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, 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.
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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.
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