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33 Cards in this Set

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What is orthostatic hypotension

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, 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.

Evidence increasingly suggests that disorders of postural hemodynamic control increase risk of cardiovascular disease and all-cause mortality.


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 bodies 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 (ADH) secretion cause sodium and water retention and increase circulating blood volume.

What helps maintain BP in a normal person on standing

Baroreceptors - Aortic arch

Carotid body

↗↗↗ autonomic reflexes

Sympathetic nervous system

What comes to play in prolonged standing

Increased circulating blood volume

By activation of renin angiotensin aldosterone system

Vasopressin secretion

Na and water retention


What can go wrong

Autonomic reflexes

Cardiac contractility

Vascular response

Presence of hypovolemia

Hormonal responses are faulty

Aetiology 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.Causes differ depending on whether symptoms are acute or chronic.

The most common causes of acute orthostatic hypotension include

HypovolemiaDrugsProlonged bed restAdrenal insufficiency

The most common causes of chronic orthostatic hypotension include

Age-related changes in BP regulation


Autonomic dysfunction

Postprandial orthostatic hypotension is also common.

What causes postprandial orthostatic hypotension

It may be caused by the insulin response to high-carbohydrate meals and blood pooling in the GI tract; this condition is worsened by alcohol intake.

Diagnostic criteria

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.

Features in the History

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

What are the symptoms of autonomic insufficiency

symptoms of autonomic insufficiency such as

visual impairment (due to mydriasis and loss of accommodation),

incontinence or urinary retention,


heat intolerance (due to impaired sweating), and

erectile dysfunction.

History should look for

Presence of autonomic symptoms

Parkinson disease

Multiple system atrophy

GI haemorrhage


Cardiovascular disease

Other neurologic disorders



Other important symptoms include tremor, rigidity, and difficulty walking (Parkinson disease, multiple system atrophy);

weakness and fatigue (adrenal insufficiency, anemia); and black, tarry stool (GI hemorrhage).

Other symptoms of neurologic and cardiovascular disorders and cancer are noted.

Things to dig into

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), particularly antihypertensives and nitrates

A family history of orthostatic symptoms suggests possible familial dysautonomia.

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.

The skin and mucosae are inspected for signs of dehydration and for pigment changes suggestive of Addison disease (eg, hyperpigmented areas, vitiligo). A rectal examination is done to detect GI bleeding. During the neurologic examination, GU and rectal reflexes can be tested to evaluate autonomic function; 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

What suggests autonomic impairment

Hypotension without a compensatory increase in heart rate (< 10 beats/min) suggests autonomic impairment.

What suggests hypovolemia

Marked increase (to > 100 beats/min or by > 30 beats/min) suggests hypovolemia or, if symptoms develop without hypotension, POTS.

What are the red flags ⛳⛳⛳

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 or multiple system atrophy.

Patients with findings of peripheral neuropathy may have an apparent cause (eg, diabetes, alcoholism), but a paraneoplastic syndrome due to an occult cancer and amyloidosis must be considered.

Patients who have only peripheral autonomic symptoms may have pure autonomic failure

Testing and testing


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 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 min of BP assessment.

Patients with autonomic symptoms or signs require further evaluation for diabetes, Parkinson disease, and possibly multiple system atrophy and pure autonomic failure.

Other tests to assess autonomic dysfunction ⏳⌛

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-sec inspiration and a 7-sec expiration) for 1 min.

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-sec Valsalva maneuver

How do you treat orthostatic hypotension - non drug treatment

Nondrug treatmentPatients 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 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 elderly patients and in patients with impaired myocardial function; development of dependent edema without heart failure does not contraindicate continuing this approach.

How do you treat - drug treatment




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 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; 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 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 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 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

Pyridostigmine and octreotide have been effective in small clinical studies.

Geriatric essentials

Orthostatic hypotension occurs in about 20% of the elderly; 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 the elderly 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. The elderly also have decreased resting parasympathetic tone, so that cardioacceleration due to reflex vagal withdrawal is lessened

Key points

Orthostatic hypotension typically involves volume depletion or autonomic dysfunction.Some degree of autonomic dysfunction is common in the elderly, but neurologic disorders must be ruled out.Tilt table testing is sometimes done.Treatment involves physical measures to reduce venous pooling, increased Na intake, and sometimes fludrocortisone or midodrine