oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.
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 blood pressure less than 90 mm Hg or diastolic less than 60 mm Hg. A systolic below 100 mm Hg may be more appropriate if the patient normally has hypertension.
Orthostatic (postural) hypotension
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 blood pressure. They are particularly prone to postural hypotension, and the effects of drugs.
- It is defined as a drop in BP (usually >20/10 mm Hg) within three minutes of standing. Normal pooling of the blood in the lower limbs is not correctly regulated by the cardiovascular system on moving to a vertical position.
- The reported prevalence ranges from 5% to 11% in middle age. Orthostatic hypotension affects up to 30% of adults aged over 65 and frequently contributes to falls and syncopal episodes.
- In Parkinson’s disease the prevalence may be as high as 60%.
- The majority of patients with orthostatic hypotension are asymptomatic or have a few nonspecific symptoms.
- 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.
- The most common causes are medications and conditions that cause hypovolaemia, such as blood or fluid loss, diuretic or vasodilator therapy.
- 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.
Shy-Drager syndrome (now known as multiple system atrophy) and Bradbury-Eggleston syndrome (now known as pure autonomic failure) 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|
In the acute form it 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.
A fall of 10-20 mm Hg systolic, with increase in heart rate of >15 bpm on change of the patient's position, indicates a hypovolaemic cause rather than peripheral neuropathy or betablocker use.
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 down ≥20 mm Hg, diastolic 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 does not cause hypotension, as aldosterone production is largely independent of the pituitary.
- These are often associated with prolonged standing with resultant pooling of venous blood with reduced venous return to the heart. May be 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 site 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.
- Diagnosis is confirmed by tilt-table testing (see below).
- This is even more common than postural hypotension and mainly occurs in the elderly.
- Other risk factors include Parkinson's disease and autonomic neuropathy.
- Cause is unclear but is associated with high carbohydrate meals.
- Defined as fall in BP (20 mm Hg within two hours of a meal but usually occurs much sooner).
- Symptoms are the same as those for postural hypotension. It is an important cause of syncope.
First-line investigation should include:
- Fasting glucose
- Pregnancy test (if the patient is unsure)
- Echocardiogram - if suggested by a history suggestive of a cardiac problem
- Tilt-table testing for orthostatic hypotension:
- Passive tilt-testing to an angle between 60 and 80° for 3 minutes is recommended for the diagnosis of orthostatic hypotension.
- The test is considered positive if systolic blood pressure 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.
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.
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 blood pressure and 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 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.
- Can precipitate heart failure but peripheral oedema alone should not cause cessation of treatment.
- If symptoms still persist consider midodrine (not licensed for use in postural hypotension):
- This is a peripherally acting alpha-1 adrenoceptor agonist. It increases BP via vasoconstriction.
- 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 4 hours before going to sleep, blood pressure 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. 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.
For details see the separate article on Resuscitation in Hypovolaemic Shock.
- Check airways.
- Give O2 by mask.
- Place the patient head down.
- Administer IV fluids (0.9% saline) having excluded pulmonary oedema.
- Treat the underlying cause.
- Symptoms often resolve spontaneously
- Alpha agonists, beta2-blockers, disopyramide, hyoscine, ephedrine or antidepressants can be tried.
- If there is failure to respond to drugs, consider inserting a pacemaker, especially if tilt testing shows large bradycardic response.
- Patients need to take smaller, more frequent meals containing fewer sugars and starches.
- Lying down after meals needs to be balanced with risk of reflux.
- The somatostatin analogue octreotide may be effective if required (see above under management of postural hypotension).
Further reading & references
- Diagnosis and management of orthostatic hypotension; European Federation of Neurological societies (2011)
- Feldstein C, Weder AB; Orthostatic hypotension: a common, serious and underrecognized problem in hospitalized patients. J Am Soc Hypertens. 2012 Jan-Feb;6(1):27-39. doi: 10.1016/j.jash.2011.08.008. Epub 2011 Nov 17.
- Logan IC, Witham MD; Efficacy of treatments for orthostatic hypotension: a systematic review. Age Ageing. 2012 Sep;41(5):587-94. doi: 10.1093/ageing/afs061. Epub 2012 May 16.
- Fedorowski A, Melander O; Syndromes of orthostatic intolerance: a hidden danger. J Intern Med. 2013 Apr;273(4):322-35. doi: 10.1111/joim.12021.
- Lanier JB, Mote MB, Clay EC; Evaluation and management of orthostatic hypotension. Am Fam Physician. 2011 Sep 1;84(5):527-36.
- Sathyapalan T, Aye MM, Atkin SL; Postural hypotension. BMJ. 2011 Jun 16;342:d3128. doi: 10.1136/bmj.d3128.
- Rayner CK, Horowitz M; Physiology of the ageing gut. Curr Opin Clin Nutr Metab Care. 2013 Jan;16(1):33-8. doi: 10.1097/MCO.0b013e32835acaf4.
- Luciano GL, Brennan MJ, Rothberg MB; Postprandial hypotension. Am J Med. 2010 Mar;123(3):281.e1-6. doi: 10.1016/j.amjmed.2009.06.026.
- Samaras D, Carmona G, Vischer U, et al; [Postprandial hypotension: an unclear clinical entity]. Rev Med Suisse. 2006 Nov 1;2(85):2456-8, 2460-1.
- Abe H, Sumiyoshi M, Kohshi K, et al; Effects of orthostatic self-training on head-up tilt testing for the prevention of tilt-induced neurocardiogenic syncope: comparison of pharmacological therapy. Clin Exp Hypertens. 2003 Apr;25(3):191-8.
- Raj SR, Koshman ML, Sheldon RS; Outcome of patients with dual-chamber pacemakers implanted for the prevention of neurally mediated syncope. Am J Cardiol. 2003 Mar 1;91(5):565-9.
Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.
Dr Hayley Willacy
Dr Colin Tidy
Prof Cathy Jackson