Preventing and treating orthostatic hypotension: As easy as A, B, C
ABSTRACTOrthostatic hypotension is a chronic, debilitating illness that is difficult to treat. The therapeutic goal is to improve postural symptoms, standing time, and function rather than to achieve upright normotension, which can lead to supine hypertension. Drug therapy alone is never adequate. Because orthostatic stress varies with circumstances during the day, a patient-oriented approach that emphasizes education and nonpharmacologic strategies is critical. We provide easy-to-remember management recommendations, using a combination of drug and nondrug treatments that have proven efficacious.
KEY POINTS
- Treatment is directed at increasing blood volume, decreasing venous pooling, and increasing vasoconstriction while minimizing supine hypertension.
- Patient education and nondrug strategies alone can be effective in mild cases. Examples: consuming extra fluids and salt, wearing an abdominal binder, drinking boluses of water, raising the head of the bed, and performing countermaneuvers and physical activity.
- Moderate and severe cases require additional drug treatment. Pyridostigmine (Mestinon) is helpful in moderate cases. Fludrocortisone (Florinef) and midodrine (ProAmatine) are indicated in more severe cases.
PROGNOSIS DEPENDS ON CAUSE
Orthostatic hypotension is a syndrome, and its prognosis depends on its specific cause, its severity, and the distribution of its autonomic and nonautonomic involvement. In patients who have extrapyramidal and cerebellar disorders (eg, Parkinson disease, multiple system atrophy), the earlier and the more severe the involvement of the autonomic nervous system, the poorer the prognosis.9,10
In hypertensive patients with diabetes mellitus, the risk of death is higher if they have orthostatic hypotension.11 Diastolic orthostatic hypotension is associated with a higher risk of vascular death in older persons.12
MANAGEMENT: FROM A TO F
The goal of management of orthostatic hypotension is to raise the patient’s standing blood pressure without also raising his or her supine blood pressure, and specifically to reduce orthostatic symptoms, increase the time the patient can stand, and improve his or her ability to perform daily activities. No specific treatment is currently available that achieves all these goals, and drugs alone are never completely adequate.
Because the mainstays of treatment are volume expansion and vasoconstriction, it is difficult to improve the symptoms of orthostatic hypotension without inducing some degree of supine hypertension. Strategies to minimize nocturnal hypertension and to treat orthostatic hypotension in special circumstances are summarized in Table 1.
If hypovolemia is playing a major role, and the patient cannot ingest enough salt or plasma volume fails to increase despite salt supplementation, fludrocortisone (Florinef) should be considered. Untreated hypovolemia will decrease the efficacy of vasoconstrictor drugs.
Pyridostigmine (Mestinon) has a putative vasoconstrictor effect only during standing, but because its effect is modest it should be used in mild orthostatic hypotension that does not improve with nonpharmacologic measures and in moderate cases. Its effect can be enhanced with additional low doses of midodrine (ProAmatine). Midodrine with or without fludrocortisone should be used in severe orthostatic hypotension.
A: Abdominal compression
In conditions in which there is adrenergic denervation of vascular beds, there is an increase in vascular capacitance and peripheral venous pooling. Compression of capacitance beds (ie, the legs and abdomen) improves orthostatic symptoms.14 The improvement is due to a reduction of venous capacitance and an increase in total peripheral resistance.14
On standing, healthy adults experience an orthostatic shift of approximately 500 mL of blood to the lower extremities15 that, when added to an increased vascular capacitance in those with orthostatic hypotension, results in a relative state of hypovolemia.
Compression of the legs alone is not as beneficial as compression of the abdomen because the venous capacitance of the calves and thighs is relatively small compared with that of the splanchnic mesenteric bed, which accounts for 20% to 30% of total blood volume.16 Moreover, compression garments and stockings that are strong enough to produce a measurable effect on orthostatic hypotension are cumbersome to put on and uncomfortable to wear. Because some patients gain significant benefit from abdominal compression alone, this should be considered the first step in reducing venous capacitance.
In a laboratory experiment, Smit et al17 found that an elastic abdominal binder that exerted 15 to 20 mm Hg of pressure on the abdomen raised the standing blood pressure by about 11/6 mmHg, which was comparable to the effect of a gravity suit (such as those worn by fighter pilots to prevent syncope during violent aircraft maneuvers) inflated to 20 mm Hg—an increase of about 17/8 mm Hg. Higher gravity-suit pressures had a greater effect.
In practical terms, the binder should be tight enough to exert gentle pressure. It should be put on before rising from bed in the morning and taken off when lying supine, to avoid supine hypertension. Advantages are that a binder’s effects are immediate, its benefits can be easily assessed, and it can be used on an as-needed basis by patients who need it only during periods of prolonged orthostatic stress. Binders are also easy to fit and are available in most sporting good stores and on the Web (try searching for “abdominal binder”).
When abdominal compression alone is not enough, the addition of compression of the lower extremities can result in further benefits. This can be achieved by using compression garments that ideally extend to the waist or, at the least, to the proximal thigh.
