Orthostatic (postural) hypotension is an excessive fall in blood pressure (BP) when an upright position is assumed. The consensus definition is a drop of > 20 mm Hg systolic, 10 mm Hg diastolic, or both. Symptoms of faintness, light-headedness, dizziness, confusion, or blurred vision occur within seconds to a few minutes of standing and resolve rapidly on lying down. Some patients experience falls, syncope Syncope Syncope is a sudden, brief loss of consciousness with loss of postural tone followed by spontaneous revival. The patient is motionless and limp and usually has cool extremities, a weak pulse... read more , or even generalized seizures Seizure Disorders A seizure is an abnormal, unregulated electrical discharge that occurs within the brain’s cortical gray matter and transiently interrupts normal brain function. A seizure typically causes altered... read more . 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. Evidence increasingly suggests that disorders of postural hemodynamic control increase risk of cardiovascular disease and all-cause mortality.
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. POTS is defined by a heart rate of ≥ 120 beats/minute or an increase of ≥ 30 beats/minute when a patient moves from supine to a standing position. Various symptoms (eg, fatigue, light-headedness, exercise intolerance, cognitive impairment) and tachycardia occur upon standing; however, there is little or no fall in BP. The reason for symptoms is unclear.
Pathophysiology of Orthostatic Hypotension
Normally, the gravitational stress of suddenly standing causes blood (½ to 1 L) to pool in the veins of the legs and trunk. The subsequent transient decrease in venous return reduces cardiac output and thus BP. In response, baroreceptors in the aortic arch and carotid sinus activate autonomic reflexes to rapidly return BP to normal. The sympathetic nervous system increases heart rate and contractility and increases vasomotor tone of the capacitance vessels. Simultaneous parasympathetic (vagal) inhibition also increases heart rate. In most people, changes in BP and heart rate upon standing are minimal and transient, and symptoms do not occur.
With continued standing, activation of the renin-angiotensin-aldosterone system and vasopressin (antidiuretic hormone [ADH]) secretion cause sodium and water retention and increase circulating blood volume.
Etiology of Orthostatic Hypotension
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 Causes of Orthostatic Hypotension Causes of Orthostatic Hypotension ).
Causes differ depending on whether symptoms are acute or chronic.
The most common causes of acute orthostatic hypotension include
Prolonged bed rest
The most common causes of chronic orthostatic hypotension include
Age-related changes in BP regulation
Postprandial orthostatic hypotension is also common. It may be caused by the insulin response to high-carbohydrate meals and blood pooling in the gastrointestinal tract; this condition is worsened by alcohol intake.
Evaluation of Orthostatic Hypotension
Orthostatic hypotension is diagnosed when systolic BP drops by ≥ 20 mm Hg or diastolic BP drops by ≥ 10 mm Hg within 3 minutes of standing. Once orthostatic hypotension is diagnosed, a cause must be sought.
History of present illness should identify the duration and severity (eg, whether associated with syncope or falls) of symptoms. The patient is asked about known triggers (eg, drugs, bed rest, fluid loss) and the relationship of symptoms to meals.
Review of symptoms seeks symptoms of causative disorders, particularly symptoms of autonomic insufficiency such as visual impairment (due to mydriasis and loss of accommodation), incontinence or urinary retention, constipation, heat intolerance (due to impaired sweating), and erectile dysfunction. Other important symptoms include tremor, rigidity, and difficulty walking ( Parkinson disease Parkinson Disease Parkinson disease is a slowly progressive, degenerative disorder characterized by resting tremor, stiffness (rigidity), slow and decreased movement (bradykinesia), and eventually gait and/or... read more , multiple system atrophy Multiple System Atrophy (MSA) Multiple system atrophy is a relentlessly progressive neurodegenerative disorder causing pyramidal, cerebellar, and autonomic dysfunction. It includes 3 disorders previously thought to be distinct... read more ); weakness and fatigue ( adrenal insufficiency Addison Disease Addison disease is an insidious, usually progressive hypofunctioning of the adrenal cortex. It causes various symptoms, including hypotension and hyperpigmentation, and can lead to adrenal crisis... read more , anemia); and black, tarry stool (gastrointestinal hemorrhage). Other symptoms of neurologic and cardiovascular disorders and cancer are noted.
Past medical history should identify known potential causes, including diabetes, Parkinson disease, and cancer (ie, causing a paraneoplastic syndrome). The drug profile should be reviewed for offending prescription drugs (see table Causes of Orthostatic Hypotension Causes of Orthostatic Hypotension ), particularly antihypertensives and nitrates. A family history of orthostatic symptoms suggests possible familial dysautonomia.
BP and heart rate are measured after 5 minutes supine and at 1 and 3 minutes after standing; patients unable to stand may be assessed while sitting upright. Hypotension without a compensatory increase in heart rate (< 10 beats/minute) suggests autonomic impairment. Marked increase (to > 100 beats/minute or by > 30 beats/minute) suggests hypovolemia or, if symptoms develop without hypotension, POTS.
The skin and mucosae are inspected for signs of dehydration and for pigment changes suggestive of Addison disease Addison Disease Addison disease is an insidious, usually progressive hypofunctioning of the adrenal cortex. It causes various symptoms, including hypotension and hyperpigmentation, and can lead to adrenal crisis... read more (eg, hyperpigmented areas, vitiligo). A rectal examination is done to detect gastrointestinal bleeding.
During the neurologic examination, genitourinary and rectal reflexes can be tested to evaluate autonomic function Overview of the Autonomic Nervous System The autonomic nervous system regulates physiologic processes. Regulation occurs without conscious control, ie, autonomously. The 2 major divisions are the Sympathetic system Parasympathetic... read more ; assessment includes the cremasteric reflex (normally, stroking the thigh results in retraction of the testes) and the anal wink reflex (normally, stroking perianal skin results in contraction of the anal sphincter). Signs of peripheral neuropathy (eg, abnormalities of strength, sensation, and deep tendon reflexes) are assessed.
Certain findings suggest a more serious etiology:
Bloody or heme-positive stool
Abnormal neurologic examination
Interpretation of findings
In patients with acute symptoms, the most common causes—drugs, bed rest, and volume depletion—are often apparent clinically.
In patients with chronic symptoms, an important goal is to detect any neurologic disorder causing autonomic dysfunction. Patients with movement abnormalities may have Parkinson disease Parkinson Disease Parkinson disease is a slowly progressive, degenerative disorder characterized by resting tremor, stiffness (rigidity), slow and decreased movement (bradykinesia), and eventually gait and/or... read more or multiple system atrophy Multiple System Atrophy (MSA) Multiple system atrophy is a relentlessly progressive neurodegenerative disorder causing pyramidal, cerebellar, and autonomic dysfunction. It includes 3 disorders previously thought to be distinct... read more . Patients with findings of peripheral neuropathy may have an apparent cause (eg, diabetes Diabetic Neuropathy In patients with diabetes mellitus, years of poorly controlled hyperglycemia lead to multiple, primarily vascular, complications that affect small vessels (microvascular), large vessels (macrovascular)... read more , alcoholism), but a paraneoplastic syndrome Paraneoplastic Syndromes Paraneoplastic syndromes are symptoms that occur at sites distant from a tumor or its metastasis. Although the pathogenesis remains unclear, these symptoms may be secondary to substances secreted... read more due to an occult cancer and amyloidosis Amyloidosis Amyloidosis is any of a group of disparate conditions characterized by extracellular deposition of insoluble fibrils composed of misaggregated proteins. These proteins may accumulate locally... read more must be considered. Patients who have only peripheral autonomic symptoms may have pure autonomic failure Pure Autonomic Failure Pure autonomic failure results from neuronal loss in autonomic ganglia, causing orthostatic hypotension and other autonomic symptoms. (See also Overview of the Autonomic Nervous System.) Pure... read more .
ECG, serum electrolytes, creatinine, thyroid stimulating hormone (TSH), and glucose are routinely checked. However, these and other tests are usually of little benefit unless suggested by specific symptoms.
The dose of a suspected drug may be reduced or the drug stopped to confirm the drug as the cause.
Tilt table testing Tilt Table Testing Tilt table testing is used to evaluate syncope in Younger, apparently healthy patients Elderly patients when cardiac and other tests have not provided a diagnosis Tilt table testing produces... read more may be done when autonomic dysfunction is suspected; it gives more consistent results 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 minutes of BP assessment.
Patients with autonomic symptoms or signs require further evaluation for diabetes Diagnosis Diabetes mellitus is impaired insulin secretion and variable degrees of peripheral insulin resistance leading to hyperglycemia. Early symptoms are related to hyperglycemia and include polydipsia... read more , Parkinson disease Diagnosis Parkinson disease is a slowly progressive, degenerative disorder characterized by resting tremor, stiffness (rigidity), slow and decreased movement (bradykinesia), and eventually gait and/or... read more , and possibly multiple system atrophy Diagnosis Multiple system atrophy is a relentlessly progressive neurodegenerative disorder causing pyramidal, cerebellar, and autonomic dysfunction. It includes 3 disorders previously thought to be distinct... read more and pure autonomic failure Diagnosis Pure autonomic failure results from neuronal loss in autonomic ganglia, causing orthostatic hypotension and other autonomic symptoms. (See also Overview of the Autonomic Nervous System.) Pure... read more . Testing for pure autonomic failure may require plasma norepinephrine or vasopressin (ADH) measurements with the patient supine and upright.
Autonomic function can also be evaluated with bedside cardiac monitoring, although this test is not often done. When the autonomic system is intact, heart rate increases in response to inspiration. The heart is monitored as the patient breathes slowly and deeply (about a 5-second inspiration and a 7-second expiration) for 1 minute. The longest inter-beat (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, but this response to inspiration may decrease with aging. A similar variation in R-R interval should exist between rest and a 10- to 15-second Valsalva maneuver.
Treatment of Orthostatic Hypotension
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. Older patients should avoid prolonged standing. Sleeping with the head of the bed raised may relieve symptoms by promoting sodium 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 sodium and water intake may expand intravascular volume and lessen symptoms. In the absence of heart failure or hypertension, sodium intake can be increased to 6 to 10 g daily by liberally salting food or taking sodium chloride tablets. This approach risks heart failure, particularly in older patients and in patients with impaired myocardial function; development of dependent edema without heart failure does not contraindicate continuing this approach.
Fludrocortisone, a mineralocorticoid, causes sodium retention, which expands plasma volume, and often lessens symptoms but is effective only when sodium intake is adequate. Dosage is 0.1 mg orally 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; potassium supplements may be needed.
Midodrine, a peripheral alpha-agonist that is both an arterial and a venous constrictor, is often effective. Dosage is 2.5 mg to 10 mg orally 3 times a day. Adverse effects include paresthesias and itching (probably secondary to piloerection). This drug is not recommended for patients with coronary artery or peripheral arterial disease.
Nonsteroidal anti-inflammatory drugs (NSAIDs, eg, indomethacin 25 to 50 mg orally 3 times a day) may inhibit prostaglandin-induced vasodilation, increasing peripheral vascular resistance. However, NSAIDs may cause gastrointestinal symptoms and unwanted vasopressor reactions (reported with concurrent use of indomethacin and sympathomimetic drugs).
Droxidopa, a norepinephrine precursor, may be beneficial for autonomic dysfunction (reported in limited trials).
Propranolol or other beta-blockers may enhance the beneficial effects of sodium and mineralocorticoid therapy. Beta-blockade with propranolol leads to unopposed alpha-adrenergic peripheral vascular vasoconstriction, preventing the vasodilation that occurs when some patients stand.
Pyridostigmine and octreotide have been effective in small clinical studies.
Orthostatic hypotension occurs in about 20% of older adults it is more common among people with coexisting disorders, especially hypertension, and among residents of long-term care facilities. Many falls may result from unrecognized orthostatic hypotension.
The increased incidence in older adults is due to decreased baroreceptor responsiveness plus decreased arterial compliance. Decreased baroreceptor responsiveness delays cardioacceleration and peripheral vasoconstriction in response to standing. Paradoxically, hypertension may contribute to poor baroreceptor sensitivity, increasing vulnerability to orthostatic hypotension. Older adults also have decreased resting parasympathetic tone, so that cardioacceleration due to reflex vagal withdrawal is lessened.
Orthostatic hypotension typically involves volume depletion or autonomic dysfunction.
Some degree of autonomic dysfunction is common in older adults, but neurologic disorders must be ruled out.
Tilt table testing is sometimes done.
Treatment involves physical measures to reduce venous pooling, increased sodium intake, and sometimes fludrocortisone or midodrine.
Freeman R, Abuzinadah AR, Gibbons C, et al: Orthostatic hypotension: JACC state-of-the-art review. J Am Coll Cardiol 72(11):1294–1309, 2018. doi: 10.1016/j.jacc.2018.05.079
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