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Postural hypotension

Orthostatic hypotension (also known as postural hypotension and, colloquially, as head rush) is a sudden fall in blood pressure that occurs when a person assumes a standing position. more...

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Medicines

Symptoms

Symptoms, which generally occur after sudden standing, include dizziness, lightheadedness, blurred vision, and syncope (temporary loss of consciousness).

Causes

It may be caused by hypovolemia (a decreased amount of blood in the body), resulting from the excessive use of diuretics, vasodilators, or other types of drugs, dehydration, or prolonged bed rest. It can be a side effect of certain anti-depressants, such as tricyclics. The disorder may be associated with Addison's disease, atherosclerosis (build-up of fatty deposits in the arteries), diabetes, and certain neurological disorders including Shy-Drager syndrome and other forms of dysautonomia.

Treatment and management

When orthostatic hypotension is caused by hypovolemia due to medications, the disorder may be reversed by adjusting the dosage or by discontinuing the medication. When the condition is caused by prolonged bed rest, improvement may occur by sitting up with increasing frequency each day. In some cases, physical counterpressure such as elastic hose or whole-body inflatable suits may be required (such as Jobst stockings). Dehydration is treated with salt and fluids.

The prognosis for individuals with orthostatic hypotension depends on the underlying cause of the condition.

Medical management

Some drugs that are used in the treatment of orthostatic hypotension include fludrocortisone (Florinef), erythropoietin and midrodrine.

Lifestyle advice

Some suggestions for minimizing the effects include:

  • Checking blood pressure regularly with a home monitoring kit. Check when lying flat and when standing as well as when symptoms occur.
  • Standing slowly rather than quickly, as the delay can give the blood vessels more time to constrict properly. This can help avoid incidents of syncope.
  • Maintaining an elevated salt intake, through sodium supplements or electrolyte-enriched drinks. A suggested value is 10 g per day; overuse can lead to hypertension and should be avoided.
  • Maintaining a proper fluid intake to prevent the effects of dehydration.
  • As eating lowers blood pressure, eating multiple smaller meals rather than fewer larger meals. Taking extra care when standing after eating.

Read more at Wikipedia.org


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Evaluation and treatment of orthostatic hypotension
From American Family Physician, 10/1/97 by John W. Engstrom

Homeostatic control of blood pressure and heart rate requires frequent and rapid cardiovascular adjustments as an individual changes from supine to sitting and standing positions throughout the day. When these adjustments are not accomplished, orthostatic hypotension occurs. Some patients with severe orthostatic hypotension are severely incapacitated, and their families assume a significant burden in their care.

The diagnosis of orthostatic hypotension requires the occurrence of a sustained postural decrease in blood pressure that may be accompanied by symptoms of cerebral hypoperfusion. While the degree of hypotension required to produce symptoms varies, a decrease of 20 mm Hg or more in systolic blood pressure is one commonly used diagnostic criterion.[1,2]

If blood pressure is assessed for less than two minutes following a postural change, the degree of hypotension may be overstated. This is particularly true in elderly patients because blunted baroreceptor reflexes are common in otherwise normal older individuals. In one study,[3] 17 percent of normal elderly patients exhibited a fall in systolic blood pressure of more than 20 mm Hg after they had been standing for two minutes.

Blood pressure criteria are more sensitive than symptoms in detecting orthostatic hypotension. However, treatment usually is not required in the absence of symptoms. Symptoms of cerebral hypoperfusion include dimming or loss of vision, lightheadedness, dizziness, diaphoresis, diminished hearing, pallor, nausea and weakness. Severe orthostatic decreases in cerebral perfusion can cause syncope.

Classification and Clinical Features

The causes of orthostatic hypotension can be divided into neurogenic and nonneurogenic categories.[2,4] Frequent causes of nonneurogenic orthostatic hypotension are listed in Table 1. These nonneurogenic causes lead to orthostatic hypotension because of cardiac pump failure, reduced intravascular volume or venous pooling. In addition, many medications can cause or exacerbate orthostatic hypotension. Since the nonneurogenic causes of orthostatic hypotension are so common, they should be systematically reviewed in any patient who is experiencing postural decreases in blood pressure with symptoms of hypoperfusion. As a general rule, the postural drop in blood pressure with nonneurogenic etiologies is accompanied by a compensatory increase in heart rate (often exceeding 15 to 30 beats per minute). This increase in heart rate does not occur in patients with neurogenic causes of orthostatic hypotension.

[3.] Johnson RH, Smith AC, Spalding JM, Wollner L. Effect of posture on blood-pressure in elderly patients. Lancet 1965;1:731-3.

[4.] Engstrom JW, Martin JP. Disorders of the autonomic nervous system. In: Fauci AS, ed. Harrison's Principles of internal medicine. New York: McGraw-Hill. In press.

[5.] Bradbury S, Eggleston C. Postural hypotension. A report of three cases. Am Heart J 1925;1:73-86.

[6.] Shy GM, Drager GA. A neurological syndrome associated with orthostatic hypotension. A clinical-pathologic study. Arch Neurol 1960;2:511-27.

[7.] McLeod JG. Invited review: autonomic dysfunction in peripheral nerve disease. Muscle Nerve 1992;15:3-13.

[8.] Hund EF, Borel CO, Cornblath DR, Hanley DF, McKhann GM. Intensive management and treatment of severe Guillain-Barre syndrome. Crit Care Med 1993;21:433-46.

[9.] Hsu CY, Hogan EL, Wingfield W Jr, Webb JG, Perot PL Jr, Privitera PJ, et al. Orthostatic hypotension with brainstem tumors. Neurology 1984;34:1137-43.

[10.] Hilsted J, Low PA. Diabetic autonomic neuropathy In: Low PA, ed. Clinical autonomic disorders: evaluation and management. Boston: Little, Brown, 1993: 423-43.

[11.] Jansen RW, Lipsitz LA. Postprandial hypotension: epidemiology, pathophysiology, and clinical management. Ann Intern Med 1995;122:286-95.

[12.] Low PA, Pfeifer MA. Standardization of clinical tests for practice and clinical trials. In: Low PA, ed. Clinical autonomic disorders: evaluation and management. Boston: Little, Brown, 1993:287-96.

[13.] Wolfe DA, Grubb BP, Kimmel SR. Head-upright tilt test: a new method of evaluating syncope. Am Fam Physician 1993;47:149-59.

[14.] Low PA, Opfer-Gehrking TL, Proper CJ, Zimmerman I. The effect of aging on cardiac autonomic and postganglionic sudomotor function. Muscle Nerve 1990;13:152-7.

[15.] Thomson PD, Melmon KL. Clinical assessment of autonomic function. Anesthesiology 1968;29:724-31.

[16.] Benarroch EE, Sandroni P, Low PA. The valsalva maneuver. In: Low PA, ed. Clinical autonomic disorders: evaluation and management. Boston: Little, Brown, 1993:209-15.

[17.] Omboni S, Smit AA, Wieling W Twenty four hour continuous non-invasive finger blood pressure monitoring: a novel approach to the evaluation of treatment in patients with autonomic failure. Br Heart J 1995;73:290-2.

[18.] Polinsky RJ. Clinical autonomic neuropharmacology. Neurol Clin 1990;8:77-92.

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

[20.] Kaufmann H, Brannan T, Krakoff L, Yahr MD, Mandeli J. Treatment of orthostatic hypotension due to autonomic failure with a peripheral alpha-adrenergic agonist (midodrine). Neurology 1988;38:951-6.

[21.] New drugs. Facts and Comparisons drug newsletter. 1996;15(10):73.

[22.] Hollister AS. Orthostatic hypotension causes, evaluation and management. West J Med 1992;157:652-7.

JOHN W. ENGSTROM, M.D., and MICHAEL J. AMINOFF, M.D. University of California, San Francisco, School of Medicine, San Francisco, California

JOHN W. ENGSTROM, M.D. is associate professor of clinical neurology, residency program director and vice chairman for the Department of Neurology at the University of California, San Francisco, School of Medicine. Dr. Engstrom attended Stanford (Calif.) University School of Medicine, completed a residency in internal medicine at Johns Hopkins Hospital, Baltimore, and a residency in neurology at the University of California, San Francisco, School of Medicine.

MICHAEL J. AMINOFF, M.D. is professor of neurology and director of the clinical neurophysiology laboratories at the University of California, San Francisco, School of Medicine. He attended University College Hospital Medical School at the University of London and undertook residency training at the National Hospital for Neurology and Neurosurgery, also in London.

Address correspondence to John W. Engstrom, M.D., Department of Neurology (M-798), Box 0114, University of California, San Francisco, School of Medicine, San Francisco, CA 94143.

COPYRIGHT 1997 American Academy of Family Physicians
COPYRIGHT 2004 Gale Group

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