Treatment of orthostatic and postprandial hypotension

Authors
Horacio Kaufmann, MD
Roy Freeman, MD
Norman M Kaplan, MD
Section Editor
Michael J Aminoff, MD, DSc
Deputy Editor
Janet L Wilterdink, MD
Disclosures
All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Jul 2013. | This topic last updated: sep 22, 2010.
INTRODUCTION When autonomic reflexes are impaired or intravascular volume is markedly
depleted, a significant reduction in blood pressure occurs upon standing (ie, orthostatic
hypotension). Orthostatic hypotension can cause dizziness, syncope, and even angina or stroke.
Symptomatic falls in blood pressure after standing or eating are a frequent clinical problem. The
prevalence of orthostatic hypotension varies from 5 to 20 percent in different reports. Many
disorders can cause orthostatic hypotension, which can also be a symptom of acute or chronic
volume depletion. A related problem, postprandial hypotension (a fall in blood pressure occurring 15
to 90 minutes after meals) is also common in older subjects. Orthostatic hypotension can be a
disabling condition and is also a risk factor for cardiovascular and all-cause mortality, as well as falls
with attendant morbidity.
This topic will review the treatment of chronic orthostatic and postprandial hypotension. The patient
with acute orthostatic hypotension due to volume depletion should be treated with volume
replacement.
The causes and evaluation of orthostatic hypotension are discussed separately. POTS is also
discussed separately (See "Mechanisms, causes, and evaluation of orthostatic
hypotension" and "Postural tachycardia syndrome".)
NONPHARMACOLOGIC MEASURES The following sections on therapy are directed toward the
patient with chronic orthostatic hypotension due to autonomic dysfunction. The patient with acute
orthostatic hypotension due to volume depletion should be treated with volume replacement.
Nonpharmacologic measures are important components of the therapy of chronic orthostatic
hypotension. These include removal of offending agents, patient education, physical and dietary
interventions, and avoiding precipitating factors.
Removal of offending medications Recognition and removal of drugs which can cause
orthostatic hypotension is the first management step. The most common offending agents are
diuretics, antihypertensive (primarily sympathetic blockers), antianginal drugs (nitrates), alpha-
adrenergic antagonists, and antidepressants.
Lifestyle modification Patient education is very important for the management of chronic
orthostatic hypotension. Throughout the day, patients are subject to a number of orthostatic
demands for which there are simple and effective countermeasures. As a result, the time spent
emphasizing practical management principles is of inestimable value. These measures include [1]:
Arising slowly, in stages, from supine to seated to standing. This maneuver is most
important in the morning, when orthostatic tolerance is lowest.
Avoiding straining, coughing, and walking in hot weather; these activities reduce venous
return and worsen orthostatic hypotension.
Patients should be counselled to maintain hydration and avoid over-heating.
Raising the head of the bed 10 to 20 degrees decreases renal perfusion, thereby activating
the renin-angiotensin-aldosterone system and decreasing nocturnal diuresis, which can be
pronounced in these patients. These changes relieve orthostatic hypotension by expanding
extracellular fluid volume and may reduce end organ damage by reducing supine
hypertension.

Only small case series and clinical experience support the efficacy of this intervention, but
its effect in patients with autonomic failure can be dramatic [2]. In one series of nine older
inpatients with orthostatic hypotension, six inches of head of bed elevation during sleep was
associated with higher blood pressure and improved mobility after one week of treatment
[3]. A follow-up study by the same investigators found that this same intervention in 100
community-dwelling patients had no effect on symptoms or hemodynamic parameters after
six weeks [4].
The use of custom-fitted elastic stockings permits the application of graded pressure to the
lower extremities and lower abdomen, thereby minimizing peripheral blood pooling. It is
essential that such stockings extend to the waist since most peripheral pooling occurs in the
splanchnic circulation. These stockings are poorly tolerated by many patients, particularly
those with painful peripheral neuropathies or motor dysfunction and those living in hot
climates. They are difficult to take on and off.

One report of ten patients found that compression stockings in patients with orthostatic
hypotension and a history of falls reduced the average degree of orthostasis in the group as
a whole, and abolished orthostatic dizziness in seven [5]. In a cross-over study of 21
patients, use of compression bandages was associated with reduced orthostatic blood
pressure decrease and symptoms compared to control [6].
Exercise may be beneficial when cardiovascular deconditioning rather than chronic
autonomic failure is the cause of orthostatic hypotension. As an example, a small study of
five elderly patients in whom tilt-table testing at baseline resulted in symptoms showed that
an exercise regimen consisting of walking or climbing stairs for 30 to 45 minutes per day
three times per week for six months resulted in symptom disappearance during a repeat tilt-
table test [7].
Modifying meals can be helpful when symptoms appear to occur in association with eating.
(See 'Modification of meals' below.)
Physical maneuvers Specific physical maneuvers appear to be helpful in some patients [1]:
One maneuver that may be effective is tensing the legs by crossing them while actively
standing on both legs. In one series of seven patients with autonomic neuropathy, this
procedure raised the cardiac output by 16 percent and the systemic blood pressure by 13
percent [8,9]. Without leg-crossing, five of the patients reported dizziness within 10 minutes
of standing up, leg-crossing allowed all to stand for 10 minutes or more [8]. Another study
also found that tensing lower body muscles in the legs, buttocks, and abdomen before
arising from a squat position blunted the hypotensive response and clinical symptoms in a
series of 13 patients with orthostatic hypotension [10].
Isometric handgrip when standing was effective in reducing symptoms and minimizing
decreases in blood pressure and cardiac output in a case series of 14 patients (age 15 to
22 years) with orthostatic hypotension [11].
Respiratory maneuvers are under investigation as a means of treating orthostatic
hypotension [12]. Increased negative inspiratory intrathoracic pressure may reduce
orthostatic hypotension by augmenting venous return. Techniques such as inspiration
through pursed lips, inspiratory sniffing, and use of an external device causing selective
inspiratory obstruction were shown in 10 patients to improve standing blood pressure
comparable to leg muscle tensing as long as hyperventilation was avoided.
Increased salt and water intake The reduction in central blood volume associated with
autonomic insufficiency (due to increased urinary sodium and water excretion) can be attenuated by
increasing sodium and water intake [13-15].
In a study of 11 patients with severe orthostatic hypotension due to autonomic failure, blood
pressure increased significantly after drinking 480 mL of tap water in less than five minutes
from 836/533.4 mmHg at baseline, to 11430/6618 mmHg 35 minutes later [13]. After a meal,
blood pressure declined less in patients who drank water during the meal than in patients who did
not. Another study found that water drinking prior to supine exercise improved orthostatic tolerance
post-exercise [15].
The effect of water is greatest in the hour after ingestion. In addition to drinking water during meals
and before exercise, some clinicians advise keeping a pitcher of water at the bedside and drinking
rapidly before getting out of bed in the morning [1]. A target daily ingestion of 1.5 to 3 L per day is
recommended by some clinicians [16-18].
High-sodium containing foods or salt tablets also may be prescribed. While the optimal dose will
vary among patients, some have suggested a target does of 6 to 10g/day of sodium, or a target
urinary sodium level of 150 to 200 mEq [16-19].
Modification of meals Patients with autonomic failure and even normal elderly are susceptible
to significant falls in blood pressure in association with meals [20,21]. Postprandial hypotension can
be minimized by [20]:
Avoiding large meals
Ingesting meals low in carbohydrate
Minimizing alcohol intake
Drinking water with meals
Avoiding activities or sudden standing immediately after eating
PHARMACOTHERAPY Nonpharmacologic measures are often insufficient to prevent symptoms
of orthostatic hypotension, particularly in patients with moderate to severe disease. Such patients
often need pharmacologic intervention. Numerous agents from diverse pharmacological groups
have been utilized (table 1), but there is limited evidence to support the use of any of these agents
[22,23]. A step-wise approach that starts with fludrocortisone monotherapy in most patients is
presented below.
The therapeutic goal is to ameliorate symptoms while avoiding side effects. Normotension cannot
be perfectly restored. It is important to analyze symptoms rather than blood pressure values.
Patients taking medications for orthostatic hypotension should be instructed in blood pressure
recording and should provide to the clinician, for monitoring, a series of blood pressure recordings
taken over several days, including when supine, sitting, and standing upon awakening, before and
one hour after lunch, and before retiring to bed [24].
Fludrocortisone Fludrocortisone acetate (9-alpha-fluorohydrocortisone), a synthetic
mineralocorticoid, is the medication of first choice for most patients with orthostatic hypotension,
whose symptoms are not adequately controlled using nonpharmacologic measures [25]. This agent
has a long duration of action, and is well-tolerated by most patients with chronic autonomic failure.
The principal mode of action of fludrocortisone is an increase in blood volume. Enhanced sensitivity
of blood vessels to circulating catecholamines [26], and enhanced norepinephrine release from
sympathetic neurons are also suggested. A pressor effect of fludrocortisone tends to persist due to
increased peripheral vascular resistance [27].
Treatment with fludrocortisone acetate is initiated at a dose of 0.1 mg per day, administered in the
morning, which can eventually be increased up to 0.3 mg per day; little benefit is obtained by further
dosage increase. Increments should not occur more rapidly than weekly. Patients treated with
fludrocortisone must be carefully monitored for the development of edema or worsening seated or
supine hypertension, which may necessitate discontinuation or dosage reduction. Potassium
supplementation is usually required, particularly when higher doses are used. Potassium levels
should be checked within a week or two of dose adjustment.
Patients taking fludrocortisone should be instructed in blood pressure recording and should provide
to the clinician, for monitoring, a series of blood pressure recordings taken over several days
including when supine, sitting, and standing upon awakening, before and one hour after lunch, and
before retiring to bed [24].
Therapy with fludrocortisone acetate may be limited by supine hypertension resulting from the
increase in peripheral vascular resistance [27]. (See 'Supine hypertension'below.) Other side effects
include hypokalemia, ankle edema, and congestive heart failure. Edema is generally not a major
problem, in the absence of some other sodium-retaining state, because of escape from the sodium-
retaining effects of fludrocortisone. As an example, patients with primary aldosteronism do not
typically develop edema. (See "Clinical features of primary aldosteronism".) However, many elderly
patients with autonomic dysfunction do have concurrent conditions that promote edema.
Discontinuation of therapy due to side effects is common. In one study of 64 patients with
orthostatic hypotension, one-third stopped taking fludrocortisone within six months due primarily to
worsening supine hypertension, edema, and, congestive heart failure [28].
Sympathomimetic agents A direct or indirect sympathomimetic pressor agent may be added if
the patient remains symptomatic despite treatment with fludrocortisoneacetate. Pressor agents may
be used alone in those unable to tolerate fludrocortisone acetate.
The effectiveness of sympathomimetic agents is probably dependent upon the increase in
adrenergic receptor number and affinity, and the reduction in baroreflex modulation that
accompanies autonomic failure [29]. The available alpha-1 adrenoreceptor agonists include those
with:
Both direct and indirect effects. These include ephedrine (25 to 50 mg three times a day)
and pseudoephedrine (30 to 60 mg three times a day) [30,31].
Direct effects alone, such as phenylephrine and midodrine (see 'Midodrine' below).
Indirect effects alone, such as methylphenidate and dextroamphetamine sulphate [29-31].
These are no longer used in the treatment of orthostatic hypotension because of intolerable
CNS side effects.
The use of any of these medications may be complicated by tachyphylaxis, although efficacy may
be regained after a short drug holiday. Combining fludrocortisone with an alpha agonist can have
synergistic effects and allow for lower dosage of both agents [32].
Midodrine The peripheral selective alpha-1-adrenergic agonist midodrine is most often used in
the treatment of chronic orthostatic hypotension; it does not cross the blood brain barrier and has a
pressor effect due to both arterial and venous constriction. The efficacy of midodrine in the
treatment of orthostatic hypotension (and in neurocardiogenic syncope) has been shown in open-
label and double-blind studies [32-34]. As an example, in a randomized trial in 162 patients with
chronic orthostatic hypotension, midodrine 10 mg TID was associated with greater improvement in
lightheadedness and in standing systolic blood pressure than placebo [33].
Midodrine, the prodrug, is activated to de-glymidodrine, the active alpha agonist. Midodrine is
rapidly absorbed from the gastrointestinal tract and reaches a peak plasma concentration in 20 to
40 minutes; the plasma half life is 30 minutes.
Since patient sensitivity to this agent varies, the dose should be titrated from 2.5 mg to 10 mg three
times a day. Potential side effects include pilomotor reactions, pruritus, supine hypertension,
gastrointestinal complaints, and urinary retention. The sympathomimetic side effects, such as
anxiety, tremulousness and tachycardia, that accompany the use of adrenergic agents that cross
the blood brain barrier do not occur with midodrine.
Midodrine should not be used in patients with severe heart disease, uncontrolled hypertension, or
urinary retention. Supine hypertension, which occurs both as a consequence of baroreceptor
denervation even in untreated patients with autonomic failure and as a side effect of
antihypotensive treatment, often limits therapeutic intervention. Raising the head of the bed 10 to 20
degrees may protect the brain against supine hypertension. Eccentric dosing to avoid
administration within four hours of bedtime is also advised [1].
Patients taking midodrine should be instructed in blood pressure recording and should provide to
the clinician, for monitoring, a series of blood pressure recordings taken over several days including
when supine, sitting, and standing upon awakening, before and one hour after lunch, and before
retiring to bed [24].
Supplementary agents Pyridostigmine, nonsteroidal antiinflammatory drugs, caffeine, and
erythropoietin may be used in combination therapy with first or second line agents in patients with
persistent symptoms.
Erythropoietin Recombinant human erythropoietin increases standing blood pressure and
improves orthostatic tolerance in patients with the anemia that often occurs in autonomic failure
[35,36]. In one series of eight patients, for example, erythropoietin increased the mean hematocrit
from 34 to 45 percent and the standing blood pressure from 81/46 to 100/63 [35]. Orthostatic
dizziness improved in six patients; three developed supine hypertension. The elevation in blood
pressure may be mediated by increases in red cell mass and central blood volume and by direct or
indirect neurohumoral effects on the vascular wall. (See "Hypertension following erythropoietin in
chronic kidney disease".)
A trial of erythropoietin should be used in all patients with orthostatic hypotension and anemia who
have low serum erythropoietin concentrations. Recombinant human erythropoietin, epoetin alpha, is
administered subcutaneously or intravenously at doses between 25 to 75 U/kg three times a week
until a hematocrit that approaches normal is attained. Lower maintenance doses (approximately
25 U/kg three times a week) may subsequently be used. Iron supplementation is usually required,
particularly during the period when the hematocrit is increasing. (See "Iron balance in non-dialysis,
peritoneal dialysis, and home hemodialysis patients" and "Use of iron preparations in hemodialysis
patients".)
Caffeine The methylxanthine, caffeine, has a well-established pressor effect that is in part due to
blockade of vasodilating adenosine receptors. Caffeine improves orthostatic hypotension and may
attenuate postprandial hypotension in patients with autonomic failure. Typical doses are 100 to 250
mg three times a day with meals, either as tablets or caffeinated beverages (one cup of coffee and
tea contains approximately 85 and 50 mg of caffeine, respectively) [37].
Pyridostigmine Acetylcholine is a neurotransmitter in the autonomic ganglia.
Acetylcholinesterase inhibition could thereby enhance ganglionic neurotransmission, increase the
release of norepinephrine by postganglionic sympathetic nerves, and ameliorate orthostatic
hypotension. Because postganglionic sympathetic nerves are activated mainly during orthostatic
stress, acetylcholinesterase inhibition may ameliorate orthostatic hypotension without inducing
supine hypertension, a common side effect of midodrine and other sympathomimetics.
There is limited evidence of efficacy for this treatment. In one double-blind, randomized, four-way
crossover study in 58 patients, a single dose of 60 mg of pyridostigmine, an acetylcholinesterase
inhibitor, alone or with midodrine, resulted in a small reduction of orthostatic hypotension (mean
diastolic BP fall of 27.2 mmHg versus 34 mmHg in placebo), without increasing supine blood
pressure [38]. However, in a single-blind randomized crossover trial of 31 patients with severe
autonomic failure, a single dose of 60 mg of pyridostigmine did not increase the standing diastolic
blood pressure [39].
Pyridostigmine is usually initated at a dose of 30 mg three times daily, up to a maximum dose of 90
mg three times daily.
Nonsteroidal antiinflammatory drugs The NSAIDs are rarely effective as monotherapy, but
can supplement treatment with fludrocortisone or a sympathomimetic agent. They probably act to
limit the vasodilating effects of circulating prostaglandins and arachidonic acid derivatives. They
may also increase blood volume and enhance vascular sensitivity to norepinephrine [40].
Third line and experimental agents Occasional patients require third-line or experimental
therapy to ameliorate the symptoms of orthostatic hypotension. Such agents include vasopressin
analogues, yohimbine, somatostatin, dihydroergotamine, dopamine antagonists
(eg, metoclopramide), monoamine oxidase inhibitors, and dihydroxyphenylserine. Beta blockers
and clonidine are no longer recommended.
Vasopressin analogues - Vasopressin analogues have a limited role in orthostatic
hypotension. Both V1 and V2 receptor agonists have been used. Their mechanism of action
may be enhanced by supersensitivity to vasopressin among patients with autonomic failure
because of reduced postural release of this hormone. V1 and V2 receptor agonists have
different modes of action.
The synthetic vasopressin analogue desmopressin (dDAVP) acts on the V2 receptors in
the collecting tubules but has no V1 receptor vasoconstricting potential. dDAVP, which
can be taken via the nasal or oral route, prevents nocturia and overnight weight loss
and reduces the morning postural fall in blood pressure in patients with autonomic
failure [41]. Careful and continued monitoring of serum Na concentration is required. If
hyponatremia develops, treatment with dDAVP should be stopped.
The V1 receptor agonists, such as lysine-vasopressin nasal spray and intramuscular
triglycyl-lysine vasopressin, may increase blood pressure and peripheral vascular
resistance due to a direct vasopressor effect, thereby improving symptoms of
orthostatic hypotension [42]. No controlled clinical trial has been conducted and
therefore the use of V1 receptor agonists cannot be recommended.
Yohimbine - Yohimbine is a centrally active, selective alpha-2 antagonist that increases
sympathetic nervous system efferent output by blocking central and/orpresynaptic alpha-2
receptors. In subjects with residual sympathetic nervous system outflow, yohimbine (8 mg
TID) produces a modest pressor effect [43]. Side effects include anxiety, tremor,
palpitations, diarrhea, and supine hypertension. Yohimbine has limited availability in the
United States.

In a single-blind randomized crossover treatment trial in 31 patients with severe autonomic
failure, a single dose of yohimbine (5.4 mg) was associated with an average 11 mm Hg
improvement in standing diastolic blood pressure compared with placebo-treated patients
[39]. Patients also reported an improvement in presyncopal symptoms.
Somatostatin - Somatostatin and somatostatin analogues such as octreotide attenuate the
pancreatic and gastrointestinal hormone response to food ingestion and other stimuli by
inhibiting the release of vasoactive gastrointestinal peptides. They also enhance cardiac
output, and increase forearm and splanchnic vascular resistance. The net effect is
attenuation of the fall in the postprandial blood pressure in patients with autonomic failure
[44].

Subcutaneous doses of octreotide range from 25 to 200 g. Side-effects of nausea and
abdominal cramps limit the use of these agents.
Dihydroergotamine - Dihydroergotamine, an ergot alkaloid that interacts with alpha-
adrenergic receptors, has a selective venoconstrictor effect. As a result, it may increase
venous return in patients with orthostatic hypotension without producing a significant
increase in peripheral vascular resistance. Although dihydroergotamine is an effective
pressor intravenously and intramuscularly, low oral bioavailability results in an inconsistent
effect when it is taken orally [45].

Ergotamine/caffeine (1 mg/100 mg) combination is available in tablet form for the treatment
of migraine and may be tried as occasional symptomatic treatment or up to twice daily
dosing in patients with orthostatic hypotension [16].
Dihydroxyphenylserine - DL and L-dihydroxyphenylserine (DOPS, droxidopa) are
synthetic, non-physiologic, amino acid norepinephrine precursors that are decarboxylated
by the ubiquitous L-amino acid decarboxylase to norepinephrine. The important role played
by norepinephrine in the maintenance of upright blood pressure and the successful
implementation of precursor therapy for Parkinson disease provide the rationale for the use
of this agent to treat neurogenic orthostatic hypotension. Of the four stereoisomers, D- and
L-threo-DOPS and D- and L-erythro-DOPS, only L-threo-DOPS is pharmacologically
active.

Since the conversion of DOPS to norepinephrine bypasses the dopamine beta-
hydroxylation step of catecholamine synthesis, DOPS is the ideal therapeutic agent for
patients with dopamine beta-hydroxylase deficiency; such individuals are unable to
synthesize norepinephrine and epinephrine in the central and peripheral nervous system.
This agent may also be of benefit in patients with familial amyloid polyneuropathy,
Parkinson disease, multiple system atrophy, and pure autonomic failure [46]. In small,
short-term treatment trials in patients with orthostatic hypotension in the setting of pure
autonomic failure or multiple system atrophy, administration of L-DOPS was associated
with increased blood pressure and improved orthostatic tolerance [47,48]. A randomized
trial in 263 patients with neurogenic hypotension, found that after seven days of treatment,
droxidopa treatment was associated with blood pressure and symptom improvement [49].
Droxidopa is not yet approved by the US FDA.
Dopamine antagonists - The dopamine
antagonists, metoclopramide and domperidone (which is not approved by the US FDA),
may be effective in chronic orthostatic hypotension [50]. Most likely, these agents inhibit the
vasodilating and natriuretic effect of dopamine or increase noradrenaline release by
blocking prejunctional inhibitory dopamine receptors. These should not be used in patients
with parkinsonism. The risk of tardive dyskinesia and other extrapyramidal side effects
limits their long-term use.
Monoamine oxidase inhibitors - Initial reports of combination therapy consisting of the
indirect acting agent tyramine (which releases norepinephrine from neuronal storage pools)
and a monoamine oxidase inhibitor (which prevents the breakdown of the released
norepinephrine) were optimistic. Unfortunately, this combination can cause severe supine
hypertension, an unpredictable response, and, in some cases, fails to abolish orthostatic
symptoms.
Ambulatory norepinephrine infusion - In selected patients with refractory orthostatic
hypotension due to primary autonomic failure, ambulatory, patient-controlled infusion of
norepinephrine may be an effective therapy [51]. In one series of six patients, four had a
continued benefit from this therapy, without side effects, for up to 19 months [52].
SUPINE HYPERTENSION A common problem in patients with orthostatic hypotension is the
concurrent presence of supine hypertension. Drugs effective in managing hypertension may
exacerbate orthostatic hypotension, while treatment of orthostatic hypotension may increase supine
hypertension. In many such patients, the best that can be achieved is to maximize
nonpharmacologic measures and to use drugs that might raise the supine blood pressure only to
the degree that permits the patient to ambulate.
Supine hypertension in patients with chronic autonomic failure can result in end organ damage
[53,54]. It is uncertain what threshold of blood pressure requires treatment in this setting.
No treatment approach to supine hypertension has been systematically evaluated. To offset supine
hypertension, patients should avoid lying down during the day, and, if tired, should rest in a seated
position. At night, patients should sleep in a semisitting position. One strategy is to treat supine
hypertension at night with a transdermalnitroglycerin patch (0.025 to 0.1 mg/hour), which is
removed in the morning prior to the assumption of an upright position [55,56]. Other short-acting
antihypertensive agents (eg, captopril, hydralazine) may also be tried [16]. Significant hypotension
may result in some patients, thus the dose must be individually tailored. To avoid syncope and
dangerous falls, patients should be cautioned to be extremely careful if they must arise at night,
since orthostatic symptoms will be exacerbated.
TREATMENT OF POSTPRANDIAL HYPOTENSION In postprandial hypotension, blood
pressure falls occur within one to two hours after a meal. As with orthostatic hypotension,
postprandial hypotension is common in older patients. (See "Mechanisms, causes, and evaluation
of orthostatic hypotension", section on 'Postprandial hypotension'.)
Optimal therapy of symptomatic postprandial hypotension has not been defined. The same
principles noted above for orthostatic hypotension (such as avoidance of volume depletion and
certain drugs) should also be applied to patients with postprandial symptoms. As an example,
among 20 patients with postprandial hypotension and heart failure but preserved left ventricular
systolic function, the successful withdrawal of furosemide in 13 significantly lessened the maximum
fall in both the systolic (-25 to -11 mmHg, P<0.001) and diastolic blood pressures (-18 to -9 mmHg,
P=0.01) [57].
Modification of meals (avoiding large and high carbohydrate meals) as suggested above may also
be helpful in selected patients [20] (See 'Modification of meals' above.)
Lying semirecumbent for 90 minutes after meals may be necessary for some patients. Patients
should try to walk in between meals.
Acarbose, an alpha-glucosidase inhibitor, oral hypoglycemic agent, was found to attenuate
postprandial hypotension in a small trial of patients with autonomic failure [58].
The somatostatin analogue octreotide can minimize postprandial hypotension, perhaps by
increasing splanchnic vascular resistance, thereby preventing pooling of blood in the gut [20].
However, octreotide must be given subcutaneously (50 g, 30 minutes before each meal), is
expensive, and often leads to side effects such as diarrhea and pain at the injection site. It should
therefore be reserved for the most severely symptomatic patients.
Caffeine has also been thought to be effective in this disorder. However, a controlled trial in patients
with postprandial syncope showed no benefit [59].
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Here are the patient education articles that are relevant to this topic. We encourage you to print or
e-mail these topics to your patients. (You can also locate patient education articles on a variety of
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Basics topics (see "Patient information: Orthostatic hypotension (The Basics)")
SUMMARY AND RECOMMENDATIONS
The initial treatment of orthostatic hypotension should focus on nonpharmacologic
measures: removal of offending medications, liberalizing salt and fluid intake, using elastic
stockings, physical maneuvers, and exercise (table 1). (See 'Nonpharmacologic
measures' above.)
We suggest step-wise pharmacologic treatment starting with fludrocortisone for patients
with disabling symptoms despite nonpharmacologic measures (Grade 2B). A
sympathomimetic pressor agent, such as midodrine, can be subsequently added or
substituted in patients who remain symptomatic on or cannot tolerate
fludrocortisone. (See 'Fludrocortisone' above and 'Midodrine' above.)
When medications such as fludrocortisone and midodrine are used, patients should be
instructed in blood pressure recording. They should provide to the clinician, for monitoring,
a series of blood pressure recordings taken over several days, including when supine,
sitting, and standing upon awakening, before and one hour after lunch, and before retiring
to bed. (See 'Pharmacotherapy' above.)
Further treatment should be graded to the patients symptoms and their impact on daily
function. A number of other modalities may be beneficial (see 'Supplementary
agents' above):
Caffeine in the morning is probably helpful to most patients
A trial with recombinant erythropoietin should be attempted in patients with anemia
Nonsteroidal antiinflammatory drugs may be useful supplementary agents in those with
refractory symptoms
A small number of patients have persistent orthostatic symptoms despite these modalities.
Medication trials of agents with less clear evidence of benefit can be attempted in these
patients (table 1). (See 'Third line and experimental agents' above.)
Supine hypertension may be a treatment-limiting complication and may require specific
interventions. (See 'Supine hypertension' above.)
Postprandial hypotension may respond to similar nonpharmacologic measures. Smaller
meals, with low carbohydrate and salt content may also ameliorate symptoms. Rare
patients will require pharmacologic intervention. (See 'Treatment of postprandial
hypotension' above.)
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