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Treatment of almost all medical conditions has been affected by the COVID-19 pandemic. NICE has issued rapid update guidelines in relation to many of these. This guidance is changing frequently. Please visit https://www.nice.org.uk/covid-19 to see if there is temporary guidance issued by NICE in relation to the management of this condition, which may vary from the information given below.

Blood pressure (BP) is a variable with a continuous and unimodal variation. One can only consider normal and abnormal against the circumstances of the individual in question, with regard to age/sex, conditions in which it was measured, and other relevant factors.

Hypotension is therefore a BP that is much lower than usual and which may be causing symptoms such as dizziness or light-headedness. It is often defined as systolic BP less than 90 mm Hg or diastolic BP less than 60 mm Hg. A systolic BP below 100 mm Hg may be more appropriate if the patient normally has hypertension.

This is very common, especially in the elderly, due to a number of underlying problems with BP control. The baroreflex mechanisms which control heart rate and vascular resistance decline with age (particularly in patients with hypertension) who thus display lability in BP. They are particularly prone to postural hypotension and to the effects of drugs.

  • It is defined as a drop in BP (usually >20/10 mm Hg) within three minutes of standing[1]. Normal pooling of the blood in the lower limbs is not correctly regulated by the cardiovascular system on moving to a vertical position.
  • The prevalence is age-dependent, ranging from 5% in patients under 50 years of age to 30% in those over 70 years of age[2].
  • Orthostatic hypotension frequently contributes to falls and syncopal episodes[3].
  • In Parkinson's disease the prevalence may be as high as 60%[1].
  • The majority of patients with orthostatic hypotension are asymptomatic or have a few nonspecific symptoms[4].
  • Common symptoms include dizziness, light-headedness, blurred vision, weakness, fatigue, nausea, palpitations and headache. Less common symptoms include syncope, dyspnoea, chest pain and neck and shoulder pain[5].
  • The most common causes are medications and conditions that cause hypovolaemia, such as blood or fluid loss, diuretic or vasodilator therapy[6].
  • It can also be associated with prolonged bed rest and drugs that affect reflex control of BP, including antidepressants, phenothiazine antipsychotics, levodopa, barbiturates, alcohol and vincristine.

Multiple system atrophy (Shy-Drager syndrome) and pure autonomic failure (Bradbury-Eggleston syndrome) are primary neuropathies that cause severe orthostatic hypotension as a result of widespread damage to the autonomic system:

  • The condition is often worse in the morning and after food or exercise.
  • It is associated with other signs of parasympathetic failure - eg, dry mouth and eyes, impotence, loss of sweating and atonic bowel, bladder or stomach.
  • In mild-to-moderate cases the patient presents with some or all of the following: feeling faint or dizzy, light-headedness, confusion and blurred vision.
  • In more severe cases there may be a history of syncope or fits.

Conditions producing orthostatic hypotension






  • Pregnancy
  • Severe varicose veins

Although commonly associated, hypotension is not synonymous with shock. Normal BP can be present during shock in people with hypertension, and normal tissue perfusion can exist among hypotensive individuals. The cause of hypotension and shock among traumatic patients is often hypovolaemia due to blood loss[7].

In the acute form, hypotension can be a serious clinical feature that may cause renal, cerebral and myocardial hypoxic damage. It is often associated with the different forms of shock including:

  • Septic - Gram-negative septicaemia.
  • Cardiogenic - following MI.
  • Hypovolaemia - blood loss (haemorrhage), plasma loss (burns), dehydration (diarrhoea and/or vomiting), pooling of unavailable fluids (eg, pancreatitis).
  • Anaphylactic - type I IgE-mediated hypersensitivity reaction.
  • Neurogenic - caused by trauma to the spine or as an adverse effect of an epidural anaesthetic. Also, it can result from pain or fear via reflex vagal stimulation.

Other causes include:

  • Vasodilatation - from antihypertensive drugs, heat exposure.
  • Drugs such as narcotic analgesics, alcohol, some antidepressants and anxiolytics.
  • Cardiac dysfunction - eg, arrhythmia, MI, aortic regurgitation, tamponade.
  • Pulmonary embolism.
  • Autonomic nervous system failure (systolic BP down ≥20 mm Hg, diastolic BP down ≥10 mm Hg inside three minutes of standing without increase in pulse rate).
  • Micturition syncope.

Primary acquired disease of the adrenals: Addison's disease (autoimmune adrenal failure). This is perhaps the best remembered cause of hypotension. Systolic BP is rarely >110 mm Hg, symptoms of postural hypotension are common and reactive hypoglycaemia after carbohydrates may masquerade as postprandial hypotension.

NB: secondary adrenal insufficiency causes hypotension. The clinical features are similar to Addison's disease but usually with less pronounced hypovolaemia.

  • These are often associated with prolonged standing with resultant pooling of venous blood with reduced venous return to the heart. There may be a brief period of sweating and pre-syncope symptoms before collapse. Reduced cerebral perfusion causes loss of consciousness. Consciousness returns relatively quickly.
  • When due to pain, emotional stress or sight of blood, there is central reflex activation.
  • They affect all age groups, varying from infrequent attacks with an obvious trigger to frequent episodes with no apparent cause.
  • There have been multiple studies of permanent pacemakers for vasovagal faints, with wildly varying results. A pacemaker may be required if severe bradycardia or asystole is shown during a faint using an implantable loop recorder[9].
  • 40-80% of people with autonomic dysfunction will have postprandial hypotension.
  • This is often defined as a decline in systolic arterial pressure of 20 mm Hg or a systolic arterial pressure less than 90 mm Hg (with a pre-meal systolic arterial pressure greater than 100 mm Hg), within two hours of consuming a meal.
  • Ambulatory blood pressure monitoring can aid in the diagnosis of postprandial hypotension.
  • One study found that meals with higher glucose load were found to lower blood pressure more significantly than meals with higher fat content. Higher protein content was associated with the least amount of BP change, when compared to a high glucose or lipid meal.
  • The initial treatment approach to postprandial hypotension is non-pharmacological. Patients with postprandial hypotension should be advised to take in smaller more frequent meals. If this is not adequate then patients should be instructed to decrease the carbohydrate load in their diet.
  • Although non-pharmacological approaches are usually adequate, medications may sometimes be required.
  • One study found that acarbose, a glucosidase inhibitor which decreases glucose absorption in the small intestine, significantly reduced the fall in blood pressure after eating in patients with postprandial hypotension.
  • An alternative is subcutaneous octreotide.

First-line investigation should include:

  • FBC.
  • U&E.
  • Fasting glucose.
  • Pregnancy test (if the patient is unsure).
  • ECG.
  • Echocardiogram - if suggested by a history suggestive of a cardiac problem.
  • Tilt-table testing for orthostatic hypotension[1]:
    • Passive tilt-testing to an angle between 60° and 80° for three minutes is recommended for the diagnosis of orthostatic hypotension.
    • The test is considered positive if systolic BP falls below 20 mm Hg and diastolic BP below 10 mm Hg of baseline.
    • If symptoms occur, the patient should be tilted back to the supine position immediately.

Postural hypotension

The key to managing this condition is individually tailored therapy. The goal of treatment is to improve the patient's functional capacity and quality of life, preventing injury, rather than to achieve a target BP. Cardiology referral is indicated if heart disease or abnormal ECG is present or suspected[1].

Most patients will improve with simple measures and these should be tried first:

  • The patient (and carers) should be educated about the various factors that affect BP and about the special aspects that have to be avoided - eg, foods, habits, positions and drugs.
  • Avoid triggers - eg, high-temperature environments.
  • Review any medication being taken.
  • Advise the elderly on standing slowly, dorsiflexing the feet first and even crossing the legs whilst upright.
  • Raising the head of the bed, which helps prevent diuresis and supine hypertension caused by fluid shifts.
  • Physical counterpressure with compression hosiery, or whole-body inflatable suits may be required.
  • A morning dose of caffeine as coffee or in tablet form can be effective.

More severely affected patients may require further interventions. Further interventions must be tailored to the individual needs of the patient and the benefits and risks carefully considered and discussed. Some of the further interventions used for hypotension have the potential to cause significant harm and so should be used with caution.

Initial intervention is to increase intravascular fluid volume by large daily salt intake, either added to food or as salt tablets:

  • Continue with this until weight has increased by 1.3-2.3 kg; then can consider giving fludrocortisone, if necessary, to increase sodium retention. Dose is 0.1- 0.2 mg/day[1].
  • Can precipitate heart failure but peripheral oedema alone should not cause cessation of treatment.

If symptoms still persist, consider medication. Medications used for orthostatic hypotension include midodrine, fludrocortisone, droxidopa, octreotide and pyridostigmine[1, 11]:

  • Fludrocortisone is recommended as first-line drug monotherapy:
    • Full benefit requires a high dietary salt and adequate fluid intake. The combination of a high-salt diet, head-up tilt sleeping (20-30 cm) and a low dose of fludrocortisone is often effective.
    • Supine hypertension is a common (25%) adverse effect and may be severe. The last dose should be administered at least four hours before going to sleep and BP should be monitored.
  • Alpha-receptor agonists:
    • Midodrine is recommended for monotherapy or combined therapy (eg, with fludrocortisone).
    • Supine hypertension is common (25%) and may be severe.
    • The last dose should be administered at least four hours before going to sleep; BP should be monitored.
    • Some patients become worse on midodrine and it is contra-indicated in heart disease, renal failure, phaeochromocytoma and thyrotoxicosis.
  • Dihydroxyphenylserine (DOPS) is a prodrug which is converted to noradrenaline (norepinephrine). It reduces orthostatic hypotension. It is the only effective treatment of dopamine beta-hydroxylase deficiency.
  • The somatostatin analogue octreotide:
    • Inhibits release of gastrointestinal peptides, some of which may cause vasodilatation.
    • Subcutaneous doses given 30 minutes before a meal may be used to reduce postprandial orthostatic hypotension. It does not increase supine hypertension. Nausea and abdominal cramps may occur.
  • Pyridostigmine, a cholinesterase inhibitor, often only has a modest effect on orthostatic hypotension but does not aggravate supine hypertension.

Acute hypotension

See separate Resuscitation in Hypovolaemic Shock article.

  • Check airways.
  • Give O2 by mask.
  • Place the patient head down.
  • Administer intravenous fluids (0.9% saline) having excluded pulmonary oedema.
  • Treat the underlying cause.

Vasovagal faints[8]

  • Symptoms often resolve spontaneously. Non-pharmacological therapy is often effective in preventing vasovagal syncope.
  • Education, hydration and physical counter-measures (eg, leg crossing and clenching buttocks as soon as possible after the start of the vasovagal prodrome) are often effective.
  • Any medications that could potentially worsen symptoms should be removed if possible. Common agents that could worsen symptoms include diuretics (decreased preload) and vasodilators (decreased afterload).
  • Drugs may be needed in only a small minority of patients. Midodrine and fludrocortisone are the main drugs used.

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Further reading and references

  1. Diagnosis and management of orthostatic hypotension; European Federation of Neurological societies (2011)

  2. Ricci F, De Caterina R, Fedorowski A; Orthostatic Hypotension: Epidemiology, Prognosis, and Treatment. J Am Coll Cardiol. 2015 Aug 1866(7):848-60. doi: 10.1016/j.jacc.2015.06.1084.

  3. Logan IC, Witham MD; Efficacy of treatments for orthostatic hypotension: a systematic review. Age Ageing. 2012 Sep41(5):587-94. doi: 10.1093/ageing/afs061. Epub 2012 May 16.

  4. Fedorowski A, Melander O; Syndromes of orthostatic intolerance: a hidden danger. J Intern Med. 2013 Apr273(4):322-35. doi: 10.1111/joim.12021.

  5. Lanier JB, Mote MB, Clay EC; Evaluation and management of orthostatic hypotension. Am Fam Physician. 2011 Sep 184(5):527-36.

  6. Sathyapalan T, Aye MM, Atkin SL; Postural hypotension. BMJ. 2011 Jun 16342:d3128. doi: 10.1136/bmj.d3128.

  7. Holler JG, Bech CN, Henriksen DP, et al; Nontraumatic hypotension and shock in the emergency department and the prehospital setting, prevalence, etiology, and mortality: a systematic review. PLoS One. 2015 Mar 1910(3):e0119331. doi: 10.1371/journal.pone.0119331. eCollection 2015.

  8. Coffin ST, Raj SR; Non-invasive management of vasovagal syncope. Auton Neurosci. 2014 Sep184:27-32. doi: 10.1016/j.autneu.2014.06.004. Epub 2014 Jun 21.

  9. Raj SR, Coffin ST; Medical therapy and physical maneuvers in the treatment of the vasovagal syncope and orthostatic hypotension. Prog Cardiovasc Dis. 2013 Jan-Feb55(4):425-33. doi: 10.1016/j.pcad.2012.11.004.

  10. Jones PK, Shaw BH, Raj SR; Orthostatic hypotension: managing a difficult problem. Expert Rev Cardiovasc Ther. 2015 Nov13(11):1263-76. doi: 10.1586/14779072.2015.1095090. Epub 2015 Oct 1.

  11. Low PA, Tomalia VA; Orthostatic Hypotension: Mechanisms, Causes, Management. J Clin Neurol. 2015 Jul11(3):220-6. doi: 10.3988/jcn.2015.11.3.220.