The orthostatic (position-dependent) hypotension is accompanied by an excessive drop in blood pressure, if an upright posture is assumed. The generally accepted definition is a drop of> 20 mmHg systolic, 10 mmHg diatolisch or both. Symptoms of pallor, dizziness, drowsiness, confusion or blurred vision occur within seconds to a few minutes while standing and improve rapidly when lying down. Some patients experience falls, syncope or even generalized seizures. Physical exertion or heavy foods can exacerbate symptoms. Most other associated symptoms and discomfort associated with the cause. Orthostatic hypotension is the appearance of a pathological blood pressure regulation due to various conditions, but no specific illness. Postural orthostatic tachycardia syndrome (POTS) The POTS (postural and autonomic tachycardia or chronic idiopathic orthostatic intolerance called) is a syndrome of orthostatic intolerance in younger patients. Various symptoms (eg. As fatigue, dizziness, exercise intolerance, cognitive disorders) and tachycardia occur upon standing. However, the blood pressure drops only slightly or not at all from. The cause of the symptoms is unclear. Normally pathophysiology leads gravity during sudden standing to the fact that blood (½-1 L) is accumulated in the capacitance veins of the legs and the trunk. The following temporary drop in venous return reduces cardiac output and blood pressure. In response, activate baroreceptors in the aortic arch and carotid body automatic reflexes to bring blood pressure to normal state. The sympathetic nervous system increases heart rate and contractility and increases the vasomotor tone of Kapazitanzgefäße. In parallel, the inhibition of parasympathetic (vagal) increases the heart rate. In most people, the changes in blood pressure and heart rate while standing are minimal and temporary and there are no symptoms. After some time, the activation of the renin-angiotensin-aldosterone system and vasopressin ADH secretion lead to sodium and water retention and increase the circulating blood volume. Etiology The homeostatic mechanisms may be insufficient to compensate for the low blood pressure when afferent, central or efferent portions of the autonomic reflex are disrupted by disease or medication if myocardial contractility or vascular reactivity are lowered when hypovolemia is present and if the hormonal incorrect answers are (see table: causes of orthostatic hypotension). The reasons differ depending on whether the symptoms are acute or chronic. Among the most common causes of acute orthostatic hypotension are hypovolemic medicines Extended bed rest adrenal insufficiency of the most common causes of chronic orthostatic hypotension include age-related changes in the regulation of blood pressure medicines Autonomous dysfunction Postprandial orthostatic hypotension is also common. It can be caused by the insulin response in carbohydrate-rich foods and blood accumulation in the gastrointestinal tract. This condition is worsened by alcohol consumption. Causes to the orthostatic hypotension cause Examples Neurological (including autonomic dysfunction) Central system atrophy Parkinson’s disease stroke (multiple) spinal cord tabes dorsalis transverse myelitis tumors peripheral amyloidosis diabetic, alcohol-related, or dietary neuropathy familial dysautonomia (Ril ey-Day syndrome) Guillain-Barre syndrome paraneoplastic syndromes isolated autonomous insufficiency Surgical sympathectomy Cardiovascular hypovolemia adrenal hemorrhage dehydration Verschlechteter vasomotor tone bed rest (extended) hypokalemia Deteriorated cardiac output aortic stenosis Constrictive pericarditis heart failure myocardial infarction tachyarrhythmias or bradyarrhythmias Other hyperaldosteronism * Peripheral venous insufficiency pheochromocytoma * drug vasodilators, calcium-channel blockers, nitrates Autonom active alpha-blocker (prazosin, phenoxybenzamine) antihypertensive agents (clonidine, methyldopa, reserpine, [rare] Beta blockers) antipsychotics (in particular phenothiazines) monoamine oxidase inhibitors (MAO inhibitor) Tricyclic or tetracyclic antidepressants alcohol barbiturates levodopa (Parkinson’s Disease in ince [rare]) loop diuretics (eg. As furosemide) quinidine vincristine (neurotoxic) * disorder causing hypertension in the supine position. symptoms occur more frequently when treatment is started. The assessment of orthostatic hypotension is diagnosed when a significant drop in the measured blood pressure and symptoms that indicate a hypotension, are provoked by standing up and disappear by lying down. A reason for this must be given. History The history of this disease should the duration and severity (eg. As whether it is associated with syncope or falls) to identify the symptoms. The patient is known triggers (eg. Medication, bed rest, fluid loss) asked and the relationship of symptoms to meals. The assessment of the symptoms examined for symptoms of the disease-causing, especially symptoms of autonomous insufficiency such as Visusstörung (due to mydriasis and loss of accommodation), incontinence or urinary retention, constipation, heat intolerance (due to a disturbed perspiration) and erectile dysfunction. Other important symptoms include tremor, rigidity and difficulty walking (Parkinson’s disease, multiple system atrophy), weakness and fatigue (adrenal insufficiency, anemia) and black, tarry stools (GI bleeding). Other symptoms of neurological and cardiovascular disease and cancer are noted. The medical history (h a paraneoplastic syndrome d.. Causing) should known potential causes such as diabetes, Parkinson’s disease and cancer identified. The drug profile should be checked for inducing prescription drugs (see table: causes of orthostatic hypotension), especially antihypertensive agents and nitrates. A family history of orthostatic symptoms suggesting a possible familial dysautonomia nahe.Körperliche study are blood pressure and heart rate after 5 minutes lying down and measured 1 and 3 minutes after Hinstehen. Patients who are unable to stand, can be examined in an upright sitting position. Hypotension without compensatory increase in heart rate (<10 beats / min) indicates an autonomous impairment. Striking increases (to> 100 beats / min or> 30 beats / min) put hypovolemia or when the symptoms without hypotension develop POTS close. The skin and mucous membranes are examined for signs of dehydration and pigmentation changes that are suggestive of Addison’s disease (z. B. hyperpigmented areas, vitiligo). A rectal exam is performed to detect GI bleeding. During the neurological examination Urogenitaltrakt- and Rektalreflexe can be tested to evaluate the autonomous functioning. The investigation includes the cremasteric (usually dissolves coating the inner thigh of a retraction of the testes), and the anal reflex (usually leads brushing the perianal skin to a contraction of the anal sphincter) tools. Signs of peripheral neuropathy (. Eg anomalies of strength, sensation and deep Tendonreflexes) are bewertet.Warnzeichen Certain findings indicate a more serious etiology out: Bloody or heme-positive stool Abnormal neurological examination interpretation of the findings in patients with acute symptoms are the most common causes – drugs, bed rest and volume loss – often clinically evident. In patients with chronic symptoms, it is an important goal to recognize any neurological disorder that causes autonomic dysfunction. Patients with movement disorders can Parkinson’s disease or multiple system atrophy have. Patients with findings of peripheral neuropathy can cause a recognizable (eg. As diabetes, alcoholism), but have a paraneoplastic syndrome by an occult cancer and amyloidosis must be considered. Patients who have only peripheral autonomic symptoms can a purely autonomous failure haben.Tests EKG, serum electrolytes and blood sugar are checked by default. However, these and other studies are of little use if there are no specific symptoms for it. The dosage of the suspected drug can be reduced or the drug is stopped to confirm the causal significance of the drug. The tilt table test can be performed when autonomic dysfunction is suspected. It provides more consistent results than the determination of blood pressure in supine and upright and closes the increase in venous return by the tension of the leg muscles from. The patient may remain for 30-45 minutes for measuring blood pressure in the upright position. Patients with autonomic symptoms and complaints need further clarification in relation to diabetes mellitus, Parkinson’s disease and possibly a multiple system atrophy and pure autonomic failure. Tests on pure autonomic failure, measurements of plasma norepinephrine or – require vasopressin (ADH), with the patient lying on his back and upright. The autonomous function can also be evaluated with a cardiac monitor on the side of the bed, even if this test is not often done. If the autonomous system is intact, the heart rate increases during inspiration. The heart is monitored while the patient is breathing slowly and deeply (about 5 seconds inspiration and 7 seconds exhalation) for 1 minute. The longest RR interval between heartbeats during expiration is usually at least 1.15 times as long as the smallest RR interval during inspiration. A shorter interval suggests autonomic dysfunction, but this response to the inspiration may decrease with age. A similar variation of the RR interval should exist between the rest condition and a 10-15-second Valsalva maneuver. Treatment Non-drug treatment patients who require prolonged bed rest should sit every day and if possible work out in bed. Patients should rise slowly from lying or sitting position, take plenty of fluids, limit alcohol consumption or avoid and where practicable also exercise regularly. Regular exercise moderate intensity promotes the general vascular tone and reduces the venous pooling. Elderly patients should avoid prolonged standing. Sleeping with the head elevated part can ease the symptoms by promoting sodium retention and reduce nocturnal diuresis. Postprandial hypotension can often be prevented by reducing the size and carbohydrate content of meals by limiting alcohol intake and by avoiding sudden getting up. Waist high elastic pants adapted to venous return, increase cardiac output and blood pressure after Hinstehen. In severe cases, inflatable aviator suit similar antigravity suits, but these are often poorly tolerated, may be necessary to bring about an adequate leg and Abdomengegenpulsation. An increase in sodium and water intake can increase the intravascular volume and alleviate the symptoms. There is no heart failure or hypertension, sodium intake can be increased daily at 6-10 g over by permissive salts or by ingestion of sodium chloride tablets. This approach can lead to heart failure, particularly in elderly patients and in patients with impaired cardiac function. The emergence of dependent edema without heart failure does not speak against the continuation of this Ansatzes.Medikamentöse treatment fludrocortisone, a mineralocorticoid causes sodium retention, which increases the plasma volume and often alleviates the symptoms; but this is only effective when the sodium intake is adequate. The dosage is 0.1 mg p.o. for sleep time, increased weekly up to 1 mg or to peripheral edema arise. This drug can improve a sympathetic stimulation and peripheral Vasokonstriktorantwort. It can cause hypertension lying down, heart failure and hypokalemia. A Kaliumsupplementation may be required. Midodrine, a peripheral alpha-agonist, which is both an arterial and venous constrictor, is often effective. The dosage is 2.5-10 mg p.o. 2 times a day. Side effects include paresthesia and itching (probably secondary to the hair root erection) a. This drug is not recommended in patients with coronary artery disease or peripheral arterial disease. NSAIDs (eg. B. indomethacin 25-50 mg p.o. 2 times daily) may prevent the prostaglandin-induced vasodilation by an increase in peripheral vascular resistance. However, NSAIDs can also gastrointestinal symptoms and unwanted Vasopressorreaktionen (reported with concomitant use of indomethacin and sympathomimetic drugs) cause. L-dihydroxyphenylserine, a norepinephrine precursor, can have a favorable effect on the autonomic dysfunction (as in limited studies reported). Propranolol or other beta blockers can support the beneficial effect of sodium or Mineralocorticoidtherapie. A beta-blockade with propranolol leads to alpha-adrenergic peripheral vasoconstriction without backlash and thus the vasodilation is prevented, which occurs in some patients while standing. Central geriatric aspects Orthostatic hypotension occurs in about 20% of the elderly. It is more common in those with concomitant diseases, especially in hypertension and in patients in long term care. Many crashes can be caused by an unnoticed orthostatic hypotension. The increased incidence in elderly patients is due to a reduced responsiveness of the baroreceptors along with a decreased arterial compliance. The decreased responsiveness of the baroreceptors a delayed cycle reaction, and a peripheral vasoconstriction when standing up. Paradoxically, the high pressure can contribute to poor responsiveness of the baroreceptors and increase susceptibility to orthostatic hypotension. Older people also have a lower parasympathetic tone at rest, so that cycle reaction is reduced due to the Vagusreflexentzuges. Summary of orthostatic hypotension typically includes volume depletion, or autonomic dysfunction. Some degree of autonomic dysfunction is common in older patients, but a neurological disorder must be excluded. Kipptischtests are sometimes performed Treatment involves physical measures to reduce venous pooling, increased sodium intake and sometimes fludrocortisone or midodrine.