Postural hypotensionBMJ 2011; 342 doi: https://doi.org/10.1136/bmj.d3128 (Published 16 June 2011) Cite this as: BMJ 2011;342:d3128
- 1Academic Endocrinology, Diabetes and Metabolism, Hull-York Medical School, Hull Royal Infirmary, Hull HU3 2RW, UK
- Correspondence to: Professor Stephen L Atkin, Head of Academic Endocrinology, Diabetes and Metabolism, Hull York Medical School, Michael White Diabetes Centre, Hull, HU3 2RW
Postural hypotension is an abnormal fall in blood pressure—of at least 20 mm Hg systolic and 10 mm Hg diastolic—within three minutes of standing upright
The commonest causes of postural hypotension are medications and conditions that cause hypovolaemia
The patient’s history is of particular importance and has a high diagnostic value
Even after extensive evaluation, about a third of patients with persistent, consistent postural hypotension have no identified cause
A 70 year old man presents with recurrent lightheadedness for two to three weeks when getting up at night to pass urine over. On questioning, he reports having occasional episodes of lightheadedness when standing for prolonged periods. Three months previously he had been started on the α adrenergic blocker alfuzosin 2.5 mg three times daily, after complaining of urinary frequency and a poor urinary stream; physical examination had found an enlarged prostate along with a value for prostate specific antigen within the normal range. His other medical history includes well controlled type 2 diabetes, for which he is taking metformin 500 mg three times daily and simvastatin 40 mg daily.
On physical examination, his blood pressure was 130/80 mm Hg (right arm supine) and 105/69 mm Hg (right arm standing) with the patient complaining of lightheadedness after standing up. His heart rate was a regular 88 beats/min supine and did not rise with standing. Physical examination was otherwise unremarkable.
Postural (also known as orthostatic) hypotension is an abnormal decrease in blood pressure—of at least 20 mm Hg systolic and 10 mm Hg diastolic—within three minutes of standing upright.1 The prevalence of postural hypotension increases with age,2 and among elderly people it ranges from 6% (in those who are healthy)3 to 68% (in those in hospital geriatric wards).4 In a prospective cohort study (n=33 346, 67.3% men, mean age 45.7 (standard deviation 7.4) years, and mean follow-up 22.7 (6.0) years) mortality and risk of a coronary event were significantly higher in those whose systolic blood pressure fell by ≥30 mm Hg (hazard ratio for mortality 1.6 (95% confidence interval 1.3 to 1.9, P<0.0001) and for risk of a coronary event 1.6 (1.2 to 2.1, P=0.001)); the study also found significantly higher mortality and risk of a coronary event in those whose diastolic blood pressure fell by ≥15 mm Hg (1.4 (1.1 to 1.9, P=0.024) and 1.7 (1.1 to 2.5, P=0.01)).5 Patients often present with postural intolerance and recurrent falls, which are an important risk factor for hip fracture and head trauma.
What is the next investigation?
A detailed history and examination will be the next step. Measuring lying and standing blood pressures is the mainstay of evaluation.
The most common symptom is dizziness, often also described as lightheadedness, on standing, with or without gradual fading of consciousness.6 Other associated symptoms include weakness, fatigue, lethargy, palpitations, sweating, and visual and hearing disturbances.7 Hypoperfusion of the coronary circulation may aggravate angina pectoris and precipitate cardiac arrhythmias. Reduced sweating, symptoms related to gastroparesis, incontinence or urinary retention, constipation, erectile dysfunction, and ejaculatory dysfunction suggest that autonomic dysfunction is contributing to postural hypotension. In older patients symptoms of postural hypotension often arise after excessive nocturia or after a meal, and may worsen during exercise owing to autonomic dysfunction.
The patient’s history is of particular importance and has a high diagnostic value. A medication history may indicate the cause of postural hypotension. If symptoms of postural hypotension are of acute onset ranging from days to weeks, the postural hypotension is probably secondary to fluid or blood loss or a medication effect. Even after extensive evaluation, about a third of patients with persistent, consistent postural hypotension have no identified cause.8 The box outlines studies showing the role of medication, comorbities, sex, volume depletion, and autonomic disorders in postural hypotension.
Risk factors for postural hypotension
In a 1992 study conducted in elderly (aged 65 years or over) outpatients in general practice, current medication was found to be the most common risk factor for postural hypotension: diuretics (taken by 46% of almost 4000 study participants), sedatives (17%), centrally acting adrenergic blockers (15%), peripheral acting adrenergic blockers (10%), vasodilators (9%), β blockers (5%), and nitrates (5%).9 Alcohol intake can cause postural hypotension.9
Comorbidities and sex
The same study found that additional risk factors included a history of heart failure (19%), varicose veins (25%), diabetes mellitus (14%), ongoing acute illness (10%), anaemia (2%), and Parkinson’s disease (2%).9 In another study, postural hypotension has been associated with increasing age, particularly in women, and with the presence of hypertension, antihypertensive treatment, diabetes, and current smoking in the general population.5 In patients with diabetes, the presence of poor glycaemic control and hypertension are associated with an increased risk of postural hypotension, probably owing to autonomic dysfunction.10
Hypovolaemia and intravascular fluid depletion can contribute to postural hypotension.11 12 Common causes of fluid volume depletion include gastrointestinal losses (such as vomiting, diarrhoea, or gastrointestinal bleed) and skin losses owing to excessive sweating. Although rare in primary care setting, postural hypotension is one of the commonest presentations (12%) of Addison’s disease.13
The next step is to measure blood pressure and heart rate after 10 minutes of supine rest, repeated at three minutes after standing. If the patient cannot stand or is bedridden, a sitting measurement can be taken, but the sensitivity of the test may be reduced. Postural hypotension is considered clinically important if a reduction in blood pressure (≥20 mm Hg in systolic, ≥10 mm Hg in diastolic) is sustained at or beyond three minutes or the original symptoms are reproduced during active or passive standing.17 The heart rate normally rises on standing, but an excessive rise (≥30 beats/min) is diagnostic of postural tachycardia syndrome, which suggests autonomic dysfunction. Lack of a rise in heart rate also suggests autonomic dysfunction or medication such as β blockers.17
Assessment of fluid volume status that finds dry mucosa, reduced skin turgor, delayed capillary refill, and low jugular venous pressure suggests dehydration.
In the evaluation of adults with suspected blood loss, the presence of postural dizziness has a sensitivity for moderate blood loss of only 22% (95% confidence interval 6% to 48%) but a much greater sensitivity for large blood loss of 97% (91% to 100%); the corresponding specificity is 98% (97% to 99%). Supine hypotension and tachycardia are often absent, even after as much as 1150 mL of blood loss (sensitivity 33% (21% to 47%) for supine hypotension).18 In patients with vomiting, diarrhoea, or decreased oral intake, the presence of a dry axilla supports the diagnosis of hypovolaemia (positive likelihood ratio 2.8 (1.4 to 5.4)), and moist mucous membranes and a tongue without furrows argue against it (negative likelihood ratio 0.3 (0.1 to 0.6) for both findings).18 In adults, the capillary refill time and poor skin turgor have no proved diagnostic value.18
Pallor suggests anaemia and blood loss. Murmurs or signs of congestive cardiac failure on cardiovascular examination suggest that structural or ischaemic heart disease is contributing to the postural hypotension.
A focused neurological examination will find any evidence of previous cerebral vascular disease, neuropathy, dementia, and movement disorders such as Parkinson’s disease, which may coexist with postural hypotension. Any new neurological features, especially extrapyramidal signs, suggest a neurogenic cause of the postural hypotension and merits a specialist referral.
Postural hypotension may be suspected from the initial assessment if the patient has no features such as syncope that suggest alternative diagnosis and if the history is typical19 (such as side effects of medication and conditions that can cause hypovolaemia through diarrhoea, vomiting, inadequate fluid intake, or haemorrhage).
In a patient who is anaemic—with or without a history of blood loss—a reduced haemoglobin concentration, reduced packed cell volume, and microcytic hypochromic anaemia suggest that the postural hypotension is likely to be caused by blood loss. An inappropriately raised urea concentration in relation to creatinine suggests dehydration that is caused by fluid or blood loss or diuretics and which results from the active reabsorption of urea in the proximal tubule. A raised white cell count and inflammatory markers suggest that intercurrent infection is causing postural hypotension. Hyponatraemia or hyperkalaemia may point towards hypocortisolaemia as the cause of the postural hypotension. A short Synacthen (tetracosactide) test with a peak cortisol concentration of ≥540 nmol/L 30 minutes after 250 µg of tetracosactide excludes Addison’s disease.20 Raised fasting glucose concentration (≥7 mmol/L) or a postprandial hyperglycaemia of ≥11.1 mmol/L with or without osmotic symptoms suggests diabetes,21 which can cause autonomic dysfunction and postural hypotension.
After the patient stopped taking alfuzosin following the first consultation, he still had postural symptoms. His symptoms of a bladder outlet obstruction did not worsen. At a return visit two weeks later, the blood pressure was 126/80 mm Hg (right arm supine) and 102/68 mm Hg (right arm standing) with a heart rate of 78 beats/min, which rose to 88 beats/min on standing. He had no pallor and clinically he was euvolaemic. Focused neurological examination showed tremor at rest. His full blood count and biochemical profile was normal. He was referred for neurological evaluation.
Cite this as: BMJ 2011;342:d3128
This series of occasional articles provides an update on the best use of key diagnostic tests in the initial investigation of common or important clinical presentations. The series advisers are Steve Atkin, professor, head of department of academic endocrinology, diabetes, and metabolism, Hull York Medical School; and Eric Kilpatrick, honorary professor, department of clinical biochemistry, Hull Royal Infirmary, Hull York Medical School. To suggest a topic for this series, please email us at.
Contributors: All authors have contributed to drafting as well revising the article and were involved in final approval of the paper.
Competing interests: authors have completed the ICMJE uniform disclosure form at www.icmje.org/coi_disclosure.pdf (available on request from the corresponding author) and declare: no support from any organisation for the submitted work; no financial relationships with any organisations that might have an interest in the submitted work in the previous three years; no other relationships or activities could appear to have influenced the submitted work.
Provenance and peer review: Commissioned; externally peer reviewed.
Patient consent not required (patient anonymised, dead, or hypothetical)