и да, побольше соли - соль задерживает воду и повышает АД

SUMMARY AND RECOMMENDATIONS

●Treatment should be geared to the patients' symptoms and their impact on daily function rather than a target blood pressure. Persistent orthostatic blood pressure falls are common. (See 'Treatment goals' above.)

●The initial treatment of orthostatic hypotension should focus on nonpharmacologic measures: removal of offending medications (table 1), increasing salt and fluid intake, using elastic stockings or an abdominal binder, physical maneuvers, and exercise (table 2). (See 'Nonpharmacologic measures' above.)

●For patients with persistent symptoms despite nonpharmacologic measures, we suggest step-wise pharmacologic treatment starting with low-dose fludrocortisone (0.1 mg/day) for patients with volume depletion and disabling symptoms despite nonpharmacologic measures (Grade 2C). A sympathomimetic pressor agent, such as midodrine or droxidopa, can be added or substituted in patients who remain symptomatic on or cannot tolerate fludrocortisone. (See 'Fludrocortisone' above and 'Midodrine' above and 'Droxidopa' above.)

●When medications such as fludrocortisone, midodrine, or droxidopa are used, patients should be instructed in avoiding the flat position, sleeping with the head of the bed raised 30 to 45 degrees, and measuring their own blood pressure. 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.)

●A number of other modalities may be beneficial (see 'Supplementary agents' above):

•Caffeine in the morning is probably helpful in many patients

•A trial with recombinant erythropoietin should be attempted in patients with neurogenic orthostatic hypotension and anemia

●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 2). (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 'Postprandial hypotension' above.)

(See 'Fludrocortisone' above and 'Midodrine' above and 'Droxidopa' above.)

Вот как раз Мидодрин пью. Спасибо.

От кофеина только хуже становится

Такое ощущение, что сосуды спазмируются значительно, холодеют конечности и начинаю потеть.

на первом месте образ жизни

тревожное расстройство

При чем тут это?

от мидодрина спазмируются, это его механизм действия

Midodrine — The peripheral selective alpha-1-adrenergic agonist midodrine was the first drug specifically approved by the FDA for the treatment of orthostatic hypotension; midodrine 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 has been suggested in some open-label and double-blind studies [41-45]. Systematic reviews have concluded that the available data warranted only low confidence that midodrine improves symptoms in patients with orthostatic hypotension, in part because most studies were designed to assess an effect on blood pressure and not on symptoms [45,46].

Midodrine, the prodrug, is activated to desglymidodrine, 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 to 10 mg three times a day. The maximum dose should not exceed 40 mg/day. Patients should not take midodrine within four to five hours of bedtime in order to limit supine hypertension. (See 'Supine hypertension' below.)

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. Other potential side effects include pilomotor reactions, pruritus, supine hypertension, gastrointestinal complaints, and urinary retention [45]. 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.

Systematic reviews have concluded that the available data warranted only low confidence that midodrine improves symptoms in patients with orthostatic hypotension, in part because most studies were designed to assess an effect on blood pressure and not on symptoms [45,46].

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. Caffeine may exacerbate an existing tremor, however.

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) [57]. Because of the diuretic effect of caffeine, care should be taken to replenish fluids and avoid dehydration.

Third-line and experimental agents — Occasional patients require third-line or experimental therapy to ameliorate the symptoms of orthostatic hypotension. Because data regarding these agents are quite limited, patients should be so-advised and carefully monitored for adverse effects. Such agents include atomoxetine, vasopressin analogues, yohimbine, and others as discussed below. Beta blockers and clonidine are no longer recommended due to their hypotensive effects.

●Atomoxetine – Atomoxetine is a selective norepinephrine reuptake inhibitor that can be used to treat attention deficit hyperactivity disorder in children, adolescents, and adults. In a trial in 65 patients with severe autonomic failure, administration of atomoxetine (18 mg) produced a greater pressor response in upright systolic blood pressure and had a greater effect on symptoms compared with the administration of midodrine (5 to 10 mg) or placebo [63]. Further study is required before it is certain whether this agent has a more routine role in the treatment of orthostatic hypotension.

●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 can be taken via the nasal or oral route. In a three-day trial, DDAVP prevented nocturia and overnight weight loss and reduced the morning postural fall in blood pressure in five patients with autonomic failure [64]. Careful and continued monitoring of serum Na concentration is required before and after initiating therapy. 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 [65]. 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-adrenergic antagonist that increases sympathetic nervous system efferent output by blocking central and/or presynaptic alpha-2-adrenergic receptors (which are inhibitory). In subjects with residual sympathetic nervous system outflow, yohimbine (8 mg three times daily) produces a modest pressor effect [66]. 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 mmHg improvement in standing diastolic blood pressure compared with placebo-treated patients [59]. 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 [67].

Subcutaneous doses of octreotide range from 25 to 200 mcg. 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 [68].

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 [23]. No control trials support their efficacy.

●Dopamine antagonists – The dopamine antagonists, metoclopramide and domperidone (which is not approved by the FDA), may be effective in chronic orthostatic hypotension [69]. 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 [70]. In one series of six patients, four had a continued benefit from this therapy, without side effects, for up to 19 months [71].

Orthostatic hypotension is more common in older patients and may affect up to 20 percent of patients over the age of 65 years. (See 'Epidemiology and risk factors' above.)

●Orthostatic and postprandial hypotension are features of autonomic dysfunction that may result from certain neurodegenerative diseases affecting the central and peripheral nervous system as well as certain peripheral neuropathies. (See 'Autonomic failure' above.)

●Orthostatic hypotension may result from volume depletion (due to diuretics, hemorrhage, or vomiting). (See 'Volume depletion' above.)

he initial treatment of orthostatic hypotension should focus on nonpharmacologic measures: removal of offending medications (table 1), increasing salt and fluid intake, using elastic stockings or an abdominal binder, physical maneuvers, and exercise (table 2). (See 'Nonpharmacologic measures' above.)

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