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Section 11. Cardiovascular Disorders
Chapter 86. Hypotension
Topics:    Introduction | Orthostatic Hypotension | Postprandial Hypotension

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Orthostatic Hypotension

A reduction of >= 20 mm Hg in systolic blood pressure or of >= 10 mm Hg in diastolic blood pressure on standing upright.

Orthostatic hypotension occurs in 15 to 20% of community-dwelling and in about 50% of institutionalized elderly persons. Its prevalence increases with age and with basal blood pressure elevation and is higher among patients with cardiovascular disease. Many elderly persons have wide variations in postural blood pressure, which is closely associated with basal supine systolic blood pressure; ie, when basal supine systolic blood pressure is highest, the decline in postural systolic blood pressure is greatest. Among elderly nursing home residents, orthostatic hypotension is most prevalent in the morning when residents first arise, after basal supine systolic blood pressure has been highest.

Orthostatic hypotension is a significant risk factor for syncope, falls, and all causes of mortality in the elderly, even for those without other evidence of autonomic nervous system dysfunction.


Orthostatic hypotension in the elderly may be due to age-related physiologic changes in blood pressure regulation, to certain disorders, or to use of certain drugs (see Table 86-1).

When due to aging, orthostatic hypotension varies dramatically from day to day and is associated with the exaggerated plasma norepinephrine response to postural change that is characteristic of aging. Orthostatic hypotension is often provoked by common hypotensive stresses such as dehydration, use of hypotensive drugs, or the Valsalva maneuver during voiding. Although generally asymptomatic, orthostatic hypotension in otherwise healthy elderly persons may be sufficient to compromise cerebral blood flow and cause dizziness or syncope. Prolonged bed rest may further compromise blood pressure homeostasis, resulting in severe orthostatic hypotension.

The most common cause of acute orthostatic hypotension is dehydration during an acute illness. Excessive cardioacceleration on standing (which suggests dehydration as the cause of orthostatic hypotension in younger patients) may not occur in elderly patients because cardioacceleration is often blunted with age. A much less common cause of acute orthostatic hypotension is adrenocortical insufficiency accompanied by hyponatremia and hyperkalemia.

Chronic orthostatic hypotension is usually due to disorders of the autonomic nervous system and is associated with symptoms of autonomic nervous system dysfunction (eg, a fixed heart rate, incontinence, constipation, inability to sweat, heat intolerance, impotence, fatigability).

Drugs--even when given in therapeutic doses--are a common cause of orthostatic hypotension (see Table 86-1). Drugs that reduce venous return, particularly nitrates and diuretics, commonly produce orthostatic hypotension in the elderly. The elderly depend on adequate venous return to generate a normal cardiac output because of age-related impairments in ventricular diastolic filling. Drugs that slow heart rate can also precipitate orthostatic hypotension.

If no cause is identified, orthostatic hypotension is usually due to pure autonomic failure (previously called idiopathic orthostatic hypotension). Compared with other causes of orthostatic hypotension, pure autonomic failure produces lower basal plasma norepinephrine levels in the supine position, no increase in norepinephrine levels on standing, a lower threshold for the pressor response to infused norepinephrine, and an increased pressor response to tyramine despite the release of less norepinephrine at sympathetic nerve endings.


A clinician should not assume that an elderly patient who reports postural dizziness and light-headedness has orthostatic hypotension. Blood pressure and pulse rate should be measured after the patient has been recumbent for at least 5 minutes and after the patient has been standing quietly for 1 minute and then for 3 minutes. A hypotensive response may be immediate or delayed. Measurements after a longer period of standing or a tilt test may be needed to detect a delayed hypotensive response.


Symptoms can usually be reduced or eliminated, even without completely correcting orthostatic hypotension. Regardless of the cause, orthostatic hypotension should be managed in the following stepwise fashion:

Nonpharmacologic therapy: Patients with acute orthostatic hypotension due to dehydration should be treated with fluid replacement therapy. Patients with chronic orthostatic hypotension should be instructed to rise slowly after lying in bed or sitting in a chair for a long time. Dorsiflexing the feet before standing often promotes venous return to the heart, accelerates the pulse, and increases blood pressure. Crossing the legs while upright may also help increase blood pressure. A high-salt diet aimed at producing a modest weight gain blunts the symptoms of orthostatic hypotension in many patients. Elastic compression stockings that cover the calf and thigh may be effective; abdominal binders help some patients. Elevating the head of the bed 5 to 20° prevents the diuresis and supine hypertension caused by nocturnal shifts of interstitial fluid from the legs to the rest of the circulation.

Pharmacotherapy: Patients who remain symptomatic may require drug therapy. Fludrocortisone, a mineralocorticoid, appears to be effective for mild to moderately severe orthostatic hypotension due to most conditions. The dose is increased gradually from 0.1 mg/day po up to 1.0 mg/day until orthostatic hypotension resolves or trace pedal edema develops. Fludrocortisone increases extracellular fluid and plasma volume and sensitizes blood vessels to the vasoconstrictive effect of norepinephrine. Complications include supine hypertension, heart failure, and hypokalemia. Supine blood pressure and serum potassium should be measured every few months during therapy. If a patient has supine systolic blood pressure > 180 mm Hg, the dose may have to be reduced. Fludrocortisone should not be given in the evening before bed.

If patients taking fludrocortisone remain symptomatic, midodrine, a direct alpha1-agonist, often helps. The starting dose is 2.5 mg po tid; the dose is increased 2.5 mg each week up to a total dose of 10 mg tid. Because the drug can cause supine hypertension, the evening dose should be given before the evening meal and at least 3 hours before bedtime. Other adverse effects include paresthesias, pruritus, and urinary retention.

Other drugs that may be helpful include nonsteroidal anti-inflammatory drugs, the central alpha2-antagonist yohimbine, the alpha2-agonist clonidine, and beta-blockers that block beta2-vasodilator receptors or have intrinsic sympathomimetic activity (eg, pindolol). Yohimbine can increase central sympathetic nervous system outflow. When such outflow is reduced (as in patients with multiple system atrophy), alpha2-agonists, which inhibit central sympathetic outflow in healthy persons, can act on peripheral alpha2-receptors in the veins. This action promotes venoconstriction, thereby increasing venous return.

Caffeine 200 to 250 mg each morning as two cups of brewed coffee or a 200-mg tablet can be effective and can be used safely by the elderly. Ergot alkaloids, including oral ergotamine tartrate and dihydroergotamine given subcutaneously with oral caffeine, help some patients. Sympathomimetics such as ephedrine and phenylephrine are not consistently useful. For severe, unresponsive cases, erythropoietin may be useful.

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