Author(s): Ibiza Nevares, MD
Originally published: December 28, 2012 Last updated: February 12, 2026
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Disease/Disorder

Definition

Orthostatic Hypotension (OH) is diagnosed by comparing blood pressure readings in the supine and standing positions. The threshold of change in blood pressures within 3 minutes of standing or head-up tilt table to at least 60 degrees.1

  • A reduction of 20 mm Hg or more in systolic pressure, and/or
  • A reduction of 10 mm Hg or more in diastolic pressure

Orthostatic hypotension is a physical sign that warrants diagnosis of its underlying etiology.

The three common variants of OH2

  • Classical OH (COH)-sustained reduction of at least 20 mm Hg of SBP or 10mm Hg of DBP within 3 minutes of standing or head up-tilt table.
  • Delayed OH (DOH)-sustained reduction in BP that occurs after 3 minutes of standing or upright tilt.
  • Initial OH (IOH)-transient reduction in BP, defined as a reduction of greater than or equal to 40 mm Hg SBP and/or greater than or equal to 20 mm Hg DBP within 15 seconds of standing.

The two pathophysiological subtypes of OH (see Patho/anatomy/physiology section)

  • Neurogenic- Baroreflex dysfunction.
  • Non-Neurogenic- adequate reflexes but reduced preload or excessive vasodilation.

Etiology

Neurogenic OH (NOH)

Primary Causes

  • Primary neurodegenerative disorders – (Synucleinopathies: Parkinsons’ disease, Dementia with Lewy Bodies, MSA-P, MSA-C, Pure Autonomic Failure).
  • Other neurodegenerative/CNS disorders – (SCI especially above T6, MS).
  • Peripheral neuropathies with autonomic involvement – Diabetic autonomic neuropathy, Amyloidosis, Autoimmune autonomic ganglionopathy, paraneoplastic autonomic neuropathy, infectious/drugs/toxin neuropathies, GBS, small fiber peripheral neuropathies.
  • Genetic/hereditary autonomic disorders – familial dysautonomia (Riley-Day syndrome), acquired amyloidosis, mitochondrial disorders with dysautonomia, familial autonomic ganglionopathy.
  • Other – age related reduced baroreceptor sensitivity

Secondary Causes

  • CKD, DM, Autoimmune diseases (Sjogren’s syndrome, SLE with autonomic neuropathy), Vitamin B12 deficiency, Adrenal insufficiency, Hypothyroidism, Sarcoidosis, Porphyria.

Non-Neurogenic OH

  • Severe volume depletion – acute, subacute or chronic3
  • Adverse effects of medications – In a meta analysis of 69 trials that included more than 27,000 patients, medications associated with the highest odds of orthostatic hypotension were beta adrenergic blockers and tricyclic antidepressants.4 Alpha adrenergic antagonists, centrally acting alpha adrenergic agonists and second-generation antipsychotic medications were also associated with increased odds of OH. Sodium-glucose co transported 2 (SGLT2) inhibitors were also associated with a modestly increased odds of OH in this analysis. 
  • Chronic hypertension – Even though antihypertensive drugs can be the culprit of orthostatic hypotension, chronic hypertension which is not treated properly may be associated with the development of OH. This may occur partly due to age related baroreceptor dysfunction and by nocturnal hypovolemia from hypertension induced pressure natriuresis.
  • Others – Cardiac pump failures (aortic stenosis, pericarditis, myocarditis, arrhythmias), Adrenal insufficiency/pheochromocytoma.5
Orthostatic Hypotension – Figure 1

Epidemiology including risk factors and primary prevention

Epidemiology

The reported prevalence of orthostatic hypotension varies with age and clinical setting. In the Cardiovascular Health Study by Rutan GH, Hermanson B, et al,6 the prevalence of asymptomatic OH in patients 65 y/o, or older, was found to be 16.2%, and the presence of symptomatic OH was 18.2%.

The prevalence of OH in Long Term Residential settings vs Community-Dwelling older People – incorporating the quality of the studies (six studies with a sample of 2,694) into the pooled analysis revealed a prevalence of 22.2% vs 18.4% respectively.7

OH is a common cause of syncope in the elderly, with a prevalence reported as high as 30% among those aged > 75 y/o, and up to 50% among frail elderly adults living in nursing homes.8,9

OH is common in patients with DM, affecting an estimated 25-30% of individuals.2

OH occurs in up to 74% of SCI patients with acute high-level SCI.10

Risk factors – advanced age, polypharmacy, autonomic nervous system disorders, neurological injury (SCI-especially cervical or T6 and above and complete, CVA, peripheral neuropathies), CVD (CHF, MI, arrhythmias, AS), volume depletion, electrolyte imbalance,  prolonged bed rest, rapid postural changes, heat exposure, ETOH, Renal disease and other comorbidities as listed under primary and secondary causes of OH.

Primary Prevention – educate patients on gradual postural changes, hydration, small frequent meals, avoid alcohol, head up sleeping 10-20 degrees, abdominal binder + thigh high compression stockings, leg crossing, squatting, tensing leg muscles before standing (in non SCI patients and if patient is able), assess medications, monitor orthostatic vital signs

Patho-anatomy/physiology

Normal Blood pressure response to standing1

  • Rapid decrease in venous return to the heart
  • The ensuing reduced ventricular filling results in diminished cardiac output and blood pressure
  • The fall in blood pressure and thoracic volume provokes a compensatory reflex involving the central and peripheral nervous system that increases sympathetic and reduces parasympathetic outflow (i.e. baroreflex).
  • The increase in sympathetic outflow raises peripheral vascular resistance, venous return, and cardiac output, thereby limiting the fall in blood pressure.

In a person without NOH with intact compensatory mechanism, when the patients assumes an erect posture this normally leads to a small fall in SBP (5-10mmHg) and increase in DBP (5-10 mmHg), and an increase in in HR (10-25 b/m).

In patients with NOH – one or more of these compensatory mechanisms fail leading to a decline in BP with assumption of upright posture.  When there is baroreflex mediated sympathetic activation failure this leads to: inadequate NE release, impaired vasoconstriction, reduced HR response on standing.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

The natural history of OH depends on the underlying cause

  • Neurogenic- can be chronic and progressive, symptoms can worsen gradually, risk of falls and syncope, may precede other neurodegenerative symptoms. Age related OH can increase fall risk, cognitive decline, cardiovascular events and can be associated with frailty.
  • Non Neurogenic-Can be reversible, improves once offending cause is withdrawn or addressed (i.e. medications, hydration)

Clinical features

The main feature of symptomatic OH is that it is correlated with postural changes, exacerbated by standing and relieved by sitting or lying flat. Symptoms can be described as dizziness, shortness of breath, neck cramping on standing “coat hanger headache”, vertigo, chest pain, difficulty concentrating, lightheadedness, and/or blurry vision. Symptoms can be exacerbated by increased temperature, prolonged standing, and standing quickly. In patients with supine hypertension and autonomic failure, symptoms tend to be worse in the early morning hours, therefore these patients are at risk of falling when getting out of bed in the morning. Loss of Consciousness could also occur. Some patients can be asymptomatic due to cerebral autoregulation that allows them to maintain cerebral perfusion despite low peripheral arterial BP’s.11,12

Orthostasis is associated with an increased risk of cardiovascular disease, stroke, coronary artery disease and chronic kidney disease, as well as all-cause mortality among those aged 55 years and older.

Because of a more active parasympathetic system, higher estrogen levels and a lower center of gravity, women compensate less effectively to orthostasis.13

Specific secondary or associated conditions and complications>

Post Prandial Hypotension – fall in SBP >20 mm Hg, or a decrease to less than or equal 90 mm Hg when the pre-prandial BP is greater than or equal to 100 mm Hg within 2 hrs of a meal.

Supine Hypertension -condition that occurs while lying horizontally, unlike typical arterial HTN, which is present irrespective of body positioning.

Orthostatic Hypertension – HTN in response to standing due to a lack of afferent inhibition of sympathetic outflow in patients with baroreflex dysfunction.

Reflex Syncope (Neurocardiogenic syncope) -i.e. vasovagal, neurocardiogenic, carotid sinus hypersensitivity and syncope associated with micturition and/or defecation. In reflex syncope, the failure of sympathetic efferent vasoconstriction (and hypotension) occurs episodically and typically in response to a trigger (i.e. emotional, stress, noxious stimuli). Whereas in OH sympathetic efferent activity is chronically impaired and upon standing BP always falls.

Postural Orthostatic Tachycardia Syndrome (POTS) – patients have symptoms of OH while standing with an exaggerated tachycardia and no fall in blood pressure.

Additional Complications Decline in cognitive performance, Falls, Syncope, Chronic Orthostatic Intolerance- (COI) increased risk of Stroke, Myocardial ischemia.

Essentials of Assessment

History

A detailed history should be obtained including medication, weight loss and nutritional intake, falls, volume loss, and comorbidities causing autonomic dysfunction. Include in history urinary retention, constipation, decreased secretions and erectile dysfunction that could point towards a possibility of a widespread neurological disorder. An autonomic, neurologic, cardiovascular, and endocrine review of systems should be performed. Include family history and medications as follows.

Medications

Antihypertensives -i.e. diuretics, alpha-blockers, beta blockers, vasodilators

Psychotropics – antidepressants, antipsychotics

Parkinson’s medications – Levodopa, dopamine agonists

Other – drugs affective volume or vascular tone i.e. nitrates, opioids, alcohol

Family History

Cardiovascular/autonomic disorders, Genetic conditions affecting autonomic function

Physical examination

Blood pressure and heart rate are taken in all 3 positions, supine, sitting, and standing, with 3-5 minutes interval.

It is important to note that initial orthostatic hypotension occurs too soon to be detected with conventional blood pressure measurements.14

Supine hypertension screening is recommended as it could affect management.14

Physical examination should be comprehensive, including a neurologic examination to assess for Parkinson’s disease, cognitive impairment, depression, stroke, and peripheral neuropathy.

Volume should be assessed by examining mucosa, skin turgor, and jugular venous pressure. The carotid arteries should be examined for bruits. Because of murmurs in idiopathic hypertrophic cardiomyopathy, and mitral valve prolapse may be more prominent in standing, the heart must me auscultated in standing too.

Functional assessment

Timed Up and Go (TUG) test, Gait assessment, Orthostatic Hypotension questionnaire (OHQ)=symptom assessment scale (OHSA) + Daily Activities Scale (OHDAS).

Low and colleagues described functional classes of orthostatic hypotension

Journal of the American College of Cardiology, 66 (2015) 848-860. doi:10.1016/j.jacc.2015.06.1084

Laboratory studies

Basic – CBC with diff, CMP, fasting glucose, Hgb A1c, Urinalysis, TSH +/- free T4

Targeted labs – guided by comorbidities and clinical suspicion

Imaging and other tests

Guided by clinical suspicion -i.e. Cardiovascular-EKG, Echocardiogram, CNS-Brain CT, Brain MRI.

Early predictors of outcomes

Falls efficacy scale (FES), TUG test, OHQ, Older age > 65 y/o, frailty, prior falls, polypharmacy, symptom severity, postural triggers, magnitude of heart rate drop, supine hypertension, neurodegenerative disease, other autonomic dysfunction, blunted heart rate response, anemia, renal dysfunction.

Environmental

Factors that can affect management of patients with OH are heat exposure, humidity, cold environment, limited access to fluids/meals/snacks/salt, postprandial dehydration, uneven surfaces, slippery floors, poor lighting, lack of handrails or support, prolonged standing, rapid postural changes, heaving lifting or exertion, crowded spaces, travel/long car or plane rides, high altitude exposures, very hot drinks, lack of adaptive equipment.

Social role and social support system

The patient’s family/caregivers should have education about OH symptoms, fall risk/prevention, medications and triggers.

Orthostatic Hypotension – Figure 3

Professional issues

OH can significantly impact work safety, productivity, and career choices. Early recognition, early specialist referrals as needed (i.e. Cardiology, Neurology, etc.), work accommodation as needed, collaborative management with the patients, and the healthcare team is essential to assist patients to maximize their functioning in their professional environment.

Rehabilitation Management and Treatments

Non pharmacologic

Education is the cornerstone of the management of neurogenic OH2 (i.e. triggering factors, sudden transitional moves, avoiding ingestion of large meals). It is also helpful to provide orthostatic standing training, avoid supine position during the day, raising the head of bed at night by 10 to 20 degrees especially in patients with hypertension.15,16

Physical maneuvers to raise BP – leg crossing prior to standing, dorsiflexion of feet prior to upright posture, squatting, tensing muscles of arms, legs, abdomen and buttocks.17

Support garments – the available evidence shows that full length compression (calves, thighs and abdomen) and compression of solely the abdomen are superior to knee length and thigh length compression.18

Physical activity – to avoid deconditioning which is well recognized to exacerbate Orthostatic intolerance.19 Case report Tilt table isometrics.20

Medication readjustment -(where possible) of reversible causes of OH. Medications such as diuretic agents, antihypertensive agents, antianginal agents, alpha adrenoreceptor antagonists to treat benight prostatic hyperplasia, antiparkinsonian agents, and antidepressants are the most common offending agents.21

Volume expansion – central blood volume can be increased by increasing high sodium intake (high sodium foods or salt tablets) and fluid ingestion. However, caution must be used with patients with other comorbidities such as cardiac conditions and risk of volume overload, renal disease, etc.

Sleeping with the head of the bed elevated15,16,22– this intervention reduces supine hypertension and may decrease the nocturnal diuresis and increased orthostatic intolerance.

Acute tap water ingestion – Rapid ingestion of approximately 500 ml of tap water (e.g., over 3 to 4 minutes) elicits a marked pressor response and improvement in symptoms in patients with autonomic failures with increase BP 33-37 mm Hg.23

Pharmacotherapeutics interventions include the following2

Agents to Increase Central Blood Volume

Fludrocortisone – synthetic steroid with mineralocorticoid activity. It increases reabsorption of sodium from renal tubules and urinary excretion of potassium with hydrogen exchange. Side effects include supine hypertension, hypokalemia, and edema. Monitor Electrolytes.

Desmopressin – synthetic analog of an endogenous pituitary hormone. It is also known as anti-diuretic hormone. Patients that could benefit from Desmopressin are those with OH and nocturnal polyuria, with worsening OH in the morning. Adverse events include water intoxication and hyponatremia.

Erythropoietin – Can benefit patients who have normochromic anemia with OH, by increasing standing BP and improving orthostatic intolerance.

Sympathomimetic agents2

First line

Midodrine – is a prodrug that is hydrolyzed to its active form desglymidodrine. The mechanism of action consists of constricting peripheral arterial and venous vessels through its peripheral alpha 1 adrenoreceptor agonistic effects. It also increases standing BP in a dose dependent pattern. The peak efficacy is 1 hour after oral administration. Side effects are dose dependent and can include supine hypertension, itching, urinary retention and headaches. Avoid nighttime dosing.

Droxidopa – is a synthetic amino acid that is metabolized by DOPA decarboxylase to yield NE. It increases peripheral vasoconstriction. The USFDA has approved it for treatment for OH. Possible side effects are supine hypertension, dizziness, headaches, and nausea.

Other agents/Second line

Pyridostigmine – is a reversible cholinesterase inhibitor with low permeability across the blood brain barrier.  It increases BP and peripheral vascular resistance in standing. Its efficacy is relatively small, thus it is often used as an adjunctive drug.

Atomoxetine – is a selective NE transporter. It is theoretically more useful in patients with autonomic failure with residual sympathetic activity. 

Coordination of care

The roles of each member of the interdisciplinary team should be established along with specific precautions and goals in the POC.

Orthostatic Hypotension – Figure 4

Patient and family education

Patients should be made aware of their condition, triggers, prevention and pharmacologic and non-pharmacologic treatments that are in place.

For Family Education please refer to the OHSA tool see figure 3.

Emerging/unique interventions

Wearable devices (portable abdominal binders with biofeedback, smart wearable monitors with alerts for drop in bp,24 telehealth monitoring, pharmacologic agents under study (ampreloxetine, yohimbine), rehabilitation & exercise, tilt table training with gradual orthostatic stress, recumbent and semi recumbent aerobic training, lower extremities functional electrical stimulation (FES), autonomic neuromodulation,25 (vagus or baroreflex stimulation, respiratory and biofeedback training).

Translation into practice: “Pearls”/performance improvement in practice/changes in clinical practice behaviors and skills   

The first step in caring for patients with OH is to have an index of suspicion for those cases which have not been identified and/or whom are apparently asymptomatic (i.e. patients with history of falls, post prandial symptoms, polypharmacy, and comorbidities) and do a thorough H & P of both the diagnosed and newly diagnosed patients with OH.

It is also important to have accurate and consistent orthostatic blood pressure measurement. The recommended gold standard measurement of OH includes having patients rest in the supine position for at least 5 min and then stand for 3 min, with blood pressure measurements taken just prior to standing and at both 1 and 3 min of standing.26

The IPOC should be guided to the specific conditions that the patient has and etiology of OH- See Coordination of care tool figure 4

The ratio between the increase in heart rate and the fall in blood pressure provides the most sensitive and specific bedside differentiator between NOH and Non-Neurogenic OH. An increase of greater than or equal to 0.5 beats/minute for every 1 mm Hg drop in SBP during tilt table testing or active standing may be useful for diagnosing NOH.27

Cutting Edge/Emerging and Unique Concepts and Practice

  • Cardiovascular Autonomic Dysfunction in Post Covid Syndrome.28,29,30,31 – Some patients who recover from the acute phase of Covid 19 may be left with chronic symptoms of chest pain and dyspnea. Recent evidence suggests that patients with some of these chronic symptoms may have autonomic dysfunction (AD) with features of postural orthostatic tachycardia syndrome (POTS) and/or inappropriate sinus tachycardia (IST).
  • Wearable and continuous monitoring can capture real-time orthostatic changes and detect subtle pre-syncopal events.30
  • Autonomic biomarkers – research into plasma norepinephrine kinetics, heart rate variability (HRV) and baroreflex sensitivity as early predictors of OH severity.31
  • Imaging/Autonomic testing integration – tilt table testing combined with cerebral blood flow monitoring, fNIRS) to quantify brain perfusion during OH.32
  • Robotic tilt-table therapy – devices that progressively mobilize patients with real time feedback, exergaming/virtual reality rehab, compression technology 2.0 /e.g. servo-controlled stockings.33 AI driven environmental monitoring and adjustments, targeted hydration therapy guided by bioimpedance or wearable hydration monitors.34

Gaps in the Evidence-Based Knowledge

There is a lack of consistency and standardization of orthostatic assessments and analysis techniques for interpreting blood pressure data.35

References

  1. Freeman R, Wieling W, Axelrod FB, et al. Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and postural tachycardia syndrome. Clin. Aut res 2011;21:69
  2. Freeman R, Ahmad R., Abuzinadah, et al. Orthostatic Hypotension JACC State of the Art Review. Vol 72 no 11. 2018
  3. DiBona GF. Renal Neural activity in hepatorenal syndrome. Kidney Int 1984;25:841
  4. Bhanu C, Nimmons D, Peterson I, et al.  Drug induced orthostatic hypotension: a systematic review and metal analysis of randomized controlled trials. PLoS Med 2021;18:e1003821
  5. Perlmuter LC, Sarda G, Casavant V, Mosnalm AD. A review of the etiology associated comorbidities and treatment of orthostatic hypotension. Am J Ther 2013;20:279
  6. Rutan GH, Hermanson B, Bild DE, et al. Orthostatic Hypotension in older adults. The Cardiovascular Health Study. CHS Collaborative Research Group. Hypertension 1992; 19:508
  7. Nor L’zzati Saedon, MBBS, Maw Pin Tan, MD, James Frith, PhD. The prevalence of Orthostatic Hypotension: A systematic Review and Meta Analysis. The Gerontological Society of America. 2020. Vol 75, No 117-122
  8. Gupta V, Lipsitz LA. Orthostatic hypotension in the elderly: diagnosis and treatment. The American Journal of Medicine. October 2007. Vol 120 Issue 10 P. 841-847
  9. Parag Goyal, Mathew S Maurer. Syncope in older adults. Journal of Geriatric cardiology . (2016) 13: 380-386.
  10. Claydon VE, Krassioukov AV. Orthostatic hypotension after spinal cord injury: clinical features and management: Spinal Cord 2006; 44:341-351  
  11. Novak V, Novak P, Spies JM, Low PA. Autoregulation of cerebral blood flow in orthostatic hypotension. Stroke 1998;29:104-11
  12. Lagi A. Bacalli S, Cencetti S, Paggetti C, ColziL. Cerebral autoregulation in orthostatic hypotension. A transcranial Doppler study. Stroke 1994;25: 1771-5
  13. Chen YC. Gender differences in orthostatic hypotension. Americal Journal of Medical Science 2011;342:221-225.
  14. Wieling, et al. Diagnosis and treatment of orthostatic hypotension. Lancet Neurol 2022;21:735-46
  15. Mac Lean AR, Allen EV, Orthostatic Hypotension and orthostatic tachycardia. Treatment with the “head- up” bed. Jama 1940;115:2162-7
  16. Wieling W, Raj SR, Thijs RD. Are small observational studies sufficient evidence for a recommendation of head-up sleeping in all patients with debilitating orthostatic hypotension? Mac Lean and Allen revisited after 70 years. Clin Auton Res 2009;19:8-12. 
  17. Wieling W, van Dijk N, Thijs RD, de Lange FJ, Krediet CT, Halliwill JR. Physical countermeasures to increase orthostatic tolerance. J Intern Med 2015; 277:69-82.
  18. Smeenk H.E., Koster M. J, Faaij R. A., de Geer D.B., Hamaker M.E. Compression therapy in patient with orthostatic hypotension: a systematic review. Netherlands The Journal of Medicine. February 2014, Vol 72. No 2.
  19. Parsaik A, Allison TG, Singer W, et al. Deconditioning in patient with orthostatic intolerance. Neurology 2012;79:1435-9
  20. Hoeldtke RD, et al. Case report Treatment of orthostatic hypotension: interaction of pressor drugs and tilt table conditioning. Arch Phys Med Rehabilitation 1988 Oct. 69:895-898.
  21. Poon IO, Braun U. High Prevalence of orthostatic hypotension and its correlation with potentially causative medications among elderly veterans. J Clin Pharm Ther 2005;30:173-8.
  22. Fan CW, Walsh C, Cunningham CJ. The effect of sleeping with the head of the bed elevated six inches on elderly patients with orthostatic hypotension: an open randomized controlled trial. Age Ageing 2011;40:187-92
  23. Jordan J, Shannon JR, Black BK, et al. The pressor response to water drinking in  humans: a sympathetic reflex? Circulation 2000;101:504-9.
  24. Kehnemouyi YM, Coleman TP et al Emerging wearable technologies for multisystem monitoring and treatment of Parkinson’s disease: a narrative review. Frontiers in Network Physiology. Feb 13, 2024. 1354211
  25. Squair JW,  Berney M, et al. Implanted system for Orthostatic Hypotension in Multiple -System Atrophy, NEJM 2022;386:1339-1334
  26. Shibao C, Lipsitz LA, Biaggioni I, American Society of Hypertension Writing Group (2013) Evaluation and treatment of orthostatic hypotension. J Am Soc Hypertens 7(4):317–324.
  27. Fanciulli a, Kerer K, Leys F. et al Validation of NOH Ratio with active standing. Ann Neurology 2020;88:643.
  28. Johansson M, Stahlberg M. et al. Long- Haul Post-Covid 19 symptoms presenting as a variant of postural orthostatic tachycardia syndrome: the Swedish experience. JACC Case Rep. 2021;3:573-580.
  29. Desai AD, Boursiquot BC et al. Autonomic Dysfunction post-acute COVID 19 infection. Heart Rhythm Case rep. 2021.11.019.
  30. Shouman K., Vanichkachorn G., et al. Autonomic Dysfunction following Covid-19 infection; an early experience. Clin. Auton Res. 2021;31:385-394
  31. Nalbandian A. et al. Post Acute Covid 19 Syndrome. Nat. Med. 2021:27:601-615
  32. Gropelli A, Rafanelli M. et al Feasibility of blood pe measurement (watch-type) monitor during impending syncopal episodes. JAMA Vol 11, Issue 16. 16 August 2022 
  33. Hsieh Dong-Yi, Lai Yun-Ru, et al. Baroreflex sensitivity as a surrogate biomarker for concurrently assessing the severity of arterial stiffness and cardiovascular autonomic neuropathy in individuals with type 2 Diabetes. Journal of Personalized medicine. 2024, 14, 491
  34. Khan MS, Miller A, et al. Cerebral blood flow in Orthostatic intolerance. Journal of the American Heart Association. Vol 14. Issue 3, February 2025.
  35. Okamoto LE, Diedrich A, et al. Efficacy of servo-controlled splanchnic venous compression in the treatment of orthostatic hypotension. A randomized comparison with midodrine. Hypertension 2016 August;68 (2) : 418-426
  36. Kamran F, Le VC et al. Noninvasive Estimation of Hydration status in athletes using wearable  sensor and data-driven approach based on orthostatic changes. Sensors. 2021. 21,4469
  37. Shaw BH, Claydon VE. The relationship between orthostatic hypotension and falling in older adults. Clinical Autonomic Research. 2013;24.1:3-13.

Original Version of the Topic

Deepthi S. Saxena, MD. Orthostasis. 12/28/2012.

Previous Revision(s) of the Topic

Sarah Wagers, MD. Orthostasis. 7/5/2018

Marielisa Lopez, MD. Orthostatic Hypotension. 12/21/2022

Author Disclosure

Ibiza Nevares, MD
Nothing to Disclose