URL of this page: https://medlineplus.gov/genetics/condition/orthostatic-hypotension/
Orthostatic hypotension is a drop in blood pressure that occurs when moving from a laying down (supine) position to a standing (upright) position. The word "orthostasis" means to stand up, so the condition is defined as low blood pressure (hypotension) that occurs upon standing. When standing up, gravity moves blood from the upper body to the lower limbs. As a result, there is a temporary reduction in the amount of blood in the upper body for the heart to pump (cardiac output), which decreases blood pressure. Normally, the body quickly counteracts the force of gravity and maintains stable blood pressure and blood flow. In most people, this transient drop in blood pressure goes unnoticed. However, this transient orthostatic hypotension can cause lightheadedness that may result in falls and injury, particularly in older adults. The body has difficulty achieving stable blood pressure in people with orthostatic hypotension, resulting in a prolonged drop in blood pressure that occurs within minutes after moving from laying down to standing. The vast majority of people with orthostatic hypotension do not experience symptoms related to the condition; it may be detected incidentally during routine medical testing. When measuring blood pressure, orthostatic hypotension is defined as a decrease in blood pressure by at least 20mmHg systolic or 10mmHg diastolic within 3 minutes of standing. When signs and symptoms of orthostatic hypotension do occur, they are usually the result of a reduction in blood flow (hypoperfusion) to tissues, particularly the brain. Affected individuals may have fatigue, confusion, dizziness, blurred vision, or fainting episodes (syncope). Less frequently, affected individuals can experience muscle pain in the neck and shoulders (known as "coat hanger pain"), lower back pain, or weakness. During an episode of orthostatic hypotension, symptoms are often increased in severity by physical activity, warm temperatures, eating large meals, or standing for long periods of time. In people with orthostatic hypotension, hypoperfusion to other organs contributes to an increased risk of life-threatening health problems, including heart attack or heart failure, a heart rhythm abnormality called atrial fibrillation Orthostatic hypotension is a common condition that affects about 6 percent of the population. This condition is especially common in older adults, affecting at least 10 to 30 percent of people in this group. Orthostatic hypotension has two forms that result from two main causes. The neurogenic form is caused by problems with the autonomic nervous system, which controls involuntary body functions, including blood pressure. Normally when someone stands up, processes regulated by the autonomic nervous system make the heart beat faster and the blood vessels narrow, which increases blood pressure and blood flow in the body to compensate for gravity's effect on blood movement. Disorders that affect the autonomic nervous system can impair the adjustment of blood pressure, leading to orthostatic hypotension. These disorders often have a strong genetic component and may affect multiple members of a family. Neurogenic orthostatic hypotension often occurs along with nervous system disorders such as Parkinson disease, dementia with Lewy bodies, multiple system atrophy, pure autonomic failure, diabetes, Guillain-Barré syndrome, dopamine beta-hydroxylase deficiency, or infections that cause disturbances in nerve function (neuropathy). The non-neurogenic form of orthostatic hypotension is often caused by environmental or health factors that impair the body's mechanisms to stabilize blood pressure upon standing. These factors include heart disease, low blood volume (hypovolemia), alcohol use, or advanced age. Certain medications can also contribute to non-neurogenic orthostatic hypotension, such as antipsychotic or antidepressant drugs, drugs that treat high blood pressure by widening blood vessels (vasodilators), or drugs that help remove water and salt from the body (diuretics). The non-neurogenic form of orthostatic hypotension is more common than the neurogenic form, but in about 40 percent of people with orthostatic hypotension the underlying cause is unknown (idiopathic). Orthostatic hypotension is a complex condition and is usually not inherited. However, having a close relative with orthostatic hypotension likely increases a person's risk of developing the condition. When orthostatic hypotension occurs as part of a genetic syndrome, this feature follows the inheritance pattern of the syndrome. Learn how to cite this page
Orthostatic hypotension is defined as a decrease in systolic blood pressure of 20 mm Hg or a decrease in diastolic blood pressure of 10 mm Hg within three minutes of standing compared with blood pressure from the sitting or supine position. Alternatively, the diagnosis can be made by head-up tilt-table testing at an angle of at least 60 degrees.1 Orthostatic hypotension is often found in older patients and in those who are frail.2 It is present in up to 20 percent of patients older than 65 years.3 In one study, the prevalence of orthostatic hypotension was 18 percent in patients older than 65 years, but only 2 percent of these patients were symptomatic.3
In the absence of volume depletion, younger patients with orthostatic hypotension usually have chronic autonomic failure. A related problem, postprandial hypotension, is common in older patients and those with autonomic dysfunction. In postprandial hypotension, there is a decrease in systolic blood pressure of at least 20 mm Hg within 75 minutes of a meal.4
A normal hemodynamic response to changes in posture requires normal function of the cardiovascular and autonomic nervous systems. Standing results in blood pooling of approximately 500 to 1,000 mL in the lower extremities and splanchnic circulation. This initiates an increase in sympathetic outflow, which increases peripheral vascular resistance, venous return, and cardiac output, thereby limiting the decrease in blood pressure.
These compensatory mechanisms result in a decrease in systolic blood pressure (5 to 10 mm Hg), an increase in diastolic blood pressure (5 to 10 mm Hg), and an increase in pulse rate (10 to 25 beats per minute). However, orthostatic hypotension may result if there is inadequate intravascular volume, autonomic nervous system dysfunction, decreased venous return, or inability to increase cardiac output in response to postural changes.5 Decreased cerebral perfusion produces the neurologic symptoms of orthostatic hypotension.5
Clinical Presentation and Evaluation
Orthostatic hypotension may be acute or chronic. Patients may present with light-headedness, blurred vision, dizziness, weakness, and fatigue, or with syncope (in the acute care setting).6 Less commonly, they may present with neck and shoulder pain, orthostatic dyspnea, and chest pain.7 Table 1 outlines the differential diagnosis of orthostatic hypotension, which may be caused by a number of things, including dehydration, blood loss, medication, or a disorder of the neurologic, cardiovascular, or endocrine system.8–10 Evaluation of suspected orthostatic hypotension begins by identifying reversible causes and underlying associated medical conditions. Table 2 lists historical features that suggest a specific diagnosis in the patient with orthostatic hypotension.7,8 In addition to assessing for symptoms of orthostasis, the physician should elicit symptoms of autonomic dysfunction involving the gastrointestinal and genitourinary systems.7
Key physical examination findings in the evaluation of suspected orthostatic hypotension are listed in Table 3.11,12 A detailed assessment of the motor nervous system should be performed to evaluate for signs of Parkinson disease, as well as cerebellar ataxia.7 Blood pressure and pulse rate should be measured in the supine position and repeated after the patient has been standing for three minutes. As many as two-thirds of patients with orthostatic hypotension may go undetected if blood pressure is not measured while supine.13 However, a retrospective review of 730 patients found that orthostatic vital signs had poor test characteristics (positive predictive value = 61.7 percent; negative predictive value = 50.2 percent) when compared with tilt-table testing for the diagnosis of orthostatic hypotension.14 Head-up tilt-table testing should be ordered if there is a high index of suspicion for orthostatic hypotension despite normal orthostatic vital signs, and it may be considered in patients who are unable to stand for orthostatic vital sign measurements.6,14
A description of head-up tilt-table testing and its indications are outlined in Table 4,6,9 and Figure 1 shows a patient undergoing the testing. The procedure is generally considered safe, but serious adverse events such as syncope and arrhythmias have been reported. All staff involved in performing tilt-table testing should be trained in advanced cardiac life support, and resuscitation equipment should be readily available.6 Four common abnormal patterns can be seen in response to tilt-table testing (Table 5).15 The test may be useful in distinguishing orthostatic hypotension from other disorders that can present with symptoms of orthostasis, such as neurocardiogenic syncope.7 Sensitivity of tilt-table testing for diagnosing neurocardiogenic syncope is as high as 65 percent, and specificity is as high as 100 percent.15
Certain patients may not present with classic historical features of orthostatic hypotension. In older patients, a report of dizziness upon standing may not correlate with the finding of orthostatic hypotension. A prospective study of older women found that use of anxiolytics or sleeping aids once weekly and cigarette smoking were more closely associated with postural dizziness without orthostatic hypotension than with a finding of orthostatic hypotension on tilt-table testing.16 In patients with Parkinson disease, classic symptoms of orthostatic hypotension are not reliably present in those who have autonomic dysfunction.17,18 A study of 50 patients with Parkinson disease found that only one-half of the patients who developed orthostatic hypotension during tilt-table testing were symptomatic.17 The study also found that patients with Parkinson disease who undergo tilt-table testing may need to be tested for longer than the recommended three minutes because only nine of 20 patients who developed orthostatic hypotension did so within three minutes. Extending the test to 11 minutes resulted in 15 of 20 patients being diagnosed, whereas 29 minutes was necessary to detect orthostatic hypotension in all patients.17
In acute care settings (Figure 2), syncope may be the initial presentation of orthostatic hypotension. A prospective study of 611 patients presenting to an emergency department following a syncopal episode found that 24 percent had orthostatic hypotension.19 Patients with syncope should be admitted if they have known cardiovascular disease, associated chest pain, an abnormal electrocardiogram, suspected pulmonary embolism, or new cardiovascular or neurologic findings on examination.20
For patients without loss of consciousness, or those who are not considered at high cardiac or neurologic risk despite syncope, the evaluation shifts to rapidly identifying and treating reversible causes. If there is no evidence of intravascular volume depletion, or no response to volume resuscitation, then other causes should be considered. Several laboratory, imaging, and ancillary tests may be indicated (Table 6).7,18,20
Those who seek evaluation as outpatients are likely to have chronic etiologies of orthostatic hypotension (Figure 3), or they may have been referred for further testing upon discharge from the emergency department or hospital. They may be more likely to present with undifferentiated descriptions of dizziness as a symptom. If possible, potentially contributing medications (Table 18–10 ) should be discontinued and the patient reevaluated. If orthostatic hypotension persists, laboratory testing for underlying causes should include a complete blood count, basic metabolic panel, vitamin B12 level, and morning cortisol (Table 67,18,20 ).7 Orthostatic hypotension is often neurogenic in patients whose history, physical examination, and laboratory testing do not suggest another cause. Magnetic resonance imaging can be used to assess for possible etiologies of neurogenic orthostatic hypotension (Table 7).7 If the cause still is not apparent, autonomic testing may be indicated. The autonomic test most often used is the head-up tilt-table test.
Acute orthostatic hypotension generally resolves with treatment of the underlying cause. In patients with chronic orthostatic hypotension, pharmacologic and nonpharmacologic treatments may be beneficial. All patients with chronic orthostatic hypotension should be educated about their diagnosis and goals of treatment, which include improving orthostatic blood pressure without excessive supine hypertension, improving standing time, and relieving orthostatic symptoms.21
Nonpharmacologic treatment should be offered to all patients initially. If potentially contributing medications cannot be discontinued, then patients should be instructed to take them at bedtime when possible, particularly antihypertensives.7 Patients should avoid large carbohydrate-rich meals (to prevent postprandial hypotension), limit alcohol intake, and ensure adequate hydration.6,22 Patients should be encouraged to keep a symptom diary and avoid identified precipitating factors. Older patients should consume a minimum of 1.25 to 2.50 L of fluid per day to balance expected 24-hour urine losses. Water boluses (one 480-mL glass of tap water in one study and two 250-mL glasses of water in rapid succession in another study) have been shown to increase standing systolic blood pressure by more than 20 mm Hg for approximately two hours.22
Sodium may be supplemented by adding extra salt to food or taking 0.5- to 1.0-g salt tablets. A 24-hour urine sodium level can aid in treatment. Patients with a value of less than 170 mmol per 24 hours should be placed on 1 to 2 g of supplemental sodium three times a day and be reevaluated in one to two weeks, with the goal of raising urine sodium to between 150 and 200 mEq.21 Patients on sodium supplementation should be monitored for weight gain and edema.
Lower-extremity and abdominal binders may be beneficial. A randomized, single-blind controlled study using tilt-table testing demonstrated effective management of orthostatic hypotension by application of lower-limb compression bandages.23
An exercise program focused on improving conditioning and teaching physical maneuvers to avoid orthostatic hypotension has proven to be beneficial.24 Patients should actively stand with legs crossed, with or without leaning forward. Squatting has been used to alleviate symptomatic orthostatic hypotension.24 Other maneuvers include isometric exercises involving the arms, legs, and abdominal muscles during positional changes or prolonged standing.10 Toe raises, thigh contractions, and bending over at the waist are recommended.21
In patients who do not respond adequately to nonpharmacologic therapy for orthostatic hypotension, medication may be indicated.
Fludrocortisone. Fludrocortisone, which is a synthetic mineralocorticoid, is considered first-line therapy for the treatment of orthostatic hypotension. Dosing should be titrated within the therapeutic range until symptoms are relieved, or until the patient develops peripheral edema or has a weight gain of 4 to 8 lb (1.8 to 3.6 kg).9,24 Adverse effects include headache, supine hypertension, and congestive heart failure. Hypokalemia, which is dose-dependent and can appear within one to two weeks of treatment, may occur.9,24 In one study, hypokalemia developed in 24 percent of participants taking fludrocortisone, with a mean onset of eight months.25
Midodrine. Midodrine, a peripheral selective alpha-1-adrenergic agonist, significantly increases standing systolic blood pressure and improves symptoms in patients with neurogenic orthostatic hypotension.26 Patients should not take the last dose after 6:00 p.m. to avoid supine hypertension. Adverse effects include piloerection, pruritus, and paresthesia. Its use is contra-indicated in patients with coronary heart disease, urinary retention, thyrotoxicosis, or acute renal failure. The U.S. Food and Drug Administration has issued a recommendation to withdraw midodrine from the market because of a lack of post-approval effectiveness data.27 Continued approval of the drug is currently under review. Its use generally should be restricted to subspecialists. It is believed to have a synergistic effect when combined with fludrocortisone.
Pyridostigmine (Mestinon). Pyridostigmine is a cholinesterase inhibitor that improves neurotransmission at acetylcholine-mediated neurons of the autonomic nervous system. In a double-blind crossover study, patients were randomized to groups receiving 60 mg of pyridostigmine; 60 mg of pyridostigmine with 2.5 mg of midodrine; 60 mg of pyridostigmine with 5 mg of midodrine; or placebo.28 Compared with the placebo group, treatment groups demonstrated a decreased drop in standing diastolic blood pressure without worsening supine hypertension. Adverse effects include loose stools, diaphoresis, hypersalivation, and fasciculations.24
Table 8 outlines nonpharmacologic and pharmacologic options for the management of orthostatic hypotension.9,10,21–24,26,28,29
Data Sources: A PubMed search was completed using the MeSH function with the key phrases “orthostatic hypotension,” “evaluation,” and “treatment.” The search included meta-analyses, randomized controlled trials, clinical trials, and reviews. Also searched were the Agency for Healthcare Research and Quality evidence reports, Bandolier, the Canadian Task Force on Preventive Health Care, the Database of Abstracts of Reviews of Effects, the Effective Health Care Program, the Institute for Clinical Systems Improvement, the Cochrane Database of Systematic Reviews, the National Center for Complementary and Alternative Medicine, the National Guideline Clearinghouse database, the U.S. Preventive Services Task Force Web site, Clinical Evidence, and UpToDate. Search date: May 31, 2010. |
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