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Orthostatic (postural) hypotension is an excessive fall in BP (typically > 20/10 mm Hg) when an upright position is assumed. Faintness, light-headedness, dizziness, confusion, or blurred vision occurs within seconds of standing. Some patients experience syncope (see Approach to the Cardiac Patient: Syncope) or even generalized seizures. Exercise or a heavy meal may exacerbate symptoms. Most other associated symptoms and signs relate to the cause. Orthostatic hypotension is a manifestation of abnormal BP regulation due to various conditions, not a specific disorder.

Orthostatic hypotension occurs in about 20% of the elderly; it is more common among those with coexisting disorders, especially hypertension, and among residents of long-term care facilities. Many falls may result from unrecognized orthostatic hypotension. Symptoms tend to be more severe shortly after eating and after vagal stimulation (eg, urination, defecation).

Postural orthostatic tachycardia syndrome (POTS): POTS (also called postural autonomic tachycardia or chronic or idiopathic orthostatic intolerance) is a syndrome of orthostatic intolerance in younger patients. Although tachycardia and various symptoms (eg, fatigue, light-headedness, exercise intolerance, cognitive impairment) occur with standing, there is little or no fall in BP. The reason for symptoms is unclear.

Pathophysiology

Normally, the gravitational stress of suddenly standing causes blood (¹⁄₂ to 1 L) to pool in the capacitance veins of the legs and trunk. The subsequent transient decrease in venous return reduces cardiac output and thus BP. The first effects are those of cerebral hypoperfusion; however, decreased BP does not always produce cerebral hypoperfusion.

Baroreceptors in the aortic arch and carotid bodies respond to hypotension by activating autonomic reflexes to rapidly normalize BP. The sympathetic system increases heart rate and contractility. Then, vasomotor tone of the capacitance vessels increases. Simultaneous parasympathetic (vagal) inhibition also increases heart rate. With continued standing, activation of the renin-angiotensin-aldosterone system and ADH secretion cause Na and water retention and increase circulating blood volume.

Etiology

Homeostatic mechanisms may be inadequate to restore low BP if afferent, central, or efferent portions of the autonomic reflex arc are impaired by disorders or drugs, if myocardial contractility or vascular responsiveness is depressed, if hypovolemia is present, or if hormonal responses are faulty (see Table 6: Approach to the Cardiac Patient: Causes of Orthostatic Hypotension).

Table 6
Causes of Orthostatic Hypotension Cause Examples Neurologic (involving autonomic dysfunction) Central Multiple system atrophy (previously Shy-Drager syndrome)   Parkinson's disease   Strokes (multiple) Spinal cord Tabes dorsalis   Transverse myelitis   Tumors Peripheral Amyloidosis   Diabetic, alcoholic, or nutritional neuropathy   Familial dysautonomia (Riley-Day syndrome)   Guillain-Barré syndrome   Paraneoplastic syndromes   Pure autonomic failure (formerly called idiopathic orthostatic hypotension)   Surgical sympathectomy Cardiovascular Hypovolemia Adrenal insufficiency   Dehydration   Hemorrhage Impaired vasomotor tone Bed rest (prolonged)   Hypokalemia Impaired cardiac output Aortic stenosis   Constrictive pericarditis   Heart failure   MI   Tachyarrhythmias or bradyarrhythmias Other Hyperaldosteronism*   Peripheral venous insufficiency   Pheochromocytoma* Drugs Vasodilators Ca channel blockers   Nitrates Autonomically active α-Blockers ( prazosin Some Trade Names MINIPRESS Click for Drug Monograph , phenoxybenzamine Some Trade Names DIBENZYLINE Click for Drug Monograph )   Antihypertensives ( clonidine Some Trade Names CATAPRES Click for Drug Monograph , methyldopa Some Trade Names ALDOMET Click for Drug Monograph , reserpine Some Trade Names SERPASIL Click for Drug Monograph , [rarely] β-blockers)†   Antipsychotics (particularly phenothiazines)   Monoamine oxidase inhibitors (MAOIs)   Tricyclic or tetracyclic antidepressants Other Alcohol   Barbiturates   Levodopa (in Parkinson's [rarely])   Loop diuretics (eg, furosemide Some Trade Names LASIX Click for Drug Monograph )   Quinidine Some Trade Names CARDIOQUIN QUINAGLUTE Click for Drug Monograph   Vincristine Some Trade Names ONCOVIN Click for Drug Monograph (neurotoxic) *Causes supine hypertension. †Symptoms are more common when treatment is begun.

The most common cause in the elderly is decreased baroreceptor responsiveness plus decreased arterial compliance. Decreased baroreceptor responsiveness delays cardioacceleration in response to standing. Paradoxically, hypertension may contribute to poor baroreceptor sensitivity, increasing vulnerability to orthostatic hypotension. Postprandial orthostatic hypotension is also common. It may be caused by the insulin Some Trade Names
HUMULIN
NOVOLIN
Click for Drug Monograph
response to high-carbohydrate meals and blood pooling in the GI tract; this condition is worsened by alcohol intake.

Evaluation

Orthostatic hypotension is diagnosed when a marked fall in measured BP and symptoms suggesting hypotension are provoked by standing and relieved by lying down. A cause must be sought.

History: The patient is asked about known triggers (eg, drugs, bed rest, fluid loss) and symptoms of autonomic insufficiency (eg, visual impairment [due to mydriasis and loss of accommodation], incontinence, constipation, heat intolerance [due to impaired sweating], impotence). Other symptoms of neurologic, cardiovascular, and malignant disorders are noted.

Physical examination: BP and heart rate are measured after 5 min supine and at 1 and 3 min after standing; patients unable to stand may be assessed while sitting upright. Hypotension without a compensatory increase in heart rate (< 10 beats/min) suggests autonomic impairment; marked increase (to > 100 beats/min) suggests hypovolemia or, if symptoms develop without hypotension, POTS. Other findings suggesting autonomic impairment include parkinsonism.

Testing: ECG and serum electrolytes and glucose are routinely checked. However, these and other tests are usually of little benefit unless suggested by specific symptoms.

Autonomic function can be evaluated. With an intact autonomic system, heart rate increases in response to inspiration. The heart is monitored as the patient breathes slowly and deeply (about 5 sec inspiration and 7 sec expiration) for 1 min. The longest interbeat (R-R) interval during expiration is normally at least 1.15 times the minimum R-R interval during inspiration; a shorter interval suggests autonomic dysfunction. A similar variation in R-R interval should exist between rest and a 10- to 15-sec Valsalva maneuver. Patients with abnormal R-R intervals or with autonomic symptoms or signs require further evaluation for diabetes, Parkinson's disease, and possibly multiple system atrophy (see Autonomic Nervous System: Multiple System Atrophy) and pure autonomic failure (see Autonomic Nervous System: Pure Autonomic Failure); the last may require plasma norepinephrine Some Trade Names
LEVOPHED
Click for Drug Monograph
or vasopressin Some Trade Names
PITRESSIN
Click for Drug Monograph
measurements with the patient supine and upright.

Tilt table testing (see Cardiovascular Tests and Procedures: Tilt Table Testing) varies less than supine and upright BP assessment and eliminates augmentation of venous return by leg muscle contraction. The patient may remain upright for 30 to 45 min of BP assessment. It may be done when autonomic dysfunction is suspected. The dose of a suspected drug may be reduced or the drug withdrawn to confirm the drug as the cause.

Prevention and Treatment

Patients requiring prolonged bed rest should sit up each day and exercise in bed when possible. Patients should rise slowly from a recumbent or sitting position, consume adequate fluids, limit or avoid alcohol, and exercise regularly when feasible. Regular modest-intensity exercise promotes overall vascular tone and reduces venous pooling. Elderly patients should avoid prolonged standing. Sleeping with the head of the bed raised may relieve symptoms by promoting Na retention and reducing nocturnal diuresis.

Postprandial hypotension can often be prevented by reducing the size and carbohydrate content of meals, minimizing alcohol intake, and avoiding sudden standing after meals.

Waist-high fitted elastic hose may increase venous return, cardiac output, and BP after standing. In severe cases, inflatable aviator-type antigravity suits, although often poorly tolerated, may be needed to produce adequate leg and abdominal counterpressure.

Increasing Na intake may expand intravascular volume and lessen symptoms. In the absence of heart failure or hypertension, Na intake can be increased 5 to 10 g above the usual dietary level by liberally salting food or taking NaCl tablets. This approach risks heart failure, particularly in elderly patients and patients with impaired myocardial function; development of dependent edema without heart failure does not contraindicate continuing this approach.

Fludrocortisone Some Trade Names
FLORINEF
Click for Drug Monograph
, a mineralocorticoid, causes Na retention, which expands plasma volume, and often lessens symptoms but is effective only when Na intake is adequate. Dosage is 0.1 mg po at bedtime, increased weekly to 1 mg or until peripheral edema occurs. This drug may also improve the peripheral vasoconstrictor response to sympathetic stimulation. Supine hypertension, heart failure, and hypokalemia may occur; K supplements may be needed.

Midodrine Some Trade Names
ORVATEN
PROAMATINE
Click for Drug Monograph
, a peripheral α-agonist that is both an arterial and venous constrictor, is often effective. Dosage is 2.5 mg to 10 mg po tid. Adverse effects include paresthesias and itching (probably secondary to piloerection). This drug is not recommended for patients with coronary artery or peripheral arterial disease.

NSAIDs (eg, indomethacin Some Trade Names
INDOCIN
Click for Drug Monograph
25 to 50 mg po tid) may inhibit prostaglandin-induced vasodilation, increasing peripheral vascular resistance. However, NSAIDs may cause GI symptoms and unwanted vasopressor reactions (reported with concurrent use of indomethacin Some Trade Names
INDOCIN
Click for Drug Monograph
and sympathomimetic drugs).

L-dihydroxyphenylserine, a norepinephrine Some Trade Names
LEVOPHED
Click for Drug Monograph
precursor, may be beneficial for autonomic dysfunction (reported in limited trials).

Propranolol Some Trade Names
INDERAL
Click for Drug Monograph
or other β-blockers may enhance the beneficial effects of Na and mineralocorticoid therapy. β-Blockade with propranolol Some Trade Names
INDERAL
Click for Drug Monograph
leads to unopposed α-adrenergic peripheral vascular vasoconstriction, preventing the vasodilation that occurs when some patients stand.

Last full review/revision November 2005

Content last modified November 2005