Postural hypotension

Orthostatic hypotension, which is a physical finding, not a disease, may be symptomatic or asymptomatic. (1) The American Autonomic Society (AAS) and the American Academy of Neurology (AAN) define orthostatic hypotension as a systolic blood pressure decrease of at least 20 mm Hg or a diastolic blood pressure decrease of at least 10 mm Hg within three minutes of standing up. (1) [Evidence level C, consensus/expert guidelines] The AAS and AAN also provide a tilt-table definition. (1) This determination has limited usefulness for the approach outlined in this article and appears to have a high rate of false-positive results. (2,3)

Orthostatic hypotension has been observed in all age groups, but it occurs more frequently in the elderly, especially in persons who are sick and frail. (4,5) It is associated with several diagnoses, conditions, and symptoms, including lightheadedness soon after standing, an increased rate of falls, and a history of myocardial infarction or transient ischemic attack (6); it also may be predictive of ischemic stroke. (7)

Pathophysiology

When an adult rises to the standing position, 300 to 800 mL of blood pools in the lower extremities. (8,9) Maintenance of blood pressure during position change is quite complex; many sensitive cardiac, vascular, neurologic, muscular, and neurohumoral responses must occur quickly. (9) If any of these responses are abnormal, blood pressure and organ perfusion can be reduced. As a result, symptoms of central nervous system hypoperfusion may occur, including feelings of weakness, nausea, headache, neck ache, lightheadedness, dizziness, blurred vision, fatigue, tremulousness, palpitations, and impaired cognition. (1) Vertigo also has been reported. (10)

When a person moves from a horizontal to a vertical position, muscle contraction in the legs and abdomen compresses veins. Because veins are equipped with one-way valves, normally blood is moved back to the heart to counter the gravitational tendency for blood to pool, and the veins constrict. In euvolemic persons, extra blood is held in the venous system, providing an additional reservoir of compensatory blood volume.

The autonomic nervous system plays an important role in maintaining blood pressure when a person changes position. The sympathetic nervous system adjusts the tone in arteries, veins, and the heart. Baroreceptors located primarily in the carotid arteries and aorta are exquisitely sensitive to changes in blood pressure. When the baroreceptors sense the slightest drop in pressure, a coordinated increase in sympathetic outflow occurs. Arteries constrict to increase peripheral resistance and blood pressure, and heart rate and contractility increase. All of these responses are aimed at maintaining blood pressure and perfusion. (9,11) Other physiologic mechanisms may be involved, including low-pressure receptors in the heart and lungs, the renin-angiotensin-aldosterone system, vasopressin, and the systemic release of norepinephrine. (9,11,12)

Normally, when a person moves to an upright position, blood pressure and heart rate change so quickly that continuous electronic monitoring is required to detect the differences, (9) and ordinary clinical observations lag behind the physiologic changes. The line between normal and pathologic changes in blood pressure and heart rate is not easy to define clinically. Although heart rate measurement is not included in the AAS/AAN definition of orthostatic hypotension, it can be determined easily and may be helpful, especially in patients who do not meet the blood pressure criteria of orthostatic hypotension. An elevation in heart rate that occurs when a patient moves from recumbency to standing may indicate compensation for decreased stroke volume. However, clinical decisions should be guided more by symptoms of decreased cerebral perfusion than by absolute blood pressure or heart rate measurements. (13,14)

A discussion of the pathophysiology of each reported cause of orthostatic hypotension is beyond the scope of this article, but a few comments are important. In general, all parts of the cardiovascular and nervous systems must work together. If there is inadequate intravascular volume, impairment of the autonomic nervous system, reduction of venous return, or inability of the heart to beat more rapidly or with greater power, orthostatic hypotension may result.

Differential Diagnosis

Orthostatic hypotension can be classified as neurogenic, non-neurogenic, or iatrogenic (e.g., caused by medication). (12,15) An algorithm to guide evaluation is given in Figure 1. Some of the etiologies of orthostatic hypotension are shown in Table 1. (11-13,15) Clinical clues to help direct the evaluation are given in Tables 2 and 3. (1,11,15,16)

[FIGURE 1 OMITTED]

Although measurements for orthostatic hypotension are not part of the standard physical examination, they should be taken if a patient's history suggests symptoms of cerebral hypoperfusion or a disease associated with orthostatic hypotension. Because orthostatic hypotension may be symptomatic or asymptomatic, symptoms and blood pressure measurements should be considered.

Diseases not related to orthostatic hypotension can cause similar symptoms (e.g., lightheadedness, dizziness). If a patient has posturally induced symptoms without blood pressure changes, the physician should consider other conditions. If a patient has posturally induced symptoms and a decrease in blood pressure but does not meet the strict definition for orthostatic hypotension, the physician still should consider orthostatic hypotension as a possible problem.

When the cause of orthostatic hypotension (e.g., hemorrhage, profound volume loss) is not immediately obvious, medications, the most common cause of orthostatic hypotension, should be considered before other etiologies. If symptoms appeared shortly after a medication reached steady state, it is likely that the medication is the cause. If the medication was started some time before the symptoms began, it may not be fully responsible (although it may play a part in the development of symptoms).

For example, after starting a medication, a patient may develop an illness that causes orthostatic hypotension, or a patient may have a condition that causes mild or asymptomatic orthostatic hypotension that becomes symptomatic when a new medication is added. If the patient is taking a potentially causative medication, the drug should be discontinued if possible. If it is not possible to stop the medication, other causes might be considered; it also may be necessary to treat the orthostatic hypotension pharmacologically or by some other method (Table 4). (8,12-15)

If medication does not appear to be fully or partly responsible for a patient's symptoms, non-neurogenic etiologies should be considered, and intravascular volume should be determined. If a patient is volume-depleted, hydration may improve symptoms; if a patient is euvolemic, other non-neurogenic causes should be considered. The patient's history and physical examination should direct further evaluation.

If medication and non-neurogenic etiologies are ruled out, neurogenic causes should be considered, using the patient's history and physical examination to direct the evaluation. Many of the neurogenic etiologies of orthostatic hypotension are difficult to diagnose and treat, and neurologic consultation may be necessary. Although it is not part of the formal definition of orthostatic hypotension, the absence of a significant increase in heart rate along with a significant postural decrease in blood pressure may suggest an autonomic cause. (13)

The evaluation and management of orthostatic hypotension must be carried out in the context of the patient's unique clinical circumstances. In some patients, stopping a medication may cause more harm than benefit if the hypotension symptoms are mild.

Orthostatic hypotension may have more than one cause; a patient with mild neurogenic orthostatic hypotension who becomes dehydrated or starts taking a new medication could develop symptomatic orthostatic hypotension. Because orthostatic hypotension is associated with several other morbidities, its diagnosis or onset should prompt the physician to consider other conditions, especially if the patient is elderly.

Treatment

The first steps in treatment of orthostatic hypotension are diagnosis and management of the underlying cause. A patient with symptomatic orthostatic hypotension who has a disease with no complete or specific cure may benefit from nonpharmacologic interventions. Increasing salt and fluid intake often is an initial step, although it may be difficult to undertake in some patients, such as those with severe congestive heart failure. Nonsteroidal anti-inflammatory drugs can be used to increase intravascular volume.

The mineralocorticoid fludrocortisone (Florinef) may be used in some patients to expand intravascular volume. (8,13-15) This agent should be used judiciously; in addition to the risk of volume overload, many patients taking fludrocortisone also develop hypokalemia or hypomagnesemia. Additional side effects of this medication include headache, edema, weight gain, and supine hypertension. (14,15)

Midodrine (ProAmitine), a vasoconstrictor, is effective in some cases of orthostatic hypotension. (17) [Evidence level A, randomized controlled trial] The most common side effects are pupillary dilation, piloerection, paresthesias, and pruritus. Midodrine also can cause supine hypertension. (14,15)

Erythropoietin has been used to treat autonomic failure associated with decreased red cell mass or anemia. (18) The goal is to bring the hematocrit level within the normal range. Increased appetite is a common side effect, along with an increased sense of well-being. (14,15)

REFERENCES

(1.) Consensus statement on the definition of orthostatic hypotension, pure autonomic failure, and multiple system atrophy. The Consensus Committee of the American Autonomic Society and the American Academy of Neurology. Neurology 1996;46:1470.

(2.) Petersen ME, Williams TR, Gordon C, Chamberlain-Webber R, Sutton R. The normal response to prolonged passive head up tilt testing. Heart 2000;84:509-14.

(3.) Sumiyoshi M, Mineda Y, Kojima S, Suwa S, Nakata Y. Poor reproducibility of false-positive tilt testing results in healthy volunteers. Jpn Heart J 1999;40:71-8.

(4.) Mader SL, Josephson KR, Rubenstein LZ. Low prevalence of postural hypotension among community-dwelling elderly. JAMA 1987;258:1511-4.

(5.) Ooi WL, Barrett S, Hossain M, Kelley-Gagnon M, Lipsitz LA. Patterns of orthostatic blood pressure change and their clinical correlates in a frail, elderly population. JAMA 1997;277:1299-304.

(6.) Rutan GH, Hermanson B, Bild DE, Kittner SJ, LaBaw F, Tell GS. Orthostatic hypotension in older adults. The Cardiovascular Health Study. CHS Collaborative Research Group. Hypertension 1992;19:508-19.

(7.) Eigenbrodt ML, Rose KM, Couper DJ, Arnett DK, Smith R, Jones D. Orthostatic hypotension as a risk factor for stroke: the atherosclerosis risk in communities (ARIC) study, 1987-1996. Stroke 2000;31:2307-13.

(8.) Lipsitz LA. Orthostatic hypotension in the elderly. N Engl J Med 1989;321:952-7.

(9.) Weiling W, VanLieshout JJ. Maintenance of postural normotension in humans. In: Low PA. Clinical autonomic disorders: evaluation and management. Boston: Little, Brown, 1993:69-77.

(10.) Low PA, Opfer-Gehrking TL, McPhee BR, Fealey RD, Benarroch EE, Willner CL, et al. Prospective evaluation of clinical characteristics of orthostatic hypotension. Mayo Clin Proc 1995;70:617-22.

(11.) Grubb BP, Karas B. Clinical disorders of the autonomic nervous system associated with orthostatic intolerance: an overview of classification, clinical evaluation, and management. Pacing Clin Electrophysiol 1999;22:798-810.

(12.) Mathias CJ. Orthostatic hypotension: causes, mechanisms, and influencing factors. Neurology 1995;45(4 suppl 5):S6-11.

(13.) Hollister AS. Orthostatic hypotension: causes, evaluation, and management. West J Med 1992;157:652-7.

(14.) Robertson D, Davis TL. Recent advances in the treatment of orthostatic hypotension. Neurology 1995;45(4 suppl 5):S26-32.

(15.) Engstrom JW, Aminoff MJ. Evaluation and treatment of orthostatic hypotension. Am Fam Physician 1997;56:1378-84.

(16.) Harrison TR, Brunwald E. Harrison's Principles of internal medicine. 15th ed. New York: McGraw-Hill, 2001.

(17.) Low PA, Gilden JL, Freeman R, Sheng KN, McElligott MA. Efficacy of midodrine vs placebo in neurogenic orthostatic hypotension. A randomized, double-blind multicenter study. Midodrine Study Group. [Published erratum appears in JAMA 1997;278:388]. JAMA 1997;277:1046-51.

(18.) Hoeldtke RD, Streeten DH. Treatment of orthostatic hypotension with erythropoietin. N Engl J Med 1993;329:611-5.

Members of various family practice departments develop articles for "Problem-Oriented Diagnosis." This is one in a series from the Department of Family and Community Medicine at Southern Illinois University School of Medicine, Springfield. Guest editor of the series is John G. Bradley, M.D., professor and director of the Decatur Family Practice Residency Program.

The authors thank Robert M. Wesley, M.A., for assistance in editing the manuscript.

The authors indicate that they do not have any conflicts of interests. Sources of funding: none reported.

JOHN G. BRADLEY, M.D., is professor and associate chair in the Department of Family and Community Medicine at Southern Illinois University School of Medicine, Decatur, and director of the Decatur Family Practice Residency Program. Dr. Bradley received his medical degree from the University of Missouri School of Medicine, Columbia, and completed a residency at Southern Illinois University-Springfield Family Medicine Residency Program.

KATHY A. DAVIS, R.N., is a researcher in the Department of Family and Community Medicine at Southern Illinois University School of Medicine. Ms. Davis earned her nursing degree at Millikin University, Decatur. She is a member of the Association of Clinical Research Professionals and a certified clinical research coordinator.

Address correspondence to John G. Bradley, M.D., Southern Illinois University School of Medicine, Decatur Family Practice Center, 250 W. Kenwood Ave., Decatur, IL 62526 (e-mail: jbradley@siumed.edu). Reprints are not available from The authors.

JOHN G. BRADLEY, M.D., and KATHY A. DAVIS, R.N. Southern Illinois University School of Medicine, Decatur, Illinois

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