dopaminomimetic therapy. This rarely leads to fainting unless the person has developed true autonomic failure or has an unrelated heart problem. Another disease, dopamine beta hydroxylase deficiency, also thought to be underdiagnosed, causes loss of sympathetic noradrenergic function and is characterized by low or extremely low levels of norepinephrine, but an excess of dopamine.[21]


Causes

Some causes of orthostatic hypotension include neurodegenerative disorders, low blood volume (e.g. caused by dehydration, bleeding, or the use of diuretics), drugs that cause vasodilation, other types of drugs (notably, narcotics and marijuana), discontinuation of vasoconstrictors, prolonged bed rest (immobility), significant recent weight loss, anemia,[22] vitamin B12 deficiency, or recent bariatric surgery.[23]

Medication

Tetrahydrocannabinol

Orthostatic hypotension can be a side effect of certain antidepressants, such as tricyclics[24] or monoamine oxidase inhibitors (MAOIs)[25] Alcohol can potentiate orthostatic hypotension to the point of syncope.[26] Orthostatic hypotension can also be a side effect of alpha-1 blockers (alpha1 adrenergic blocking agents). Alpha1 blockers inhibit vasoconstriction normally initiated by the baroreceptor reflex upon postural change and the subsequent drop in pressure.[27] Other antihypertensive medications may also cause orthostatic hypotension, in addition to anticholinergics, dopaminergic drugs, opiates and psychoactive medications.[28]

Other factors

Mechanism

Orthostatic hypotension happens when gravity causes blood to pool in the lower extremities, which in turn compromises venous return, resulting in decreased cardiac output and subsequent lowering of arterial pressure. For example, changing from a lying position to standing loses about 700 ml of blood from the thorax, with a decrease in systolic and diastolic blood pressures.[29] The overall effect is insufficient blood perfusion in the upper part of the body.

Diagnosis

Orthostatic hypotension can be confirmed by measuring a person's blood pressure after lying flat for 5 minutes, then 1 minute after standing, and 3 minutes after standing.[30] Orthostatic hypotension is defined as a fall in systolic blood pressure of at least 20 mmHg or the diastolic blood pressure of at least 10 mmHg between the supine reading and the upright reading. Also, the heart rate should be measured for both positions. A significant increase in heart rate from supine to standing may indicate a compensatory effort by the heart to maintain cardiac output. A related syndrome, postural orthostatic tachycardia syndrome (POTS), is diagnosed when at least a 30 bpm increase in heart rate occurs with little or no change in blood pressure. A tilt table test may also be performed.[31]

Definition

Orthostatic hypotension (or postural hypotension) is a drop in blood pressure upon standing. One definition (AAFP) calls for a systolic blood pressure decrease of at least 20 mm Hg or a diastolic blood pressure decrease of at least 10 mm Hg within 3 minutes of standing.[32] A common first symptom is lightheadedness upon standing, possibly followed by more severe symptoms: narrowing or loss of vision, dizziness, weakness, and even syncope (fainting).

Subcategories

Orthostatic hypotension can be subcategorized into three groups – initial, classic, and delayed.[33][34][35]

Initial orthostatic hypotension is frequently characterized by a systolic blood pressure decrease of ≥40 mmHg or diastolic blood pressure decrease of ≥20 mmHg within 15 seconds of standing.[33] Blood pressure then spontaneously and rapidly returns to normal, so the period of hypotension and symptoms is short (<30 s).[33] Only continuous beat-to-beat BP measurement during an active standing-up maneuver can document this condition.[33]

Classic orthostatic hypotension is frequently characterized by a systolic blood pressure decrease of ≥20 mmHg or diastolic blood pressure decrease of ≥10 mmHg between 30 seconds and 3 min of standing.[34]

Delayed orthostatic hypotension is frequently characterized by a sustained systolic blood pressure decrease of ≥20 mm Hg or a sustained diastolic blood pressure decrease ≥of 10 mm Hg beyond 3 minutes of standing or upright tilt table testing.[35]

Management

Lifestyle changes

Apart from treating underlying reversible causes (e.g., stopping or reducing certain medications, treating autoimmune causes), several measures can improve the symptoms of orthostatic hypotension and prevent episodes of syncope (fainting). Even small increases in the blood pressure may be sufficient to maintain blood flow to the brain on standing.[34]

In dysautonomic patients who do not have a diagnosis of high blood pressure, drinking 2–3 liters of fluid a day and taking 10 g of salt can improve symptoms, by maximizing the amount of fluid in the bloodstream.[34] Another strategy is keeping the head of the bed slightly elevated. This reduces the return of fluid from the limbs to the kidneys at night, thereby reducing nighttime urine production and maintaining fluid in the circulation. Various measures can be used to improve the return of blood to the heart; the wearing of compression stockings and exercises ("physical counterpressure maneuvers" or PCMs) can be undertaken just before standing up (e.g., leg crossing and squatting), as muscular contraction helps return blood from the legs to the upper body.[34]

Medications

The medication midodrine, an α1-adrenergic receptor agonist, can benefit people with orthostatic hypotension,[34][36] with the main side effect being piloerection ("goose bumps").[36] Fludrocortisone, a mineralocorticoid, is also used, although based on more limited evidence.[34]

Droxidopa (L-DOPS), a norepinephrine prodrug and hence non-selective adrenergic receptor agonist, has been shown to be effective as well,[37] with few, mostly mild side effects reported.[38]

Atomoxetine, a norepinephrine reuptake inhibitor (NRI), has been studied and used in the treatment of orthostatic hypotension.[39][40][41] While acutely effective, tachyphylaxis has been found to occur with continuous administration.[39][40] The reasons for this tolerance are unclear.[39] Another NRI, ampreloxetine (TD-9855), is in late-stage development for treatment of the condition.[42][43] Bupropion, a norepinephrine–dopamine reuptake inhibitor (NDRI), may be helpful as well.[44]

Amezinium metilsulfate is approved and widely used for the treatment of orthostatic hypotension in Japan.[45][46][47] It has a unique mechanism of action of acting as a dual monoamine oxidase inhibitor (MAOI) and NRI.[46][45][47]

Norepinephrine releasing agents (NRAs) like ephedrine, pseudoephedrine, and phenylpropanolamine have been used to treat orthostatic hypotension, though evidence is limited.[48][49]

Findings are mixed for the α2-adrenergic receptor antagonist yohimbine.[48][50]

A number of other measures have slight evidence to support their use, including indomethacin, fluoxetine, dopamine antagonists like metoclopramide and domperidone, ergot alkaloids like ergotamine and dihydroergotamine (α-adrenergic agonists), monoamine oxidase inhibitors (MAOIs) with tyramine (can produce severe hypertension), the NRA oxilofrine, the α1-adrenergic receptor agonist norfenefrine, and potassium chloride.[50][48]

Other

Robotic devices, such as the Erigo medical device, have been proven to help orthostatic hypotension in some patients. These machines adjust a patient's position from 0 degrees to 90 degrees in progressive increments, allowing the blood pressure to adjust more slowly.[51]

Prognosis

Orthostatic hypotension may cause accidental falls.[12] It is also linked to an increased risk of cardiovascular disease, heart failure, and stroke.[52][28] Also, observational data suggest that orthostatic hypotension in middle age increases the risk of eventual dementia and reduced cognitive function.[53]

See also

References

  1. ↑ "Orthostatic Hypotension: A Practical Approach to Investigation and Management". The Canadian Journal of Cardiology 33 (12): 1725–1728. December 2017. doi:10.1016/j.cjca.2017.05.007. PMID 28807522. 
  2. ↑ "Orthostatic hypotension" at Dorland's Medical Dictionary
  3. ↑ "headrush" (in en), Wiktionary, the free dictionary, 2024-08-19, https://en.wiktionary.org/w/index.php?title=headrush&oldid=81158361, retrieved 2026-02-02 
  4. ↑ "Orthostatic Hypotension: Epidemiology, Prognosis, and Treatment". Journal of the American College of Cardiology 66 (7): 848–860. August 2015. doi:10.1016/j.jacc.2015.06.1084. PMID 26271068. 
  5. ↑ "Orthostatic Hypotension Information Page | National Institute of Neurological Disorders and Stroke". https://www.ninds.nih.gov/disorders/all-disorders/orthostatic-hypotension-information-page. 
  6. ↑ "Small vessel disease pathological changes in neurodegenerative and vascular dementias concomitant with autonomic dysfunction". Brain Pathology 30 (1): 191–202. January 2020. doi:10.1111/bpa.12769. PMID 31357238. 
  7. ↑ "Orthostatic hypotension and cognitive impairment: a dangerous association?". Neurological Sciences 35 (6): 951–957. June 2014. doi:10.1007/s10072-014-1686-8. PMID 24590841. 
  8. ↑ 8.0 8.1 8.2 Bradley, JG; Davis, KA (15 December 2003). "Orthostatic hypotension.". American Family Physician 68 (12): 2393–8. PMID 14705758. 
  9. ↑ 9.0 9.1 9.2 Ringer, Matthew; Lappin, Sarah L. (2024). "Orthostatic Hypotension". StatPearls (StatPearls Publishing). PMID 28846238. https://www.ncbi.nlm.nih.gov/books/NBK448192/. 
  10. ↑ "Relationships between orthostatic hypotension, frailty, falling and mortality in elderly care home residents". BMC Geriatrics 19 (1). March 2019. doi:10.1186/s12877-019-1082-6. PMID 30866845. 
  11. ↑ "Orthostatic Hypotension and Falls in Older Adults: A Systematic Review and Meta-analysis". Journal of the American Medical Directors Association 20 (5): 589–597.e5. May 2019. doi:10.1016/j.jamda.2018.11.003. PMID 30583909. https://research.vu.nl/ws/files/101284496/Orthostatic_Hypotension_and_Falls_in_Older_Adults.pdf. 
  12. ↑ 12.0 12.1 "Continuous noninvasive orthostatic blood pressure measurements and their relationship with orthostatic intolerance, falls, and frailty in older people". Journal of the American Geriatrics Society 59 (4): 655–665. April 2011. doi:10.1111/j.1532-5415.2011.03352.x. PMID 21438868. 
  13. ↑ Harrison's principles of internal medicine. 2 (19th ed.). New York: McGraw-Hill Medical Publishing Division. 2015. p. 2639. ISBN 978-0-07-180215-4. 
  14. ↑ "The effects of postural changes of baroreflex gain in normal and hypertensive pregnancies". Clinical and Experimental Hypertension 24 (1–2): 23–31. 2002-01-01. doi:10.1081/CEH-100108712. PMID 11848166. 
  15. ↑ "Impairment in cardiac autonomic regulation preceding arterial hypertension in humans: insights from spectral analysis of beat-by-beat cardiovascular variability". Circulation 106 (21): 2673–2679. November 2002. doi:10.1161/01.CIR.0000039106.89299.AB. PMID 12438292. 
  16. ↑ "The hemodynamic effects of orthostatic stress during pregnancy". Obstetrics and Gynecology 72 (4): 550–552. October 1988. PMID 3419734. 
  17. ↑ "Pregnancy and the endocrine regulation of the baroreceptor reflex". American Journal of Physiology. Regulatory, Integrative and Comparative Physiology 299 (2): R439–R451. August 2010. doi:10.1152/ajpregu.00059.2010. PMID 20504907. 
  18. ↑ "Acute intermittent porphyria associated with postural hypotension". Canadian Medical Association Journal 121 (7): 845–846. October 1979. PMID 497968. 
  19. ↑ Lee, Cassie; Greenwood, Darren C.; Master, Harsha; Balasundaram, Kumaran; Williams, Paul; Scott, Janet T.; Wood, Conor; Cooper, Rowena et al. (1 March 2024). "Prevalence of orthostatic intolerance in long covid clinic patients and healthy volunteers: A multicenter study" (in en). Journal of Medical Virology 96 (3). doi:10.1002/jmv.29486. ISSN 0146-6615. PMID 38456315. https://onlinelibrary.wiley.com/doi/10.1002/jmv.29486. 
  20. ↑ "Is long COVID linked with orthostatic intolerance?". NIHR Evidence. 24 September 2024. https://evidence.nihr.ac.uk/alert/is-long-covid-linked-with-orthostatic-intolerance/. 
  21. ↑ "Dopamine Beta-Hydroxylase Deficiency". GeneReviews. University of Washington, Seattle. September 2003. https://www.ncbi.nlm.nih.gov/books/NBK1474/. 
  22. ↑ "What Causes Hypotension? -". National Heart, Lung, and Blood Institute (NHLBI). U.S. National Institutes of Health. https://www.nhlbi.nih.gov/health/low-blood-pressure. 
  23. ↑ "The effects of body weight status on orthostatic intolerance and predisposition to noncardiac syncope". Obesity Reviews 18 (3): 370–379. March 2017. doi:10.1111/obr.12501. PMID 28112481. 
  24. ↑ "Antidepressant therapy in patients with ischemic heart disease". American Heart Journal 150 (5): 871–881. November 2005. doi:10.1016/j.ahj.2005.01.041. PMID 16290952. 
  25. ↑ "Cardiovascular system effects of marijuana". Journal of Clinical Pharmacology 42 (S1): 58S–63S. November 2002. doi:10.1002/j.1552-4604.2002.tb06004.x. PMID 12412837. 
  26. ↑ "Alcohol potentiates orthostatic hypotension: implications for alcohol-related syncope". Circulation 101 (4): 398–402. February 2000. doi:10.1161/01.CIR.101.4.398. PMID 10653831. 
  27. ↑ "Orthostatic Hypotension". Merck Manual. https://www.msdmanuals.com/professional/cardiovascular-disorders/symptoms-of-cardiovascular-disorders/orthostatic-hypotension. 
  28. ↑ 28.0 28.1 Kim, Michael J.; Farrell, Jennifer (January 2022). "Orthostatic Hypotension: A Practical Approach". American Family Physician 105 (1): 39–49. ISSN 1532-0650. PMID 35029940. https://www.aafp.org/pubs/afp/issues/2022/0100/p39.html. 
  29. ↑ Idiopathic Orthostatic Hypotension and other Autonomic Failure Syndromes at eMedicine
  30. ↑ "Measurement of lying and standing blood pressure: A brief guide for clinical staff". 2017-01-13. https://www.rcplondon.ac.uk/projects/outputs/measurement-lying-and-standing-blood-pressure-brief-guide-clinical-staff. 
  31. ↑ "Provocation of hypotension during head-up tilt testing in subjects with no history of syncope or presyncope". Circulation 92 (1): 54–58. July 1995. doi:10.1161/01.CIR.92.1.54. PMID 7788917. 
  32. ↑ "Orthostatic hypotension". American Family Physician 68 (12): 2393–2398. December 2003. PMID 14705758. https://www.aafp.org/afp/2003/1215/p2393.html. 
  33. ↑ 33.0 33.1 33.2 33.3 "Initial orthostatic hypotension: review of a forgotten condition". Clinical Science 112 (3): 157–165. February 2007. doi:10.1042/CS20060091. PMID 17199559. 
  34. ↑ 34.0 34.1 34.2 34.3 34.4 34.5 34.6 "Guidelines for the diagnosis and management of syncope (version 2009)". European Heart Journal 30 (21): 2631–2671. November 2009. doi:10.1093/eurheartj/ehp298. PMID 19713422. 
  35. ↑ 35.0 35.1 "Delayed orthostatic hypotension: a frequent cause of orthostatic intolerance". Neurology 67 (1): 28–32. July 2006. doi:10.1212/01.wnl.0000223828.28215.0b. PMID 16832073. 
  36. ↑ 36.0 36.1 "Midodrine for orthostatic hypotension and recurrent reflex syncope: A systematic review". Neurology 83 (13): 1170–1177. September 2014. doi:10.1212/WNL.0000000000000815. PMID 25150287. 
  37. ↑ "L-dihydroxyphenylserine (Droxidopa) in the treatment of orthostatic hypotension: the European experience". Clinical Autonomic Research 18 (Supplement 1): 25–29. March 2008. doi:10.1007/s10286-007-1005-z. PMID 18368304. 
  38. ↑ "Droxidopa for neurogenic orthostatic hypotension: a randomized, placebo-controlled, phase 3 trial". Neurology 83 (4): 328–335. July 2014. doi:10.1212/WNL.0000000000000615. PMID 24944260. 
  39. ↑ 39.0 39.1 39.2 "Norepinephrine Reuptake Inhibition, an Emergent Treatment for Neurogenic Orthostatic Hypotension". Hypertension 81 (7): 1460–1466. July 2024. doi:10.1161/HYPERTENSIONAHA.124.22069. PMID 38766862. 
  40. ↑ 40.0 40.1 "Atomoxetine on neurogenic orthostatic hypotension: a randomized, double-blind, placebo-controlled crossover trial". Clin Auton Res 34 (6): 561–569. December 2024. doi:10.1007/s10286-024-01051-2. PMID 39294522. 
  41. ↑ "Evaluating the effectiveness of atomoxetine for the treatment of primary orthostatic hypotension in adults". J Clin Hypertens (Greenwich) 20 (4): 794–797. April 2018. doi:10.1111/jch.13260. PMID 29569329. 
  42. ↑ "Ampreloxetine - Theravance Biopharma". 21 November 2023. https://adisinsight.springer.com/drugs/800026474. 
  43. ↑ "Ampreloxetine Versus Droxidopa in Neurogenic Orthostatic Hypotension: A Comparative Review". Cureus 15 (5). May 2023. doi:10.7759/cureus.38907. PMID 37303338. 
  44. ↑ "Orthostatic hypotension: definition, diagnosis and management". J Cardiovasc Med (Hagerstown) 16 (2): 75–81. February 2015. doi:10.2459/01.JCM.0000446386.01100.35. PMID 24933201. 
  45. ↑ 45.0 45.1 "From depression to neurodegeneration and heart failure: re-examining the potential of MAO inhibitors". Expert Rev Clin Pharmacol 5 (4): 413–425. July 2012. doi:10.1586/ecp.12.29. PMID 22943121. "Amezinium metilsulfate (risumic, supratonin, amezinin and ryzmilate) is an indirectly acting sympathomimetic drug available in Japan, which reversibly inhibits intraneuronal MAO-A and MAO-B, as well as the reuptake of NE at postganglionic sympathetic terminals [120,121]. Amezinium is indicated for the treatment of essential hypotension, orthostatic hypotension and hypotension during dialysis [208].". 
  46. ↑ 46.0 46.1 "Treatment of orthostatic hypotension". Curr Opin Pharmacol 2 (6): 740–747. December 2002. doi:10.1016/s1471-4892(02)00213-8. PMID 12482740. "Amezinium metilsulfate is one of the most popular drugs in Japan for the treatment of OH. It has a unique mechanism of vasoconstriction. The drug inhibits monoamine oxidase (MAO) activity and norepinephrine (noradrenaline) uptake, and, therefore, enhances norepinephrine activity resulting in an increase in blood pressure [59]. Amezinium is especially recommended [60,61] in selected patients with asympathotonic (deficiency of sympathetic stimulation) OH [62••].". 
  47. ↑ 47.0 47.1 "Treatment of neurogenic orthostatic hypotension with amezinium metilsulfate, a new indirect sympathomimetic drug". Neurology 38 (7): 1095–1099. July 1988. doi:10.1212/wnl.38.7.1095. PMID 3386828. 
  48. ↑ 48.0 48.1 48.2 "Evidence-based treatment of neurogenic orthostatic hypotension and related symptoms". J Neural Transm (Vienna) 124 (12): 1567–1605. December 2017. doi:10.1007/s00702-017-1791-y. PMID 29058089. 
  49. ↑ "Postural orthostatic tachycardia syndrome: clinical presentation, aetiology and management". J Intern Med 285 (4): 352–366. April 2019. doi:10.1111/joim.12852. PMID 30372565. 
  50. ↑ 50.0 50.1 "Efficacy of treatments for orthostatic hypotension: a systematic review". Age and Ageing 41 (5): 587–594. September 2012. doi:10.1093/ageing/afs061. PMID 22591985. 
  51. ↑ "ERIGO: a possible strategy to treat orthostatic hypotension in progressive supranuclear palsy? A feasibility study". Functional Neurology 34 (2): 93–97. Apr–Jun 2019. PMID 31556389. 
  52. ↑ "Cardiovascular morbidity and mortality related to orthostatic hypotension: a meta-analysis of prospective observational studies". European Heart Journal 36 (25): 1609–1617. July 2015. doi:10.1093/eurheartj/ehv093. PMID 25852216. 
  53. ↑ "Abstract 28: Orthostatic Hypotension is Associated With 20-year Cognitive Decline and Incident Dementia: the Atherosclerosis Risk in Communities (ARIC) Study". Circulation 135 (suppl_1). 7 March 2017. doi:10.1161/circ.135.suppl_1.28. 
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