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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mitra Chitsazan, M.D.[2]; Sogand Goudarzi, MD [3]; Norina Usman, M.B.B.S[4]

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


Orthostatic hypotension or postural hypotension is defined as a reduction of systolic blood pressure of at least 20 mm Hg or 10 mm Hg in diastolic blood pressure within 3 minutes of standing. A similar fall during head-up tilt test at 60 degrees also defines orthostatic hypotension. Orthostatic hypotension may be asymptomatic or may cause symptoms of lightheadedness, dizziness, blurred vision or cognitive impairment. It may have acute or chronic causes. Management of orthostatic hypotension may be challenging, in particular in patients with orthostatic hypotension and concomitant supine hypertension. [1][2][3]


Initial orthostatic hypotension (iOH)

  • It is most common in healthy adolescents
  • It 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 resolved 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)

Cardiovascular orthostatic hypotension (cOH)

Orthostatic pseudohypotension (pOH)



Common causes of orthostsic hypotension include: [13][14][15][16]

Causes of orthostatic hypotension
Cardiac diseases
Intravascular volume depletion
Venous pooling/venous vasodilation
Autonomic nervous system disorders

Medication-induced Orthostatic Hypotension
Vasodilation through Alpha-1 blockade
Vasodilation (Others)
Volume depletion
Sympathetic blockade
Dopamin agonists and other anti-Parkinsonian medications

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 assessment
Neurally mediated hypotension + + + - + + + + - + - + - - - -
  • Clinical assessment
'Postural Orthostatic Tachycardia Syndrome (POTS) + + + - - - - - + - - - - - + -
  • Clinical assessment
Neurologic syncope + - + - + +/- + - - - + +/- - - - -
  • Clinical assessment
Cardiac syncope + + + _ + + + + + +/- + + - - + -
Situational syncope + + + - + + + +/- +/- +/- + +/- - - - -
  • Clinical assessment syncope occurs during defecation, micturition, or coughing
Vasovagal syncope (also known as cardio-neurogenic syncope) + + + - + +/- + + - + + +/- - + + -

Epidemiology and Demographics


  • 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]


  • 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]



Risk Factors

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


Natural History, Complications, and Prognosis

Natural History


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



Diagnostic study of choice

History and Symptoms

  • Symptoms of orthostatic hypotension are prominent immediately upon standing, might improve in sitting position, and disappear in the supine position (i.e., postural symptoms). [43][44]
  • Symptoms may also be seen in association with meals, exercise, and prolonged standing
  • Symptoms are due to cerebral hypoperfusion
  • Symptoms usually last for few minutes
  • The most common symptoms are lightheadedness and dizziness upon standing.
  • Other symptoms include:

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. [45]

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. [42] These tests include those that access the underlying cause that may be altered in patients suffering from orthostatic hypotension.


An ECG may be helpful in the diagnosis of cardiovascular causes of orthostatic hypotension.


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


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 decreased right chamber volume. [46]

CT scan

A CT scan may be helpful in the diagnosis of orthostatic hypotension. Findings on a CT scan diagnostic of orthostatic hypotension include the presence of a cerebral tumor or communicating hydrocephalus. [47]


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

Other Imaging Findings

There are no other diagnostic studies associated with orthostatic hypotension.

Other Diagnostic Studies

There are no other diagnostic studies associated with orthostatic hypotension.


  • Asymptomatic hypotension is a common finding in practice and does not require any treatment.
  • There is no specific target blood pressure goals in the management of orthostatic hypotension.
  • However, management is targeted to alleviate symptoms, prevention of future falls, and excessive supine hypertension.
  • Management of orthostatic hypotension can be categorized into lifestyle modifications and medical therapy.
  • Education of the patient and non-pharmacological treatments are the cornerstone of treatment of orthostatic hypotension.
Drop of systolic BP > 20 mmHg (30 for hypertensive patients)
Non-pharmacological treatment
Observation and follow-up
Persistence of symptoms
Pharmacological Treatment
No supine hypertension or chronic heart failure
Supine hypertension or chronic heart failure:

Non-Pharmacological Therapy

  • Education of the patient and non-pharmacological treatments are the cornerstone of treatment of orthostatic hypotension.[48][49][50][51][52][1][53]
  • Cessation of orthostatic hypotension inducing drugs such as anti-hypertensivess in patients with a mean blood pressure below target value is recommended.
  • Avoidance of certain factors that aggravate hypotension such as heat, and alcohol intake.
  • Consumption of large meals induces splanchnic vasodilation thereby resulting in hypotension postprandially.
    • Fractionated meals are recommended in patients with postprandial symptoms.
Non-Pharmacological methods Mechanism of alleviating hypotension Recommendations
Elastic stockings
  • Elastic stockings expanding up to the waist are recommended.
  • Leg compression alone is not considered effective.
    • Due to the minor venous capacitance of legs relative to the abdomen.
  • Separate abdominal and leg compression is recommended to avoid patient discomfort.
Physical Maneuvers
  • Transiently increase venous return and peripheral vascular resistance
  • Contraction of a group of muscles
  • Leg crossing
  • Toe raising
  • Bending at the waist
Head up tilt sleeping
  • Enhance orthostatic tolerance upon the first morning rise
  • Results in reduction in supine hypertension, pressure-natriuresis
Intravascular volume
  • Tubular loss of salt and fluid
  • Decreased vascular tone creates relative hypovolemia
  • Volume expansion can alleviate symptoms even in the presence of normal intravascular volume.
    • 2 liters of water and 6 g of salt
    • Twenty-four-hour urine collection is helpful to guide treatment and follow-up
Intake of cold water
  • Increase systolic orthostatic hypotension by more than 30 mmHg
    • Via gastropressor response
  • Rapid drinking of approximatively 500 mL of cold water, independent of daily water intake

Medical Therapy

Initial Therapy

  • Preferred regimen (1): Fludrocortisone acetate at a dose of 0.1 mg per day, administered in the morning, which can eventually be increased up to 0.3 mg per day.
  • Preferred regimen (2): Midodrine 2.5 to 10 mg three times a day.
    • Max dose should not exceed 40 mg/day.
  • Preferred regimen (2): Droxidopa starts at 100 mg and escalates to 600 mg three times per day.
    • Patients should not take droxidopa within four to five hours of bedtime in order to limit supine hypertension.

Second-line Therapy

  • Preferred regimen (1): Erythropoietin is administered SC or IV at doses between 25 to 75 units/kg three times a week.
  • Preferred regimen (1): Methylxanthine caffeine 100 to 250 mg three times a day with meals.
  • Preferred regimen (1): Pyridostigmine initiated at a dose of 30 mg three times daily, up to a maximum dose of 90 mg three times daily.
  • Preferred regimen (1): Non-steroidal anti-inflammatory drugs are rarely effective as monotherapy
    • They can supplement treatment with fludrocortisone or a sympathomimetic agent.

Third-line Therapy

  • Preferred regimen (1): Atomoxetine
  • Preferred regimen (1): Vasopressin analogs (desmopressin (DDAVP))
  • Preferred regimen (1): Yohimbine a single dose of yohimbine (5.4 mg).
    • Yohimbine has limited availability in the United States.
  • Preferred regimen (1): Somatostatin subcutaneous doses range from 25 to 200 mcg.
  • Preferred regimen (1): Ergotamine-caffeine (1 mg/100 mg) up to twice-daily dosing in patients with orthostatic hypotension.
  • Preferred regimen (1): Metoclopramide and domperidone

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


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nl:Orthostatische hypotensie