Orthostatic hypotension is a chronic, debilitating illness associated with common neurologic conditions (eg, diabetic neuropathy, Parkinson disease). It is common in the elderly, especially in those who are institutionalized and are using multiple medications.
Treatment can be challenging, especially if the problem is neurogenic. This condition has no cure, symptoms vary in different circumstances, treatment is nonspecific, and aggressive treatment can lead to marked supine hypertension.
This review focuses on the prevention and treatment of neurogenic causes of orthostatic hypotension. We emphasize a simple but effective patient-oriented approach to management, using a combination of nonpharmacologic strategies and drugs clinically proven to be efficacious. The recommendations and their rationale are organized in a practical and easy-to-remember format for both physicians and patients.
WHAT HAPPENS WHEN WE STAND UP?
When we stand up, the blood goes down from the chest to the distensible venous capacitance system below the diaphragm. This fluid shift produces a decrease in venous return, ventricular filling, cardiac output, and blood pressure.1
This gravity-induced drop in blood pressure, detected by arterial baroreceptors in the aortic arch and carotid sinus, triggers a compensatory reflex tachycardia and vasoconstriction that restores normotension in the upright position. This compensatory mechanism is termed a baroreflex; it is mediated by afferent and efferent autonomic peripheral nerves and is integrated in autonomic centers in the brainstem.2
Orthostatic hypotension is the result of baroreflex failure (autonomic failure), end-organ dysfunction, or volume depletion. Injury to any limb of the baroreflex causes neurogenic orthostatic hypotension, although with afferent lesions alone, the hypotension tends to be modest and accompanied by wide fluctuations in blood pressure, including severe hypertension. Drugs can produce orthostatic hypotension by interfering with the autonomic pathways or their target end-organs or by affecting intravascular volume. Brain hypoperfusion, resulting from orthostatic hypotension from any cause, can lead to symptoms of orthostatic intolerance (eg, lightheadedness) and falls, and if the hypotension is severe, to syncope.
A DECREASE OF 20 MM HG SYSTOLIC OR 10 MM HG DIASTOLIC
The consensus definition of orthostatic hypotension is a reduction of systolic blood pressure of at least 20 mm Hg or a reduction of diastolic blood pressure of at least 10 mm Hg within 3 minutes of erect standing.3 A transient drop that occurs with abrupt standing and resolves rapidly suggests a benign condition, such as dehydration, rather than autonomic failure.
In the laboratory, patients are placed on a tilt table in the head-up position at an angle of at least 60 degrees to detect orthostatic changes in blood pressure. In the office, 1 minute of standing probably detects nearly all cases of orthostatic hypotension; however, standing beyond 2 minutes helps establish the severity (a further drop in blood pressure).4 Orthostatic hypotension developing after 3 minutes of standing is uncommon and may represent a reflex presyncope (eg, vasovagal) or a mild or early form of sympathetic adrenergic dysfunction.4, 5
NEUROGENIC AND NONNEUROGENIC CAUSES
Orthostatic hypotension may result from neurogenic and nonneurogenic causes.
Neurogenic orthostatic hypotension can be due to neuropathy (eg, diabetic or autoimmune neuropathies) or to central lesions (eg, Parkinson disease or multiple system atrophy). Its presence, severity, and temporal course can be important clues in diagnosing Parkinson disease and differentiating it from other parkinsonian syndromes with a more ominous prognosis, such as multiple system atrophy and Lewy body dementia.
Nonneurogenic causes include cardiac impairment (eg, from myocardial infarction or aortic stenosis), reduced intravascular volume (eg, from dehydration, adrenal insufficiency), and vasodilation (eg, from fever, systemic mastocytosis).
Common drugs that cause orthostatic hypotension are diuretics, alpha-adrenoceptor blockers for prostatic hypertrophy, antihypertensive drugs, and calcium channel blockers. Insulin, levodopa, and tricyclic antidepressants can also cause vasodilation and orthostatic hypotension in predisposed patients. Poon and Braun,6 in a retrospective study in elderly veterans, identified hydrochlorothiazide, lisinopril (Prinivil, Zestril), trazodone (Desyrel), furosemide (Lasix), and terazosin (Hytrin) as the most common culprits.
ORTHOSTATIC HYPOTENSION IS COMMON IN THE ELDERLY
The prevalence of orthostatic hypotension is high in the elderly and depends on the characteristics of the population studied, such as age, use of medications, and comorbidities known to be associated with this problem. Orthostatic hypotension is more common in institutionalized elderly people (up to 68%)7 than in those living in the community (6%).8 The high prevalence among institutionalized patients likely reflects multiple disease processes, including neurologic and cardiac conditions, as well as medications associated with orthostatic hypotension.
CLINICAL MANIFESTATIONS ARE DUE TO HYPOPERFUSION, OVERCOMPENSATION
Symptoms are related to cerebral hypoperfusion, with resulting lack of cerebral oxygenation (causing lightheadedness, dizziness, weakness, difficulty thinking, headache, syncope, or feeling faint) and a compensatory autonomic overreaction (causing palpitations, tremulousness, nausea, coldness of extremities, chest pain, and syncope).
Lightheadedness is a common symptom, but subtler issues such as difficulty thinking, weakness, and neck discomfort are also common in the elderly. Recurrent or unexplained falls in older adults may be a manifestation of syncope due to orthostatic hypotension.