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==Differentiating Orthostatic Hypotension from Other Diseases==
==Differentiating Orthostatic Hypotension from Other Diseases==
Orthostatic hypotension must be differentiated from [[neurogenic syncope]], [[cardiogenic syncope]], [[situational syncope]], [[multiple system atrophy]] with orthostatic hypotension, [[neurally mediated hypotension]], [[postural Orthostatic Tachycardia Syndrome]] (POTS) and [[vasovagal syncope]]<ref name="pmid25498732">{{cite journal| author=Poewe W, Seppi K, Fitzer-Attas CJ, Wenning GK, Gilman S, Low PA | display-authors=etal| title=Efficacy of rasagiline in patients with the parkinsonian variant of multiple system atrophy: a randomised, placebo-controlled trial. | journal=Lancet Neurol | year= 2015 | volume= 14 | issue= 2 | pages= 145-52 | pmid=25498732 | doi=10.1016/S1474-4422(14)70288-1 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25498732  }} </ref><ref name="pmid15875516">{{cite journal| author=Brignole M| title=Neurally-mediated syncope. | journal=Ital Heart J | year= 2005 | volume= 6 | issue= 3 | pages= 249-55 | pmid=15875516 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15875516  }} </ref><ref name="pmid24630686">{{cite journal| author=Trahair LG, Horowitz M, Jones KL| title=Postprandial hypotension: a systematic review. | journal=J Am Med Dir Assoc | year= 2014 | volume= 15 | issue= 6 | pages= 394-409 | pmid=24630686 | doi=10.1016/j.jamda.2014.01.011 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24630686  }} </ref><ref name="pmid26198889">{{cite journal| author=Garland EM, Celedonio JE, Raj SR| title=Postural Tachycardia Syndrome: Beyond Orthostatic Intolerance. | journal=Curr Neurol Neurosci Rep | year= 2015 | volume= 15 | issue= 9 | pages= 60 | pmid=26198889 | doi=10.1007/s11910-015-0583-8 | pmc=4664448 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26198889  }} </ref><ref name="pmid28375909">{{cite journal| author=Cheshire WP| title=Syncope. | journal=Continuum (Minneap Minn) | year= 2017 | volume= 23 | issue= 2, Selected Topics in Outpatient Neurology | pages= 335-358 | pmid=28375909 | doi=10.1212/CON.0000000000000444 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28375909  }} </ref><ref name="pmid3528810">{{cite journal| author=Dohrmann ML, Cheitlin MD| title=Cardiogenic syncope. Seizure versus syncope. | journal=Neurol Clin | year= 1986 | volume= 4 | issue= 3 | pages= 549-62 | pmid=3528810 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3528810  }} </ref><ref name="pmid21160608">{{cite journal| author=Aydin MA, Salukhe TV, Wilke I, Willems S| title=Management and therapy of vasovagal syncope: A review. | journal=World J Cardiol | year= 2010 | volume= 2 | issue= 10 | pages= 308-15 | pmid=21160608 | doi=10.4330/wjc.v2.i10.308 | pmc=2998831 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21160608  }} </ref>.
Orthostatic hypotension must be differentiated from [[neurogenic syncope]], [[cardiogenic syncope]], [[situational syncope]], [[multiple system atrophy]] with orthostatic hypotension, [[neurally mediated hypotension]], [[postural orthostatic tachycardia syndrome]] (POTS) and [[vasovagal syncope]]<ref name="pmid25498732">{{cite journal| author=Poewe W, Seppi K, Fitzer-Attas CJ, Wenning GK, Gilman S, Low PA | display-authors=etal| title=Efficacy of rasagiline in patients with the parkinsonian variant of multiple system atrophy: a randomised, placebo-controlled trial. | journal=Lancet Neurol | year= 2015 | volume= 14 | issue= 2 | pages= 145-52 | pmid=25498732 | doi=10.1016/S1474-4422(14)70288-1 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25498732  }} </ref><ref name="pmid15875516">{{cite journal| author=Brignole M| title=Neurally-mediated syncope. | journal=Ital Heart J | year= 2005 | volume= 6 | issue= 3 | pages= 249-55 | pmid=15875516 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15875516  }} </ref><ref name="pmid24630686">{{cite journal| author=Trahair LG, Horowitz M, Jones KL| title=Postprandial hypotension: a systematic review. | journal=J Am Med Dir Assoc | year= 2014 | volume= 15 | issue= 6 | pages= 394-409 | pmid=24630686 | doi=10.1016/j.jamda.2014.01.011 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24630686  }} </ref><ref name="pmid26198889">{{cite journal| author=Garland EM, Celedonio JE, Raj SR| title=Postural Tachycardia Syndrome: Beyond Orthostatic Intolerance. | journal=Curr Neurol Neurosci Rep | year= 2015 | volume= 15 | issue= 9 | pages= 60 | pmid=26198889 | doi=10.1007/s11910-015-0583-8 | pmc=4664448 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26198889  }} </ref><ref name="pmid28375909">{{cite journal| author=Cheshire WP| title=Syncope. | journal=Continuum (Minneap Minn) | year= 2017 | volume= 23 | issue= 2, Selected Topics in Outpatient Neurology | pages= 335-358 | pmid=28375909 | doi=10.1212/CON.0000000000000444 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28375909  }} </ref><ref name="pmid3528810">{{cite journal| author=Dohrmann ML, Cheitlin MD| title=Cardiogenic syncope. Seizure versus syncope. | journal=Neurol Clin | year= 1986 | volume= 4 | issue= 3 | pages= 549-62 | pmid=3528810 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3528810  }} </ref><ref name="pmid21160608">{{cite journal| author=Aydin MA, Salukhe TV, Wilke I, Willems S| title=Management and therapy of vasovagal syncope: A review. | journal=World J Cardiol | year= 2010 | volume= 2 | issue= 10 | pages= 308-15 | pmid=21160608 | doi=10.4330/wjc.v2.i10.308 | pmc=2998831 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21160608  }} </ref>.


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sogand Goudarzi, MD [2]; Norina Usman, M.B.B.S[3]

Synonyms and keywords: Postural hypotension; orthostatic intolerance; head rush; dizzy spell

Overview

Orthostatic hypotension is a physical finding demarcated by the American Academy of Neurology and the American Autonomic Society as a reduction in systolic blood pressure of 20 mm Hg or a drop of 10 mm Hg in diastolic blood pressure within three minutes of standing compared with blood pressure from the sitting or supine position. Orthostatic hypotension is frequently found in frail patients and those who are older.It is noticed in up to 20 percent of patients older than 65 years [1][2][3].

Classification

Initial orthostatic hypotension (iOH)

It is most common in healthy adolescents and is demarcated as a brief BP decrease of >40 mmHg systolic or >20 mmHg diastolic with symptomatic cerebral hypoperfusion within five to fifteen seconds after standing, typically resolves by twenty seconds.

Neurogenic orthostatic hypotension (nOH)

In Neurogenic orthostatic hypotension, the sympathetic noradrenergic nerves continually fail to facilitate the reflexive cardiovascular responses essential to sustain blood pressure in response to orthostatic stress. It is described as a constant BP decrease of >20 mmHg systolic or >10 mmHg diastolic, without or with symptoms, within three minutes of head-up tilt or standing.

Delayed orthostatic hypotension (dOH)

Delayed orthostatic hypotension (dOH) is demarcated as a fall in blood pressure that accomplishes neurogenic orthostatic hypotension criteria but ensues after three minutes.

Neurally mediated syncope (vOH)

It is also recognized as vasodepressor or vasovagal syncope, It involves a paroxysmal extraction of sympathetic vasopressor tone, frequently during prolonged standing, in patients with an effective autonomic nervous system.

Cardiovascular orthostatic hypotension (cOH)

Cardiovascular orthostatic hypotension occurs from intravascular hypovolemia or reduced cardiac output along with compensatory tachycardia.

Orthostatic pseudohypotension (pOH)

It is stated as apparent orthostatic hypotension when baseline supine blood pressure is raised, which may be due to a short time at rest to create a valid baseline, related recumbent hypertension, or fluctuation of baseline blood pressure with labile hypertension[4][5][6][7].

Pathophysiology

Causes

Common Causes

Common causes of orthostatic hypotension may include:

Differentiating Orthostatic Hypotension from Other Diseases

Orthostatic hypotension must be differentiated from neurogenic syncope, cardiogenic syncope, situational syncope, multiple system atrophy with orthostatic hypotension, neurally mediated hypotension, postural orthostatic tachycardia syndrome (POTS) and vasovagal syncope[17][18][19][20][21][22][23].

Disease History and Physical Examination Diagnostic approach
Lightheadedness Fatigue Autonomic symptoms Fever Nausea/vomiting Diminished Vision Dizziness Slurred Speech Tachycardia Altered mentation Loss of Consciousness Weakness Neurological Deficit Labs and CSF findings ECG CT/MRI Gold standard test
Multiple system atrophy with orthostatic hypotension + + + - - + + + - + - + + - - Atrophy of brain stem and cerebellum Clinical assesment
Neurally mediated hypotension + + + - + + + + - + - + - - - - Clinical assesment
Postural Orthostatic Tachycardia Syndrome (POTS) + + + - - - - - + - - - - - + - Clinical assesment
Neurologic syncope + - + - + +/- + - - - + +/- - - - - Clinical assessment
Cardiac syncope + + + _ + + + + + +/- + + - - + - ECG, Holter monitor, Echocardiography
Situational syncope + + + - + + + +/- +/- +/- + +/- - - - - Clinical assessment syncope occurs during defecation, micturition or coughing
Vasovagal syncope (also known as cardio-neurogenic syncope) + + + - + +/- + + - + + +/- - + + - ECG, Echocardiogram, Exercise stress test.

Differential Diagnosis

Intravascular volume depletion: Blood loss

Cardiovascular:

Neurologic Causes:

Drugs:

Endocrine Causes:

Miscellaneous:

Epidemiology and Demographics

Incidence

  • The approximation of orthostatic hypotension‐associated hospitalization is 36 per 100,000 adults, and the rate can be as high as 233 per 100,000 patients >75 years of age[24].

Prevalence

  • The overall prevalence of orthostatic hypotension depends on age as it increases with age in the general population.
  • The prevalence ranges from 5% in patients <50 years of age to 30% in those >70 years of age.
  • It is ~20% in > 65-year-old patients[25][26].

Age

  • Orthostatic Hypotension is commonly seen in individuals older than 50 years of age.

Gender

  • Orthostatic hypotension affects men and women equally.

Risk Factors

Common risk factors in the development of orthostatic hypotension include:[27][28]

Screening

  • Orthostatic hypotension, screening consists of blood pressure measurements in supine (or sitting) and standing position during clinical consultations[29].

Natural History, Complications, and Prognosis

Natural History

Complications

Common complications of orthostatic hypotension include:[31][32]

Prognosis

  • Depending on the underlying condition of orthostatic hypotension at the time of diagnosis, the prognosis may vary.

Diagnostic study of choice

  • Orthostatic vitals are the best diagnostic tests that are simple and easy to perform in a clinical setting.

History and Symptoms

  • Symptoms are predominant when standing, less often when sitting, and they subside when lying down[33][34].
  • Symptoms of orthostatic hypotension may include the following:

Physical Examination

Common physical examination findings of orthostatic hypotension include checking the blood pressure, pulse, and symptoms while having the patient in the standing and sitting position[35].

Diagnosis

Laboratory Findings

There are no diagnostic laboratory findings associated with orthostatic hypotension. While the definitive diagnosis of orthostatic hypotension is made clinically, other tests contribute to understanding the risks of disease and may provide clues to the selection of treatment options. These tests include those that access the underlying cause that may be altered in patients suffering from orthostatic hypotension. Addressing these conditions may improve the quality of life of a patient.

Electrocardiogram

An ECG may be helpful in the diagnosis of orthostatic hypotension. Findings on an ECG suggestive of orthostatic hypotension include:[36]

X-ray
  • There are no x-ray findings associated with orthostatic hypotension.
Echocardiography

Echocardiography may be helpful in the diagnosis of orthostatic hypotension. Findings on an echocardiography diagnostic of orthostatic hypotension include cardiac structural changes such as left ventricular hypertrophy, development of diastolic dysfunction, and decrease right chamber volume[37].

CT scan

CT scan may be helpful in the diagnosis of orthostatic hypotension. Findings on CT scan diagnostic of orthostatic hypotension include the presence of a cerebral tumor or communicating hydrocephalus[38].

MRI

MRI of a brain may be helpful in the diagnosis of orthostatic hypotension. Findings on MRI suggestive of orthostatic hypotension include:

Other Imaging Findings
  • There are no other diagnostic studies associated with [disease name]

Treatment

Medical Therapy

Pharmacological: Some drugs that are used in the treatment of orthostatic hypotension include fludrocortisone (Florinef), erythropoietin, midodrine and Pyridostigmine bromide (Mestinon)

Non-phamacological: Avoid triggers: large meals, hot bath, prolong standing[39][40][41][42]

Steps to approach a patient[43][1][44]
When we should suspect orthostatic hypotension?:
Unexplained fall/syncope
Typical symptoms (dizziness, lightheadedness, confusion, fatigue, gait disorder, neck pain, and vision disturbance)
Patient history (age, neurodegenerative disorder, renal failure, amyloidosis, autoimmune disease, heart disease, hypertension, autoimmune disease)
Current pharmacological treatment (vasodilator, alpha-and beta-blockers, diuretics, tricyclic-antidepressants
Initial assessment (outpatient clinic. ED and hospital):
Physical examination
Laboratory assessment (Hb, electrolytes, glucose, TSH, creatinine)
Bedside BP supine/standing test (after 1-3.5 min)
Cardiac assessment (ECG, telemetry or Holter-ECG, echocardiography, exercise-ECG, angiography if indicated i.e., history or signs of cardiac disease)
Neurological assessment (neurological status, and brain imaging if indicated, i.e., history of trauma and neurological symptoms)
Orthostatic Hypotension confirmed:
Nonpharmacological methods+ drug modification (mild-moderate cases)
Pharmacological/compression therapy (severe cases)
Advanced cardiac and autonomic assessment (investigation unit led by an expert):
Head-up tilt test with continuous BP monitoring plus active standings, carotid sinus massage, and Valsalva test (if positive, indicates neurogenic orthostatic hypotension); neuroendocrine assessment (supine and standing epinephrine/norepinephrine; other biomarkers such as vasopressin, renin, endothelin-1, the natriuretic peptide can be considered)
24 -h-ambulatory BP monitoring (BP variability pattern? Non-dipping? Reversed dipping? Diurnal hypotension period? Overtreatment? White Coat Syndrome?)
Long-term ECG monitoring if indicated (Cardiac arrhythmia? Chronotropic insufficiency?)
Cardiac sympathetic neuroimaging (PET or MIBG, optional if available)
Specialist consultation/referrals (if indicated):
Cardiologist (OH with concurrent cardiac arrhythmia, structural heart disease, and/or severe hypertension)
Neurologist (neurogenic OH and/or concurrent neurodegenerative diseases such as pure autonomic failure, Parkinson's disease, or multiple system atrophy)
Endocrinologists (patient with suspected or confirmed endocrine disorder such as hypothyroidism, electrolyte abnormalities, or adrenal diseases)
Geriatrician (older patient with special needs and comorbidities, dementia, cognitive impairment, fall tendency)
Otolaryngologist ("dizziness" with preserved hemodynamic parameters or typical vertigo)

Lifestyle Advice

Some suggestions for minimizing the effects include:[45][46][47][48]

  • Checking blood pressure regularly with a home monitoring kit. Check when lying flat and when standing as well as when symptoms occur.
  • Standing slowly rather than quickly, as the delay can give the blood vessels more time to constrict properly. This can help avoid incidents of syncope (fainting).
  • Take a deep breath and flex your abdominal muscles while rising to maintain blood and oxygen in the brain. This, however, may be contraindicated in individuals with Stage 3 hypertension.
  • Usually, medical personnel has their patients "dangle" before rising from bed to decrease dizziness/falling due to orthostatic hypotension. The dangling is done by having the patient sit on the side of their bed for about a minute so they do not have the sudden dizziness.
  • Maintaining an elevated salt intake, through sodium supplements or electrolyte-enriched drinks. A suggested value is 10 g per day; overuse can lead to hypertension and should be avoided.
  • Maintaining a proper fluid intake to prevent the effects of dehydration.
  • As eating lowers blood pressure, eat multiple smaller meals rather than fewer more substantial meals. Take extra care when standing after eating.
  • When orthostatic hypotension is caused by hypovolemia due to medications, the disorder may be reversed by adjusting the dosage or by discontinuing the medication.
  • When the condition is caused by prolonged bed rest, improvement may occur by sitting up with increasing frequency each day. In some cases, physical counterpressure, such as an elastic hose or whole-body inflatable suits, may be required.

Intervention

The mainstay of treatment for Orthostatic hypotension is medical therapy and lifestyle changes.

Primary Prevention

Effective measures for the primary prevention of orthostatic hypotension include:

ABCDEF method


  • A. Abdominal compression: Wear an abdominal binder when out of bed
  • B. A bolus of water/elevate Bed: On bad days, drink two 8-ounce glasses of cold water prior to prolonged standing and sleep with the head of the bed raised about 4 inches
  • C. Counter-maneuvers: While standing, contract the lower abdominal muscles for about 30 seconds
  • D. Drugs: Midodrine, Pyridostigmine, or Fludrocortisone can be used to elevate blood pressure (acknowledge any medications currently taken that can lower blood pressure)
  • E. Education & Exercise: Note any symptoms that indicate a fall in blood pressure while standing, recognize conditions that lower blood pressure (i.e. heavy metals, temperature changes, exercise, change in position)
  • F. Fluids: Stay hydrated

References

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  6. Freeman R, Wieling W, Axelrod FB, Benditt DG, Benarroch E, Biaggioni I; et al. (2011). "Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome". Clin Auton Res. 21 (2): 69–72. doi:10.1007/s10286-011-0119-5. PMID 21431947.
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  18. Brignole M (2005). "Neurally-mediated syncope". Ital Heart J. 6 (3): 249–55. PMID 15875516.
  19. Trahair LG, Horowitz M, Jones KL (2014). "Postprandial hypotension: a systematic review". J Am Med Dir Assoc. 15 (6): 394–409. doi:10.1016/j.jamda.2014.01.011. PMID 24630686.
  20. Garland EM, Celedonio JE, Raj SR (2015). "Postural Tachycardia Syndrome: Beyond Orthostatic Intolerance". Curr Neurol Neurosci Rep. 15 (9): 60. doi:10.1007/s11910-015-0583-8. PMC 4664448. PMID 26198889.
  21. Cheshire WP (2017). "Syncope". Continuum (Minneap Minn). 23 (2, Selected Topics in Outpatient Neurology): 335–358. doi:10.1212/CON.0000000000000444. PMID 28375909.
  22. Dohrmann ML, Cheitlin MD (1986). "Cardiogenic syncope. Seizure versus syncope". Neurol Clin. 4 (3): 549–62. PMID 3528810.
  23. Aydin MA, Salukhe TV, Wilke I, Willems S (2010). "Management and therapy of vasovagal syncope: A review". World J Cardiol. 2 (10): 308–15. doi:10.4330/wjc.v2.i10.308. PMC 2998831. PMID 21160608.
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